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Group1 Flashcards

1
Q

principle causes of ESRD (2)

A

44% diabetes, 27% HTN

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2
Q

glomerular barrier parts (3)

A

fenestrated capillary endothelium, basement membrane, podocyte foot processes with slit diaphragms made up of nephrin

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3
Q

normal urine proteins (amount, % of two major) and what level of proteinuria is nephrotic?

A

Normal urine has < 150 mg/day proteins: 45% Tamm Horsfall (secreted by TAL epithelium), 35% albumin (escapes reabsorption in PCT); if urine has more than 3.5 g/day it must be glomerular in origin

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4
Q

selective proteinuria: urine findings, mechanism, pathophys

A

pathophys: minimal change disease; mechanism: foot process effacement (loss of charge barrier?); urine: albumin, transferrin, no IgG (too big)

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5
Q

non-selective proteinuria

A

pathophys: most glomerulopathy other than min change disease; mechanism: foot process effacement (loss of size barrier?); urine: albumin, transferrin, IgG

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6
Q

proximal tubular dysfn proteinuria: urine findings, mechanism, pathophys

A

mech: decr reabs of filtered protein; pathophys: tubulo-interstitial dis, Fanconi; urine: <3 g day proteinuria (B2 microglobulin, lysozyme, albumin) along w/ other signs of PCT dysfn (glucose, bicarb, AA, etc.)

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7
Q

overload proteinuria: urine findings, mechanism, pathophys

A

pathophys: plasma cell dyscrasias (multiple myeloma); mech: incr # small, abnormal filterable serum proteins, these proteins can cause PCT toxicity/cast formation (prevent reabs of albumin); urine: <3 g day (non-glomelular), normal urine dipstick for protein (altho poss incr albumin), lots of IgG light chains (Bence Jones protein)

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8
Q

orthostatic proteinuria: urine findings, pathophys

A

pathophy: not pathological (seen in healthy teens/young adults); <2 g day proteinuria that appears in first morning urine when pt becomes upright

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9
Q

functional proteinuria

A

not pathological, seen in pts w/ high fever, CHF, cold exposure, resolves w/ resolution of precipitating event

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10
Q

best method for long term follow-up of proteinuria

A

spot urine protein:creatinine ratio

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11
Q

spot urine protein:creatinine ratio

A

best method for long-term follow-up; detects all protein; Upr/Ucr ~ 24 hr protein excretion (nl <.15) b/c Ucr ~ 1000 mg/day; this underestimates Upr in muscular men and overestimates Upr in elderly pts, but still useful for tracking vs time b/c Ucr shouldn’t change

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12
Q

nephrotic syndrome

A

non-inflammatory glomerulopathy (seen in CKD); syndrome: glomerular proteinuria (>3.5 g/day), hypoproteinemia, edema, hyperlipidemia

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13
Q

diff dx of edema (5)

A

proteinuria, renal failure, CHF, liver failure, protein malnutrition

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14
Q

complications of nephrotic syndrome (3)

A

hypercoagulability (due to loss of antithrombin proteins), infection, atherogenesis

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15
Q

histopathologies of nephrotic syndrome (3)

A

minimal change disease; focal segmental glomerulosclerosis; membranous glomerulopathy

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16
Q

mechs of injury in nephrotic syndrome (3)

A

minimal change -> unclear (T/B mediated); FSGS -> podocyte injury; MGN -> in-situ immune complex to some antigen on podocytes

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17
Q

minimal change disease: type of what, LM/FM/EM, etiology, demographics, tx (2), prognosis (3)

A

type of histopath in nephrotic syndrome; normal cx on LM, negative FM, but EM shows foot process effacement; etiology either primary (poss B/T cell mediated) or secondary (NSAIDs, lymphoma); seen mostly in kids; tx w/ corticosteroids for 6 weeks (90-95% remission) -> may give kids steroid trial rather than biopsy if they have nephrotic syndrome w/o HTN and hematuria and w/ normal GFR and C3; 33% never relapse after tx, 33% occasionally relapse, and 33% frequently relapse (>3 in 6 mos)

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18
Q

FSGS: type of what, LM/FM/EM, pathogenesis, FSGS factor, demographics (2)

A

type of histopath in nephrotic syndrome; LM has focal (some glomeruli) segmental (parts of these glomeruli) scleroris (too much ECM) w/ segmental collapse w/ adhesions to Bowman’s capsule, FM has IgM and C3 in mesangium of collapsed segments, EM has foot process effacement, focal podocyte injury or denudation of GBM, collapse of cap loops w/ accumulation of hyalin; pathogenesis: final common pathway for glom injury, due to podocyte injury w/ loss of podocytes in urine -> segmental sclerosis; may be due to uPAR (circulating factor, explains why transplanted kidneys can get FSGS in FSGS pts); common in elderly (infantile FSGS is monogenetic)

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19
Q

uPAR

A

circulating FSGS factor (explains why pts w/ FSGS can get FSGS in donated kidneys)

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20
Q

what disease has no findings on LM or FM but has foot process effacement on EM?

A

minimal change disease

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21
Q

what disease is assoc w/ injury and loss of podocytes?

A

FSGS

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22
Q

what disease has FM of IgM and C3 in mesangium?

A

FSGS

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23
Q

what disease has EM of foot process effacement, focal podocyte injury or denudation of GBM, collapse of capillary loops w/ accumulation of hyalin

A

FSGS

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24
Q

what nephrotic syndrome is common in kids?

A

minimal change disease

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25
Q

what nephrotic syndrome is common in elderly?

A

FSGS

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26
Q

when do we try a steroid trial?

A

kids w/ nephrotic syndrome w/o HTN and hematuria and w/ normal GFR and C3 -> way to avoid biopsy if we believe they may have minimal change disease

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27
Q

membranous glomerulopathy: type of, LM/FM/EM, etiology (7), natural hx (3)

A

type of histopath in nephrotic syndrome; LM: thickened glomerular cap loops (thickened BM) w/ BM spikes seen on PAS and subepithelial deposits seen in trichrome, FM: IgG and C3 in granular cap loop deposits (secondary MGN has both cap loop and mesangial deposits of more proteins), EM: foot process effacement, subepithelial electron dense deposits w/ variable amounts of BM surrounding them, secondary MGN may have subendothelial and mesangial deposits too; primary MGN: subepithelial immune complexes form in situ against podocyte membrane antigen (assoc w/ HLA types); secondary: infx (hep B/C, malaria), neoplasms (lung, colon, gastric, breast), meds (gold salts, penicillinamine), SLE; natural hx: 20% spontaneous remission, 60% persistent proteinuria w/o GFR decline; 20% progressive w/ GFR decline

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28
Q

etiology of MGN

A

primary MGN: subepithelial immune complexes form in situ against podocyte membrane antigen (assoc w/ HLA types); secondary: infx (hep B/C, malaria), neoplasms (lung, colon, gastric, breast), meds (gold salts, penicillinamine), SLE

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29
Q

what disease can be caused by hep B/C?

A

MGN

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30
Q

what disease can be caused by HIV?

A

FSGS

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31
Q

what disease can be caused by malaria?

A

MGN

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32
Q

what disease can be caused by gold salts?

A

MGN

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33
Q

what disease can be caused by penicillamine?

A

MGN

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34
Q

what disease can be caused by neoplasm?

A

lung/colon/gastric/breast cancer -> MGN; lymphoma -> minimal change disease

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35
Q

what disease can be caused by NSAIDS?

A

minimal change disease and interstitial nephritis; NSAIDS also cause GFR decline (no afferent dilation)

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36
Q

what disease has LM of: thickened glomerular cap loops w/ BM spikes seen on PAS and subepithelial deposits seen in trichrome

A

MGN

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37
Q

what disease of EM of: foot process effacement, subepithelial electron dense deposits w/ variable amounts of BM surrounding them

A

MGN

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38
Q

what disease has FM of: IgG and C3 in granular cap loop deposits

A

MGN (can have mesangial and other staining in secondary MGN), post-strep (w/ mesangial deposits too), lupus (w/ mesangial deposits and positive w/ other stains too)

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39
Q

FM in nephrotic syndromes

A

minimal change disease: no staining; FSGS: IgM/C3 in mesangium; MGN: IgG/C3 in granular cap loop deposits (secondary MGN can have more proteins in granular loop and mesangial deposits)

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40
Q

hematuria/proteinuria differential dx

A

glomerular disease likely if hematuria and proteinuria (either inflammatory glomerulonephritis aka nephritic syndrome or diabetic nephropathy or heriditary GBM disease); non-glomerular disease likely if hematuria only (if >40 yo, consider cancer, stones, infx; if <40 yo, consider stones, infx, trauma); nephrotic syndrome likely if proteinuria only

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41
Q

nephritic syndrome

A

inflammatory glomerulonephritis (seen in acute and subacute renal failure); syndrome: microscopic hematuria (RBC casts, dysmorphic RBCs), proteinuria (not as high as nephrotic syndrome), HTN, edema

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42
Q

nephritic syndrome mnemonic

A

PHARAOH = Proteinuria, Hematuria, Azotemia, RBC casts, Anti-strep titres (if post-strep), Oliguria, Hypertension

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43
Q

nephritic vs nephrotic

A

nephritic is inflammatory, acute, has hematuria (dysmorphic RBC/RBC casts) and mild proteinuria (3.5 g proteinuria w/o hematuria; nephritic assoc w/ HTN; nephrotic assoc w/ hyperlipidemia and hypoalbuminemia; both have edema (nephrotic due to hypoalbuminemia, nephritic due to Na retention b/c nephritic assoc. w AKI)

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44
Q

Rapidly Progressive Glomerulonephritis

A

2 nested clinical syndromes: subacute rise in Pcr w/ nephritic syndrome

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45
Q

pathophys of nephritic syndrome (5 events and timeline)

A

Capillary wall injury -> proliferation w/in 24 hrs (influx of immune cells to glomerular tuft, not prolif of endogenous glom. cells = hypercellularity on LM) -> acellular crescent formation (4 days, made up of fibrinogen) -> cellular crescent formation (7 days, immune cells and fibroblasts gel onto acellular crescent)-> glomerular and interstitial scarring by fibroblasts (30 days -> irreversible nephron loss)

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46
Q

nephritic syndrome diff dx

A

antibody mediated (anti GBM/Goodpasture’s); immune complex mediated (post-strep, lupus, IgA/HSP); pauci-immune glomerulonephritis (ANCA positive small vessel vasculitis)

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47
Q

antibody mediated nephritic syndrome etiology

A

IgG against type IV collagen in GBM

48
Q

Goodpasture’s syndrome: type of what, what is it, how does it present, LM/FM/GM,tx (3)

A

antibody-mediated nephritic syndrome; anti-GBM (IgG against type IV collagen) pulmonary-renal syndrome: presents w/ RPGN and hemoptysis; LM: hypercellular glomeruli w/ fibrin and crescents in Bowman’s space; FM: linear GBM staining w/ IgG and C3 w/ stringy fibrin staining in Bowman’s space; EM: compressed glomerular tuft, fibrin in Bowman’s space, no deposits; tx: plasma exchange, immunosuppression, rituximab (anti CD20)

49
Q

FM in: minimal change disease, FSGS, MGN, anti-GBM, post-strep, lupus, HSP, vasculitis

A

minimal change dis: no FM staining (LM also normal); FSGS: IgM and C3 in mesangium; MGN: IgG and C3 in granular cap loop deposits; anti-GBM: linear cap loop staining of IgG and C3 w/ stringy fibrin in Bowman’s space; post-strep: granular cap loop and mesangial IgG and C3; lupus: granular cap loop and mesangial “full house” deposits (IgG, IgA, IgM, C1q, C4, C3); HSP: mesangial IgA and C3; vasculitis: no FM staining (despite inflamm infiltrate on LM)

50
Q

what disease has normal LM?

A

minimal change disease

51
Q

what disease has nothing staining on FM?

A

minimal change disease, vasculitis (altho MCD has nothing on LM while vasculitis has inflammation of LM)

52
Q

what disease has FM: linear cap loop staining of IgG and C3

A

anti-GBM (also has stringy fibrin in Bowman’s)

53
Q

which disease has FM: granular cap loop and mesangial IgG and C3

A

post-strep GN; lupus (also has more positive stains); MGN has cap loop IgG/C3 but no mesangial unless secondary MGN)

54
Q

which disease has FM: granular cap loop and mesangial “full house” deposits (IgG, IgA, IgM, C1q, C4, C3)

A

lupus

55
Q

which disease has FM: mesangial IgA and C3

A

Henoch Schoenlein Purpura (IgA nephropathy variant)

56
Q

what disease has LM: hypercellular glomeruli w/ fibrin and crescents in Bowman’s space

A

anti-GBM -> no PNMs like in post-strep

57
Q

what disease has EM: compressed glomerular tuft, fibrin in Bowman’s space, no deposits

A

anti-GBM

58
Q

post-strep GN: type of what, presentation, LM/FM/EM, tx

A

type of immune complex mediated nephritic syndrome; presents 21 days post-infx w/ RPGN; LM: diffuse hypercellularity w/ LOTS of PNMs (specific feature), accentuation of lobar architecture, occasional subepi deposits; FM: granular cap loop and mesangial IgG and C3; EM: large discrete subepi deposits w/o sclerotic reaction (diagnostic), subendo and mesangial deposits present but not diagnostic; tx: supportive care (self-limited)

59
Q

what disease has LM: hypercellular glomeruli w/ PNMs, accentuation of lobar architecture, occasional subepi deposits

A

post-strep GN (PNMs are specific)

60
Q

what disease has EM: large discrete subepi deposits w/o sclerotic reaction, also subendo and mesangial deposits

A

post-strep GN (subepi deposits diagnostic)

61
Q

lupus: type of what, serology (3), LM/FM, tx (2)

A

type of immune complex mediated nephritic syndrome; serology: ANA, anti-dsDNA, hypocomplementemia; LM variable: can be prolif GM limited to mesangium, severe diffuse prolif GN similar to post-infx but w/ fewer PNMs, or combo of these w/ MGN, often see “wire loops” due to thickening of cap loops and extensive subendo or subepi deposits; FM: full house granular cap and mesangial deposits; tx: immunosuppression (achieves remission but w/ freq relapses), poss ACEI/ARB for BP control

62
Q

hypocomplementemia seen in?

A

lupus, post-infectious

63
Q

what has LM with “wire loops”?

A

lupus

64
Q

subendo deposits seen in

A

lupus (extensive), secondary MGN (w/ subepi and mesangial)

65
Q

subepi deposits seen in

A

lupus (extensive), post-strep (large, discrete), MGN (with variable BM surrounding)

66
Q

Henoch Schoenlein Purpura: type of what, presents (4), demographics, LM/FM/EM, Tx

A

type of IgA nephropathy (immune-mediated nephritic syndrome); presents w/ systemic vasculitis (RPGN, purpuric skin rash, colitis, arthritis); presents in childhood; LM: mesangial hypercellularity, focal cellular crescents; FM: mesangial IgA and C3 deposits; EM: mesangial electron dense deposits; Tx: us. supportive, poss immunosuppresion

67
Q

what disease has LM: mesangial hypercellularity, focal cellular crescents

A

HSP

68
Q

pauci-immune glomerulonephritis

A

aka “mechanism X” form of nephritic syndrome; LM has inflammatory infiltrate altho FM shows no staining

69
Q

ANCA positive small vessel vasculitis: aka (2), type of what, LM/FM/EM, tx

A

either Wegner’s or microscopic polyangitis; form of pauci-immune glomerulonephritis form of nephritic syndrome; LM: vasculitis w/ fibrinoid necrosis is diagnostic but rarely seen, focal necrotizing GN w/ crescents is commonly seen but not specific; FM: negative Ig/complement (hence pauci-immune), w/ fibrin in Bowman’s space; EM: collapse of glom tuft, no immune deposits; also positive for ANCA on serology; tx w/ immunosuppresion (95% remit w/ freq relapses)

70
Q

serologies (6)

A

ANCA positive in pauci-immune GN due to vasculitis; anti-dsDNA, ANA, hypocomplementemia positive in lupus; hypocomplementemia positive in post-infx; ASO positive in post-strep

71
Q

consequences of tubulointerstitial disease (8)

A

reduced GFR (AKI or CKD), Fanconi syndrome, RTA, tubular (small molecular weight) proteinuria (<2 g/day), polyuria, isothenuria (Uosm = Posm b/c tubules can’t concentrate or dilute), hyperkalemia (no K secretion), salt wasting (no Na reabsorption)

72
Q

ATN etiologies

A

ATN is most common cause of AKI; due to ischemia or toxins (drugs, heme pigements, contrast agents)

73
Q

acute interstitial nephritis LM

A

inflammation (mostly T cells) in interstitium; can cause tubulitis; assoc w/ edema that separates tubules; spares glomeruli and vessels (altho can be affected in chronic interstitial nephritis)

74
Q

thyroidization occurs in

A

chronic interstitial nephritis -> atrophic, dilated tubules filled w/ proteinacious material

75
Q

AIN etiology (7)

A

drug reaction (allergic) is most common, infection (direct renal infx or systemic); immunologic (lupus, Sjogrens, sarcoidosis, allograft rejection); idiopathic (tubulointerstitial nephritis-uveitis syndrome)

76
Q

allergic interstitial nephritis presentation

A

classic triad (rash, fever, peripheral eosinophilia) is rare, us. one or two of those sx w/ malaise, fatigue, arthralgias, flank pain; these sx occur 10-14 days after first drug exposure or sooner after repeat exposure and are not dose-dependent

77
Q

serum and urine in allergic interstitial nephritis

A

serum: elevated BUN/creatinine, eospinophilia; urine: lots of WBCs and WBC casts, occasional RBCs, mild proteinuria (can see nephrotic range w/ NSAIDs b/c they cause minimal change disease), eosinophiluria (>1% of WBCs, seen best w/ Hansel’s, not sensitive or specific), NO BACTERIA

78
Q

diff dx of pulm-renal syndrome (3)

A

Goodpasture’s, SLE, ANCA positive small vessel vasculitis

79
Q

diff dx of eosinphiluria (4)

A

AIN, RPGN, atheroemboli syndrome, transplant rejection

80
Q

drugs that lead to AIN (12)

A

antibiotics (pencillin analogues esp methicilin, cephalosporins, sulfonamides, rifampin, quinolones), NSAIDs, salicylates, loop and thiazide diuretics, phenytoin, allopurinol, cimetidine, omeprazole

81
Q

AIN LM, pathophys

A

LM: dense inflammatory infiltrate (mostly lymphocytes w/ some eosinophils), occasional granulomas (sparse and non-necrotic); most drug-induced AIN is cell mediated (lots of T cells, no immune deposits)

82
Q

when do we see “SICK” kidneys, and what does SICK stand for?

A

drug-induced (us. analgesic) chronic interstitial nephritis; SICK is small, indented, calcified gross kidneys

83
Q

common cause of chronic interstitial nephritis: what is it, demographics, disease development, assoc w/, similar disease

A

analgesic nephropathy due to combo meds (aspirin + pehnacetin + caffeine); most common in women w/ chronic pain; assoc w/ papillary necrosis (-> polyuria due to vasa recta damage) and chronic interstitial nephritis -> progressive kidney failure and hypertension; incr. incidence of transitional cell carcinoma of uroepithelium; Aristolochic acid nephropathy (Chinese herbal nephropathy) has similar features

84
Q

what disease has papillary necrosis and chronic interstitial nephritis?

A

analgesic nephropathy, Chinese herbal nephropathy (aristolochic acid nephropathy)

85
Q

acute pyelonephritis: us. caused by, settings (3), LM, consequences, viral causes (2)

A

us. caused by gram negative directly invading kidney via ascending route; commonly settings: UT obstruction, reflux, pregnancy, diabetes; LM: pus casts in renal tubules, microabscesses on surface or w/in parenchyma; us. don’t impair renal fn unless associated w/ V depletion or sepsis; viral causes: BK polyoma, cytomegalovirus

86
Q

vesicouteral reflux: types, predisposes to what

A

primary VUR is due to incompetent or inadequate closure of uterovesical junction during micturition (common in kids); secondary VUR is due to high bladder P that results in UVJ closure failure (aka urethral obstruction); VUR predisposes to pyelonephritis, esp. at renal poles due to more compound papillae

87
Q

chronic pyelonephritis

A

due to VUR; renal poles more affected (more compound papillae); focal scars over blunted calyces at poles; can occur w/o infx just due to sterile urine reflux

88
Q

multiple myeloma cast nephropathy LM, gross

A

tubules distended by homogenous, eosinophilic, fractured casts surrounded by multinucleated giant cells; Myeloma kidney is waxy and large w/ preserved cortex (one of few diseases w/ enlarged kidneys in CKD)

89
Q

multiple myeloma can affect kidney how (7)

A

misc: dehydration, hypercalcemia, hyperuricemia (tumor lysis syndrome), infection; light chain mediated: cast nephropathy, light chain glomerulopathy, amyloidosis

90
Q

MM light chain glomerulopathy LM/FM, sx (3)

A

LM: light chains deposit in mesangium -> nodular glomerulopathy that resembles diabetic nephropathy, poss chains depositing in tubular BM (PAS would show thickening of BM); FM: monoclonal light chains in glomeruli and poss tubular BM; sx: proteinuria (poss nephrotic range), microscopic hematuria, renal failure, less commonly Fanconi’s

91
Q

MM amyloidosis: involve what part of kidney (2), sx (2)

A

us involve glomeruli and blood vessels; pts present w/ heavy proteinuria and renal insufficiency

92
Q

main histologic feature of chronic interstitial nephritis

A

interstitial fibrosis w/ tubular atrophy

93
Q

normal urine

A

0-3 RBC/hpf, 0-2 WBC/hpf, few epithelial cells, 0-1 hyaline cast/lpf, up to 150 mg/day protein (+1 on dipstick if urine is concentrated)

94
Q

diff dx of red-brown urine

A

if sediment red (RBCs) then hematuria; if supernatant red and dipstick neg, then beeturia, phanazopyridine, porphyria; if supernatant red and dipstick positive, then myoglobin or hemoglobin; if hemoglobin then plasma should be red, if myoglobin then plasma should be clear; brown urine can be due to acid in urine turning hemoglobin into brown methemoglobin

95
Q

turbidity of urine diff dx

A

normal: contaminating mucus, precipitating urate/phosphate crystals (esp if refrigerated); abnormal: microorganisms, cells, casts, crystals, lipids; foamy: heavy proteinuria

96
Q

microalbuminuria

A

albuminuria ( > 20 mcg/min or > 30 mg/day) w/o proteinuria ( < 150 mg/day); highly predictive of clinical nephropathy in DM and CV dis in T2DM and nondiabetics; need special assay to detect (RIA or ELISA)

97
Q

urine epithelial cells

A

squamous (large, flat, small nucleus) due to urogenital contamination; tubular (1.5-3x bigger than WBC, round nucleus) due to ATN, exercise, GN

98
Q

Maltese cross

A

if heavy proteinuria present, tubular epithelial cells can undergo fatty degeneration and form Maltese crosses under polarized light -> fatty casts seen in glom disease w/ heavy proteinuria (>3 g/day)

99
Q

Casts (7 - what are they, describe them, due to)

A

hyaline casts (colorless cylinders), waxy and broad casts (high optical density, may have cracks, seen in advanced renal failure), granular casts (degen cells or aggregated serum proteins in many diseases) or muddy brown cigar casts (seen in ATN), epithelial cell casts (ATN, tubulointerstitial disease), RBC cases (GN), WBC casts (tubulointerstitial dis, pyelonephritis, acute GN), fatty casts (glom disease w/ heavy proteinuria aka nephrotic syndrome -> Maltese cross under polarized light)

100
Q

conditions favoring casts (4)

A

acidic urine, concentrated urine, urine stasis, proteinuria

101
Q

crystals (5 - what are they)

A

uric acid, calcium oxalate, struvite, calcium phosphate, cystine

102
Q

uric acid crystal: description (3), pH, seen in (4)

A

yellow or reddish-brown; may cause cloudy pink urine on precipitation; pleomorphic, rosettes, needles, or diamond shaped; found in acidic urine; seen in gout, fever, cytotoxic therapy for lymphoma (marked increase in uric acid production), amorphous urate is common and not clinically significant

103
Q

calcium oxalate crystals: description (2), pH, seen in (6)

A

envelopes (oXalate = X on envelope) or dumbbells, independent of pH; found in increased oxalate production (ethylene glycol ingestion, methoyxflurane anesthesia, glycerol infusion, primary hyperoxaluria) or absorption (chronic diarrhea w/ malabsorption), renal failure

104
Q

struvite crystals: aka (2), description, pH, seen in (2)

A

aka magnesium ammonium phosphate aka triple phosphate; coffin-lids; alkaline urine; assoc w/ UTI w/ urease producing bacteria (Proteus mirabilis), assoc w/ staghorn calculi

105
Q

calcium phosphate crystals: description (3), pH, seen in

A

pleomorphic, amorphous, stellate; seen in alkaline urine; seen commonly

106
Q

cystine crystals: description, pH, seen in

A

hexagonal, us. independent of pH although less common at pH > 7.4; seen in cystinuria

107
Q

crystals in acidic urine (3)

A

uric acid (acid urine only), calcium oxalate (all pHs), cystine (all pHs but less common above 7.4)

108
Q

crystals in alkaline urine (4)

A

calcium phosphate, struvite, calcium oxalate (all pHs), cystine (all pHs but less common above 7.4)

109
Q

coffin-lid crystals

A

struvite crystals

110
Q

envelope crystals

A

calcium oxalate crystals

111
Q

dumbbell crystals

A

calcium oxalate crystals

112
Q

cloudy pink urine on precipitation

A

uric acid crystals

113
Q

pleomorphic, rosettes, needles, or diamond shaped crystals

A

uric acid crystals

114
Q

pleomorphic, amorphous, stellate crystals

A

calcium phosphate crystals

115
Q

hexagonal crystals

A

cystine crystals

Renal (8 decks)

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