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Renal Pathology > Structural Renal Pathology > Flashcards

Structural Renal Pathology Flashcards

1
Q

Name 4 general types of Glomerular Disease

A
  1. Podocyte
  2. Immune Complex
  3. GBM Disease
  4. Vascular Injury
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2
Q

Name 2 specific podocyte glomerular diseases

A
  1. Minimal change disease

2. Focal Segmental Glomerulosclerosis

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3
Q

Name 4 specific Immune Complex glomerular diseases

A
  1. APSGN (subepithelia)
  2. Membranous Nephropathy (subepithelia)
  3. MPGN (subendothelial)
  4. IgA Nephropathy (Mesangial)
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4
Q

Name 4 specific GBM diseases

A
  1. Anti-GBM Disease
  2. Goodpastures
  3. Alport’s Syndrome
  4. Thin Basement Membrane
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5
Q

Name 6 specific Vascular Injury glomerular diseases

A
  1. ANCA-associated glomerulonephritis
  2. Pauci-Immune glomerulonephritis
  3. Hemolytic Uremic Syndrome/TTP (TMA)
  4. Wegener’s Granulomatous
  5. SLE
  6. Scleroderma/Systemic Sclerosis
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6
Q

What is the etiology of Focal Segmental Glomerulosclerosis?

A

Primary: Idiopathic
Secondary: Reduced nephron mass

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7
Q

What are some of the causes of reduced nephron mass in Focal Segmental Glomerulosclerosis?

A
  1. Familial Sporadic Mutations
  2. HIV, Parvovirus
  3. Heroin, lithium, IFN-alpha
  4. Chronic kidney disease
  5. suPAR
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8
Q

What is the mechanism of the suPAR subtype of FSGS?

A

suPAR - circulating factor from WBCs that activate B3 integrin (anchor for podocytes to GBM), high activity of B3 integrin&raquo_space; podocyte dysfunction

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9
Q

Name and describe the 5 sub-types of Focal Segmental Glomerulosclerosis

A
  1. Collapsing
  2. Cellular
  3. Tip
  4. Perihilar
  5. Not otherwise specified
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10
Q

Which subtypes of FSGS presents with heavy proteinuria?

A

Collapsing & Tip

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11
Q

Which subtype of FSGS has the best prognosis?

A

Tip: more likely to achieve remission

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12
Q

Which FSGS has the worst prognosis and what causes it?

A

Collapsing: heavy proteinuria, worst renal survival

—- HIV (glomerular tuft collapse)

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13
Q

What Familial Sporadic Mutations cause Focal Segmental Glomerulosclerosis?

A

Mutations in:

  • podocin
  • nephrin
  • alpha-actinin-4
  • transient receptor channel 6
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14
Q

What is the clinical presentation of Focal Segmental Glomerulosclerosis?

A
  • Nephrotic syndrome (second most common in adults)
  • Non-specific loss of proteins (albumin AND globins)
  • HIV patient (FSGS is most common cause of glomerular disease in HIV patients)
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15
Q

What are the Light Microscopy characteristics of FSGS?

A
  • scarring
  • Obliterated capillary lumen (hyalinosis)
  • Areas of adhesion to Bowman’s capsule
  • Expansion of mesangial matrix
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16
Q

What is the immunohistochemistry of FSGS?

A

Normal; easy to confuse w/ MCD

+/- non-specific Ig+

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17
Q

What is the EM of FSGS?

A

Effacement / fusion of foot processes

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18
Q

How do you treat FSGS?

A
  • Corticosteroids (less likely to remit)
  • Calcinuerin inhibitors
  • Mycophenolate Mofetil
  • Sirolimus
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19
Q

What is the etiology of Acute Post-infections Glomerulonephritis

A

Post-immune response to nephritogenic Group A streptococcal strains

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20
Q

Which bacteria, viruses and parasites cause Acute Post-infections Glomerulonephritis?

A

Bacterial: Group A beta-hemolytic streptococci - nephritogenic
Virus: HBV, EBV, mumps
Parasites: malaria, toxoplasmosis

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21
Q

Acute Post-Infections Glomerulonephritis follows the “Filtered Cationic Antigen” theory. Explain this theory.

A

cation filters through endothelial but charge restricted sub-podocyte. Antibodies localize and target.

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22
Q

What is the clinical presentation of Acute Post-infections Glomerulonephritis?

A
  • Nephritic
  • Gross hematuria (tea/cola colored)
  • 1-3 weeks after URI
  • throat, skin, strep infections
  • school children
  • edema
  • hypertension
  • pulm/GI symptoms
  • Ascites 2:1 males to females
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23
Q

Light microscopy of Acute Post-infections Glomerulonephritis?

A
  • Proliferation

- Inflammation = membranoproliferative disease

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24
Q

Immunohistochemistry of Acute Post-infections Glomerulonephritis?

A

C3+

IgG+

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25
Q

EM of Acute Post-infections Glomerulonephritis?

A

Subepithelial Humps (immune complexes)

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26
Q

Lab profile of Acute Post-infections Glomerulonephritis?

A
  • Hypocomplementemia (low C3, but normal C4 = alternate pathway activation)
  • Low cryoglobulinemia
  • Anti-streptolysin O titers elevated (throat)
  • Anti-DNAase/hyaluronidase titers elevated (skin)
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27
Q

What is the treatment of Acute Post-infections Glomerulonephritis?

A
  • Treat underlying infection
  • Hypertension: loop diuretics
  • Renal replacement therapy if severe dysfunction
  • may resolve spontaneously
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28
Q

What is Membraneous Nephropathy?

A

Autoimmune disease w/ Ab directed at podocyte protein

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29
Q

What is the Primary/Idiopathic etiology of Membranous Nephropathy?

A

In-situ immune complex formation

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30
Q

What is the Primary/Idiopathic pathogenesis of Membranous Nephropathy?

A

In-situ immune complex formation

  • podocyte damage from MAC (complement)
  • Autoantibody to M Type Phospholipase A2 receptor (PLA2R)
  • — receptor expressed by podocytes in normal glomeruli
  • — colocalizes with IgG4
  • locally generated antigen + filtered antibody
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31
Q

What is the secondary etiology of Membranous Nephropathy?

A
  • SLE, hepB, occult carcinoma

- Rx: gold preparations, penicillamine

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32
Q

What is the secondary pathogenesis of Membranous Nephropathy?

A
  • in-situ formation in sub-podocyte epithelial space
  • Recruits complement, but NOT nephritic because sheds complement into urine and also is sub epithelium – no contact w/ inflammatory cells
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33
Q

What is the clinical presentation of Membranous Nephropathy?

A
  • Most common cause of nephrotic syndrome in caucasians, males
  • No serological abnormalities
  • Hypertension
  • Azotemia
  • Thromboembolic complications
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34
Q

What is the light microscopy characteristics of Membranous Nephropathy?

A
  • Thickening of capillaries
  • Thickening of mesangial matrix
  • Subepithelial deposits (thick GBM)
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35
Q

What is the immuno profile of Membranous Nephropathy?

A
  • IgG+
  • C3+
  • C4+ (not nephritic)
  • lumpy, bumpy fluorescence
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36
Q

What is the EM profile of Membranous Nephropathy?

A
  • layer of subepithelial deposits
  • Retraction and effacement of foot processes
  • Spikes of GBM on capillary walls
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37
Q

How do you treat Membranous Nephropathy?

A
  • Give ACE inhibitor for BP & proteinuria

- Cytotoxic + steroids

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38
Q

What is the prognosis for Membranous Nephropathy?

A
  • Spontaneous remission (40%)
  • Progressive renal failure (30%)
  • Persistent proteinuria +/- renal failure
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39
Q

What are the buzz words for Membranous nephropathy?

A

Diffuse thickening of capillary walls

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40
Q

What disease does “diffuse thickening of capillary walls” describe?

A

Membranous nephropathy

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41
Q

What glomerular disease is associated with subendothelial deposits?

A

Membranoproliferative Glomerulonephritis

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42
Q

What are the 2 types of Membranoproliferative Glomerulonephritis?

A

Type 1 - Most common

Type 2 - Dense Deposit disease

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43
Q

What is the etiology of Membranoproliferative Glomerulonephritis Type I?

A
  • Idiopathic
  • Secondary to hepC > hepB infections
  • Damage occurs from activation of both complement pathways
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44
Q

What is the pathogenesis of Membranoproliferative Glomerulonephritis?

A

Damage = cytokines/autocoids released w/ complement&raquo_space; increase endothelial adhesion to circulating immune complexes&raquo_space; inflammation

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45
Q

Type I Membranoproliferative Glomerulonephritis is characterized by subendothelial deposits caused by endothelial injury. What are three causes of endothelial injury in general?

A
  • Deposition of immune complexes in subendothelial space
  • Thrombotic microangiopathies
  • Entrapment of paraproteins (myeloma, plasma cell)
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46
Q

What is the clinical presentation of Type I Membranoproliferative Glomerulonephritis?

A
  • Nephritic syndrome + Nephrotic syndrome
  • rapidly progressing glomerulonephritis
  • anti-hepC antibody
  • low C3 complement levels
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47
Q

What is the immunohistochemistry profile of Type I Membranoproliferative Glomerulonephritis?

A

C3 + Ig

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48
Q

What is the EM profile of Type I Membranoproliferative Glomerulonephritis?

A
  • Thickened BM

- Hypercellular: expansion of capillaries and mesangial matrix, thickening of capillary loops

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49
Q

What is the LM profile of Type I Membranoproliferative Glomerulonephritis?

A

Capillary wall&raquo_space; tram track appearance

— duplicated basement membrane b/c of immune complex deposits and infiltrating mesangial cells

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50
Q

What is the treatment for Membranoproliferative Glomerulonephritis?

A

No concensus on treatment

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51
Q

What is the prognosis for Membranoproliferative Glomerulonephritis?

A
  • Spontaneous remission may occur

- Usually slow progression to end stage renal disease

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52
Q

What autoantibody is associated with Type 2 Membranoproliferative Glomerulonephritis?

A

C3NeF - C3 Nephritic Factor

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53
Q

What is another name for Type 2 Membranoproliferative Glomerulonephritis?

A

Dense Deposit Disease

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54
Q

What is the mechanism of Type 2 Membranoproliferative Glomerulonephritis?

A

C3NeF autoantibody binds to C3 convertase (C3Bb) preventing degradation of C3 convertase&raquo_space; constant, low level complement activation

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55
Q

Type 1 vs. Type 2 Membranoproliferative Glomerulonephritis. Which has a worst prognosis?

A

Type 2 has a worst prognosis than Type I

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56
Q

What is the clinical presentation of Membranoproliferative Glomerulonephritis Type II?

A
  • Similar to Type I
  • Macular deposits in eye
  • partial lipodystrophy (loss of upper body cutaneous fat)
  • common in transplant patients
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57
Q

What is the immuno profile of type 2 Membranoproliferative Glomerulonephritis?

A

C3 deposition “lining” caps

NO Ig

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58
Q

What is the LM characteristics of type 2 Membranoproliferative Glomerulonephritis?

A

Same as Type I&raquo_space; tram track appearance

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59
Q

What is the EM profile of Type 2 Membranoproliferative Glomerulonephritis?

A
  • Splitting of capillary BM from deposits

- “Split” = dense deposits + mesangial cytoplasm

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60
Q

What is the buzz word for Type 2 Membranoproliferative Glomerulonephritis?

A

Ribbon-like appearance

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61
Q

What disease is associated with the buzz word “ribbon like appearance”?

A

Type 2 Membranoproliferative Glomerulonephritis

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62
Q

What disease is associated with mesangial deposits of Galactose deficient IgA1?

A

IgA Nephropathy (Berger’s Disease)

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63
Q

What is the etiology of IgA Nephropathy?

A

1-2 days post URI or GI infection

  • – The exact etiology is unknown
  • – We do know that IgA is the main immunoglobin of MUCOSAL SURFACES
  • – both pharyngeal & GI have large mucosal surfaces
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64
Q

What is the pathogenesis of IgA Nephropathy?

A

URI or GI infection&raquo_space; underglycosylation of O-linked glycans of IgA1&raquo_space; N-linked glycan recognized by circulating immune complexes&raquo_space; mesangial deposits of Galactose deficient IgA1

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65
Q

What is Secondary IgA Nephropathy called?

A

Henoch-Schonlein Purpura

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66
Q

What diseases are associated with Henoch-Schonlein Purpura?

A

GI gastroenteritis + Liver disease

  • Cirrhosis
  • Irritable bowel disease
  • Celiac disease
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67
Q

What is the clinical presentation of IgA Nephropathy?

A
  • Most common primary glomerulonephritis
  • 1-2 days post URI
  • hypertension
  • macroscopic hematuria
  • Nephritic > Nephrotic presentation
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68
Q

What are the risk factors for IgA Nephropathy?

A
  • Proteinuria/edema
  • decreased GFR
  • older age
  • HPTN
  • crescent (rapidly progressive glomerulonephritis)
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69
Q

What is the LM profile of IgA Nephropathy?

A
  • Mesangioproliferative

- May be crescent formation

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70
Q

What is the immuno profile of IgA Nephropathy?

A

IgA+ (only in 50% of patients)

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71
Q

What is the EM profile of IgA Nephropathy?

A

Mesangial deposits

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72
Q

What’s the name for systemic Anti-glomerular basement membrane disease?

A

Goodpasture’s Syndrome

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73
Q

What’s the etiology of Goodpasture’s Syndrome?

A

Autoantibodies against alpha-3 subunit of Type 4 collagen (non-collagenous portion)

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74
Q

What are the diseases associated with Goodpasture’s Syndrome?

A
  • Pulmonary hemorrhage
  • Renal failure
  • Disproportional anemia
  • Arthritis
  • HPTN
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75
Q

What is the prognosis of Goodpasture’s Syndrome?

A
  • rapid development of kidney failure
  • glomerulosclerosis
  • Crescent formation (rapid progresive glomerulonephritis)
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76
Q

What is the clinical presentation of Goodpasture’s syndrome?

A
  • Nephritic syndrome
  • no correlation between titers and disease activity
  • might confuse with Wegener’s but more azotemia in goodpasture’s
  • Goodpasture’s is seen in smokers or in cases where there is already some damage to lung— this is because the antibodies have to be able to access the collagen in that tissue
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77
Q

What is the LM profile of Goodpasture’s syndrome?

A

necrotizing
crescenting
— crescenting is proliferation of BC parietal cells into urinary space

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78
Q

What are seen in the lungs of patients with Goodpasture’s syndrome?

A

Full of hemosiderin and fluid accumulation from hemorrhage

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79
Q

What is the immunohistochemistry profile of Goodpasture’s syndrome?

A

Linear anti-GBM IgG appearance

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80
Q

What is the treatment for Goodpasture’s Syndrome?

A

Corticosteroids
Plasma exchange
Cytotoxic drugs

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81
Q

What what is the pathogenesis of Rapidly Progressive Glomerulonephritis (crescentic)?

A

Accumulation and proliferation of parietal cells&raquo_space; compress glomerular tuft&raquo_space; renal failure

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82
Q

How does Rapidly Progressive Glomerulonephritis (crescentic) cause renal failure?

A

Allows RBC, WBC, Fibrinogen and other plasma components to enter the urinary space&raquo_space; increase proliferation of mononuclear cells and parietal cells

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83
Q

How is Rapidly Progressive Glomerulonephritis (crescentic) initially characterized?

A

Initially characterized as segmental proliferative necrotizing lesions&raquo_space; cellular crescent&raquo_space; fibrocellular crescents&raquo_space; fibrous crescents

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84
Q

What diseases are most commonly associated with Rapidly Progressive Glomerulonephritis (crescentic)?

A

Goodpasture’s
Wgener’s
Other ANCA+ disease

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85
Q

What is the clinical presentation of Rapidly Progressive Glomerulonephritis (crescentic)?

A

Nephritic
Rapid loss of renal function
Oliguria
Death with no treatment

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86
Q

What are the 3 types of Rapidly Progressive Glomerulonephritis (crescentic)?

A

Type I - Linear
Type II - Granular
Type III - Pauci-Immune

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87
Q

What are the differences between the 3 types of Rapidly Progressive Glomerulonephritis (crescentic)?

A

Type I - Linear
— Usually anti-GBM diseases

Type II - Granular

  • – Usually immune complex disease
  • – Lumpy, bumpy w/necrosis & mesangial proliferation

Type III - Pauci-Immune

  • – little immune deposition: negative immune
  • – Wegener’s and ANCA-associated vasculitis
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88
Q

What are the LM/EM profile of Rapidly Progressive Glomerulonephritis (crescentic)?

A

Look for polys and fibrin

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89
Q

What’s another name for Hereditary Nephritis?

A

Alport’s Syndrome

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90
Q

What is the genetics of Hereditary Nephritis (Alport’s Syndrome)?

A 
Defective Alpha-5 collagen Type 4
- X-linked (alpha-5)
Can also be AR, AD
- Ch 13: alpha 1,2
- Ch 2: alpha 3,4
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91
Q

What is the pathogenesis of Hereditary Nephritis (Alport’s Syndrome)?

A

Collagen 4A5 mutation prevents collagen heterotrimer formation

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92
Q

Where is collagen Type 4 - Alpha 5 located?

A

GBM, lens of the eye & cochlea

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93
Q

What other disease can Hereditary Nephritis (Alport’s Syndrome) protect you against?

A

Cool fact: Patients with Ch 2 (alpha 3 mutation of Collagen Type 4) are protected from Goodpasture’s Disease!

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94
Q

What is the clinical presentation of Hereditary Nephritis (Alport’s Syndrome)?

A

Males have persistent hematuria, proteinuria, end stage renal disease, sensoneural hearing loss, lens abnormalities, platelet defects, esophageal defects

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95
Q

What does the SEEK pneumonic stand for in Hereditary Nephritis (Alport’s Syndrome)?

A

Skin
Eyes
Ears
Kidney

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96
Q

How are heterozygous females with Hereditary Nephritis (Alport’s Syndrome) affected?

A

may have hematuria and thin basement membranes

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97
Q

What is the EM profile of Hereditary Nephritis (Alport’s Syndrome)?

A
  • Splitting of lamina densa
  • Basket weave appearance
  • – split basement membrane
  • – can also do skin biopsy to see same collagen
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98
Q

What is the etiology of Thin Basement Membrane Disease?

A

Defect in alpha 3,4 Type 4 collagen

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99
Q

What is the pathogenesis of Thin Basement Membrane Disease?

A

GBM thickness is reduced about 1/2 normal size

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100
Q

What is the inheritance pattern of Thin Basement Membrane Disease?

A

Autosomal dominant

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101
Q

What is the clinical presentation of Thin Basement Membrane Disease?

A

Usually diagnosed at routine checkup, benign as long as heterozygous

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102
Q

What is another name for Thin Basement Membrane Disease?

A

Benign Familial Hematuria

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103
Q

What is the prognosis for Thin Basement Membrane Disease patients?

A

If compound or homozygous = bad prognosis

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104
Q

What is the general pathogenesis of vascular disorders?

A
  • Inflammation of blood vessels (vasculitis)&raquo_space; loss of thromboresistance (pro-clot formation seen in thrombotic microangiopathies)
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105
Q

What is the pathogenesis of Poalyarteritis nodosa?

A

MEDIUM VESSEL disease&raquo_space; ANCA negative&raquo_space; fibrinoid necrosis of vasculature&raquo_space; glomerular ischemia

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106
Q

What are the important facts distinguishing Pauci immune Glomerulonephritis?

A

Crescent glomerulonephritis w/negative immunofluorescence

— often ANCA-positive with extrarenal findings

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107
Q

What is the pathogenesis of ANCA-Associated Glomerulonephritis?

A

Pathogeneic contact & adhesion to vascular endothelium&raquo_space; creates target for inflammatory cells

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108
Q

What causes the loss of thromboresistance in ANCA-Associated Glomerulonephritis?

A

ANCA can bind to PMN toxic component (PR3) preventing inactivating proteins (alpha-1-antitrypsin) from inactivating
— deposition of ANCA-PR3 on endothelium causes loss of thromboresistance

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109
Q

What are the 2 types of ANCA-Associated Glomerulonephritis?

A

cANCA = cytoplasmic; proteinase 3 target
—– WEGENER’S!

pANCA = perinuclear; lysosomal MPO target

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110
Q

What is the immuno profile of ANCA-Associated Glomerulonephritis?

A

cANCA - fine cytoplasmic staining

pANCA - perinuclear staining

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111
Q

What are the similarities and differences between Goodpasture’s and Wegner’s Gramulomatous?

A
  • Both have lung involvement

- Wegener’s has fewer presentations of azotemia

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112
Q

What is the etiology of Wegner’s Gramulomatous?

A

cANCA positive

- anti-nuclear cytoplasmic antibodies for Proteinase 3

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113
Q

What is the prognosis of Wegner’s Gramulomatous?

A

80-90% mortality if untreated

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114
Q

What is the clinical presentation of Wegner’s Gramulomatous?

A

URI, rhinnorrhea, sinusitis, nasopharyngeal irritation, LUNG INVOLVEMENT, nephritic symptoms, granulomas in lungs, nose, and sinus, MULTIPLE SKIN LESIONS
=== sinopulmonary renal syndrome
+ arthritis, arthralgia, myalgia, fatigue

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115
Q

What is the LM profile of Wegner’s Gramulomatous?

A

Granulomatous vasculitis; renal may show segmental issue&raquo_space; crescent

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116
Q

What is the IF profile of Wegner’s Gramulomatous?

A

Pauci-immune glomulonephritis (crescent) Type 3

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117
Q

What is the treatment for Wegner’s Gramulomatous?

A

Oral cyclophhosphamide
steroids
plasma exchange

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118
Q

What is the pathogenesis of Thrombotic Microangiopathy?

A

endothelial cell damage&raquo_space; Loss of thromboresistance of endothelial cells&raquo_space; widespread microvascular thrombosis&raquo_space; deposition of platelet and fibrin thrombi in lumen

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119
Q

What is the etiology of Thrombotic Microangiopathy?

A

Endothelial cell damage from:

  • verotoxin from Ecoli H7
  • auto-antibodies
  • chemotherapy
  • radiation
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120
Q

What diseases are associated with Thrombotic Microangiopathy?

A
  • TTP - vWF disease
  • Childhood hemolytic uremic syndrome
  • — Shiga toxin
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121
Q

What is clinical presentation of Thrombotic Microangiopathy?

A 
Bleeding
MAHA
Thrombocytopenia
Children for HUS
--- McDonald's >> kids (HUS) like hamburgers (Shiga/Ecoli) and onion rings (light microscopy) but don't want thrombi (TTP/DIC)
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122
Q

What is the endothelial appearance of Thrombotic Microangiopathy?

A

Onion skin appearance
Swelling
Microthrombi

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123
Q

What is the DDx of TTP vs. DIC?

A
    • TTP = normal PT and PTT because this ia a platelet disorder, not clotting disorder
    • DIC has prolonged PT/PTT
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124
Q

What is the treatment for Thrombotic Microangiopathy?

A
  • Dialysis for HUS

- Plasmapheresis for TTP

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125
Q

What is the etiology of Lupus Nephritis?

A

SLE is a system disease caused by autoimmune antibodies (ANCA, Anti-dsDNA)

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126
Q

Name and distinguish the 4 types of Lupus Nephriits?

A 
Lupus Nephriits Type I
Lupus Nephriits Type II
---- mesangial proliferative
---- increased mesangial matrix & cells
Lupus Nephriits Type III 
---- focal proliferative
---- often w/ crescent (rapid prog. GN)
Lupus Nephriits Type IV
---- diffuse proliferative
---- worst prognosis
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127
Q

What is the clinical presentation of Lupus Nephriits?

A

Systemic disease sparing no organ system, begins with arthritis, rash on face, renal failure; Brazil

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128
Q

What is the immuno profile of Lupus Nephriits?

A
  • Subendothelial deposits
  • Full House / Kitchen sink
  • – contains positive signals for C3, C4, IgA, IgG, IgM
  • – has eerything
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129
Q

What is the treatment for Lupus Nephriits?

A

FDA approved: aspirin, glucocorticoids, hydroxychloroquine

Immunosuppressive: Cyclophosphomide mycophenolate mofetil

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130
Q

What is the etiology of Scleroderma systemic sclerosis?

A

unknown

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131
Q

What is the pathogenesis of Scleroderma systemic sclerosis?

A

Connective tissue fibrosis

Vascular occlusion of microvasculature

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132
Q

What are the 2 types of Scleroderma systemic sclerosis?

A 
(LC) Limited cutaneous
- few constitutional symptoms
- severe Raynaud's finding
(DC) Diffuse cutaneous
- present at 5 years
- many constitutional symptoms (heart, lungs, kidneys)
- Mild Raynaud
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133
Q

What is the clinical presentation of Scleroderma systemic sclerosis?

A

Females, AA, mild renal involvement, HPTN, proteinuria

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134
Q

What is the risk factors for Scleroderma systemic sclerosis?

A

Scleroderma renal crisis
Arterial HPTN
Oliguric renal failure
Luminal narrowing of arcuate arteries

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135
Q

What is the LM profile for Scleroderma systemic sclerosis?

A

Luminal occlusion
systemic changes in blood vessels
- onion skin appearance

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136
Q

What does the glomerulus look like in a patient with Scleroderma systemic sclerosis?

A

No inflammation
Ischemia
Increased glomerular hydrostatic pressure from increased resistance

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137
Q

What is the treatment for Scleroderma systemic sclerosis?

A

ACE inhibitors for renal crisis

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138
Q

What is cause of sickling in Sickle Cell Nephropathy?

A

RBC prone to sickling in hypoxic, hypertonic, acidic medulla

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139
Q

What is the mechanism of RBC sickling’s effect on medullary function in Sickle Cell Nephropathy?

A

Medulla becomes hypoxic as it descends&raquo_space; deoxygenated HbS sickles&raquo_space; increase polymerization of RBC&raquo_space; vasa recta become attenuated (trait) or absent (SCD)&raquo_space; loss of medullary funciton&raquo_space; loss of ability to dilute and concentrate urine

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140
Q

What is the mechanism of Sickle Cell Nephropathy?

A

increased GFR + increased RPF = hyperfiltration&raquo_space; proximal tubule increases function&raquo_space; hyperfiltration persists from birth till 40s when disease presents w/ low GFR

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141
Q

Why would some patients with no other associated renal dysfunction have milder form of Sickle Cell Nephropathy if both are homozygous?

A

Disease affects mainly juxtamedullary nephrons; cortical nephrons tubular system barely enters hypoxic medulla

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142
Q

What is the incidence of Sickle Cell Nephropathy?

A
  • decline in 40s-50s when low GFR
  • 4-12% of patients&raquo_space; ESRD
  • other complications can kill before (CVD)
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143
Q

What is the clinical presentation of Sickle Cell Nephropathy?

A

60% microalbuminuria
20% proteinuria
Hematuria
Hyperphosphatemia

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144
Q

What is the histopathology of Sickle Cell Nephropathy?

A

Due to increased GFR (hemodynamic)

  • Early
  • — glomerular hypertrophy, hemosiderin (transfusions), focal damage
  • Later
  • — interstitial inflammation + tubular atrophy
  • End stage
  • — Glomerular enlargement, FSGS
  • Renal artery thrombosis
  • Microthrombi of glomerulus an dvasa recta
  • Glomerulosclerosis, mesangial expansion
  • papillary necrosis - less blood flow down medulla – also seen in DM, chronic pyelonephritis, and NSAID abuse TIN
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145
Q

What are the 4 types of Amyloidosis?

A
  1. AL Amyloidosis (Primary)
  2. AA Amyloidosis (Secondary- systemic)
  3. Abeta2M Amyloidosis
  4. Hereditary Amyloidosis
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146
Q

What is the classification of the 4 types of Amyloidosis?

A

Primary: idiopathic, B-cell abnormality, AL
Secondary: chronic inflammatory disease (RA), AA (inflammatory amyloid protein)
Familial: inherited mutation, AA, ATTR, Acys, Abeta (Alzheimer protein)
Isolated (focal) Amyloidosis: deposits in single tissue/organ, Abeta, AiAPP (diabetes), ATTR

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147
Q

What is the mechanism of all Amyloidosis types?

A

Interstitial deposits of insoluble B-pleated fibrils

— disease specific fragment w/ B-pleated conformation

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148
Q

How are pathogenic proteins misfolded in Amyloidosis?

A
  • Intrinsic pathogenic property of protein
  • single amino acid replacement (familial)
  • proteolytic remodeling of a protein precursor
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149
Q

What is the consequence of misfolded pathogenic proteins in amyloidosis?

A

Enlarged kidney from deposits
Vascular involvement
Interstitial deposits&raquo_space; fibrosis&raquo_space; tubular damage (think nephrogenic diabetes, ion imbalance)

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150
Q

How do you diagnose Amyloidosis?

A

SPEP/IF or Serum Light Chain Assay

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151
Q

How do you treat Amyloidosis?

A

Eprodisate - limits interaction btw GAG + Amyloid

Low dose melphalan/dexamethasone OR transplant

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152
Q

What is the overall morphology of Amyloidosis?

A
  • Homogenous + glassy appearance
  • Congo red&raquo_space; apple green bifringence
  • Major components:
  • — Fibrillogenic protein (B-pleat) + Amyloid P (donut) + PG (Heparan Sulfate) + Apoprotein E
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153
Q

Is Amyloidosis nephritic or nephrotic?

A

NEPHROTIC - non-inflammatory

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154
Q

What is primary Amyloidosis called?

A

AL Amyloidosis

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155
Q

What is the etiology of AL Amyloidosis?

A

Secondary to multiple myeloma, B-cell lymphoma, plasma cell diseases

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156
Q

What is the mechanism of AL Amyloidosis?

A

Plasma cell light chain (lambda&raquo_space;>kappa)

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157
Q

What is the clinical presentation of AL Amyloidosis?

A

64 y/o
Weakness, weight loss, nephrotic syndrome
Renal insufficiency, Bence Jones (proteinuria)
Enlarged kidneys
Myocardial dysfunction, sick sinus syndrome
Bleeding diathesis

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158
Q

What is secondary Amyloidosis called?

A

AA Amyloidosis (systemic)

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159
Q

What is the etiology of AA Amyloidosis?

A

Secondary to chronic inflammatory disease (RA, Familial Mediterranean Fever)

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160
Q

What are the affected organs in Amyloidosis?

A

Kidney + GI malabsorption

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161
Q

What is the pathogenesis of AA Amyloidosis?

A

Serum amyloid A (SAA) increased w/ inflammation&raquo_space; Amyloid Enhancing Factor (AEF) changes SAA processing by macrophages and endothelial cells&raquo_space; BM disturbances are required so SAA can bind&raquo_space; apoE + SAA + AEF + BM&raquo_space; amyloid AA

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162
Q

What is the clinical presentation of AA Amyloidosis?

A 
Chronic inflammatory condition
Renal insufficiency
GI insufficiency
\+Kidney biopsy
Vascular (coronary artery, renal)
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163
Q

What is the name of the Amyloidosis associated with diabetes?

A

Abeta2M Amyloidosis

— will use B for beta from now on

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164
Q

What is the precursor for AB2M Amyloidosis called?

A

B2 Microglobulin

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165
Q

Which patients have elevated B2 Microglobulin?

A

Patients with chronic dialysis

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166
Q

What is the clinical presentation of patients with AB2M Amyloidosis?

A

Deposits in bones and joints

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167
Q

What is the inherited form of Amyloidosis called?

A

Hereditary Amyloidosis

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168
Q

What are the test results for Hereditary Amyloidosis?

A

Negative for heavy/light chains

Positive for fibrinogen, transthyretin, apolipo, lysozyme

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169
Q

How do you treat patients with Hereditary Amyloidosis?

A

Liver transplant

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170
Q

What is another name for light chain disease?

A

Non-amyloid monoclonal Ig deposition disease (MIDD)

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171
Q

What makes the etiology of light chain disease (MIDD) different from Amyloidosis?

A

Not just the B-pleated sheet, entire Ig

– Kappa&raquo_space; lambda

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172
Q

What makes the diagnosis of light chain disease (MIDD) different from Amyloidosis?

A

Light chain disease

  • neg Congo red (B-sheet is still in Ig; no fibrils)
  • No fibrillar organization
  • precipitation of light chains
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173
Q

What is the clinical presentation of Light Chain disease, nephritic or nephrotic?

A

Nephrotic

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174
Q

What is the clinical presentation of Light Chain disease?

A 
Proteinuria + renal failure (nephrotic-like)
HEpatomegaly
CVD (CHF, conduction disturbance)
Peripheral neuropathy
GI disturbances
Pulmonary nodules
Sicca (Sjogren's) syndrome
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175
Q

What is the morphology of light chain disease?

A

Nodular glomerulosclerosis (classic)
Expansion of mesangial matrix
Light chain deposits in glomerulus, tubules and mesangial matrix

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176
Q

What are the 2 types of virus associated kidney diseases?

A

HIV-associated Nephropathy

Cryoglobulinemia

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177
Q

What is the pathogenesis of HIV-associated Nephropathy?

A

direct infection from HIV-1 of renal epithelial cells

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178
Q

What are the risk factors for HIV-associated Nephropathy?

A

The infection must occur in a genetically susceptible host

  • Common in African Americans w/o ApoL1 (Ch.22) allele
  • Mutation in ApoL1 protects against Trypanosoma brucie rhodesiese (African sleeping sickness)
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179
Q

What is the clinical presentation of HIV-associated Nephropathy?

A

Late stage HIV with rapid onset of proteinuria

- no edema, no HPTN

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180
Q

What is the morphology of HIV-associated Nephropathy?

A 
Collapsing FSGS
Tubular dilation (full of protein-like material)
Podocyte de-differentiation and proliferation
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181
Q

Name diseases associated with proximal tubule defects

A

Hereditary Renal Glucosuria
Cystinuria
Hypophosphatemia
Hypo/Hyperuricemia

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182
Q

What is the etiology of Hereditary Renal Glucosuria?

A

Autosomal recessive; 1/20,000

Mutation in SGLT2 glucose transporter

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183
Q

What is the pathogenesis of Hereditary Renal Glucosuria?

A

Defective glucose reabsorption&raquo_space; glucose concentration overcomes threshold&raquo_space; renal glucosuria

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184
Q

What are the 2 renal glucose transporters?

A

SGTL1 - found on enterocytes, unaffected

SGTL2

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185
Q

People with what disease would benefit from having Hereditary Renal Glucosuria?

A

We would want SGLT2 mutation in diabetics - we give SGTL2 inhibitors to diabetic patients

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186
Q

What is the etiology of Cystinuria?

A

Mutation in brush border transporter of CYSTINE, ORNITHINE, LYSINE, ARGININE

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187
Q

What is the mechanism of Cystinuria

A

Defective amino acid reabsorption

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188
Q

What is found in the urine of patients with Cystinuria?

A

cystine stones, cystine crystals (hexagonal)

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189
Q

What is the mechanism of Hypophosphatemia?

A

Defective phosphate reabsorption

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190
Q

What are the inherited causes of Hypophosphatemia?

A
  1. X-linked Hypophosphatemia (PHEX mutation)
    - — Rickets in kids; osteomalacia in adults
  2. Autosomal Dominant Rickets (FGF-23 mutation)
  3. Autosomal Recessive Hypophosphatemic Rickets (FGF-23 OR Na/Pi IIc transporter)
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191
Q

What are the acquired causes of Hypophosphatemia?

A
  1. Oncogenic Hypophosphatemic Osteomalacia (increased FGF-23 production)
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192
Q

What is the pathogenesis of Hypophosphatemia?

A
  • PHEX mutation decreases FGF-23 degradation
  • increased FGF-23 down regulates phosphate transporter activity (not a mutation in transporter)&raquo_space; FGF lowers calcitrol = increases PTH&raquo_space; lowers P = hpophosphatemia&raquo_space; also inhibits activation of vit. D
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193
Q

What are the two diseases characterized by defective uric acid handling in the kidney?

A

Hypouricemia

Hyperuricemia

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194
Q

What is the mechanisms of hypo and hyperuricemia?

A

— Uric acid —
Decreased reabsorption = hypouricemia
Defective secretion = hyperuricemia

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195
Q

What is the generalized PT dysfunction in Faconi’s syndrome, acquired vs. inherited?

A

acquired > inherited

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196
Q

What are the possible mechanisms of Faconi’s syndrome?

A
  • Defecting binding of Na to transport proteins
  • defecting inserting of carriers
  • Leaky membrane tight junctions
  • inhibit Na/K ATPase
  • impaired mitochondria energy generation
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197
Q

What are the metabolic abnormalities associated with Faconi’s syndrome?

A
  1. aminoaciduria
  2. glucosuria (normal serum glucose)
  3. Hypophosphatemia (multifactorial: decreased Na/P carrier, decreased Vit D)
  4. Increased bicarb excretion = metabolic acidosis
  5. Hypokalemia (more delivery to distal tubule)
  6. Uricosuria
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198
Q

What is the clinical presentation of Faconi’s syndrome?

A 
Polyuria/polydipsia form osmotic diuresis
Volume depletion
Cardiac issues (K+)
Proteinuria
Rickets
Renal stones
Growth retardation
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199
Q

What are the drug-induced etiologies of Faconi’s Syndrome?

A

Tenofovir (anti-HIV)
Lead
Toluene (toxin)
Aristolochic Acid (weight loss)

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200
Q

What types of diseases are associated with loop of Henle and distal tubule defects?

A

Sodium disorders
Hypokalemia
Hyperkalemia
Renal tubular acidosis

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201
Q

Name the 3 Sodium disorders?

A

Bartter’s Syndrome
Gittelman’s Syndrome
Liddle’s syndrome

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202
Q

What is the etiology of Bartter’s Syndrome?

A

Mutation in Na, k, 2Cl in TALH

- Autosomal recessive

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203
Q

What is Neonatal Bartter’s Syndrome?

A

Polyhydraminous: high PGE2, give COX-1

– volume depletion&raquo_space; excess fetal urine&raquo_space; failure to thrive

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204
Q

What is the clinical presentation of Bartter’s syndrome?

A
  • Low blood Ca, Mg, Cl, K - metabolic alkalosis
  • Na wasting disorder
    Increased K+ and H+ secretion
    —– due to increased luminal negative transepithelial potential downstream due to increased Na delivery and increased ENaC from aldosterone
  • High renin, aldosterone - volume depletion
  • crave pickle juice
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205
Q

How do you treat Bartter’s syndrome?

A

K+ supplements
Mg supplements
high salt intake

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206
Q

What is the etiology of Gittelman’s Syndrome?

A

Mutation in thiazide sensitive NCCT in DCT

    • autosomal recessive
    • Na wasting disorder
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207
Q

Bartter’s vs. Gittelman’s, which is more severe?

A

Patients have more normal growth with Gittelman’s compared to Bartter’s because less sodium in wasted with this mutation

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208
Q

What are the findings in Gittelman’s syndrome?

A
  • Hypochloremic, hypokalemia metabolic alkalosis
  • Low Mg
  • Hypercalcemia (b/c PTH effect)
  • High renin, aldosterone
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209
Q

What is the etiology of Liddle’s Syndrome?

A

ENaC channel beta/gamma mutations

Autosomal dominant

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210
Q

What is the pathogenesis of Liddle’s Syndrome?

A

ENaC channel is always open

  • gain of function mutation
  • low renin and aldosterone
  • high Na will increase lumen negative transepithelial charge&raquo_space; low K+ retention&raquo_space; hypokalemia
  • high K+ in lumen will provide substrate to alpha-intercalated K/H+ATPase&raquo_space; increase H+ excretion&raquo_space; metabolic alkalosis
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211
Q

What is the clinical presentation of Liddle’s Syndrome?

A
  • Hypertension

- Mirror image of Pseudohypoaldosternism Type I

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212
Q

Name the three diseases that are associated with Hypokalemia

A
  1. Primary and Secondary Hyperaldosteronism
  2. Glucocorticoid Remediable Aldosteronism (GRA)
  3. Apparent Mineralcorticoid Excess (AME)
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213
Q

What is the etiology of primary Hyperaldosteronism?

A

Adrenal tumors

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214
Q

What is the etiology of secondary Hyperaldosteronism?

A

dehydration, pyloric stenosis (Barfer’s), Bartter’s/Gittelman

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215
Q

What are the clinical findings in dehydration and pyloric stenosis Hyperaldosteronism??

A
  • Pyloric stenosis is common in first born males with increase vomit&raquo_space; dehydration&raquo_space; increase aldosterone
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216
Q

What are the clinical findings in Bartter’s/Gittelman Hyperaldosteronism?

A
  • increase urinary chloride because this is a genetic defect in Cl- transport
  • important for differentiating between these secondary causes for hyperaldosteronism
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217
Q

What is the pathogenesis of Glucocorticoid Remediable Aldosteronism (GRA)?

A

Recombination of aldosterone synthase and 11-Beta-hydroxy-dehydrogenase&raquo_space; increase aldosterone in response to stress

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218
Q

What are the clinical findings in Glucocorticoid Remediable Aldosteronism (GRA)?

A
  • low renin – aldosterone not created by RAAS
  • increase Na&raquo_space; increase lumen negative transepithelial charge&raquo_space; low K+ retention&raquo_space; increase hypokalemia
  • increase K+ in lumen will provide substrate to alpha-intercalated K+/H+ATPase&raquo_space; increase H+ excretion&raquo_space; metabolic acidosis
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219
Q

What is the treatment for Glucocorticoid Remediable Aldosteronism (GRA)?

A

Glucocorticoids

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220
Q

What is the pathogenesis of Apparent Mineralcorticoid Excess (AME)?

A

Mutated enzyme 11BHD2&raquo_space; increased activation of aldosterone receptor&raquo_space; increase ENaC

221
Q

What is the function of the enzyme 11BHD2?

A

Enzyme 11-Beta-hydroxy-dehydrogenase 2 exists to prevent glucocorticoids from binding to aldosterone receptors

222
Q

What happens to the mutated enzyme 11BHD2 in Cushing’s Syndrome?

A

In cases of excess glucocorticoids (Cushing’s Syndrome), 11BHD2 is overwhelmed

223
Q

What is the clinical findings in Apparent Mineralcorticoid Excess (AME)?

A
  • low renin, aldosterone
  • increase Na will increase lumen negative transepithelial charge&raquo_space; low K+ retention&raquo_space; increase hypokalemia
  • increase K+ in lumen will provide substrate to alpha-intercalated K+/H+ATPase&raquo_space; increase H+ excretion&raquo_space; metabolic alkalosis
224
Q

What is the treatment for - increase K+ in lumen will provide substrate to alpha-intercalated K+/H+ATPase&raquo_space; increase H+ excretion&raquo_space; metabolic acidosis?

A

Glucocorticoids

225
Q

What are the 3 diseases associated with hyperkalemia?

A
  1. Hypoaldosteronism
  2. Pseudohypoaldosteronism Type I
  3. Pseudohypoaldosteronism Type II
226
Q

What are the 3 diseases that cause Hypoaldosteronism?

A
  • congenital adrenal hypoplasia
  • congenital adrenal hyperplasia
  • autoimmune disease
227
Q

What diseases are associated with hypoaldosteronism and adrenal insufficiency?

A
  • Congenital adrenal hypoplasia

- Addison’s disease

228
Q

What is the main problem in both congenital adrenal hypoplasia and Addison’s disease?

A

no aldosterone

229
Q

What is congenital adrenal hyperplasia and how is it related to Cushing’s syndrome?

A
  • disorder of steroid synthesis pathway (21 hydroxylase most common)
  • also could create excess cortisol activation of aldosterone receptor as in cushing’s syndrome
230
Q

What are 3 autoimmune diseases associated with Hypoaldosteronism?

A

IDD
Hypothyroidism
Addison’s Disease

231
Q

What is the pathogenesis of hypoaldosteronism?

A
  • low aldosterone and decreased activation of ENaC&raquo_space; decrease lumen negative transepithelial charge&raquo_space; increased K+ retention&raquo_space; hyperkalemic metabolic acidosis
232
Q

What is the etiology of Pseudohypoaldosteronism Type I?

A
  • AD mutation in mineralcorticoid receptor OR

- AR ENaC mutation (loss of function > stuck closed > opposite of Liddle)

233
Q

What is the dysfunction in Pseudohypoaldosteronism Type I?

A

Tubular disorder - have aldosterone, but doesn’t work right

234
Q

What are the clinical findings in Pseudohypoaldosteronism Type I?

A
  • high renin to high Na retention
  • Hyperkalemia, hyponatremia (aldosterone dysfunction)
  • prone to volume depletion
235
Q

What are 2 other names for Pseudohypoaldosteronism Type II?

A

Gordon’s syndrome

Chloride shunt syndrome

236
Q

What is the etiology of Pseudohypoaldosteronism Type II?

A

Mutation in WNK 4 (regulator of NCCT) or WNK1 (regulator of WNK 4) of NCCT

237
Q

What is the pathogenesis of Pseudohypoaldosteronism Type II?

A
  • high Na reabsorption in DCT
  • This is proximal compared to other hyperkalemic diseases, which means you have less delivery of Na to the CD, so no extra excretion of K+
  • hyperkalemia
238
Q

What are the clinical findings in Pseudohypoaldosteronism Type II?

A
  • low RAAS b/c increased Na reabsorption
  • hyperkalemic
  • hyperchloremic
  • metabolic acidosis
  • mirror image of Gittelman syndrome
239
Q

What is the treatment for Pseudohypoaldosteronism Type II??

A

thiazide diuretics

240
Q

What are the 3 types of Renal Tubular Acidosis? (stones, bones, aldosterone)

A
  1. Type I RTA - Classical distal RTA
  2. Type 2 RTA - Proximal Tubule defect
  3. Type 4 RTA - Secondary to hypoaldosteronism
241
Q

What is the major dysfunction in Type I RTA - Classical distal RTA?

A

Inability of distal tubule to secrete H+

242
Q

What diseases are associated with Type I RTA - Classical distal RTA?

A

Nephrolithiasis (stones) and amphotercin

Failure to thrive

243
Q

Is the K+ high or low in Type I RTA - Classical distal RTA?

A

Hypokalemia - no H+ secretion, no K+ reabsorption

244
Q

What is the major dysfunction in Type 2 RTA - Proximal Tubule defect?

A

Inability of PT to resorb HCO3-

245
Q

What diseases are associated with Type 2 RTA - Proximal Tubule defect?

A

Faconi’s Syndrome

Ricket’s and multiple myeloma (bones)

246
Q

Is the K+ high or low in Type 2 RTA - Proximal Tubule defect?

A

Hypokalemia

247
Q

What is the pathogenesis of Type 4 RTA - Secondary to hypoaldosteronism?

A

low aldosterone&raquo_space; low Na reabsorption&raquo_space; high K+ retention&raquo_space; hyperkalemia

248
Q

What is the primary defect in Type 4 RTA - Secondary to hypoaldosteronism?

A

considered a distal tubule issue, but actually has to do with NH3 secretion proximally

249
Q

How does hyperkalemia lead to low NH4 formation in Type 4 RTA - Secondary to hypoaldosteronism?

A

hyperkalemia&raquo_space; increased K+ movement intracellularly&raquo_space; increase H+ movement out of cell&raquo_space; increase pH in cell&raquo_space; decrease NH3 production to restore pH&raquo_space; decrease NH4 formation

250
Q

For all RTA types, are the plasma and urinary anion gaps normal?

A

All RTA types are NORMAL plasma anion gap & positive urinary anion gap acidosis

251
Q

What are the 4 tests for distinguishing RTA types?

A
  1. Fractional Excretion of Bicarb
  2. Urine pH
  3. Urine anion Gap (UNa + UK+ - UCI-)
  4. U-B PCO2
252
Q

For the Fractional Excretion of Bicarb test, which RTA type can you identify?

A
  • high HCO3 excretion in Type 2

- normal in other types

253
Q

For the urine pH test, which RTA type can you identify?

A

pH < 5.5 in type 2

    • because defect is proximal before acidification
    • pH > 5.5 in other types
254
Q

Is the urine ion gap test + or - in RTA? Why?

A

Positive

  • in RTA, low H+ secretion&raquo_space; no NH4+
  • therefore, Na + K > Cl = positive
255
Q

What are the results for a normal urine ion gap test and why?

A

Normally: high H+ secretion&raquo_space; high NH4+
- because NH4+ is not measured in urine anion gap, and elevated NH4+ will require that Cl- increases to maintain neutrality, thus Cl > Na + K

256
Q

How do you perform the U-B PCO2 test and what does it measure?

A
  • Give HCO3- + acetozolamide
  • HCO3- cannot be absorbed in PT
  • In DT/CD it will rect with H+&raquo_space; H2O+CO2&raquo_space; measure the CO2
257
Q

For the U-B PCO2 test, which RTA type can you identify and why?

A
  • Normal in Type 2

- Low in Type 1 & 4 because no H+ to react

258
Q

What is the etiology of Papillary Necrosis?

A

Focal ischemia + infection

259
Q

How does infection cause Papillary Necrosis?

A

Increased metabolic needs from infection / toxicity&raquo_space; inflammation w/ metabolic demands&raquo_space; micro/macro angiopathy induced ischemia

260
Q

What diseases are associated with Papillary Necrosis?

A

UTI, diabetes, UT obstruction, analgesic nephropathy

261
Q

What is the difference between ATN and Papillary Necrosis?

A

Focal ischemia in Papillary Necrosis vs. diffuse ischemia in ATN

262
Q

What is the clinical presentation of Papillary Necrosis?

A
  • Azotemia
  • fever
  • renal pain
263
Q

What will the urinalysis show in Papillary Necrosis?

A
  • macroscopic hematuria

- passage of tissue shreds

264
Q

what is another name for Pseudohyperaldosteronism?

A

Liddle’s Syndrome

265
Q

What is the etiology of Liddle’s Syndrome (Pseudohyperaldosteronism)?

A

ENaC channel is always open due to beta/gamma mutations

- autosomal dominant

266
Q

What is the pathogenesis of Liddle’s Syndrome (Pseudohyperaldosteronism)?

A
  • low renin & aldosterone
    » high Na will increase lumen negative transepithelial charge&raquo_space; low K+ retention&raquo_space; high hypokalemia
    » high K+ in lumen will provide substrate to alpha-intercalated K/H+ATPase&raquo_space; high H+ excretion&raquo_space; metabolic acidosis
267
Q

How do you treat Liddle’s Syndrome (Pseudohyperaldosteronism)?

A

Triamterene or amiloride (K+ sparing ENaC inhibitors)

268
Q

What are 3 water and salt balance disorders that are associated with edema?

A
  1. CHF
  2. Liver cirrhosis
  3. Nephrotic syndrome
269
Q

In congestive heart failure (CHF), how does low CO lead to edema?

A

Low CO&raquo_space; low EABV&raquo_space; RAAS + SNS + AVP/ADH&raquo_space; increased Na + water reabsorption&raquo_space; increase plasma volume&raquo_space; increase vascular hydrostatic pressure&raquo_space; edema

270
Q

What is the clinical presentation of CHF?

A 
Edema
bibasilar rales
Cardiac enlargement
Neck vein distention
Pulmonary edema
271
Q

What is the basic 3 steps in the pathogenesis of edema in CHF?

A

increased plasma volume&raquo_space; increased hydrostatic pressure&raquo_space; edema

272
Q

How does liver cirrhosis lead to edema?

A
  1. increased hydrostatic pressure&raquo_space; increased PV

2. liver failure&raquo_space; low albumin&raquo_space; decreased capillary oncotic pressure

273
Q

What is the pathogenesis of liver cirrhosis?

A

Splanchnic vasodilation&raquo_space; low EABV&raquo_space; RAAS + SNS + AVP/ADH&raquo_space; increased Na + water reabsorption&raquo_space; increase plasma volume&raquo_space; increase vascular hydrostatic pressure&raquo_space; edema

274
Q

What is the clinical presentation of liver cirrhosis?

A 
liver failure
hepatosplenomegaly
concurrent persistent liver infection
hypoalbuminemia
edema
275
Q

What is the pathogenesis of Nephrotic syndrome?

A

leaky glomerulus&raquo_space; increased loss of albumin through excretion&raquo_space; decreased capillary oncotic pressure

276
Q

What is the clinical presentation of Nephrotic syndrome?

A

signs of kidney failure

edema

277
Q

What hormone directly stimulates ADH/AVP?

A

Angiotensin II

278
Q

What medications stimulate ADH/AVP despite low osmolarity?

A

Pain & nausea meds

279
Q

What is the pathogenesis of Hypovolemic Hyponatremia?

A

decrease in TBNa that exceeds decrease in TBW

280
Q

What is the clinical presentation of Hypovolemic Hyponatremia?

A

Low BP
poor skin turgor
absence of dependent edema (no skin recoil)
prerenal azotemia (disproportionate increase in BUN relative to serum creatinine)

281
Q

What are the renal causes of Hypovolemic Hyponatremia?

A

diuretics, aldosterone deficit

282
Q

What are the GI causes of Hypovolemic Hyponatremia?

A

diarrhea, vomiting, bleeding

283
Q

What are the skin causes of Hypovolemic Hyponatremia?

A

burns, sweating

284
Q

How do you differentiate renal vs. extra-renal sodium loss?

A

Renal Na loss: urine Na > 20

Extra-renal Na loss: urine Na < 20

285
Q

Why is urine Na higher in renal vs. extra-renal causes of Na loss?

A

If hyponatremic, kidneys should be reabsorbing as much Na as possible, not excreting it… unless renal damage is the cause

286
Q

What are the 2 types of hyponatremia?

A

Euvolemic Hyponatremia

Hypervolemic Hyponatremia

287
Q

In Euvolemic Hyponatremia, what is the relationship between TBW and TBNa?

A
  • increase in TBW

- no change in TBNa

288
Q

What is the clinical presentation of Euvolemic Hyponatremia?

A
  • decreased serum osmolality
  • inappropriate urinary concentration
  • high urinary Na
  • anti-psychotic drugs
  • glucocorticoid deficiency
289
Q

What is the treatment for Euvolemic Hyponatremia?

A

Loop diuretics

290
Q

How do you distinguish Euvolemic Hyponatremia and SIADH?

A

If there is no change in TBNa, but TBW increases&raquo_space; this means that there is something released that only increases TBW = ADH/AVP

291
Q

In Hypervolemic Hyponatremia, what is the relationship between TBW and TBNa?

A

increase in TBW that exceeds decrease in TBNa

- increase in TBNa < increase in TBW

292
Q

What is the clinical presentation of Hypervolemic Hyponatremia?

A
  • EDEMA
  • heart failure
  • liver failure
  • kidney failure
    Diseases: CHF, liver cirrhosis, nephrotic syndrome
293
Q

Regarding clinical symptoms, how do you differentiate acute vs. chronic hyponatremia?

A

Acute: has constitutional symptoms
—- nausea, malaise, headache, seizures, coma
Chronic: has few symptoms
—- cerebral edema

294
Q

In chronic hyponatremia, how does too much water affect the brain?

A

too much water&raquo_space; cerebral edema&raquo_space; brain responds by losing intra/extra cellular solutes to make room for H2O

  • – brain adapts to chronic hyponatremia
  • – avoid demylination syndrome by altering treatment (.5 mEq/L/hr)
295
Q

What are the 3 types of Hypernatremia?

A

Hypovolemic Hypernatremia
Euvolemic Hypernatremia
Hypervolemic Hypernatremia

296
Q

What is the relationship between TBW and TBNa in Hypovolemic Hypernatremia? Use very high, high, low, very low for each and compare the two.

A

very low TBW > low TBNa

297
Q

Describe the amount of TBW in Euvolemic Hypernatremia? Use very high, high, low, very low for each and compare the two.

A

very low TBW

298
Q

What is the relationship between TBW and TBNa in Hypervolemic Hypernatremia? Use very high, high, low, very low for each and compare the two.

A

very high TBNa > high TBW

299
Q

What is the clinical presentation of Hypovolemic Hypernatremia?

A

lethargy, weakness, irritable, seizure, coma

300
Q

What is the main problem and how do you treat Hypovolemic Hypernatremia?

A

– very low TBW > low TBNa
Give isotonic saline
— volume loss (Na) is more important

301
Q

What is the main problem and treatment for Euvolemic hypernatremia?

A

– very low TBW
treat underlying cause
replace with water

302
Q

What is the main problem and treatment for hypervolemic hypernatremia?

A

– very high TBNa > high TBW
Get Na out of the body
- furosemide
- dialysis

303
Q

What are the 2 types of diabetes insipidus?

A

Central diabetes insipidus

Nephrogenic diabetes insipidus

304
Q

What is the problem with ADH in Central diabetes insipidus compared to Nephrogenic diabetes insipidus?

A

Central diabetes insipidus
—- No ADH
Nephrogenic diabetes insipidus
—- ADH resistance

305
Q

What is the etiology of Central diabetes insipidus?

A

trauma, tumor, congenital

306
Q

What is the treatment for Central diabetes insipidus?

A

DDAVP (exogenous vasopressin)

307
Q

What is the etiology of Nephrogenic diabetes insipidus?

A

V2 receptor mutation, cAMP defect

308
Q

How do the V2 receptor mutation, and cAMP defect in Nephrogenic diabetes insipidus affect ADH?

A

causes ADH resistance

309
Q

What is the clinical presentation of Nephrogenic diabetes insipidus?

A 
CKD
hypokalemia
lithium
demeclocycline
sickle cell disease
PREGNANCY (VASOPRESSINASE)
310
Q

How do you treat Nephrogenic diabetes insipidus?

A

thiazides

311
Q

What is the method used to differentiate diabetes insipidus and primary polydipsia?

A

withhold water source and watch the urine osmolarity increase

312
Q

What is the method used to differentiate central DI vs. nephrogenic DI?

A

give DDAVP and look for change (no change will occur in nephrogenic)

313
Q

What molecules are low in metabolic acidosis?

A

very low HCO3-

also, low CO2 by hyperventilation as compensatory mechanism

314
Q

What anion gap do you always measure in metabolic acidosis?

A

Plasma anion gap

315
Q

In metabolic acidosis, what does a high anion gap indicate?

A 
unmeasured anion (MUDPILES)
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Inborn errors of metabolism
Lactic acidosis
Ethylene glycol
Salicyates
316
Q

If the plasma anion gap is normal in metabolic acidosis, what do you measure next?

A

Urinary anion gap

317
Q

What cause does a (+) urinary ion gap indicate in metabolic acidosis?

A

RTA

318
Q

What cause does a (-) urinary ion gap indicate in metabolic acidosis?

A

diarrhea, etc.

319
Q

In metabolic acidosis, what are the causes of decreased renal acid secretion?

A
  • renal function impairment
  • impaired NH4+ formation
  • RTA Type 1 and 4 (high urinary anion gap)
320
Q

What are the 3 general etiologies for metabolic acidosis?

A
  1. Decreased renal acid secretion
  2. Direct bicarbonate loss
  3. Acid generation
321
Q

What are 2 examples of direct bicarbonate loss in metabolic acidosis?

A

GI loss

Type 2 RTA

322
Q

What are 5 examples of acid generation in metabolic acidosis?

A 
Shock
Lactic acidosis
Ketoacidosis
Aspirin
Methanol, ethylene glycol
323
Q

What do you measure to determine respiratory acidosis?

A

pCO2

324
Q

Is pCO2 high or low in respiratory acidosis?

A

very high pCO2

325
Q

Why do you have elevated HCO3- in respiratory acidosis?

A

high HCO3- as compensatory kidney mechanism

326
Q

In respiratory acidosis you have a compensatory kidney mechanism. Is this a fast or slow response?

A

slow process because kidney takes time to respond

327
Q

What is an important question to ask with respiratory acidosis?

A

acute or chronic?

328
Q

What causes acute respiratory acidosis?

A
  • anything that decreases breathing = increased CO2 retention
  • anesthesia
  • cardiac arrest
  • pneumothorax
329
Q

What causes chronic respiratory acidosis?

A
  • prolonged decreased breathing = high CO2 retention
  • obstructive pulmonary disease
  • Myopathy (chest fall dysfunction)
  • barbituates, opioids, benzodiazapenes
330
Q

Compare and contrast the changes in pH and HCO3 in acute vs. chronic respiratory acidosis?

A 
Acute = high pH change & low HCO3 change
Chronic = low pH change & high HCO3 change
331
Q

What is the mechanism of respiratory alkalosis?

A

low pCO2

- also, low HCO3 as compensatory kidney mechanism, slow process

332
Q

What is the most common cause of respiratory alkalosis?

A

anxiety (hyperventilation)

333
Q

What causes respiratory alkalosis?

A

Anything that causes increased breathing = low CO2 retention

  • Gram(-) bacteria (endotoxin)
  • Pregnancy
  • Trauma
  • hypoxia
  • Aspirin
334
Q

How does pregnancy cause respiratory alkalosis?

A

progesterone and estrogen overstimulate the respirator center&raquo_space; more CO2 is expelled per breath

335
Q

Why do people breathe into paper bags during anxiety attacks?

A

Breathing into a bag gets all the expelled CO2 back in

336
Q

What is the relationship between CO2, carbonic anhydrase reactions and HCO3- in the proximal tubule?

A

Think about the role of CO2 in the carbonic anhydrase related reactions in the PT.
– More CO2 (which can diffuse into epithelial cell from basolateral side) means more substrate for that reaction&raquo_space; more HCO3-

337
Q

What is the mechanism of metabolic alkalosis?

A

elevated HCO3-

- also high CO2 by hypoventilation

338
Q

What 2 things should you always check in metabolic alkalosis?

A

plasma & urine ion gap

339
Q

What is main cause of metabolic alkalosis?

A

Mainly loss of acid

– GI tract loss = vomiting/diarrhea - loss of H+

340
Q

What are other causes of metabolic alkalosis?

A
  • excessive urinary acid excretion
  • Hyperaldosteronism
  • movement of acid into cells
341
Q

How do you determine if metabolic alkalosis is Cl responsive or Cl resistant?

A

Urine [Cl-] < 20 = Cl responsive
Urine [Cl-] > 20 = Cl resistant
–same concept as checking if renal vs. extra-renal

342
Q

Name 6 causes of dehydration

A
  • water deprivation
  • extensive perspiration
  • severe diarrhea
  • comatose patient
  • infants
  • random rare “trapped in earthquake”
343
Q

How do you treat dehydration?

A

Water + glucose

344
Q

What is the mechanism of dehydration?

A

decrease volume in both compartments&raquo_space; increase in osmolarity of both compartments, ECF, ICF

345
Q

Outline the movement of water and changes in osmolarity in ECF/ICF when there is a loss of water from ECF.

A

loss of water from ECF&raquo_space; relative increase of solutes in ECF&raquo_space; increase in ECF osmolarity&raquo_space; ICF volume moves to ECF due to osmotic gradient&raquo_space; relative increase in solutes in ICF&raquo_space; increase in ICF osmolarity

346
Q

When would you give a patient an infusion of isotonic salt solution (saline infusion)?

A

If a patient is hypovolemic
— may have similar findings to dehydration
Trauma patients
Bleeding

347
Q

What is the purpose of giving a patient an infusion of isotonic salt solution (saline infusion)?

A

Increase ECF volume

- no increase in osmolarity is because isotonic solutions will not change the number of osmotically active particles

348
Q

What causes gain of water?

A
  1. drinking large amounts of water

2. infusion of fluid for nutritive purposes (glucose solution)

349
Q

In gain of water, how does addition of volume to ECF lead to decrease in ICF osmolarity?

A

Addition of volume to ECF&raquo_space; decrease in ECF osmolarity&raquo_space; while initially in ECF, it moves quickly to ICF b/c permeable cell membrane&raquo_space; decrease in ICF osmolarity

350
Q

What is Gain of Salt and what does it cause?

A

Excessive salt consumption&raquo_space; hypernatremia (elevated plasma sodium)

351
Q

In Gain of Water, what happens to the volume and osmolarity of ECF and ICF?

A

increase in volume of ECF and ICF

decrease osmolarity

352
Q

What is the specific steps in gain of salt that starts with excess NaCl and leads to increased ICF osmolarity

A

Excess NaCl remains in the ECF&raquo_space; ECF osmolarity increases&raquo_space; water moves from ICF to ECF&raquo_space; ECF volume increases & ICF volume decreases&raquo_space; ICF osmolarity increases

353
Q

In Gain of Salt, what happens to the volume and osmolarity of ECF and ICF?

A

Increases ECF volume and osmolarity
Decrease ICF volume
Increase ICF osmolarity

354
Q

What is Loss of salt and what causes it?

A

Hyponatremia (low plasma sodium)

Excess water consumption after sweating

355
Q

What is the specific steps in loss of salt that starts with low NaCl and leads to decreased ICF osmolarity

A

Low NaCl&raquo_space; decrease ECF osmolarity&raquo_space; water moves from ECF to ICF (to balance osmotic pressure)&raquo_space; decrease ECF volume&raquo_space; increase ICF volume&raquo_space; decreased ICF osmolarity

356
Q

In Loss of Salt, what happens to the volume and osmolarity of ECF and ICF?

A

osmolarity decreases overall

357
Q

What is the cause of infusion of isotonic urea?

A

intentional infusion

358
Q

What is the specific steps in infusion of isotonic urea that starts with added urea and leads to no change in osmolarity

A

isotonic urea infusion&raquo_space; increase urea in ECF&raquo_space; readily diffuses in ICF&raquo_space; ICF and ECF volumes increase&raquo_space; isotonic, no change in osmolarity

359
Q

In infusion of isotonic urea, what happens to the volume and osmolarity of ECF and ICF?

A

increase in volume in all compartments

360
Q

Sickle Cell Nephropathy - what 3 conditions in the medulla cause RBCs to sickle?

A 
RBC are prone to sickling in 
- hypoxic
- hypertonic
- acidic
Medulla
361
Q

What is the mechanism of Sickle Cell Nephropathy?

A

medulla become increasingly hypoxic as it descends&raquo_space; deoxygenated HbS sickles&raquo_space; increase polymerization of RBC&raquo_space; vasa recta become attenuated (trait) or absent (SCD)&raquo_space; loss of medullary function&raquo_space; loss of ability to dilute & concentrate urine

362
Q

Primary tumors in the ureter are rare or common?

A

rare

363
Q

What is the cellular origin of benign ureter tumors?

A

mesenchymal origin

364
Q

What are 2 examples of benign primary tumors in the ureter?

A

Fibroepithelial polyps

Leiomyoma

365
Q

What are the malignant ureter tumors called?

A

transitional cell carcinoma (urothelial)

366
Q

Name 2 other places transitional cell carcinoma (urothelial) can be found.

A

renal pelvis

bladder

367
Q

Malignant transitional cell carcinoma rarely appears alone in the ureter. Where do concurrent neoplasms usually exist?

A

bladder
renal calyx
(field effect)

368
Q

What is the greatest risk factor for ureter cancer?

A

smoking

369
Q

What are the odds that a smoker will get urothelial/transitional cell carcinoma?

A

~100% chance, 70s-80s

370
Q

Is the ureter more like an artery or intestines?

A

the ureter is a muscular tube

- active peristaltic contraction

371
Q

What are the 3 cellular layers of the ureter?

A
  • mucosa
  • muscularis (smooth)
  • adventitia
372
Q

What kind of cells line the ureter?

A

transitional epithelium

373
Q

What are intrinsic obstructive lesions of the ureter?

A
  • calculi
  • strictures
  • neoplasms
  • blood clots
  • neurogenic bladder
  • vesiculoureteral reflux
374
Q

What are extrinsic obstructive lesions of the ureter?

A
  • pregnancy
  • preureteral inflammation
  • sclerosing retroperitoneal fibrosis (Rx-induced)
  • endometriosis
  • neoplasm
375
Q

What are the 4 types of cells in transitional epithelium?

A

Basal cells
Intermediate cells
Umbrella cells
basement membrane

376
Q

What are the “replacement” cells in transitional epithelium?

A

Basal cells + intermediate cells

377
Q

What do Umbrella cells do?

A

flatten with bladder filling, contract with emptying

378
Q

What are 7 urinary bladder diseases?

A
  • obstruction of bladder neck
  • diverticula
  • exstrophy
  • urachus
  • cystoceie
  • vesicoureteral reflux
  • neoplasm
379
Q

What do you call a decrease in ureteral lumen?

A

stricture

380
Q

What are 3 causes of ureteral strictures?

A
  • congenital
  • chronic inflammation
  • retroperitoneal fibrosis
381
Q

What can obstructive lesions of the bladder lead to?

A

Hydronephrosis

382
Q

What is the mechanism of hydronephrosis?

A

obstruction&raquo_space; increased pressure upwards toward kidney&raquo_space; dilation of renal pelvis

383
Q

If there is acute obstruction, why is there no change in BUN/creatinine?

A

obstruction causes increase pressure in medulla

– glomeruli are in the cortex

384
Q

What are the lab values in hydronephrosis?

A

normal labs

385
Q

What is neurogenic ureter?

A

interruption of neural pathways to the bladder

386
Q

How does neurogenic ureter disrupt normal urine flow?

A
  • loss of peristaltic function - easier back flow

- lack of force propelling urine to bladder

387
Q

What is the infection associated with virus-associated kidney disease?

A

Hep C

388
Q

What is the Ig associated with virus-associated kidney disease?

A

RF: Ig that binds IgG (most commonly IgM)

389
Q

What is the blood condition associated with virus-associated kidney disease?

A

cyoglobulinemia

390
Q

What are the 3 types of complexes/deposits in virus-associated kidney disease?

A
  • IgM RF (nephrotic)
  • IgG binds HepC particle (nephrotic)
  • IgM RF binds IgG bound to Hep C particle (larger complex too big&raquo_space; nephritic)
391
Q

What’s the clinical presentation of virus-associated kidney disease?

A
  • nephrotic + nephritic = mixed
  • palpable purpura
  • arthralgia
  • asthenia (weak)
  • organ involvement: renal + neuropathy
392
Q

What’s the morphology of virus-associated kidney disease?

A
  • membranoproliferative glomerulonephritis
  • expanded mesangium
  • increased cellularity
  • increase capillary thickness
  • subendothelial deposits
393
Q

What is the etiologies of Chronic TIN?

A
  • NSAIDS, anti-inflammatory
  • infection (vesicoureteral efflux)
  • SLE/Sjogren’s disease
  • secondary to light chain, myeloma, amyloidosis, sarcoidosis
394
Q

What is the progression of chronic TIN?

A

slow onset, gradual decrease in GFR + interstitial fibrosis

395
Q

What are the morphological features of chronic TIN?

A
  • large increase in interstitial fibrosis w/ few inflammatory cells
  • decrease vascularity because decrease volume of capillaries
  • tubular atrophy
  • secondary glomerulosclerosis
396
Q

What does the fibrosis lead to in chronic TIN?

A

increase fibrosis = decrease capillaries = decreased renal function

397
Q

How is UTI and pyelonephritis related?

A

Bacterial infection in the urinary tract&raquo_space; move up&raquo_space; tubular interstitial nephritis

398
Q

What are some common causes of UTI and Pyelonephritis?

A
  • pregnancy (uterus pushes on bladder)
  • instrumentation
  • vesicoureteral reflux
  • female shorter urethra
  • diabetes mellitus
  • immunodeficiency
399
Q

What is the most common cause of UTI and Pyelonephritis?

A
  • bacteria from rectum
400
Q

What is a rare cause of UTI and Pyelonephritis?

A

hematogenous (from blood)

401
Q

If left untreated, what are the complications of UTI and Pyelonephritis?

A
  • pyonephrosis (pus in renal pelvis)
  • perinephric abscess (infection spreads)
  • scar formation (thyroidisation)
  • acute papillary necrosis
402
Q

Which bacteria are associated with UTI and Pyelonephritis, and why?

A

Ecoli, proteus, kelbesiela, enterocacter

– all depends on bacterial adhesion and migration

403
Q

What is the clinical presentation of UTI and Pyelonephritis?

A

< 50 = females, short urethra
> 50 = males, BPH (decrease prostatic fluid)
- bladder is commonly infected (urethritis + cystitis)
- flank pain
- azotemia

404
Q

Compare and contrast the clinical presentation of acute vs. chronic UTI and Pyelonephritis.

A

Acute: suppurative infllammation of pelvic/calyx + parenchyma
- Chronic: scarring, more associated w/ obstructive type; loss of nephrons

405
Q

What is the macro profile of UTI and Pyelonephritis?

A
  • swollen kidneys
  • abscesses common
  • U shaped scarrine
  • hydronephrosis
406
Q

What is the micro profile of UTI and Pyelonephritis?

A
  • interstitial edema
  • increased cells between tubules
  • fibrous tissue and tubules
  • granulomas
407
Q

Name the 4 types of drugs that cause Drug-induced TIN.

A
  • B-Lactams
  • NSAIDSs/Analgesics
  • Aminoglycosides
  • Chinese herb
408
Q

Name the 5 types of Drug-induced TIN.

A
  • B-Lactams: Immunogenic interstitial nephritis from B-lactams (penicillin)
  • NSAIDSs/Analgesics: prolonged administration&raquo_space;phenacetic/acetaminophen toxicity
  • Aminoglycosides: direct cytotoxic effect on IS (rifampin)
  • Balken Endemic Nephropathy (slow) Aristolochic Acid toxicity
  • Chinese Herb nephropathy: (FAST) Aristolochic Acid toxicity
409
Q

Aristolochic Acid toxicity: Balken Endemic Nephropathy vs. Chinese Herb nephropathy. Fast or slow onset?

A

Balken - slow onset, slowly progressive

Chinese - fast onset

410
Q

Aristolochic Acid toxicity: Balken Endemic Nephropathy vs. Chinese Herb nephropathy. Which one is found in weight-reducing diets?

A

Chinese herb nephropathy

411
Q

What are the renal complications associated with Balken Endemic Nephropathy (slow) Aristolochic Acid toxicity?

A
  • renal tubular dysfunction&raquo_space; ESKD

- interstitial inflammation + carcinoma risk

412
Q

What are the clinical manifestations of Aristolochic acid toxicity?

A
  • mild proteinuria (< 1.0 g)
  • hypertension
  • gross hematuria (may be uroepithelial carcinoma)
  • normal urine sediment
413
Q

What causes the reaction in Immunogenic interstitial nephritis from B-lactams (penicillin)?

A
  • not dose dependent
  • Hapten-mediated
  • neoantigen mediated
414
Q

What is the clinical presentation of Immunogenic interstitial nephritis from B-lactams (penicillin)?

A
  • fever, rash, +/- eosinophilia
  • oliguric/non-oliguric renal failure
  • UA: hematuria, pyruria, sub-nephrotic proteinuria, eosinophiluria
  • enlarged kidney + interstitial inflammation
415
Q

What is the micro profile of Immunogenic interstitial nephritis from B-lactams (penicillin)?

A
  • Interstitial edema
  • increased cells between tubules
  • fibrous tissue and tubules
  • granulomas
416
Q

How does NSAIDSs/Analgesics: prolonged administration&raquo_space;phenacetic/acetaminophen toxicity target the kidney?

A
  • Drug accumulates and is highly concentrated in the renal medullary interstitium
417
Q

What is the pathogenesis of NSAIDSs/Analgesics: prolonged administration&raquo_space;phenacetic/acetaminophen toxicity?

A

NSAIDS&raquo_space; direct cellular damage to endothelium
Analgesics&raquo_space; tubular cell damage by oxidative stress
Both&raquo_space; hypoxia&raquo_space; lower PG&raquo_space; increase metabolic need&raquo_space; inflammation + hypoxia

418
Q

What are the clinical presentation for NSAIDSs: prolonged administration&raquo_space;phenacetic/acetaminophen toxicity?

A

NSAIDS:

  • acute impairment of renal function
  • non-nephrotic proteinuria or nephrotic range proteinuria
  • hyperkalemia (tubular dysfunction)
  • can become full nephrotic syndrome (resembles minimal change disease)
419
Q

What are the manifestations of analgesic abuse?

A
  • slow progressive impairment of renal function
  • tubular dysfunction – RTA, hyperkalemia
  • nephrogenic diabetes
  • papillary necrosis
  • uro-epithelia cancer
420
Q

What is the mechanism of Aminoglycosides: direct cytotoxic effect on IS (rifampin)?

A

direct tubular injury&raquo_space; necrosis

421
Q

What is the clinical presention of Aminoglycosides: direct cytotoxic effect on IS (rifampin)?

A
  • increase serum creatinine
  • hypokalemia (unique to this drug associated TIN)
  • renal glucoria
422
Q

Name 2 types of acquired cystic renal diseases.

A
  • simple cyst

- acquired cyst (chronic kidney disease)

423
Q

What is the incidence of simple cysts and is it serious?

A
  • common

- no clinical consequence

424
Q

How do you distinguish cancer from a simple cyst?

A
  • radiographs
425
Q

What are the radiographic features of a simple cyst?

A
  • smooth contours
  • avascular
  • fluid signal (not solid tissue signal)
426
Q

What is the etiology of acquired cysts of the kidney?

A
  • acquired with chronic renal disease&raquo_space; scarring of the kidneys
427
Q

What do you call multiple acquired cysts in the kidney?

A

multicystic

428
Q

multicystic vs. polycystic: distinguishes which origins?

A
  • acquired vs. congenital
429
Q

Name the disease and treatment asociated with acquired cysts.

A
  • end stage renal disease (ESRD)

- chronic dialysis

430
Q

What are the imaging features of acquired cysts?

A
  • hydronephrosis

- shrunken end-stage looking kidney with multiple cysts

431
Q

What is the chromosome affected in autosomal dominant polycystic kidney disease (ADPKD)?

A

ch. 16

432
Q

What are the 2 ch. 16 mutations that cause autosomal dominant polycystic kidney disease (ADPKD)?

A
  • Type 1 = polycystin 1 mutation
  • Type 2 = polycystin 2 mutation
    disease may follow the 2 hit hypothesis
433
Q

Of Type 1 and Type 2 autosomal dominant polycystic kidney disease (ADPKD), which one is more common and which has an earlier presentation?

A

Type 1 is more common, & has an earlier presentation

434
Q

What is the mechanism of autosomal dominant polycystic kidney disease (ADPKD)? What is the function of polycystin?

A

polycystin regulates tubular & vascular develpment in kidney, brain, lung, heart and pancreas

  • after second hit, tubular cells proliferate as benign neoplasm and form their cyst
  • worse w/ AVP (cAMP stimulation)
435
Q

What is the incidence of autosomal dominant polycystic kidney disease (ADPKD)?

A
  • most common form of PKD
  • 1 in 800 = 500,000 cases
  • 10% of dialysis its
  • called Adult PKD b/c presents 30-40s
436
Q

What is the presentation of autosomal dominant polycystic kidney disease (ADPKD)?

A
  • hypertension, hematuria, flank pain, recurrent UTI
  • also affects liver, pancreas, and intestine (compression/mutation)
  • heart valve defect
  • circle of willis aneurysms
437
Q

What is the etiology of autosomal recessive polycystic kidney disease (ARPKD)?

A

PKHD1 gene mutation

438
Q

What is the mechanism of autosomal recessive polycystic kidney disease (ARPKD)?

A

PKHD1 gene mutation&raquo_space; dilation of tubules + proliferation&raquo_space; dilation of tubules&raquo_space; cyst formation

439
Q

What is the epidemiology of autosomal recessive polycystic kidney disease (ARPKD)?

A
  • BABIES die at birth due to giant kidneys compression of lungs
  • 1/20,000
440
Q

Name 3 types of congenital cystic renal diseases.

A
  1. autosomal recessive polycystic kidney disease (ARPKD)
  2. Medullary Cystic Disease
  3. Nephronophthisis-Medullary Cystic Disease
441
Q

What is the etiology of Medullary cystic disease?

A
  • Type 1 = MCKD1 mutation
  • Type 2 = MCKD2 mutation
    Autosomal dominant
442
Q

What is the mechanism of Medullary cystic disease?

A

cysts restricted to medulla

443
Q

What is the presentation of Medullary cystic disease?

A
  • salt wasting
  • polyuria
  • both types are milder than ADPKD
  • seen in children
444
Q

What is the etiology of Nephronophthisis-Medullary Cystic Disease?

A
  • mutation in NPHP 1-5 genes
445
Q

What does the NPHP 1-5 genes do?

A
  • code for nephrocystins = proteins in epithelial cell cilia
446
Q

What is the mechanism of Nephronophthisis-Medullary Cystic Disease?

A

mutated nephrocystins&raquo_space; dysfunctional epithelial cell cilia&raquo_space; ciliary dysfunction

447
Q

What are the four groups/types of Nephronophthisis-Medullary Cystic Disease?

A
  • infantile
  • juvenile (most common)
  • adolescent
  • adult
448
Q

What is the presentation of Nephronophthisis-Medullary Cystic Disease?

A

extra-renal manifestation

  • retinitis pigmentosa
  • interstitial fibrosis
  • mental retardation
  • cerebellar abnormalities
449
Q

What is the histology of Nephronophthisis-Medullary Cystic Disease?

A
  • small kidneys
  • cysts at cortico-medullary junction
  • TIN
  • interstitial fibrosis
450
Q

What are the 4 types/causes of secondary hypertension?

A
  1. Aldosterone excess
  2. Glucocorticoid excess/cushing’s syndrome
  3. Pseudohyperaldosteronism
  4. Gordon’s syndrome
451
Q

What is the basic mechanism of aldosterone excess leading to secondary hypertension?

A

increase aldosterone&raquo_space; increase Na retention&raquo_space; increase vasoconstriction&raquo_space; increase SNS activation&raquo_space; increase BP

452
Q

What is the detailed mechanism of aldosterone excess leading to secondary hypertension?

A
  1. aldosterone acts on renal tubular collecting duct cell
  2. increases ENaC translocation to luminal surface
  3. increase Renin & aldosterone (exception)
  4. high Na will increase lumen negative transepithelial charge &raquo_space; low K+ retention&raquo_space; increased hypokalemia
  5. high K in lumen will provide substrate to alpha-intercalated K/H+ ATPase&raquo_space; high H+ excretion&raquo_space; metabolic alkalosis
453
Q

What is the mechanism of glucocorticoid excess & Cushing’s syndrome?

A

high glucocorticoids&raquo_space; increase activation of aldosterone receptor&raquo_space; high ENaC

454
Q

What is the pathophysiology of glucocorticoid excess & Cushing’s syndrome?

A
  1. Enzyme 11-beta-hydroxy-dehydrogenase 2 exists to prevent glucocorticoids from binding to aldosterone receptors
  2. In cases of excess glucocorticoids (Cushing’s Syndrome), 11-BHD2 is overwhelmed
    - low renin & aldosterone
    - high Na will increase lumen negative transepithelial charge&raquo_space; low K+ retention&raquo_space; hypokalemia
    - high K in lumen will provide substrate to alpha-intercalated K/H+ ATPase&raquo_space; high H+ excretion&raquo_space; metabolic alkalosis
455
Q

What causes 11-beta hydroxy dehydrogenase 2 deficiency?

A

chronic licorice ingestion inhibits 11-BHD2

456
Q

What is the mechanism of 11-beta hydroxy dehydrogenase 2 deficiency?

A

low 11-BHD2&raquo_space; high glucocorticoid activation of aldosterone receptor&raquo_space; high ENaC&raquo_space; high Na reabsorption

457
Q

In 11-beta hydroxy dehydrogenase 2 deficiency, what is the status of:

  • renin
  • aldosterone
  • Na+
  • K+
  • H+
A
  • low renin and aldosterone
  • high Na will increase lumen negative transepithelial charge&raquo_space; low K+ retention&raquo_space; high hypokalemia
  • high K+ in lumen will provide substrate to alpha-intercalated K/H+ ATPase&raquo_space; high H+ excretion&raquo_space; metabolic alkalosis
458
Q

What is the genetic mutation that causes Gordon’s syndrome?

A

Mutation in WNK 4 (regulator of NCCT) or WNK1 (regulator of WNK 4) of NCCT

459
Q

What is the mechanism of Gordon’s Syndrome?

A
  • high Na reabsorption in DCT
  • This is proximal compared to other hyperkalemic diseases, which means you have less delivery of Na to the CD, so no extra excretion of K+
  • hyperkalemia
460
Q

What are the 3 types of acute kidney injury (AKI)?

A
  1. Post-renal
  2. Pre-renal
  3. Intra-renal
461
Q

What are 3 causes of Post-renal AKI?

A

Obstruction of urine flow

  • prostate disease
  • bilateral ureter occlusion from retroperitoneal malignancies
462
Q

What is the presentation of Post-renal AKI?

A
  • voiding complaints

- PE shows distended bladder

463
Q

What do the labs show in Post-renal AKI?

A
  • normal urinalysis

- diagnosed w/ ultrasound (look for dilated calyx)

464
Q

What is the main problem in pre-renal AKI?

A

kidneys are normal, but not enough perfusion

465
Q

What are the common causes of pre-renal AKI?

A 
volume depletion
diuretics
3rd space (burns)
CHF
shock/sepsis
466
Q

What lab values suggest a pre-renal cause of AKI?

  • FeNa
  • Urine Na
  • Urine Osm
A
  • FeNa < 1% = pre-renal
  • Urine Na < 25 = body is compensating for decreased perfusion by inceased Na reabsorption
  • Urine Osm > 500 = compensatory mechanism includes high AVD/ADH&raquo_space; high urine osmolarity
467
Q

What are 3 types/causes of pre-renal AKI?

A
  • Hepatorenal syndrome
  • Bilateral RAS w/ATII and ACE-I
  • NSAID use
468
Q

What condition most commonly leads to hepatorenal syndrome?

A

cirrhosis

469
Q

What is the pathophysiology of hepatorenal syndrome?

A

Portal hypertension&raquo_space; splanchnic vasodilation&raquo_space; low ECFV&raquo_space; increase RAAS&raquo_space; high Na reabsorption + high renal vasoconstriction&raquo_space; hepatorenal syndrome

470
Q

What is the presentation of hepatorenal syndrome?

A

decreased BP despite increased extracellular fluid volume

471
Q

What are the labs for hepatorenal syndrome?

A
  • low urine sodium (<10)
  • volume infusion trial to determine pre-renal
  • rule out other causes (NSAIDS, contrast)
472
Q

What is the basic mechanism of AKI in bilateral RAS w/ATII and ACE-I?

A

bilateral RAS&raquo_space; no autoregulation &raquo_space; collapse of GFR&raquo_space; AKI

473
Q

In bilateral RAS w/ATII and ACE-I, what is the relationship and function of:

  • ACE
  • ATII
  • ACE-1
A
  • ACE allows formation of ATII
  • ATII&raquo_space; vasoconstriction of efferent arteriole to maintain GFR&raquo_space; autoregulation
  • ACE-I inhibits autoregulation
474
Q

What is the mechanism of AKI caused by NSAIDS?

A
  • NSAID use&raquo_space; inhibits autoregulation

- NSAIDS&raquo_space; COX inhibitor&raquo_space; lowers PG production&raquo_space; PG dilates afferent arteriole, so low RPF&raquo_space; AKI

475
Q

What is the presentation of NSAID induced AKI?

A

leads to AKI in patients with volume depletion, CHF, cirrhosis

476
Q

What are the 3 types of intra-renal diseases leading to AKI?

A
  • Acute tubular necrosis
  • AKI from therapeutic agents
  • Acute interstitial nephritis
477
Q

What causes acute interstitial nephritis?

A
  • allergic reaction to penicillins, cephalosporins, sulfonamides, NSAIDS
478
Q

What is the presentation of acute interstitial nephritis?

A

fever, rash, joint pain, increased eosinophils on CBC

479
Q

What does the urine labs show in acute interstitial nephritis?

A

pyuria +/- eosinophils + granulocytes

480
Q

What are the 2 therapeutic agents that cause AKI in AKI from Therapeutic Agents?

A
  • aminoglycosides

- contrast agents

481
Q

What is the mechanism of aminoglycosides causing AKI in AKI from Therapeutic Agents?

A

Aminoglycosides accumulate in proximal tubule cells and inhibit lysosomal function

482
Q

What is the mechanism of Contrast agents causing AKI in AKI from Therapeutic Agents?

A

contrast nephropathy caused by contrast’s direct vasoconstrictive effects and tubular toxicity

483
Q

How do you prevent AKI from Therapeutic Agents?

A
  • aminoglycosides: once daily dosing + monitor
  • contrast: lower amount, avoid closely spaced studies, IV for volume depletion, acetylcysteine
  • Both: avoid other nephrotoxins
484
Q

What are the 2 main types of injury that cause acute tubular necrosis (ATN)?

A

Diffuse ischemia

Toxic injury

485
Q

What 2 main types of injury that causes diffuse ischemia leading to ATN?

A
  • chronic pathological condition
  • —- leading to severe tubular damage and acute renal failure
  • Ischemic injury
  • —- secondary to prolonged pre-renal disease (ischemia)
486
Q

What are 5 examples of injury that causes diffuse ischemia in ATN?

A
  • shock (septemia)
  • hypotension (inadequate RPF)
  • Hypovolemia
  • severe burns
  • pancreatitis
487
Q

What are 8 causes of toxic injury in ATN?

A
  • hemoglobinuria (hemolysis)
  • myoglobinuria
  • heavy metals: mercury, lead
  • organic solvents: chloroform, ethylene glycol
  • drugs: clyclosporine, antibiotics
  • pesticides: paraquat, phenol
  • fungal toxins
  • contrast agents
488
Q

Describe the different parts of the renal tubule affected by ischemia and toxic substances.

A
  • ischemia affects short segments (ATP requiring)

- Toxic substances affect long limbs

489
Q

Is ATN reversible or irreversible, and why or how?

A

ATN is reversible with dialysis and supportive care

- tubular cells will be replaced, but most will be immature and cannot function normally (polyuric)

490
Q

What are the 3 phases of presentation of ATN?

A 
Oliguric phase = severe tubular damage >> less reabsorption >> decreased GFR >> decreased urinary output (prevent hyperkalemia and fluid overload)
Polyuric Phase (1-3 wks later) = tubular cells are replaced w/ immature cells >> cannot reabsorb water >> hypotonic urine (give fluids)
Recovery Phase = tubular cells become differentiated; normal
491
Q

What are the lab values of Urine Na and FeNa in ATN?

A
  • urine Na > 20 – intra-renal dysfunction

- FeNa > 1%

492
Q

What is the macro profile of ATN?

A
  • pale and swollen kidneys

- cortex is paler than medulla

493
Q

What are the urinalysis results for ATN?

A
  • muddy brown granular casts
  • — 100% indicative of intra-renal cause
  • — These are renal tubular epithelial cells that have sloughed off post-ischemic damage and combined with TH proteins&raquo_space; casts
494
Q

TIN vs ATN: what is the difference in urine casts?

A
  • TIN = white blood cell casts

- ATN = muddy brown casts

495
Q

What is the treatment of ATN?

A
  • restore perfusion
  • avoid nephrotoxins (NSAIDS, contrast, ACE-I)
  • Supportive care
496
Q

How does PTH affect Ca levels? P levels?

A

PTH = increases Ca, decreases P

497
Q

How does Calcitriol/Vit.D affect Ca levels? PTH levels?

A

increases Ca, decreases PTH

498
Q

So how does P affect PTH levels?

A

high P&raquo_space; inhibits calcitriol synthesis&raquo_space; inhibiting the inhibitor of PTH&raquo_space; high PTH

499
Q

How does FGF-23 affect calcitriol/Vit.D levels?

A

FGF-23 increases P excretion&raquo_space; lowers calcitriol/Vit.D synthesis

500
Q

How does chronic kidney disease lead to secondary hyperparathyroidism?

A

In CKD, kidney or PTH cannot compensate for excess phosphate&raquo_space; hyperphosphatemia&raquo_space; increased PTH (secondary hyperparathyroidism)

501
Q

How does increased PTH in CKD affect the bones and blood vessels?

A
  • high PTH&raquo_space; high bone turnover = osteogenesis

- Calciphylaxis = calcification of blood vessels and/or ulceration

502
Q

What is the treatment of Ca/P levels in CKD?

A
  • Phosphate binders
  • — Ca based (carbonate, acetate; cause calcification
  • — Sevelamer HCL - great but pricey
  • Lanthanum carbonate
  • — binds P as it is digested out of food
  • — 99.99% excretion
503
Q

What are 3 types of benign renal tumors?

A

Renal adenoma
Angiomylolipoma
Oncocytoma

504
Q

What are the major characteristics of a renal adenoma?

  • is it benign or metastatic?
  • what does the adenoma look like?
A
  • low metastatic potential
  • commonly associated with papillary structures
  • finger-like projections with fibrous core
505
Q

What is another name for angiomylolipoma?

A

benign harmatoma

506
Q

Why are benign harmatomas called angiomyolipoma?

A

it is composed of smooth muscle, adipose tissue and vessels

  • angio = vessels
  • myo = muscle
  • lipoma = fat
507
Q

What are the major characteristics of benighn harmatomas (angiomyolipoma)?

  • is it benign or metastatic?
  • what does the harmatoma look like?
A
  • nearly 100% benign
  • can be pre or post-renal
  • harmatoma: tissue growth of cells that are normally there, just disorganized
508
Q

Where in the body are Oncocytomas found?

A

Benign tumor of kidney, thyroid, URI

509
Q

What kind of cells are oncocytomas composed of?

A

large epithelial cells with abundant mitochondria

510
Q

Is oncocytoma benign or malignant?

A

90% benign

  • 3 histological grades
  • grade III = malignant carcinoma
511
Q

Name 5 malignant renal tumors

A
  • Clear cell carcinoma
  • chromophobe renal carcinoma
  • papillary renal cell carcinoma
  • Wilm’s tumor (nephroblastoma)
  • Transitional cell carcinoma
512
Q

What is the basic cause of clear cell carcinoma?

A

Abnormal von Hippel-Lindau (VHL) gene

513
Q

What are the genetic mutations associated with sporadic causes of clear cell carcinoma?

A
  • del(3)

- t(3;6), t(3;8), t(3;11)

514
Q

Describe what happens to VHL in the hereditary form of clear cell carcinoma.

A
  • loss of VHL

- mutated + inactivated + methylated VHL

515
Q

In the hereditary form of renal clear cell carcinoma, where are masses found?

A

familial cases have multiple masses bilaterally

516
Q

How common is clear cell carcinoma?

A
  • 80% of all renal cancers

- 2% of all adult cancers

517
Q

What is the prognosis of clear cell carcinoma?

A
  • High mortality (hematuria seen too late)

- not an aggressive cancer

518
Q

What is the presentation of renal clear cell carcinoma?

A 
60-70 y/o, smoking, obesity, HTN, high Ca, hematuria, flank pain
- May have paraneoplastic syndromes
Hypercalcemia
Hypertension
Polycythemia (EPO)
Cushing's syndrome (glucocorticoids)
519
Q

What is the macroscopic profile of clear cell carcinoma?

A

necrosis
hemorrhage
pseudocapsule

520
Q

What is the microscopic profile of clear cell carcinoma?

A

cells are not anaplastic

Oil-red O stain reveals lipid vesicles

521
Q

What is the etiology of Chromophobe Renal carcinoma?

A

Hypodiploidy - loss of multiple chromosomes

- chromosomes lost: 1,2,6,10,13,17,21

522
Q

How common is Chromophobe Renal carcinoma?

A

Rare (5% of all renal cancers)

523
Q

What is the prognosis of Chromophobe Renal carcinoma?

A

it has a better prognosis than clear cell carcinoma

524
Q

What is the histology of Chromophobe Renal carcinoma?

A
  • cells have eosinophilic cytoplasm (not clear)
  • variability in size
  • cells have distinct membranes
525
Q

What is the basic etiology of Papillary Renal Cell Carcinoma?

A

activated or mutated MET oncogene

526
Q

What are the genetic mutations that cause sporadic Papillary Renal Cell Carcinoma?

A
  • Trisomy 7, 16, 17 (mutated/activated MET)
  • Loss of Y
  • t(X;1)&raquo_space; PRCC oncogenes
527
Q

What is the genetic profile of Papillary Renal Cell Carcinoma?

A
  • Trisomy 7

- familial cases have multiple masses bilaterally

528
Q

What is the prevalence of Papillary Renal Cell Carcinoma?

A

10-15% if all cancers

529
Q

What is the presentation of Papillary Renal Cell Carcinoma?

A

hematuria
tobacco use
cystic renal disease
analgesic nephropathy

530
Q

What is the macro characteristics of Papillary Renal Cell Carcinoma?

A
  • pseudocapsule indicating slow growth
  • Hemorrhage and necrosis
  • — these occur because tumor outgrows vascular size
531
Q

What is the micro characteristics of Papillary Renal Cell Carcinoma?

A
  • Finger-like projections w/ fibrous core
  • fibrovascular core
  • eosinophilic cytoplasm
  • overlap with benign papillary tumors
  • vimentin and cytokeritin +
532
Q

What gene is mutated in Wilm’s tumor (nephroblastoma)?

A

mutated WT1 (tumor suppressor gene - Ch.11)

533
Q

How common is Wilm’s tumor (nephroblastoma)?

A

3rd most common cancer in children

534
Q

What is the prognosis of Wilm’s tumor (nephroblastoma)?

A

90% cure rate with proper St. Jude therapy

535
Q

What cell makes up Wilm’s tumor (nephroblastoma)?

A

Arises from pluripotent metanephric cells

  • kidney comes from mesenchymal cells
  • many cell types are found in Wilm’s tumor
536
Q

What is the clinical presentation of Wilm’s tumor (nephroblastoma)?

A

abdominal mass +/- hematuria, neonatal colic, < 4 yo

537
Q

What is the macro profile of Wilm’s tumor (nephroblastoma)?

A

typically large, round, fleshy white appearance

538
Q

What is the micro profile of Wilm’s tumor (nephroblastoma)?

A

many cell types b/c pluripotent origin

  • primitive cells = metanephric blastema
  • immature glomerular structures
  • epithelial tubules
  • spindle stromal/striated muscle
  • +/- cartilage, osteoid, neural tissues, sq. epith.
539
Q

Where in the urinary tract is transitional cell carcinoma found?

A

neoplasm of urothelium lining renal pelvis and lower tract

- may spread down the urinary tract by seeding

540
Q

How do stones/calculi affect transitional cells?

A

transitional cell&raquo_space; squamous cell (metaplasia) in the presence of stones/calculi

541
Q

What is the clinical presentation of Transitional cell carcinoma?

A

hematuria is seen early

smokers

542
Q

What is the mechanism of Acute TIN?

A

rapid onset; rapid decrease in GFR + interstitial edema&raquo_space; decrease ccn of urine&raquo_space; medullary/ papillary damage

543
Q

What care the 2 types of injury in Acute TIN?

A

proximal tubule injury

distal tubule injury

544
Q

What are 3 causes of proximal tubule injury in acute TIN?

A
  • antibiotics
  • multiple myeloma
  • analgesics/NSAIDs
545
Q

What does Acute TIN cause in the proximal tubule?

A

decrease reabsorption of Na, AA, glucose, etc.

546
Q

What are the 3 causes of Acute TIN affecting the distal tubule?

A

Antibiotics
immunologic disorders
analgesics/NSAIDs

547
Q

What does Acute TIN cause in the distal tubule?

A

decrease reabsorption of Na

decrease secretion of K+/H+

548
Q

What are the morphological features of Acute TIN?

A
  • increase interstitial volume from inflammatory mononuclear cell infiltration (lymphocytes, plasma, macrophages, +/- eosinophils)
  • epithelial BM disrupted, epithelial cell necrosis
549
Q

What are 4 important drugs/poisons to associate with Acute TIN and how would you detect each?

A
  • Indinavir (anti-HIV) - calcium oxalate crystals
  • Phenoytin - ppt in urine
  • Rifampin - HPTN, flank pain
  • Lead - anemia

Renal Pathology (1 decks)

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