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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
post-streptococcal glomerulonephritis LM
glomeruli enlarged and hypercellular
26
post-streptococcal glomerulonephritis IF
'starry sky' granular appearance ('lumpy bumpy') due to IgG, IgM, and C3 deposition along GBM and mesangium
27
post-streptococcal glomerulonephritis EM
sub epithelial immune complex humps
28
rapidly progressive (crescentic) glomerulonephritis
rapidly deteriorating renal function (days to weeks)
29
rapidly progressive (crescentic) glomerulonephritis LM
crescent moon shaped | - crescents consist of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophages
30
rapidly progressive (crescentic) glomerulonephritis - goodpasture syndrome IF
linear IF due to antibodies to GBM and alveolar basement membrane
31
good pasture syndrome
hematuria/hemoptysis type II hypersensitivity reaction tx: plasmapheresis
32
rapidly progressive (crescentic) glomerulonephritis - Wegener's IF
negative IF/Pauci-immune (no Ig/C3 deposition) | PR3-ANCA (c-ANCA)
33
rapidly progressive (crescentic) glomerulonephritis - microscopic polyangiitis IF
negative IF/Pauci-Immune (no Ig/C3 deposition) | MPO-ANCA/p-ANCA
34
rapidly progressive (crescentic) glomerulonephritis - PSGN or DPGN
granular IF
35
diffuse proliferative glomerulonephritis
often d/t SLE (think 'wire lupus') | DPGN and MPGN often present as nephrotic syndrome and nephritic syndrome concurrently
36
diffuse proliferate glomerulonephritis LM
'wire looping' of capillaries
37
diffuse proliferative glomerulonephritis IF
granula
38
diffuse proliferative glomerulonephritis EM
subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
39
IgA nephropathy
episodic hematuria that occurs concurrently with respiratory OR GI tract infections (IgA is secreted by mucosal linings) renal pathology of IgA vasculitis (HSP)
40
IgA nephropathy LM
mesangial proliferation
41
IgA nephropathy IF
IgA-based IC deposits in mesangium
42
IgA nephropathy EM
mesangial IC deposition
43
Alport syndrome
mutation in type IV collagen -> thinning and splitting of glomerular basement membrane X-linked dominant
44
Alport syndrome presentation
``` Eye problems (retinopathy, lens dislocation), glomerulonephritis, sensorineural deafness 'can't see, can't pee, can't hear a bee' ```
45
alport syndrome EM
basket-weave
46
membranoproliferative glomerulonephritis
nephritic syndrome that often co-presents with nephrotic syndrome
47
type I membranoproliferative glomerulonephritis
may be secondary to hepatitis B or C infection may also be idiopathic sub-endothelial IC deposits with granular IF
48
type II membranoproliferative glomerulonephritis
associated with C3 nephritic factor (IgG antibody that stabilizes C3 convertase -> persistent complement activation -> decrease C3 levels) intramembranous deposits, aka dense deposit disease
49
membranoproliferative glomerulonephritis
mesangial ingrowth -> GBM splitting -> 'tram-track' appearance on H&E and PAS stains
50
casts
indicates that hematuria/pyuria is of glomerular or renal tubular origin bladder cancer, kidney stones -> hematuria, no casts acute cystitis -> pyuria, no casts
51
RBC casts
glomerulonephritis, hypertensive emergency
52
WBC casts
tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
53
fatty casts ('oval fat bodies')
nephrotic syndrome | associated with 'Maltese cross' signs
54
granular ('muddy brown') casts
acute tubular necrosis (ATN)
55
waxy casts
end-stage renal disease/chronic renal failure
56
hyaline casts
nonspecific, can be a normal finding, often seen in concentrated urine simplex
57
Acute interstitial nephritis causes
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
acute interstitial nephritis findings
pyuria (classically eosinophils) and azotemia | fever, rash, hematuria, pyuria, and CVA tenderness, but an be asymptomatic
59
AIN mnemonic
``` P's: Pee (diuretics) Pain-free (NSAIDs) Penicillins and cephalosporins Proton pump inhibitors rifamPin ```
60
acute tubular necrosis causes
ischemic or nephrotoxic
61
ischemic ATN
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
nephrotoxic ATN
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
stages of ATN
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
key finding of ATN
granular (muddy brown) casts
65
distal renal tubular acidosis (type 1) defect
inability of α-intercalated cells to secrete H+ -> no new HCO3- is generated -> metabolic acidosis
66
RTA type 1 urine pH
> 5.5
67
RTA type 1 serum K+
decrease
68
RTA type 1 causes
amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (SLE)
69
RTA type 1 associations
increase risk of calcium phosphate kidney stones (due to increase urine pH and increase bone turnover)
70
proximal renal tubular acidosis (type 2) defect
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
RTA type 2 urine pH
< 5.5
72
RTA type 2 serum K+
decrease
73
RTA type 2 causes
Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors
74
RTA type 2 associations
increase risk for hypophosphatemic rickets (in Fanconi syndrome)
75
hyperkalemic tubular acidosis (type 4) defects
hypoaldosteronism or aldosterone resistance; hyperkalemia -> decrease NH3 synthesis in PCT -> decrease NH4+ excretion
76
RTA type 4 urine pH
< 5.5 (or variable)
77
RTA type 4 serum K+
increase
78
RTA type 4 causes
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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