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COMLEX 2 > Renal Path > Flashcards

Renal Path Flashcards

1
Q

nephrotic syndrome

A

massive proteinuria with hypoalbuminemia, resulting edema, hyperlipidemia, frothy urine with fatty casts

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2
Q

minimal change disease

A

most common cause of nephrotic syndrome in children
often primary and may be triggered by recent infection, immunization, immune stimulus,
- rarely secondary to lymphoma (cytokine-mediated damage)

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3
Q

minimal change disease LM

A

normal glomeruli (lipid may beseen in PCT cells)

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4
Q

minimal change disease IF

A

negatve

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5
Q

minimal change disease on EM

A

effacement of podocyte foot processes

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6
Q

focal segmental glomerulosclerosis

A

most common cause of nephrotic syndrome in African Americans and Hispanics
can be primary or secondary to other conditions (HIV, sickle, IVDA, obesity, IFN tx, or congenital malformations)

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7
Q

FSGS LM

A

segmental sclerosis and hyalinosis

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8
Q

FSGS IF

A

often negative, but may be positive for nonspecifci focal deposits of IgM, C3, C1

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9
Q

FSGS EM

A

effacement of foot processes similar to minimal change disease

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10
Q

membranous nephropathy

A

aka membranous glomerulonephritis
can be primary (antibodies to phospholipase A2R) or secondary to drugs (NSAIDs, penicillamine, gold), infections (HBV, HCV, syphilis), SLE, or solid tumors

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11
Q

membranous nephropathy LM

A

diffuse capillary and GBM thickening

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12
Q

membranous nephropathy IF

A

granular due to IC deposition

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13
Q

membranous nephropathy

A

‘spike and dome’ appearance of sub epithelial deposits

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14
Q

membranous nephropathy tx

A

primary disease has poor response to steroids

may progress to CKD

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15
Q

amyloidosis

A

kidney is most commonly involved organ (systemic amyloidosis)
assoc with chronic conditions that predispose to amyloid deposition (AL amyloid, AA amyloid)

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16
Q

amyloidosis LM

A

Congo red stain shows up apple-green birefringence under polarized light due to amyloid deposition in the mesangium

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17
Q

diabetic glomerulonephropathy

A

most common cause of ESRD in the US

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18
Q

how are kidneys affected in diabetes

A

hyperglycemia -> nonenzymatic glycation of tissue proteins -> mesangial expansion
GBM thickening and increase permeability
hyperfiltration (glomerular HTN and increase GFR) -> glomerular hypertrophy and glomerular scarring (glomerulosclerosis) leading to further progression of nephropathy

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19
Q

diabetic glomerulonephropathy LM

A

mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis
Kimmelstiel-Wilson lesions

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20
Q

nephritic syndrome

A

inflammatory process
glomeruli involvement -> hematuria and RBC casts in urine
associated with azotemia, oliguria, hypertension (due to salt retention), proteinuria, hypercellular/inflamed glomeruli on biopsy

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21
Q

acute poststreptococcal glomerulonephritis

A

most frequently seen in children ~2-4wks after Group A strep infection of pharynx or skin

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22
Q

acute post streptococcal glomerulonephritis prognosis

A

resolves spontaneously in children, may progress to renal insufficiency in adults

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23
Q

acute post-streptococcal glomerulonephritis immunology

A

type III hypersensitivity reaction

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24
Q

presentation of acute post-streptococcal glomerulonephritis

A

presents with peripheral and periorbital edema, cola-colored urine, HTN
+ strep titers/serologies
decrease complement (C3) levels d/t consumption

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25
Q

post-streptococcal glomerulonephritis LM

A

glomeruli enlarged and hypercellular

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26
Q

post-streptococcal glomerulonephritis IF

A

‘starry sky’ granular appearance (‘lumpy bumpy’) due to IgG, IgM, and C3 deposition along GBM and mesangium

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27
Q

post-streptococcal glomerulonephritis EM

A

sub epithelial immune complex humps

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28
Q

rapidly progressive (crescentic) glomerulonephritis

A

rapidly deteriorating renal function (days to weeks)

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29
Q

rapidly progressive (crescentic) glomerulonephritis LM

A

crescent moon shaped

- crescents consist of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophages

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30
Q

rapidly progressive (crescentic) glomerulonephritis - goodpasture syndrome IF

A

linear IF due to antibodies to GBM and alveolar basement membrane

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31
Q

good pasture syndrome

A

hematuria/hemoptysis
type II hypersensitivity reaction
tx: plasmapheresis

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32
Q

rapidly progressive (crescentic) glomerulonephritis - Wegener’s IF

A

negative IF/Pauci-immune (no Ig/C3 deposition)

PR3-ANCA (c-ANCA)

33
Q

rapidly progressive (crescentic) glomerulonephritis - microscopic polyangiitis IF

A

negative IF/Pauci-Immune (no Ig/C3 deposition)

MPO-ANCA/p-ANCA

34
Q

rapidly progressive (crescentic) glomerulonephritis - PSGN or DPGN

A

granular IF

35
Q

diffuse proliferative glomerulonephritis

A

often d/t SLE (think ‘wire lupus’)

DPGN and MPGN often present as nephrotic syndrome and nephritic syndrome concurrently

36
Q

diffuse proliferate glomerulonephritis LM

A

‘wire looping’ of capillaries

37
Q

diffuse proliferative glomerulonephritis IF

A

granula

38
Q

diffuse proliferative glomerulonephritis EM

A

subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition

39
Q

IgA nephropathy

A

episodic hematuria that occurs concurrently with respiratory OR GI tract infections (IgA is secreted by mucosal linings)
renal pathology of IgA vasculitis (HSP)

40
Q

IgA nephropathy LM

A

mesangial proliferation

41
Q

IgA nephropathy IF

A

IgA-based IC deposits in mesangium

42
Q

IgA nephropathy EM

A

mesangial IC deposition

43
Q

Alport syndrome

A

mutation in type IV collagen -> thinning and splitting of glomerular basement membrane
X-linked dominant

44
Q

Alport syndrome presentation

A 
Eye problems (retinopathy, lens dislocation), glomerulonephritis, sensorineural deafness
'can't see, can't pee, can't hear a bee'
45
Q

alport syndrome EM

A

basket-weave

46
Q

membranoproliferative glomerulonephritis

A

nephritic syndrome that often co-presents with nephrotic syndrome

47
Q

type I membranoproliferative glomerulonephritis

A

may be secondary to hepatitis B or C infection
may also be idiopathic
sub-endothelial IC deposits with granular IF

48
Q

type II membranoproliferative glomerulonephritis

A

associated with C3 nephritic factor (IgG antibody that stabilizes C3 convertase -> persistent complement activation -> decrease C3 levels)
intramembranous deposits, aka dense deposit disease

49
Q

membranoproliferative glomerulonephritis

A

mesangial ingrowth -> GBM splitting -> ‘tram-track’ appearance on H&E and PAS stains

50
Q

casts

A

indicates that hematuria/pyuria is of glomerular or renal tubular origin
bladder cancer, kidney stones -> hematuria, no casts
acute cystitis -> pyuria, no casts

51
Q

RBC casts

A

glomerulonephritis, hypertensive emergency

52
Q

WBC casts

A

tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

53
Q

fatty casts (‘oval fat bodies’)

A

nephrotic syndrome

associated with ‘Maltese cross’ signs

54
Q

granular (‘muddy brown’) casts

A

acute tubular necrosis (ATN)

55
Q

waxy casts

A

end-stage renal disease/chronic renal failure

56
Q

hyaline casts

A

nonspecific, can be a normal finding, often seen in concentrated urine simplex

57
Q

Acute interstitial nephritis causes

A

drugs act as happens, inducing hypersensitivity (diuretics, penicillin derivatives, proton pump inhibitors, sulfonamides, rifampin, NSAIDs)
less commonly secondary to other processes such as systemic infections (Mycoplasma) or autoimmune (Sjogren, SLE, sarcoidosis)

58
Q

acute interstitial nephritis findings

A

pyuria (classically eosinophils) and azotemia

fever, rash, hematuria, pyuria, and CVA tenderness, but an be asymptomatic

59
Q

AIN mnemonic

A 
P's:
Pee (diuretics)
Pain-free (NSAIDs)
Penicillins and cephalosporins
Proton pump inhibitors
rifamPin
60
Q

acute tubular necrosis causes

A

ischemic or nephrotoxic

61
Q

ischemic ATN

A

secondary to decrease renal blood flow (hypotension, shock, sepsis, hemorrhage, HF)
-> death of renal tubular cells that may slough into tubular lumen
(PCT and thick ascending limb are highly susceptible to injury)

62
Q

nephrotoxic ATN

A

secondary to injury resulting from toxic substances (ahminoglycosides, radio contrast agents, lead, cisplatin, ethylene glycol), crush injury (myoglobulinuria), hemoglobinuria
proximal tubules are particularly susceptible to injury

63
Q

stages of ATN

A
  1. inciting event
  2. maintenance phase - oliguric; lasts 1-3wks; risk of hyperkalemia, metabolic acidosis, uremia
  3. recovery phase - pyloric; BUN and serum creatinine fall; risk of hypokalemia and renal wasting of other electrolytes and minerals
64
Q

key finding of ATN

A

granular (muddy brown) casts

65
Q

distal renal tubular acidosis (type 1) defect

A

inability of α-intercalated cells to secrete H+ -> no new HCO3- is generated -> metabolic acidosis

66
Q

RTA type 1 urine pH

A

> 5.5

67
Q

RTA type 1 serum K+

A

decrease

68
Q

RTA type 1 causes

A

amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (SLE)

69
Q

RTA type 1 associations

A

increase risk of calcium phosphate kidney stones (due to increase urine pH and increase bone turnover)

70
Q

proximal renal tubular acidosis (type 2) defect

A

defect in PCT HCO3- reabsorption -> increase excretion of HCO3- in urine -> metabolic acidosis
urine can be acidified by α-intercalated cells in collecting duct, but not enough to overcome the increased excretion of HCO3- -> metabolic acidosis

71
Q

RTA type 2 urine pH

A

< 5.5

72
Q

RTA type 2 serum K+

A

decrease

73
Q

RTA type 2 causes

A

Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors

74
Q

RTA type 2 associations

A

increase risk for hypophosphatemic rickets (in Fanconi syndrome)

75
Q

hyperkalemic tubular acidosis (type 4) defects

A

hypoaldosteronism or aldosterone resistance; hyperkalemia -> decrease NH3 synthesis in PCT -> decrease NH4+ excretion

76
Q

RTA type 4 urine pH

A

< 5.5 (or variable)

77
Q

RTA type 4 serum K+

A

increase

78
Q

RTA type 4 causes

A

decrease aldosterone production (e.g. diabetic hyporeninism, ACEi, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (e.g. K+-sparing diuretics, nephropathy due to obstruction, TMP-SMX)

COMLEX 2 (37 decks)

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