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GU / GYN & Renal > B&B Renal: Nephron Disorders > Flashcards

B&B Renal: Nephron Disorders Flashcards

1
Q

Capillary Endothelium

Structure & Function

A
  • 1st barrier to filtration
  • Fenestrated –> only small (<40 nm) particles pass through
  • Repels RBCs, WBCs, platelets
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2
Q

Glomerular Basement Membrane (GBM)

Structure & Function

A
  • Composed of negatively charged molecules
    * Type IV collegen
    * Heparan sulfate (-)
  • Repels (-) molecules (e.g., albumin)
  • Also a size barrier: only small (<4 nm) molecules pass through
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3
Q

Podocytes

Structure & Function

A
  • Epithelial cells
  • Long foot process wrap around capillaries
  • Slits between foot processes filter blood
    * Further size barrier: only very small molecules pass through
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4
Q

Glomerular Diseases

Features

A

Characterized by breakdown of filtration barrier components
* Results in aberrant filtration of particles
* Findings: RBCs, proteins (albumin) in urine

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5
Q

Hematuria

Diagnosis

A
  • Urinalysis
  • Dipstick: test for presence of heme
    * Heme has peroxidase activity –> reacts with strip
    * Heme positive = hemoglobin or myoglobin
  • Microscopy: RBCs visualized
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6
Q

Glomerular Bleeding

Hematuria

A
  • RBC casts: RBCs aggregate in nephron once they squeeze past damaged filtration barrier
  • Dysmorphic RBCs: abnormally shaped RBCs resulting from squeezing past damaged filtration barrier
  • Acanthocytes: RBCs with spiked cell membrane
  • Proteinuria
  • Urine appearance: red, smoky brown
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7
Q

Proteinuria

Diagnosis

A
  • Urine dipstick
    • Color change indicates amount of protein
    • Primarily detects albumin (helpful for glomerular disease)
      * Glomerular disease: usually 4+ protein
    • Affected by urine concentration
      * Dehydration can increase concentration of normal amount of protein and produce false-positive
  • Urine protein-to-creatinine ratio: “spot urine”
    • 1st or 2nd morning urine sample after avoiding exercise
    • Normal ratio: < 0.2 mg/mng
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8
Q

Gold Standard Test for Proteinuria

Diagnosis

A

24-hour urine collection
* Measures grams/day of protein excretion
* Normal: <150 mg/day
* Disadvantages:
* Cumbersome for patients
* Errors in collection are common

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9
Q

Glomerular Disease Spectrum

A

Spectrum of diseases ranging from nephritic to nephrotic
* Nephritic syndrome
* RBC casts
* Mild proteinuria
* Renal failure
* Nephrotic syndrome
* Massive proteinuria
* Hyperlipidemia

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10
Q

Nephrotic Syndrome

Glomerular Diseases

A

Loss of protein filtration barrier (GBM)
* RBC filtration barrier remains intact
* Massive proteinuria
* Dipstick: 4+
* 24-hr urine: >3.5 g/day
* Triggers pathological cascade

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11
Q
  • Proteinuria / Frothy urine
  • Edema
  • Hyperlipidemia
  • Fatty casts / Oval fat bodies
  • Thrombosis
  • Recurrent infections

Clinical Features

A

Nephrotic Syndrome

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12
Q

Proteinuria

Nephrotic Syndrome

A

Loss of GBM results in filtration of proteins into urine
* Appearance: frothy urine

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13
Q

Edema

Nephrotic Syndrome

A
  • Loss of GBM results in loss of serum proteins via filtration into urine
  • Loss of serum albumin lowers plasma oncotic pressure
    • Low plasma oncotic pressure decreases ECV & GFR
      * Low ECV & GFR activate RAAS increasing Na+ / H2O retention & plasma hydrostatic pressure
    • Low plasma oncotic pressure results in edema via osmotic diffusion of H2O into interstitium
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14
Q

Hyperlipidemia

Nephrotic Syndrome

A
  • Loss of GBM results in loss of serum proteins via filtration into urine
  • Low serum albumin increases liver metabolic activity
  • Increased fatty acid production by liver causes hyperlipidemia
    • Serum lipids are filitered into urine producing fatty casts & oval fat bodies
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15
Q

Thrombosis

Nephrotic Syndrome

A
  • Loss of GBM results in loss of serum proteins via filtration into urine
  • Low antithrombin III (clotting factor) increases risk of thrombosis

Hypercoagulable state

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16
Q

Infections

Nephrotic Syndrome

A
  • Loss of GBM results in loss of serum proteins via filtration into urine
  • Loss of immunoglobulins increases risk of infections
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17
Q

Urine

Nephrotic Syndrome

A

Urinary lipid may be present

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18
Q

Urine

Nephrotic Syndrome

A

Urinary lipid may be present
* Can be trapped in casts: fatty casts
* Can be enclosed by plasma membrane of degenerative epithelial cells (oval fat bodies)
* Under polarized light: “Maltese cross” appearance

Maltese cross = characteristic finding

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19
Q
  • Frothy urine
  • Swelling of ankles
  • Periorbital edema
  • Often mistaken for allergic reaction
  • Serum total cholesterol: >300 mg/dL
  • Proteinuria: >3.5 mg/day

Classic Presentation

A

Nephrotic Damage

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20
Q

Nephritic Syndrome

Glomerular Disease

A

Inflammatory process damages entire glomeruli and results in loss of both RBC & protein filtration barriers
* Glomerular damage: decreased GFR
* RBCs in urine: RBC casts, dysmorphic DBCs
* Protein in urine: <3.5 g/day
* Less than nephrotic syndrome due to lower GFR

Nephritic = nephritis; inflammatory

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21
Q
  • Proteinuria
  • Oliguria
  • Edema
  • Hypertension
  • Increased BUN / Cr ratio
  • RBC casts & dysmorphic RBCs

Clinical Features

A

Nephritic Syndrome

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22
Q

Proteinuria

Nephritic Syndrome

A

Loss of GBM results in filtration of proteins into urine

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23
Q

RBC Casts, Dysmorphic RBCs

Nephritic Syndrome

A

Damaged capillary endothelium results in filtration of RBCs into urine

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24
Q

Oliguria

A

Decreased GFR due to glomerular damage
* Decreased urine production results in oliguria

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25
Q

Increased BUN / Cr Ratio

Nephritic Syndrome

A

Glomerular damage results in increased BUN / Cr ratio

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26
Q

Hypertension

A

Decreased GFR due to glomerular damage results in increased plasma hydrostatic pressure

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27
Q

Edema

Nephritic Syndrome

A
  • Decreased GFR due to glomerular damage results in increased plasma hydrostatic pressure
  • Increased hydrostatic pressure drives fluid into extracellular space
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28
Q
  • Dark urine (due to RBCs)
  • Swellnig / edema
  • Fatigue (due to uremia)
  • Proteinuria: <3.5 g/day

Presentation

A

Nephritic Syndrome

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29
Q
  • Dark urine (due to RBCs)
  • Swellnig / edema
  • Fatigue (due to uremia)
  • Proteinuria: <3.5 g/day

Presentation

A

Nephritic Syndrome

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30
Q

Sites of Glomerular Injury

Nephritic/Nephrotic

A

Major determinant of whether a disease process leads to nephritic or nephrotic syndrome is the site of injury
* Podocyte injury –> nephrotic syndrome
* Podocytes are separated from blood by GBM
* Injury does not lead to inflammation
* Results in loss of protein in urine only
* Endothelial & mesangial cells –> nephritic syndrome
* Cells are exposed to blood elements
* Injury causes inflammation (nephritis)
* Influx of inflammatory cells
* Results in loss of RBCs & protein in urine

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31
Q
  1. Post-streptococcal glomerulonephritis
  2. Berger’s (IgA) nephropathy
  3. Diffuse proliferative glomerulonephritis
  4. Rapidly progressive glomerulonephritis (RPGN)
  5. Alport syndrome
  6. Membranoproliferative glomerulonephritis

Etiology

A

Nephritic Syndrome

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32
Q

Post-Streptococcal GN

Etiology

A
  • Occurs following group A strep infection
    • Impetigo (skin)
    • Pharyngitis
  • Nephritogenic strains of GAS carry specific subtypes of M protein virulence factor
  • Immune complex deposit in glomeruli
    * Circulating ATG-AB complexes
    * In situ immune complex formation
  • Complexes fix complement & attract PMNs
    * Inflammatory response –> nephritic syndrome
    * Response depletes serum complement levels, results in hypocomplementemia
    * Also seen in SLE nephritis, MPGN
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33
Q
  • Child
  • Nephritic syndrome
  • 2-3 weeks following strep throat infection (pharyngitis)

Classic Case

A

Post-Streptococcal GN
* Takes 2-3 weeks for antibodies / immune complexes to form and deposit in kidneys

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34
Q
  • LM: enlarged, hypercellular glomeruli
  • Granular IF: stained for IgG, C3
  • EM: subepithelial “humps”

Microscopy

A

Post-Streptococcal GN

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35
Q

Post-Streptococcal GN

Prognosis

A

Depends on age
* Children: good prognosis
* 95% recover completely
* Adults: moderate prognosis
* About 60% recover
* Patients at risk for renal insufficiency
* Can occur decades after initial illness
* Patients at risk of RPGN

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36
Q

Most common form of glomerulonephritis worldwide

Epidemiology

A

IgA Nephropathy / Berger’s Disease

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37
Q

IgA Nephropathy / Berger’s Disease

A
  • Overactive immune system resulting in IgA overproduction in response to triggers
    • Respiratory infection
    • GI infection
  • IgA immune complex deposit in mesangium
    * Disease processes involving mesangium will trigger inflammation in glomeruli
    * IgA complexes activate complement via alternative & lectin pathways
    * No hypocomplementemia
  • Results in glomerular injury
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38
Q

Granular IF: stained for IgA

Microscopy

A

IgA Nephropathy / Berger’s Disease

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39
Q
  • Recurrent episodes of hematuria since childhood
  • Episodes follow URI or diarrheal illness
  • Slow decline in renal function (BUN/Cr) over time
  • Possible progression to ESRD & dialysis (>20 yrs)

Classic Case

A

IgA Nephropathy / Berger’s Disease

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40
Q

Most common childhood systemic vasculitis

Epidemiology

A

Henoch-Schonlein Purpura

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41
Q

IgA nephropathy with extra-renal involvement
* Diffuse IgA deposition
* Tissue biopsy: demonstrates IgA
* Skin: palpable purpura on buttocks, legs
* GI: abdominal pain; melena
* Joints: arthritis

A

Henoch-Schonlein Purpura

Nephritic Syndrome

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42
Q

Diffuse Proliferative GN (DPGN)

Nephritic Syndrome

A
  • Most common & severe subtype of SLE renal disease
    • Type IV Lupus Nephritis
    • Often presents with other SLE features:
      • Fever
      • Rash
      • Arthritis
  • Diffuse: > 50% of glomeruli are affected
    * < 50%: focal
  • Proliferative: increased glomerular cellularity
    • Endotheial & mesangial cell prolfieration
    • Monocyte / PMN infiltration
  • Immune complex deposition in glomeruli
    • Subendoethelial deposits trigger inflammatory response
    • Immune complexes are formed by anti-dsDNA Abs & other SLE Abs
    • ICs activate complement –> hypocomplementemia
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43
Q
  • LM: thickened capillary loops (“wire looping”)
  • Granular IF: stained for IgG, IgA, IgM, C3, or C1q
    * “Full house” pattern

Microscopy

A

Diffuse Proliferative GN
- Wire looping = classic finding

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44
Q
  • Mixed clinical presentation
    • Proteinuria (sometimes nephrotic)
    • Hematuria
    • Reduced GFR
  • Severe, often leads to ESRD

Presentation

A

Diffuse Proliferative GN

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45
Q

Rapidly Progressive GN (RPGN)

A
  • Hallmark = presence of crescents within glomeruli
    • Also called “crescentic” GN
  • Crescents formed by inflammation:
    * Monocytes / macrophages
    * Fibrin
  • Pathologic description, not a cause of glomerulonephritis
    * Common pattern of inflammation that results from various diseases
  • Severe form of glomerulonephritis
    • Progressive loss of renal function
    • Rapid onset; often presents as acute renal failure
    • Non-specific symptoms: fatigue, anorexia, etc.
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46
Q

RPGN

Diagnosis

A

Causes are distinguished based on immunofluoresence
* Type I: Linear IF
* Type II: Granular IF
* Type III: Negative IF

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47
Q

Antibody-mediated destruction of GBM
* Type II HSR: autoimmune production of anti-GBM Abs
* Linear IF: linear patter of IgG antibodies

RPGN

A

Type I RPGN

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48
Q
  • Caused by production of anti-collagen antibodies
    • Antibodies to alpha-3 chain of type IV collagen
    • Found in GBM & alveoli
  • Presentation: hemoptysis & nephritic syndrome
    • Typically in young adult male

Type I RPGN

A

Goodpasture’s Syndrome

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49
Q

Immune complex deposition
* Type III HSR
* Granular IF: “lumpy bumpy” appearance

RPGN

A

RPGN Type II

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50
Q

Immune complex kidney disorders

RPGN Type II

A
  • Post-streptococcal GN
    • Can progress to RPGN
  • Diffuse proliferative GN (type IV SLE nephritis)
    • Can progress to RPGN
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51
Q

Most common cause of rapidly progressive GN

Epidemiology

A

Post-Streptococcal GN

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52
Q
  • Negative IF: no staining for IgG, IgA, etc.
    • “Pauci-immune” pattern
  • Most patients are ANCA-positive
    • c-ANCA or p-ANCA
  • Most patients have a vasculitic syndrome

RPGN

A

RPGN Type III

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53
Q

ANCA Diseases

RPGN Type III

A

All can lead to pauci-immune nephritis
1. Wegener’s Granulomatosis: c-ANCA
2. Microscopic Polyangiitis: p-ANCA
3. Churg-Strauss Syndrome: p-ANCA

ANCA: anti-neutrophil cytoplasmic antibodies

54
Q

Alport Syndrome

Nephritic Syndrome

A

Hereditary Nephritis
* Genetic type IV collage defect
* Mutations in alpha-3, alpha-4, or alpha-5 chains
* Chains found in basement membranes of the kidneys, eyes, ears
* Inheritance: X-linked
* Classic triad:
* Hematuria
* Hearing loss
* Ocular disturbances

55
Q

Disruption of podocytes / GBM; capillary endothelium is intact
1. Minimal change disease <— cytokines
2. FSGS <— podocyte damage
3. Membranous nephropathy <— immune complexes
4. Diabetic nephropathy <— glucose
5. Amyloidosis <— amyloid
6. Membranoproliferative glomerulonephritis

Etiology

A

Nephrotic Syndrome

FSGS: focal segmental glomerulosclerosis

56
Q

Effacement (flattening) of podocyte foot processes
* Loss of GBM anion charge barrier
* Effacement of podocytes impairs function
* Inflammation triggered by cytokines damages podocytes
* Usually idiopathic
* Associated with Hodgkin Lymphoma
* May involve immunological trigger days before onset
* Viral infection (URI)
* Allergic reaction
* Recent immunization
* Presents as “selective” proteinuria
* Only albumin in urine, not immunoglobulins

Nephrotic Syndrome

A

Minimal Change Disease

Selective proteinuria = distinctive feature

57
Q

EM: effacement of foot processes

Microscopy

A

Minimal Change Disease

58
Q

Most common cause of nephrotic syndrome in children

Epidemiology

A

Minimal Change Disease

59
Q

Minimal Change Disease

Prognosis & Treatment

A
  • Responds well to steroids
    • Disease mediated by cytokines
    • Steroids are anti-inflammatory agents
  • Favorable prognosis

Prognosis & treatment are unique among nephrotic syndromes

60
Q

Focal Segmental Glomerulosclerosis (FSGS)

Nephrotic Syndrome

A
  • Glomerulosclerosis: pink/dense glomerular deposition of collagen
  • Segmental: only portion of glomerulus is involved
  • Focal: only some glomeruli are involved

Features

61
Q

Involves GBM & podocytes, but not capillary endothelium
* LM: focal, segmental sclerotic lesions
* Collapse of basement membranes
* Hyaline deposition (hyalinosis)
* IF: usually negative (no ICs)
* Sometimes IgM, C3, C1 (non-specific
* EM: effacement of foot processes

Microscopy

A

FSGS

62
Q

Most common cause of nephrotic syndrome in African-Americans

Epidemiology

A

FSGS

63
Q

FSGS

Epidemiology

A
  • Often progresses to chronic renal failure
    • 40-60% within 10-20 years
  • Severe form of Minimal Change Disease
    • Does not respond to steroids
  • Usually idiopathic (primary)
64
Q

FSGS

Associations

A
  • HIV
  • Sickle cell patients
  • Heroin users
  • Morbid obesity
  • Interferon treatment
    • Used to treat HCV & HBV
    • Some leukemias & lymphomas, melanoma
  • Loss of nephrons
    • Congenital single kidney
    • Surgical kidney removal
65
Q

FSGS

Associations

A
  • HIV
  • Sickle cell patients
  • Heroin users
  • Morbid obesity
  • Interferon treatment
    • Used to treat HCV & HBV
    • Some leukemias & lymphomas, melanoma
  • Loss of nephrons
    • Congenital single kidney
    • Surgical kidney removal
66
Q

Thick GBM w/o hypercellularity
* Thickening occurs due to immune complex deposition
* Caused by production of anti-PLA2R autoantibodies
* PLA2R is expressed on podocytes
* Typically idiopathic

Nephrotic Syndrome

A

Membranous Nephropathy
“Membranous” = thick membrane

PLA2R: phospholipase A2 receptor

67
Q
  • LM: thickening of capillary/GBM interface
    • “Spike & dome” membrane with silver stain
  • Granular IF: stained for IgG, C3
  • EM: supepithelial deposits; “electron-dense” deposits

Microscopy

A

Membranous Nephropathy

Characteristic finding: “electron-dense” deposits; “spike & dome”

68
Q

Membranous Nephropathy

Secondary Causes

A
  • SLE
    * Most lupus nephropathy is nephritic: DPGN
    * 10-15% of SLE patients develop nephrotic syndrome via membranous nephropathy
  • Solid tumors
    • Clon canxer
    • Lung cancer
    • Melanoma
  • Infections
    * HBV
    * HCV
  • Rheumatoid arthritis drugs
    * Penicillamine
    * Gold
    * NAIDs
69
Q

Most common nephrotic syndrome in adults

Epidemiology

A

Membranous Nepropathy

Caucasians > African-Americans

70
Q

Membranous Nephropathy

Prognosis

A

Depends on age
* Children: excellent prognosis
* Adults: may progress to ESRD

71
Q

Autoimmune Nephropathy

A
  • Most autoantibody-mediated disorders are nephritic
    • Auto-Abs form ICs & trigger inflammation
    • Nephritis –> nephritic syndrome
  • Membranous nephropathy is nephrotic
    • Subendothelial deposits –> podocyte disruption
      • No inflammatory response
    • Nephrotic syndrome
72
Q

Non-enzymatic glycosylation of GBM results in protein leakage
* Long-term effect: glomerulosclerosus
* Proteinuria
* Can progress to nephrotic syndrome

Nephrotic Syndromes

A

Diabetic Nephropathy

73
Q

Extracellular buildup of amyloid proteins
* Classic histological findings:
* Congo red stain: positive
* Apple-green birefringence

Nephrotic Syndromes

A

Amyloidosis

74
Q

Most commonly involved organ in systemic amyloidosis

Epidemiology

A

Kidneys

75
Q

Membranoproliferative GN (MPGN)

Nephritic / Nephrotic

A
  • Rare glomerular disorders
  • Can cause nephritic or nephrotic syndromes
  • Result in varying degrees of renal dysfunction
    • Proteinuria: +/- nephrotic rane
    • Hematuria
    • Renal failure: elevated BUN/Cr
76
Q

MPGN

Features

A

Thick GBM & hypercellular
* * “Membrano-“ = thick membrane
* Proliferative = proliferation of mesangial cells & matrix

77
Q

MPGN

Features

A

Thick GBM & hypercellular
* * “Membrano-“ = thick membrane
* Proliferative = proliferation of mesangial cells & matrix

78
Q

Subendoethelial IC deposition
* IgG –> complement activation
* Induces inflammation
* IC deposits trigger mesangial ingrowth
* Mesangium splits BM

MPGN

A

MPGN Type I

79
Q
  • LM: “tram track” appearance; common (80%)
    • “Tram track” = split GBM
  • Glandular IF: stained for IgG, C3
    • Subendothelial antibodies / immune complexes

Microscopy

A

MPGN Type I

80
Q

Assoiated with HBV & HCV infection

Etiology

A

MPGN Type I

81
Q

“Electron dense” deposits within GBM
* Mediated by complement overactivation
* IgG usually absent

MPGN

A

MPGN Type II

Dense Deposit Disease

82
Q

“Electron dense” deposits within GBM
* Mediated by complement overactivation
* IgG usually absent

MPGN

A

MPGN Type II

Dense Deposit Disease

83
Q

IF: stains for C3, not IgG

Microscopy

A

MPGN Type II

84
Q

IF: stains for C3, not IgG

Microscopy

A

MPGN Type II

85
Q

C3 Nephritic Factor (C3NF)

MPGN Type II

A

C3 Convertase Stabiliing Antibody
* Found in >80% of patients with MPGN Type II
* Overactivation of complement system
* C3 convertase activates alternative pathway
* Convertase is stabilized by C3NF
* Results in hypocomplementemia: low C3

86
Q

C3 Nephritic Factor (C3NF)

MPGN Type II

A

C3 Convertase Stabiliing Antibody
* Found in >80% of patients with MPGN Type II
* Overactivation of complement system
* C3 convertase activates alternative pathway
* Convertase is stabilized by C3NF
* Results in hypocomplementemia: low serum C3

87
Q

MPGN Type II

Epidemiology

A
  • Primarily affects children
    • Usually between ages 5-15
  • 50% develop ESRD within 10 years
88
Q

Summary

A

MPGN Type I

89
Q
  • Pathology: immune complexes
  • Location: subendothelium
  • Microscopy: tram tracks (LM)
  • Associations: hepatits (HBV, HCV)

Summary

A

MPGN Type I

90
Q
  • Pathology: complement (C3)
  • Location: GBM
  • Microscopy: dense deposits (EM)
  • Associations: children

Summary

A

MPGN Type II

91
Q

Acute Kidney Injury (AKI)

Tubulointerstitial Diseases

A

Acute fall in GFR
* Rise in serum BUN & creatinine
* Usually reversible
* Comon problem in hospitalized patients

92
Q
  1. Poor renal perfusion
  2. Acute tubular necrosis

Etiology

A

AKI

93
Q
  1. Ischemia
  2. Drugs
  3. Toxins

AKI

A

Acute Tubular Necrosis (ATN)

94
Q

Ischemia –> vasoconstriction –> decreased GFR
* Ischemia results in loss of tubular cell polarity
* Na+/K+-ATPase migrates to apical membrane
* Pumps Na+ from cells into urine
* Macula densa senses increased urinary [Na]
* MD induces vasoconstriction of afferent arterioles

ATN

A

Ischemic ATN

Affects proximal tubule, TAL

95
Q

Causes of decreased renal perfusion
1. Hypovolemia
2. Cardiogenic shock
3. Massive hemorrhage

Etiology

A

Ischemic ATN

96
Q

Toxin / Drug-Induced ATN

Etiology

A
  1. Aminoglycosides
  2. Contrast dye (i.e., for CT scans)
  3. Uric acid (tumor lysis syndrome)
  4. Myoglobin (rhabdomyolysis)
  5. Lead
  6. Cisplatin
  7. Ethylene glycol (antifreeze)

Affects proximal tubule

97
Q

ATN

Pathology

A

Sudden damage to tubular epithelial cells
* Tubular epithelial cells necrosis –> cells shed into urine
* Patchy, focal necrosis of nephron
* Epithelial cells form casts in urine
* Granular / “muddy brown” casts
* Casts occlude tubular lumen
* Urinary obstruction –> intrinsic renal failure
* GFR falls
* BUN & Cr rise

98
Q

ATN

Disease Course

A
  • Phase 1: Injury
    • Slight decline in urine output
  • Phase 2: Maintenance
    • Longest phase: may last weeks
      * Rising BUN / Cr
    • Oliguria
    • Hyperkalemia –> can be fatal if severe
    • AG metabolic acidosis
  • Phase 3: Recovery
    • Polyuria
    • Hypokalemia
99
Q

Acute Interstitial Nephritis

Tubulointerstitial Diseases

A

Inflammation of renal tubules & interstitium
* Caused by Type I HSR (allergic reaction)
* Mediated by eosinophils & neutrophils
* Main clinical feature: intrinsic renal failure
* No nephritic / nephrotic syndrome
* Usually resolves with removal of offending agent
* Rarely progresses to papillary necrosis

100
Q
  • Drugs: 75% of cases
    • Sulfonamides: TMP-SMX
    • Rifampin
    • Penicillin
    • Diuretics: loop, TZ
    • NSAIDs
  • Infections: 5-10% of cases
    • Legionella
    • Leptospira
    • CMV
    • TB
  • Systemic disease: 5-10% of cases
    • Sarcoidosis
    • Sjögren’s syndrome
    • SLE

Etiology

A

Acute Interstital Nephritis

Drugs act as haptens; bind to BM / epithelium & illicit immune response

101
Q
  • Prior exposure to trigger
  • Sx: fever, rash, malaise
  • Urine: WBC casts; eosinophilia
    • Sterile pyuria: WBCs w/o symptoms of cystitis
  • Blood: increased BUN / Cr; peripheral eosinophilia
    • ARF: increased BUN / Cr

Presentation

A

Acute Interstitial Nephritis

102
Q

Chronic Interstital Nephritis

Tubulointerstital Diseases

A

Mononuclear cell infiltration leads to fibrosis & atrophy of tubules
* Seen with longstanding NSAID use
* Presents with mild elevation of BUN / Cr
* Resolves with discontinuation of drugs

103
Q

NSAID Nephrotoxicity

Tubulointerstitial Diseases

A
  • Acute interstitial nephritis: fever, renal failure
  • Chronic interstitial nephritis: renal failure
  • ATN:
    • Blocks PG vasodilation of afferent arteriole
    • Results in ischemia
  • Membranous GN: nephrotic syndrome
  • Papillary necrosis
104
Q

NSAID Nephrotoxicity

Tubulointerstitial Diseases

A
  • Acute interstitial nephritis: fever, renal failure
  • Chronic interstitial nephritis: renal failure
  • ATN:
    • Blocks PG vasodilation of afferent arteriole
    • Results in ischemia
  • Membranous GN: nephrotic syndrome
  • Papillary necrosis
105
Q

Coagulative necrosis of renal papillae
* Sloughing of tissue
* Gross hematuria
* May obstruct urine flow
* Often painless
* In isolation, does not cause intrinsic renal failure or produce WBC casts

Tubulointerstitial Diseases

A

Papillary Necrosis

106
Q
  1. Chronice phenacetin use
  2. Diabetes
  3. Acute pyelonephritis
  4. Sickle cell anemia

Etiology

A

Papillary Necrosis

107
Q

Cortical Necrosis

Tubulointerstitial Diseases

A

Acute-onset severe renal failure due to ischemic renal cortex
* Seen in very sick patients
* Septic shock
* Major obstetric complications: abruptio placentae; fetal demise
* Cortex = location of glomeruli
* Glomerular destruction –> no filtration
* Oliguria / anuria

108
Q

Acute Renal Failure (ARF)

Definition

A

Decreased Cr clearance over days
* Often with associated symptoms
* Many causes

109
Q

Chronic Kidney Disease (CKD)

Definition

A

Slow, gradual deterioration of renal function over years
* Usually due to DM, HTN
* Symptoms only present in most severe stages

110
Q
  1. Anorexia
  2. Nausea, vomiting
  3. Platelet dysfunction (bleeding)
  4. Pericarditis
  5. Asterixis
  6. Encephalopathy

Signs & Symptoms

A

Uremia

Asterixis: tremor / flap when patients hold their hands out

111
Q

ARF Classification

ARF

A

Elevated BUN / Cr
* Pre-renal ARF: insufficient blood flow to kidneys
* Dehydration
* Shock
* Heart failure
* Post-renal ARF: bilateral urine outflow obstruction
* Kidney stones
* BPH
* Tumors
* Congenital anomalies
* Intrinsic ARF: renal dysfunction
* ATN
* Glomerulonephritis

112
Q

ARF: Key Labs

Diagnosis

A
  • Creatinine
    • Freely flitered
    • Small amount secreted
  • Blood urea nitrogen (BUN)
    * Freely filtered
    * Reabsorbed when kidney reabsorbs H2O
  • ARF: GFR falls –> BUN & Cr rise
    * Dehydration BUN rises more than Cr; resorption
113
Q

ARF Workup

Diagnosis

A

Detection of BUN / Cr elevation
1. History: medications, co-morbidities, hydration
2. Physical: low BP, dehydration, CHF, etc.
3. Urinalysis: protein, blood, casts
4. Ultrasound: hydronephrosis

114
Q

ARF Measurements

Diagnosis

A

Determine cause based on blood & urine testing
* BUN: rises in ARF
* Cr: rises in ARF
* BUN / Cr ratio –> normal = 20:1
* Urine [Na]
* Urine [Fe]
* uOsm

115
Q

ARF Measurements

Diagnosis

A

Determine cause based on blood & urine testing
* BUN: rises in ARF
* Cr: rises in ARF
* BUN / Cr ratio –> normal = 20:1
* Urine [Na]
* Fractional excretion of Na
* uOsm

116
Q

Urinary [Na]

ARF Measurements

A

Varies based on intake of Na+ & H2O
* Very low (<20 mEq/L) in Na+ / H2O retention

117
Q

Fractional Excretion of Na (F-Na)

ARF Measurements

A

Percentage of filtered Na+ that is excreted
* Very low (< 1%) during Na+ / H2O retention

118
Q

Urinary Osmolarity (uOsm)

ARF Measurements

A

Measure of urine concentration
* Very high (>550 mOsm/kg) in H20 retention

119
Q

Pre-Renal ARF

BUN / Cr

A

Decreased blood flow to kidneys
* GFR falls –> reduced BUN / Cr filtration
* Serum BUN & Cr increases
* Increased H2O resorption
* BUN is resorbed with H2O
* BUN rise > Cr rise
* Result: elevated BUN / Cr ratio

120
Q

Pre-Renal ARF

Urinary Findings

A
  • Significant H2O resorption
    • Concentrated urine –> high uOsm
  • Significant Na+ resorption
    • Low urine [Na]
    • Low F-Na
121
Q

Intrinsic ARF

BUN / Cr

A

Kidney cannot filter blood
* GFR falls –> reduced BUN / Cr filtration
* Serum BUN & Cr increases
* No additional rise in BUN from H2O resorption
* No change in BUN / Cr ratio

122
Q

Intrinsic ARF

Urinary Findings

A
  • Kidney cannot reabsorb water –> low uOsm
    • Cannot concentrate urine
  • Cannot reabsorb Na+ –> high urine [Na]; high F-Na
123
Q

Post-Renal ARF

A

Obstruction to urine outflow
* Urine backs up in kidneys
* Causes high pressure tubules:
* Impairs filtration: high hydrostatic pressure pushes blood out
* Impaired resorption: channels damaged / destroyed by high pressure
* Key features:
* Anuria
* Hydronephrosis
* Diagnostic test: ultrasound
* Shows enlarged, dilated kidneys

124
Q

Chronic Kidney Disease (CKD)

Renal Failure

A

Slow, steady fall in Cr clearance
* Blood tests show rise in BUN / Cr
* Eventually progresses to dialysis for many patients
* Most common causes:
* Hypertensive nephrosclerosis
* Diabetic nephropathy

125
Q

Stages of CKD

CKD

A
  • Stage 1: GFR >90
  • Stage 2: GFR 60-89
  • Stage 3: GFR 30-59
  • Stage 4: GFR 15-29 (approaching dialysis)
  • Stage 5 (ESRD): GFR <15 (dialysis)
126
Q
  1. Acidemia
  2. Hyperkalemia
  3. Intoxication (overdose of dialyzable substance)
  4. Volume overload (CHF)
  5. Uremic symptoms

Treatment

A

Indications for Dialysis

Mnemonic: AEIOU

127
Q

Dialysis Methods

Treatment

A
  • Hemodialysis
    • Requires vascular access
    • Blood pumped from body through filter & back
    • Done in sessions of few hours at a time
  • Peritoneal dialysis
    • Fluid is cycled through peritoneal cavity
    • Peritoneum used as dialysis membrane
  • Hemofiltration
    • Constant filtering of blood
    • Usually done at bedside for critically ill patients

q

128
Q

Vascular Access

Dialysis

A

For acute dialysis, central line can be placed
* Ideal method is fistula
* Connection between artery & vein
* Placed surgically, usually in arm
* Lowest rates of thrombosis, infection
* Fistula must “mature” for use
* Ideally placed several months before dialysis

129
Q

CKD

Complications

A
  • Anemia: due to loss of EPO production
  • Dyslipidemia: mostly triglycerides
    * Protein loss in urine –> stimulation of liver synthesis
    * Impaired clearance of chylomicrons & VLDL
  • Renal osteodystrophy
  • Growth failure (children)
130
Q

CKD

Complications

A
  • Anemia: due to loss of EPO production
  • Dyslipidemia: mostly triglycerides
    * Protein loss in urine –> stimulation of liver synthesis
    * Impaired clearance of chylomicrons & VLDL
  • Renal osteodystrophy
  • Growth failure (children)

GU / GYN & Renal (23 decks)

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