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Renal - Miscellaneous Flashcards

1
Q

What are the general symptoms of glomerulonephritis?

A

Hematuria, proteinuria, decreased GFR, HTN

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2
Q

What are the general symptoms of nephrotic syndrome?

A

Hypoalbuminemia, edema, hyperlipidemia, fatty casts, proteinuria >3.5g/24hr

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3
Q

What are the general symptoms of nephritic syndrome?

A

Hematuria, azotemia, HTN, oliguria, subnephrotic range proteinuria

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4
Q

Normal GFR = ?

A

> 90 mL/min

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5
Q

Normal urine output = ?

A

1500 mL/24 hr

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6
Q

Normal urine protein = ?

A

<150 mg/24 hr

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7
Q

Normal FeNa = ?

A

1%

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8
Q

Normal FeUrea = ?

A

35%

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9
Q

Normal specific gravity = ?

A

1.003-1.030

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10
Q

Normal urine pH = ?

A

5-8

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11
Q

Normal # of RBC on microscopy = ?

A

0-2/hpf

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12
Q

Normal # of WBC on microscopy = ?

A

0-5/hpf

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13
Q

Oliguria = ?

A

<500 mL/24 hr

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14
Q

Polyuria = ?

A

> 3000 mL/24 hr

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15
Q

Anuria = ?

A

0 mL/24 hr

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16
Q

Dysmorphic RBCs indicate an issue with…

A

Glomeruli

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17
Q

RBC casts indicate ___.

A

Glomerulonephritis

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18
Q

WBC casts indicate ___.

A

Pyelonephritis

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19
Q

Epithelial (muddy brown) casts indicate ___.

A

Acute tubular necrosis

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20
Q

Fatty casts indicate ___.

A

Nephrotic syndrome

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21
Q

Granular casts indicate ___.

A

CKD (or non-specific)

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22
Q

Hyaline casts indicate ___.

A

Dehydration, exercise, diuertics

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23
Q

Waxy casts indicate ___.

A

Advanced kidney disease

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24
Q

GFR = ?

A

([U] x V)/[P]

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25
Q

Cockcroft Gault equation - GFR = ?

A

((140 - age) x weight (kig) x 0.85 if female)/(72 x serum creatinine)

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26
Q

FeNa = ?

A

(UNa/PNa)/(UCr/PCr) x 100

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27
Q

What is a normal FF?

A

20%

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28
Q

What is the normal RPF?

A

625 mL/min

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29
Q

What is a normal urine Na?

A

20 mEq/L

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30
Q

Compare the urine Na+ in a pre-renal and renal issue.

A

Pre-renal: <20 mmol/L

Renal: >20 mmol/L

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31
Q

Compare the FeNa and FeUrea in a pre-renal and renal issue.

A

Pre-renal: <1%

Renal: >1%

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32
Q

Compare the urine specific gravity in a pre-renal and renal issue.

A

Pre-renal: >1.015

Renal: ~1.010

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33
Q

Compare the urine osmolality in a pre-renal and renal issue.

A

Pre-renal: >350 mmol/kg

Renal: <350 mmol/kg

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34
Q

Compare the casts seen in a pre-renal, renal, and post-renal issue.

A

Pre-renal: hyaline
Renal: Granular
Post-renal: hyaline

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35
Q

Compare the U/P creatinine ratio in a pre-renal and renal issue.

A

Pre-renal: >40

Renal: <20

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36
Q

Compare the serum BUN/Cr ratio in a pre-renal and renal issue.

A

Pre-renal: >20:1

Renal: <10:1

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37
Q

What are the symptoms of nephritic syndrome?

A

Acute onset of hematuria (dysmorphic RBC, RBC casts), oliguria, azotemia, HTN, edema, mild proteinuria

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38
Q

What are the four types of nephritic syndrome?

A
  1. Post-infectious GN
  2. Ig-A nephropathy
  3. Hereditary nephritis
  4. Rapidly progressive GN
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39
Q

What is systemic IgA nephropathy?

A

HSP

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40
Q

What are the symptoms of nephrotic syndrome?

A

Massive proteinuria (>3.5 g), hypoalbuminemia, generalized edema, hyperlipidemia, lipiduria

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41
Q

What are the three types of primary nephrotic syndrome?

A
  1. Membranous nephropathy
  2. Minimal change disease
  3. FSGS
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42
Q

What are the two types of nephrotic syndrome with hematuria?

A
  1. Membranoproliferative glomerulnephritis

2. Dense deposit disease

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43
Q

If pH <5, think ___.

A

Metabolic acidosis

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44
Q

If pH >5.3 in the presence of metabolic acidosis, think ___.

A

Distal RTA

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45
Q

If pH >8, think ___.

A

Presence of urea-splitting organisms

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46
Q

A specific gravity of 1.001 is very ___ and a specific gravity of 1.030 is very ___.

A

Dilute; concentrated

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47
Q

What does a specific gravity of 1.010 indicate?

A

Urine is neither concentrated nor dilute

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48
Q

If there is an acute decline in renal function and specific gravity is > 1.020, think ___.

A

Pre-renal issue (urine can still be concentrated)

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49
Q

If there is an acute decline in renal function and specific gravity is ~1.010, think ___.

A

Renal issue (urine can no longer be concentrated)

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50
Q

If there is hyponatremia, normally expect a ___ specific gravity. If there is hypernatremia, normally expect a ___ specific gravity.

A

Low; high

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51
Q

If specific gravity is > 1.010 in the setting of hyponatremia, think ____.

A

ADH secretion is occurring (urine is being concentrated)

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52
Q

If specific gravity is <1.010 in the setting of hypernatremia, think ___.

A

Diabetes inspidius (urine is being diluted)

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53
Q

If there is elevated blood glucose and glycosuria, think ___.

A

Diabetes mellitus

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54
Q

If there is normal blood glucose and glycosuria, think ___.

A

Proximal tubule dysfunction

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55
Q

If there is ketoacidosis and ketonuria, think ___.

A

Diabetic or alcoholic ketoacidosis

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56
Q

If there is no ketaocidosis and ketonuria, think ___.

A

Starvation, ketogenic diet, isopropyl alcohol ingestion

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57
Q

If there is bilirubin in the urine, think ___.

A

Hepatobiliary disease

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58
Q

If there is bilirubin in the urine without urobilinogen, think ___.

A

Biliary obstruction

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59
Q

If there is urobilinogen in the urine, think ___.

A

Liver disease

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60
Q

If there is leukocyte esterase or nitrites in the urine, think ___.

A

UTI

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61
Q

Compare the presentations of of the 4 types of nephritic syndrome.

A
  1. Acute post-infectious GN: Hematuria, edema, HTN, renal failure within 1-4 weeks of a throat/skin infection (presentation less clear in adults)
  2. IgA nephropathy: recurrent, often painless hematuria within 1-2 days of an upper respiratory, GI, or urinary infection, proteinuria
  3. Hereditary nephritis: isolated hematuria, nephritis, no infection, hearing issues and ocular issues
  4. Rapidly progressive GN: rapidly progressive loss of renal function, nephritic syndrome
    Type I - gross hematuria, oliguria, hemoptysis
    Type II - gross hematuria, oliguria
    Type III - gross hematuria, oliguria, hemoptysis/SOB
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62
Q

Compare the epidemiology of the 4 types of nephritic syndrome.

A
  1. Acute post-infectious GN: children 6-10 y/o (rare in adults)
  2. IgA nephropathy: most common glomerular disease, children and adults
  3. Hereditary nephritis: 5-20 y/o males (age of presentation)
  4. Rapidly progressive GN:
    Type I - young men
    Type II - older children/young adults
    Type III - older adults
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63
Q

Compare the etiology/pathogenesis of the 4 types of nephritic syndrome.

A
  1. Acute post-infectious GN: formation of Ag/IgG IC in circulation, deposition of IC in capillary wall, complement activation, influx of neutrophils, damage and endocapillary proliferation + in-situ IC formation
  2. IgA nephropathy: infection causes massive IgA production, IgA/Complement IC formation, deposition in mesangium, alternative complement pathway activated
  3. Hereditary nephritis: error in collagen type IV synthesis (affects GBM, cochlea, lens)
  4. Rapidly progressive GN:
    Type I - anti-glomerular basement membrane Ab
    Type II - IC formation, necrosis and breaks in glomerular BM
    Type III - ANCA (Ab to neutrophilic granules)
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64
Q

Compare the histology, IF, and EM images of the 4 types of nephritic syndrome.

A
  1. Acute post-infectious GN: Histology - capillary obliteration, endocapillary proliferation, PMN influx; EM - humps; IF: IgG + Ag/Complement
  2. IgA nephropathy: Histology - mesangial proliferation, EM - electron dense deposits; IF - IgA + complement/auto-Ab
  3. Hereditary nephritis - Histology - normal; EM - basket weave (lamina densa splitting); IF - negative
  4. Rapidly progressive glomerulonephritis - All types - Histology: crescents
    Type I: IF - linear IgG, EM - none
    Type II: IF - granular deposits (Ig + complement), EM - electron dense deposits
    Type III: IF - pauci immune, EM - pauci immune
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65
Q

What other lab tests are important in acute post-infectious GN?

A
  1. ASO titer increases
  2. Complement decreases
  3. Coca-cola, tea-colored urine
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66
Q

What other lab tests are important in IgA nephropathy?

A
  1. No decrease in complement
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67
Q

Describe the IgA nephropathy with extra-renal symptoms (systemic IgA).

A

Henoch Schonlein Purpura
Mainly seen in 3-8 y/o
IC deposits in kidney (hematuria), skin (purpuric skin lesions), GI (abdominal pain and GI bleeding), and joints (arthralgia)

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68
Q

Which nephritic syndromes do not involve immune complexes?

A

Hereditary nephritis

Type I and III rapidly progressive GN

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69
Q

What is Goodpasture disease?

A

Type I rapidly progressive GN + alveolar basement membrane involvement

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70
Q

What is the antigen attacked in Goodpasture disease?

A

NC1 (non-collagenous protein)

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71
Q

What triad is commonly affected in GPA? What type of ANCA and antigen are involved?

A

Ear/nose throat
Lungs
Kidney

c-ANCA, PR3

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72
Q

Compare the presentations of of the 3 types of nephrotic syndrome.

A

All three: nephrotic syndrome

  1. Membranous nephropathy: edema, thrombosis (loss of AT-III), infection
  2. Minimal change disease: edema
  3. FSGS: hematuria, reduced GFR, HTN
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73
Q

Compare the epidemiology of the 3 types of nephrotic syndrome.

A
  1. Membranous nephropathy: 30-60 y/o, second most common nephrotic syndrome
  2. Minimal change disease: 2-6 y/o, most common nephrotic syndrome in children, adults (10%)
  3. FSGS: adults (most common nephrotic syndrome) and children
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74
Q

Compare the etiology/pathogenesis of the 3 types of nephrotic syndrome.

A
  1. Membranous nephropathy: autoimmune response against renal Ags, IC formation, podocyte injury, NO inflammatory response, often associated with cancer
  2. Minimal change disease: reversible podocyte injury
  3. FSGS: irreverisble podoctye injury, leads to sclerosis and lumen obliteration
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75
Q

Compare the histology, IF, and EM images of the 3 types of nephrotic syndrome.

A
  1. Membranous nephropathy: Histology - normal; EM - subepithelial electron dense deposits, IF - granular deposits (IgG and C3); silver stain - spike and dome pattern (basement membrane positive - black)
  2. Minimal change disease: Histology - normal; EM - effacement/fusion of podocyte foot processes; IF - none
  3. FSGS: Histology - segemental sclerosis; EM - effacement of podocytes in all glomeruli; IF - none.
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76
Q

What are the two renal antigens targeted in membranous nephropathy?

A

PLA2R, THSD7A

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77
Q

What other lab tests are important in membranous nephropathy?

A
  1. Ab testing for PLA2R, THSD7A

2. No drop in complement

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78
Q

If you have membranous nephropathy, you must rule out ___.

A

Cancer

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79
Q

Discuss steroid treatment of minimal change disease and FSGS.

A

Minimal change disease responds to steroids. FSGS initially responds to steroids but may become resistant.

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80
Q

What are the three common etiologies of FSGS?

A
  1. Primary (idiopathic)
  2. Adaptive (response to nephron loss)
  3. APOL1 (risk alleles)
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81
Q

What are the three uncommon etiologies of FSGS?

A
  1. Genetic
  2. Medication-associated
  3. Virus-associated
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82
Q

Compare the etiology/pathogenesis of the 2 nephrotic/nephritic syndromes.

A
  1. MPGN: IC formation with classical complement activation

2. DDD: sustained activation of the alternative complement pathway (non-antibody mediated)

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83
Q

Compare the histology, IF, and EM images of the 2 types of nephrotic/nephritic syndrome.

A
  1. MPGN: Histology - lobular tufts; EM - electron dense deposits and tram tracks; IF - IgG + complement; silver stain - tram tracks
  2. DDD: Histology - none mentioned; EM - dense deposits in lamina densa; IF - C3 (no Ig)
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84
Q

What are the two major control points affecting the complement pathway in DDD?

A
  1. C3NeF is an autoantibody against C3 convertase - it stabilizes the enzyme and prevents its degradation
  2. H factor normally degrades C3 convertase; mutations/autoantibodies diminish its ability to do so
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85
Q

What is an important drug treatment for DDD?

A

Eculizumab

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86
Q

What are three systemic kidney issues and how are they categorized (nephrotic/nephritic)?

A

Nephrotic: diabetic nephropathy, amyloidosis
Nephritic: lupus nephritis (can be nephrotic 10% of the time)

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87
Q

What are the symptoms of diabetic nephropathy?

A
  1. Proteinuria
  2. Progressive decrease in GFR
  3. HTN
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88
Q

What important histologic finding is seen in diabetic nephropathy?

A

KW nodules (thickening of GBM, increased mesangial matrix)

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89
Q

Discuss the clinical presentation of TMAs.

A
  1. Microangiopathic hemolytic anemia
  2. Thrombocytopenia and thrombi in microcirculation
  3. Renal failure
  4. Diarrhea (HUS only)
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90
Q

Discuss the lab tests for TMA.

A
  1. Thrombi and endothelial injury in histology
  2. Thrombocytopenia
  3. Schistocytes on blood smear
  4. ADAMTS13 mutation
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91
Q

What are the two major categories of tubulointerstitial diseases?

A
  1. Tubulointerstitial nephritis

2. Acute tubular injury/necrosis

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92
Q

What are the primary types of tubulointerstitial nephritis?

A

Infectious: pyelonephritis (acute, chronic, papillary necrosis, viral, xanthogranulomatous)
Non-infectious:
1. Acute drug-induced (particularly NSAIDs, aristolcholic acid)
2. Metabolic (urate and oxalate nephropathies)
3. Neoplasm (multiple myeloma - uric acid, hypercalcemia, light chain casts)

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93
Q

What are the two major causes of acute tubular injury/necrosis?

A

Ischemia and toxins

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94
Q

Compare acute and chronic pyelonephritis on histology.

A

Acute: patchy interstitial suppurative inflammation (PMNs)
Chronic: lymphocytes, fibrosis, sclerosis, dilated tubules

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95
Q

What are the 4 broad causes of pre-renal AKI?

A
  1. Absolute decrease in ECV
  2. Relative decrease in ECV
  3. Low ECV + impaired renal autoregulation
  4. Vasoconstriction and occlusion
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96
Q

What causes an absolute decrease in ECV?

A

Vomiting, diarrhea, hemorrhage

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97
Q

What causes a relative decrease in ECV?

A

HF, cirrhosis

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98
Q

What causes low ECV + impaired renal autoregulation?

A

NSAIDs, ACEI/ARB

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99
Q

What causes vasoconstriction and occlusion?

A

Hypercalcemia, chemo, renal artery stenosis

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100
Q

What are some exogenous toxins that can cause acute tubular necrosis?

A

Antibiotics, chemotherapy, contrast, mannitol

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101
Q

What are some endogenous toxins that can cause acute tubular necrosis?

A

Myoglobin (rhabdo), uric acid (tumor lysis), light chains (myeloma), hemoglobin (hemolysis)

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102
Q

What is the classic triad of symptoms seen in acute interstitial nephritis?

A

Fever, rash, eosinophilia

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103
Q

What are the clinical features of contrast nephropathy?

A
  1. Increase in serum creatinine 2-3 days after contrast administration
  2. Non-oliguric
  3. Pre-renal urine indices, high specific gravity
  4. ATN eventually
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104
Q

What are some causes of high BUN?

A
  1. Pre-renal issue
  2. High dose steroids
  3. Hyper-catabolic states (fever, burns)
  4. High protein diet
  5. GI bleed
105
Q

What are some causes of low BUN or creatinine?

A
  1. Low protein diet
  2. Cachetic patients
  3. Cirrhosis (high bilirubin interferes with measurement)
106
Q

What are some causes of high creatinine?

A
  1. High muscle mass
  2. Creatinine supplements
  3. Rhabdomyolysis
  4. Diet high in animal protein
  5. Drugs blocking tubular secertion
  6. Measurement issues
107
Q

What are the general indications for dialysis?

A
  1. Acidosis
  2. Electrolytes (hyperkalemia)
  3. Intoxication (salicylate, lithium, isopropanol, methanol, ethylene glycol)
  4. Overload (volume)
  5. Uremia
108
Q

What are the 4 congenital renal abnormalities?

A
  1. Agenesis
  2. Hypoplasia
  3. Ectopic
  4. Horseshoe
109
Q

What causes renal dysplasia?

A

Immature elements in metanephric development

Leads to noncommunicating cysts of various sizes separated by dysplastic parenchyma and the absence of a normal pelvocaliceal system; associated with ureteral or ueteropelvic atresia

110
Q

What is the gross and histologic appearance of renal dysplasia?

A

Bunch of grapes; cartilage on histology

Can be uni/bilateral, non-reniform, can be segmental

111
Q

What gene is mutated in AR PCKD and what does it encode?

A

PKHD1 (encodes fibrocystin)

112
Q

What is the gross and histologic appearance of AR PCKD?

A

Gross: enlarged bilateral reniform kidneys
Histology: sponge-like cross section, dilated tubules

113
Q

What is the gross and histologic appearance of AD PCKD?

A

Gross: giant kidney
Histology: cysts, functioning nephrons

114
Q

What two complications are associated with AD PCKD?

A

Intracranial berry aneurysm, mitral valve prolapse

115
Q

What are the two benign adult renal tumors?

A
  1. Oncocytoma

2. Angiomyolipoma

116
Q

What is the classic symptom triad of RCC?

A
  1. Painless hematuria
  2. Palpable abdominal mass
  3. Dull flank pain
117
Q

Describe the pathogenesis of clear cell type RCC.

A

Loss of 3p leads to VHL inactivation; normally, VHL breaks down HIF-1a; when VHL is inactivated, HIF-1a increases and leads to tumor cell survival

118
Q

Describe the gross and histologic presentation of clear cell RCC.

A

Gross: yellow-orange, adrenal-like tumor
Histology: chicken-wire, clear cytoplasm, highly vascularized

119
Q

Describe the symptoms of Beckwith-Widemann syndrome.

A
  1. Wilms tumor
  2. Macroglossia
  3. Organomegaly
  4. Hemihypertrophy
120
Q

Describe the symptoms of the WAGR complex.

A
  1. Wilms tumor
  2. Aniridia (absence of iris)
  3. Genital abnormalities
  4. mental Retardation
121
Q

Describe the symptoms of Denys-Drash syndrome.

A
  1. Wilms tumor
  2. Gonadal dysgenesis
  3. Renal mesangial sclerosis
122
Q

What is the cause of Wilms tumors?

A

Recapitulating nephrogenesis

123
Q

Describe the histologic triphasic presentation of Wilms tumors.

A
  1. Undifferentiated blastoma
  2. Tubules
  3. Fibroblast-like stroma
124
Q

Which renal tumor is chemo resistant? Chemo sensitive?

A

Resistant: RCC
Sensitive: Wilms tumor

125
Q

Membranoproliferative GN is associated with what illness?

A

Hepatitis C

126
Q

What are the consequences of renal failure?

A

MAD HUNGER

Metabolic Acidosis
Dyslipidemia
Hyperkalemia
Uremia
Na/H2O retention
Growth retardation/developmental delay
Erythropoietin defiency
Renal osteodystrophy
127
Q

How is stage II/III CKD managed?

A

Healthy living, treat co-morbid disorders, avoid NSAIDs

128
Q

How is stage III-V CKD managed?

A

Refer to nephrology, control HTN (low sodium diet), reduce proteinuria

129
Q

How is stage IV-V CKD managed?

A
  1. Manage mineral and bone disorders
  2. Manage anemia
  3. Manage metabolic acidosis
130
Q

What are the aspects of uremic cardiovascular disease?

A
  1. Medial vascular calcification
  2. Arterial stiffness
  3. LV hypertrophy
  4. Increased risk of cardiac arrest and HF
131
Q

pH = ?

A

pKa + log [A-]/[HA] = -log[H+]

132
Q

For each 0.3 increase in pH, what happens to [H+]?

133
Q

What happens in metabolic acidosis?

A

Primary decrease in [HCO3-], relative increase in [H+], compensatory respiratory alkalosis (hyperventilation)

134
Q

What are causes of increased anion gap acidosis?

A
  1. Increased acid production/acid retention (ketoacidosis, lactic acidosis, toxin ingestion - salicylate, methanol, ethylene glycol)
  2. Failure to excrete inorganic anions (renal failure)
135
Q

What are causes of normal anion gap acidosis?

A
  1. GI loss of [HCO3-] via diarrhea
  2. Renal loss of [HCO3-] via proximal RTA, CA inhibitors
  3. Failure to excrete acid via distal RTA
  4. Administration of acid or saline
136
Q

What happens in metabolic alkalosis?

A

Primary increase in [HCO3-], relative decrease in [H+], compensatory respiratory acidosis (hypoventilation)

137
Q

What are 3 general causes of metabolic alkalosis?

A
  1. Net H+ loss from ECF
  2. Net HCO3- addition to ECF
  3. Cl- depletion
138
Q

What are 3 causes of H+ loss from ECF?

A
  1. GI loss (vomiting)
  2. Renal loss (mineralocorticoid excess, diuretics, increased Na+ distal tubule delivery)
  3. Movement to ICF (hypokalemia)
139
Q

What causes net bicarbonate addition to ECF?

A

Exogenous administration of bicarbonate, lactate, citrate, acete

140
Q

What are 2 causes of GI Cl- depletion?

A
  1. Secretion into stool (villous adenoma)

2. Reabsorption failure (congenital chloridorrhea)

141
Q

What are 3 causes of renal Cl- depletion

A
  1. Diuretics
  2. Bartter’s syndrome (defect of Na/K/2Cl transporter)
  3. Gitelman’s syndrome (defect of NaCl transporter)
142
Q

What is 1 cause of skin Cl- depletion?

A

Cystic fibrosis

143
Q

What causes maintenance of alkalosis broadly?

A

Net failure to excrete bicarbonate

144
Q

What are 4 causes of alkalotic maintenance?

A
  1. ECF depletion, decreased GFR, increased proximal tubule bicarbonate reabsorption
  2. Cl depletion, increased distal tubule bicarbonate reabsorption/decreased distal secretion
  3. Potassium depletion (lower intracellular pH, stimulate bicarbonate reabsorption)
  4. Hypercapnea (increased PCO2 decreases intracellular pH, stimulates bicarbonate reabsorption)
145
Q

Define chloride resistant alkalosis.

A

Urine chloride is high, >20 mmol/L, low renin

146
Q

Define chloride responsive alkalosis.

A

Urine chloride is low, <10 mmol/L, high renin

147
Q

How is metabolic alkalosis treated?

A
  1. Potassium
  2. Acetazolamide
  3. Volume repletion
  4. IV HCl or NH4Cl
148
Q

Anion gap = ?

A

Na - Cl - HCO3

149
Q

Normal AG = ?

A

10-12 mEq/L

150
Q

What pH indicates acidosis? Alkalosis?

A

Acidosis: <7.35
Alkalosis: >7.45

151
Q

If acidotic, what indicates metabolic versus respiratory?

A

Metabolic: HCO3- <22 mEq/L
Respiratory: PCO2 >45 mm Hg

152
Q

If metabolic acidosis, what indicates respiratory compensation?

A

PCO2 < 35 mm Hg

153
Q

If respiratory acidosis, what indicates renal compensation?

A

HCO3- >28 mEq/L

154
Q

If alkalotic, what indicates metabolic versus respiratory?

A

Metabolic: HCO3- >28 mEq/L
Respiratory: PCO2 <35 mm Hg

155
Q

If metabolic alkalosis, what indicates respiratory compensation?

A

PCO2 > 45 mm Hg

156
Q

If respiratory alkalosis, what indicates renal compensation?

A

HCO3- <22 mEq/L

157
Q

Calculate predicted compensation - metabolic acidosis.

A

Delta PCO2 = 1.2(Delta HCO3-)

158
Q

Calculate predicted compensation - metabolic alkalosis.

A

Delta PCO2 = 0.7(Delta HCO3-)

159
Q

Calculate predicted compensation - acute respiratory acidosis.

A

Delta HCO3- = 0.1(Delta PCO2)

160
Q

Calculate predicted compensation - chronic respiratory acidosis.

A

Delta HCO3- = 0.4(Delta PCO2)

161
Q

Calculate predicted compensation - acute respiratory alkalosis.

A

Delta HCO3- = 0.2(Delta PCO2)

162
Q

Calculate predicted compensation - chronic respiratory alkalosis.

A

Delta HCO3- = 0.4(Delta PCO2)

163
Q

What happens in Type I RTA?

A

Distal - intercalated cells cannot secrete H+

Urine pH >5.5

164
Q

What happens in Type II RTA?

A

Proximal - defective PT HCO3- reabsorption

Urine pH <5.5

165
Q

What happens in Type IV RTA?

A

Hypoaldosteronism

Urine pH <5.5

166
Q

What are the shapes of calcium oxalate stones?

A

Envelopes and dumbbells

167
Q

What is the shape of calcium phosphate stones?

A

Wedge prisms and needles

168
Q

What are the shapes of uric acid stones?

A

Rhomboids or rosettes

169
Q

What are the shapes of struvite stones?

A

Staghorn calculi or coffin lids

170
Q

What is the shape of cystine stones?

A

Hexagonal on micro

171
Q

What causes hypovolemic hyponatremia?

A

Decreased TBW with greatly decreased TBNa+

Diuretics, Addison’s disease, salt wasting, diarrhea, vomiting, sweating

172
Q

How is hypovolemic hyponatremia treated?

A

Physiologic saline

173
Q

What causes euvolemic hyponatremia?

A

Increased TBW with normal TBNa+

SIADH, hypothryoidism, psychogenic polydipsia, beer drinking podomania

174
Q

How is euvolemic hyponatremia treated?

A

Water restriction if severe; if symptomatic, give hypertonic saline +/- diuretics

175
Q

What causes hypervolemic hyponatremia?

A

Greatly increased TBW with increased TBNa+

CHF, cirrhosis, renal failure

176
Q

How is hypervolemic hyponatremia treated?

A

Fluid restriction and diuretics

177
Q

What causes hypovolemic hypernatremia?

A

Greatly decreased TBW with decreased TBNa+

Diuretics without water intake, tubular injury, sweating, diarrhea, vomiting with inadquate water intake

178
Q

How is hypovolemic hypernatremia treated?

A

Hypotonic fluid administration

179
Q

What causes euvolemic hypernatremia?

A

Decreased TBW with normal TBNa+

Central and nephrogenic diabetes insipidus, decreased thirst/water intake

180
Q

How is euvolemic hypernatremia treated?

A

Water administration, ADH administration in central DI

181
Q

What causes hypervolemic hypernatremia?

A

Normal TBW with increased TBNa+

Hypertonic fluid administration, mineralocorticoid excess, salt poisoning

182
Q

How is hypervolemic hypernatremia treated?

A

Water administration + diuretics or dialysis to remove Na+; rate of correction should not exceed 0.5 mEq/L/hr, can lead to brain edema

183
Q

What is a normal plasma sodium range?

A

135-145 mEq/L

184
Q

What is normal urinary Na+?

A

10-20 mmol/L

185
Q

What are the two most common adherence factors in E. coli, what do they bind to, and where are they found?

A
  1. Type 1 Fim H - bind to D-mannose on epithelial cells in bladder and lower tract
  2. PAP - p fimbriae - bind to P blood group Ag in renal pelvis and kidney
186
Q

What are the two protective urine properties?

A
  1. IgA/IgG

2. Tamm-Horsfall protein

187
Q

What are first line treatment for uncomplicated cystitis?

A
  1. Nitrofurantoin, bactrim, fosfacmyin

FQ - 2, oral beta-lactams - 3

188
Q

What are first line treatment for uncomplicated pyelonephritis?

A

FQ, Bactrim

189
Q

What are intraluminal causes of obstruction?

A

Renal calculi, blood clots, sloughed renal papilla, urothelial tumors, fungal ball

190
Q

What causes sloughed renal papilla?

A

Diabetes, sickle cell, pyelonephritis, phentactein abuse

191
Q

What are intramural causes of obstruction?

A

UPJ obstruction, structural lesions

192
Q

What are extramural causes of obstruction?

A

Prostate disease, cancer, crossing vessels, retroperitoneal fibrosis

193
Q

What are the 3 functional changes in unilateral obstruciton?

A
  1. Increased ureteral pressure decreases GFR; this decreases Na+ delivery to the macula densa. Afferent arteriole dilates to increase RBF and GFR
  2. Ureteral pressure continues to increase; efferent arteriole constricts, decreasing RBF and increasing GFR
  3. Ureteral pressure and RBF decrease due to decreased GFR and afferent arteriole constriction?
194
Q

What are the three most common sites of obstructions?

A
  1. Junction between ureter and bladder
  2. UPJ
  3. Where ureter crosses iliac muscles
195
Q

What are the 11 symptoms of lupus?

A
  1. Serositis
  2. Oral ulcers
  3. Arthritis
  4. Photosensitivity
  5. Blood disorder
  6. Renal disorder
  7. ANA
  8. Immunologic abnormalities
  9. Neurological symptoms
  10. Malar rash
  11. Discoid rash
196
Q

What are the 5 types of lupus?

A

SLE, discoid, drug-induced, neonatal, overlap with another AI disease

197
Q

What are the important lab tests for lupus?

A
  1. ANA (sensitive)
  2. Anti-DsDNA (specific)
  3. Anti-Smith
  4. Decreased C3 and C4
198
Q

What are the symptoms of Sjogren’s syndrome?

A

Exocrine glandular dysfunction due to lymphocytic infiltration

  1. Xerophthalmia (dry eyes)
  2. Xerostomia (dry mouth)
  3. Vaginal and skin dryness, constipation
  4. Parotid enlargement
  5. Joint pain
199
Q

What are the important lab tests for Sjogren’s syndrome?

A
  1. Anti-SSA/SSB
  2. Rheumatoid factor
  3. Renal tubular acidosis
200
Q

What are the symptoms of systemic sclerosis (scleroderma)?

A
  1. Raynaud
  2. Skin tightening
  3. Finger tip ulcers
  4. Joint contractures
  5. Renal HTN
  6. Dyspnea
  7. GERD
  8. Diarrhea/malabsorption
  9. Weight loss
201
Q

What are the two subtypes of systemic sclerosis?

A

Diffuse and Limited

202
Q

What are the symptoms of diffuse scleroderma?

A

Extensive skin involvement, interstitial lung disease, anti-topoisomerase I

203
Q

What are the symptoms of limited scleroderma?

A

Limited skin involvement, CREST syndrome (Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactylyl, Telangiectasia), pulmonary HTN, anti-centromere antibody

204
Q

What antibody goes with scleroderma renal crisis?

A

Anti-RNA-polymerase III

205
Q

What are the antibodies associated with anti-phospholipid syndrome?

A

aCL, anti-beta2-glycoprotein 1, lupus anticoagulant

206
Q

Anti-phospholipid syndrome can cause a false positive ___.

A

VDRL/RPR test and a prolonged PTT

207
Q

Chronic hyperphosphatemia leads to…

A

decreased renal activation of vitamin D and secondary hyperparathyroidism

208
Q

FeNa should ___ as GFR decreases.

209
Q

Describe the transporters in the cells of the PCT.

A

Lumen:

  1. Na/H exchanger (Na into cell, H into lumen)
  2. Cl/Base exchanger (Cl into cell, Base into lumen)
  3. Reaction forming H2O + CO2 –> diffuses into the cell

Cell:
1. CO2 + H2O forms H2CO3 which forms H+ and HCO3

Blood:

  1. Na/K ATPase (Na into blood, K into cell)
  2. HCO3- transporter (into blood)
210
Q

Describe the transporters in the cells of the TAL.

A

Lumen:

  1. Na/K/2CL transporter (into cell)
  2. K+ channel (into lumen)
  3. Mg/Ca paracellularly into blood

Blood:

  1. Na/K ATPase
  2. K+ channel (into blood)
  3. Cl- channel (into blood)
211
Q

Describe the transporters in the cells of the DCT.

A

Lumen:

  1. Na/Cl transporter (into cell)
  2. Ca2+ channel (into lumen)

Blood:

  1. Na/K ATPase
  2. Na/Ca2+ exchanger (Na into cell Ca2+ into blood)
  3. Cl- channel (into blood)

PTH Receptor

212
Q

Describe the transporters in the cells of the principal cell of the CCT.

A

Lumen:

  1. Cl- paracellular diffusion (into blood)
  2. H2O channel (into cell)
  3. K+ channel (into lumen)
  4. Enac chanel (into cell)

Blood:
1. Na/K ATPase

ADH and Aldosterone receptors

213
Q

Describe the transporters in the cells of the alpha-intercalated cell of the CCT.

A

Lumen:

  1. H+ ATPase (into lumen)
  2. K/H ATPase (K into cell, H into lumen)

Blood:
1. HCO3/Cl exchanger (HCO3- into blood, Cl- into cell)

Aldosterone receptor

214
Q

Describe the transporters in the cells of the beta-intercalated cell of the CCT.

A

Lumen:
1. Cl/HCO3 exchanger (Cl into cell, HCO3 into lumen)

Blood:
1. H+ ATPase (into blood)

215
Q

What is the prognosis of acute post-infectious GN?

A

Children - total recovery (95%)
Adults - slow progression to chronic GN (15-50% to ESRD)
Small subset of children and adults develop acute illness with gross hematuria and rapidly progressive renal failure

216
Q

What is the treatment of acute post-infectious GN?

A

Supportive

217
Q

True or false - IgA is a poor activator of the complement system.

218
Q

What is the prognosis of IgA nephropathy?

A

Renal failure, rarely RPGN, HSP (kids, great prognosis)

219
Q

What is the treatment of IgA nephropathy?

A

Supportive

220
Q

What is the prognosis of hereditary nephritis?

A

Overt renal failure between 20-50 year of age

221
Q

What is the treatment of hereditary nephritis?

A

Supportive, transplant

222
Q

What is the prognosis of RPGN type I?

A

Renal and pulmonary failure

223
Q

How is RPGN type I treated?

A

Plasmapheresis

224
Q

What is the prognosis of RPGN type II?

A

Chronic renal failure

225
Q

What is the treatment of RPGN type II?

A

Immunosuppression

226
Q

What is the prognosis of RPGN type III/

A

Renal and pulmonary failure

227
Q

What is the treatment of RPGN type III?

A

Immunosuppression

228
Q

What type of ANCA and antigen are involved in EPGA?

A

p-ANCA, MPO

229
Q

What is the prognosis of membranous nephropathy?

A

1/3 - spontaneous remission
1/3 - progress, require dialysis
1/3 - continued proteinuria, no progression

230
Q

How is membranous nephropathy treated?

A

Immunosuppressive drugs, treatment of underlying disease (secondary), can recur after transplant

231
Q

What is the prognosis of minimal change disease?

A

Several episodes of nephrotic syndrome, normal renal function, resolves at puberty

232
Q

What is the treatment of minimal change disease?

A

Steroid sensitive

233
Q

What is the prognosis of FSGS?

A

Progression to renal failure within 10 years

234
Q

What is the treatment of FSGS?

A

Initially steroid-responsive, progresses to steroid resistant, recurs in transplant

235
Q

What is the prognosis of MPGN?

A

Progression to renal failure

236
Q

What is the treatment of MPGN?

A

Treat underlying disease

237
Q

When a patient shows C3 by IF, but no DDD, what is this called?

A

C3 glomerulopathy

238
Q

What is the prognosis of DDD?

A

Poor, progress to renal failure

239
Q

What are the major differences between HUS and HSP?

A

HUS: thrombocytopenia, anemia with schisctocytes
HSP: rash/palpable purpura, joint pain/swelling

240
Q

What are some things that can cause papillary necrosis?

A
  1. Analgesics
  2. Diabetes
  3. Sickle cell anemia
  4. Obstruction
  5. TB
241
Q

What is seen on a kidney biopsy of acute drug-induced interstitial nephritis?

A

Interstitial inflammation, abundant eosinophils, edema

242
Q

What are the two aspects of the pathology of NSAID interstitial nephritis?

A

Interstitial nephritis and minimal change disease

243
Q

How does acute tubular injury present?

A

Rapid reduction of renal function, oliguria, uremia, signs of fluid overload, electrolyte abnormalities, acidosis; can be non-oliguric 50% of the time

244
Q

What is the most common cause of acute renal failure?

245
Q

What are some causes of combined ATN?

A
  1. Mismatched blood transfusion
  2. Hemolytic crises
  3. Skeletal muscle injury
  4. Intratubular casts and crystals
246
Q

Which of the 4 stones are radiolucent?

A

Uric acid (cystine mildly opaque)

247
Q

Discuss the three phases of the clinical course of ATN.

A
  1. Initiation (hours to days) - evolving tubular injury, potentiallyr eversible
  2. Maintenance (1-2 weeks) - established renal injury, oliguria, epithelial casts
  3. Recovery - repair and regeneration of tubules, polyuric
248
Q

What genes are mutated in APKD?

A
  1. PDK1 (earlier onset, more severe) - encodes polycystin 1, which regulates cell-cell interactions
  2. PKD2 (later onset) - encodes polycystin 2, which regulates intercellular Ca2+
249
Q

Describe oncocytoma on hsitology and EM.

A

Histology: eosinophilic cytoplasm
EM: abundant mito

250
Q

What is mutated in angiomyolipoma?

A

TSC1 and TSC2

251
Q

What is one possible targeted therapy for RCC, which is chemo-resistant?

A

mTOR inhibitors

252
Q

Analgesic nephropathy is a risk factor for ___.

A

Urothelial carcinoma

253
Q

Why are calcium oxalate stones related to hypocitraturia?

A

Citrate inhibits stone formation by forming a soluble complex with Ca2+

254
Q

Why is vitamin C problematic for calcium oxalate stones?

A

Excess vitamin C is excreted in the oxalate form

255
Q

How can calcium stones be prevented?

A
  1. Low Na+
  2. Normal dietary calcium
  3. Thiazide diuretic (decrease calcium excretion)
  4. Citrate
256
Q

How can low citrate be corrected?

A

Lemon juice

257
Q

How can uric acid stones be treated?

A
  1. Give citrate to alkalinize urine
  2. Give allopurinol, losartan
  3. Lose weight
258
Q

How can hyperoxaluria be addressed?

A
  1. Low oxalate diet
  2. Increase Ca2+
  3. Calcium carbonate
  4. Restrict vitamin C
259
Q

How can cystine stones be treated?

A

Reduce supersaturation, give chelating agents

MHD 1 (58 decks)

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