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FA Active Learning > FA - Renal Pathology > Flashcards

FA - Renal Pathology Flashcards

1
Q

What are causes of RBC casts?

A

Glomerulonephritis, ischemia, or malignant HTN

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2
Q

What are causes of WBC casts?

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

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3
Q

What are causes of fatty/oval body casts?

A

Nephrotic syndrome

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4
Q

What are causes of granular/muddy brown casts?

A

ATN

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5
Q

What are causes of waxy casts?

A

Advanced renal disease/chronic renal failure

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6
Q

What are causes of hyaline casts?

A

Non-specific and can be a normal finding

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7
Q

What defines a focal glomerular disorder and what is an example?

A

<50% of glomeruli involved, e.g. FSGS

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8
Q

What defines a diffuse glomerular disorder and what is an example?

A

> 50% of glomeruli involved, e.g. DPGN

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9
Q

What defines a proliferative glomerular disorder and what is an example?

A

Hypercellular glomeruli, e.g. mesangial proliferative

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10
Q

What defines a membranous glomerular disorder and what is an example?

A

Thickening of GBM, e.g. membranous nephropathy

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11
Q

What defines a primary glomerular disease and what is an example?

A

Involves only the glomerulus, e.g. minimal change dz

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12
Q

What defines a secondary glomerular disease and what is an example?

A

Involves glomeruli and other organs, thus a dz of another organ system or a systemic dz with renal manifestation, e.g. SLE, diabetic nephropathy

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13
Q

What are some pure nephritic syndromes?

A

Acute PSGN, RPGN, Berger’s IgA GN, Alport syndrome

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14
Q

What are some pure nephrotic syndromes?

A

Minimal change dz, FSGS, membranous nephropathy, amyloidosis, diabetic glomerulonephropathy

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15
Q

What are some mixed nephritic/nephrotic syndromes?

A

DPGN, MPGN

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16
Q

What are general features of nephrotic syndrome?

A

Proteinuria (frothy urine), hyperlipidemia, fatty casts, edema.
May also see thromboembolism (loss of AT III) and increased risk of infection (loss of Igs)

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17
Q

What are the findings in FSGS?

A

LM - segmental sclerosis and hyalinosis

EM - effacement of podocyte foot processes

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18
Q

What are common associations in FSGS?

A

Most common cause of nephrotic syndrome in adults (esp. AA, Hisp. populations)
Assoc. with HIV infection, heroin abuse, massive obesity, interferon treatment, CKD due to congenital absence or surgical removal

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19
Q

What are the findings in membranous nephropathy?

A

LM - diffuse capillary and GBM thickening
EM - “spike and dome” appearance with SUBEPITHELIAL deposits
IF - granular

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20
Q

What are common associations in membranous nephropathy?

A

Most common SLE presentation
Second most common cause of primary nephrotic syndrome in adults (esp. Caucasians)
Can be idiopathic or caused by drugs, infections, SLE, solid tumors

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21
Q

What are the findings in minimal change disease?

A

LM - normal glomeruli
EM - diffuse effacement of podocyte foot processes
Selective loss of albumins due to GBM polyanion loss

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22
Q

What are the common associations in minimal change disease?

A

Most common in children. May be triggered by a recent infection or an immune stimulus. Responds to corticosteroid Rx

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23
Q

What are the findings in amyloidosis?

A

Congo red stain shows apple-green birefringence under polarized light

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24
Q

What are the associations in amyloidosis?

A

Chronic conditions such as multiple myeloma, TB, RA

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25
Q

What are the findings in Type I MPGN?

A

EM - subendothelial “tram track” deposits (GBM splitting due to mesangial ingrowth)
IF - granular staining

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26
Q

What are the findings in Type II MPGN?

A

EM - intramembranous IC deposits (dense deposits)

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27
Q

What are the associations in Type I MPGN?

A

Associated with HBV, HCV

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28
Q

What are the associations in Type II MPGN?

A

Associated with C3 nephritic factor

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29
Q

What are the findings in diabetic glomerulonephropathy?

A

LM - nonenzymatic glycosylation of GBM –>inc. permeability and thickening, mesangial expansion, K-W lesions

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30
Q

What are the associations in diabetic glomerulonephropathy?

A

NEG of efferent arterioles –>increased GFR and mesangial expansion

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31
Q

What are general features of nephritic syndrome?

A

Inflammatory process which leads to hematuria and RBC casts in urine. Associated with azotemia, oliguria, hypertension (secondary to salt retention), proteinuria (<3.5g/day)

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32
Q

What are the findings in acute PSGN?

A

LM - glomeruli enlarged and hypercellular, neutrophils, “lumpy-bumpy” appearance
EM - subepithelial immune complex humps

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33
Q

What are the associations in PSGN?

A

Most frequently seen in children
Peripheral and periorbital edema, dark urine, hypertension
Resolves spontaneously

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34
Q

What are the findings in RPGN?

A

LM and IF - crescent moon shaped

Crescents consist of fibrin and plasma proteins (e.g. C3b) with glomerular parietal cells, monocytes, and macrophages

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35
Q

What disease processes can present like RPGN?

A 
Goodpasture's syndrome -- type II HSR, antibodies to GBM and alveolar BM with linear IF
Wegener's granulomatosis (c-ANCA)
Microscopic polyangiitis (p-ANCA)
36
Q

What are the findings in DPGN?

A

LM - wire looping of capillaries
EM - subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
IF - granular

37
Q

What are the associations in DPGN?

A

Most common cause of death in SLE

SLE and MPGN can present as nephrotic syndrome and nephritic syndrome concurrently

38
Q

What are the findings in IgA nephropathy?

A

LM - mesangial proliferation
EM - mesangial IC deposits
IF - IgA based IC deposits in the mesangium

39
Q

What are the associations in IgA nephropathy?

A

Associated with HSP (fever, petechial rash, arthalgia, GI disturbance), may follow recent illness (URI, gastroenteritis)

40
Q

What features define Alport syndrome?

A

X-linked mutation in Type IV collagen –>split BM

Presents as glomerulonephritis, deafness, eye problems (less common)

41
Q

What are the general complications of kidney stones and how can they be prevented?

A

Can lead to severe complications, such as hydronephrosis and pyelonephritis
Treat and prevent by adequate hydration, citrate (Ca++ binder) for recurrent stones

42
Q

What are the most common types of kidney stones and how do they precipitate?

A

Calcium (80%, radioopaque), precipitates as calcium phosphate at high pH, calcium oxalate at low pH (hypercalciuria + normocalcemia)

43
Q

What are some conditions that predispose to calcium stones?

A

Conditions that cause hypercalcemia (cancer, high PTH) –>hypercalciuria

44
Q

What are some conditions that predispose to calcium oxalate conditions?

A

Ethylene glycol use or Vitamin C abuse

45
Q

What are the features of ammonium magnesium phosphate (struvite) stones?

A

15% of stones, radioopaque, precipitate at high pH
Caused by infection with urease+ bugs (Proteus, Staphylococcus, Klebsiella) that hydrolyze urea to ammonia –>increased urine pH
Can form staghorn calculi –>nidus for UTI

46
Q

What are the features of uric acid stones?

A

5% of stones, radiolucent (visible on CT/US but not X-ray), precipitate at low pH
Strong association with hyperuricemia; often seen in diseases with high cell turnover. Treat by urine alkalinization.

47
Q

What are the features of cystine stones?

A

1% of stones, radioopaque, precipitate at low pH.

Most often secondary to cystinuria, hexagonal crystal. Treat by urine alkalinization.

48
Q

What are the causes of hydronephrosis?

A

Can be caused by urinary tract obstruction or vesicoureteral reflux

49
Q

What are the consequences of hydronephrosis?

A

Causes dilation of the renal pelvis and calyces proximal to obstruction. May result in parenchymal thinning in chronic, severe cases.

50
Q

What are the features of renal cell carcinoma?

A

Originates from proximal tubular cells –>polygonal clear cells filled with accumulated lipids and carbohydrates

51
Q

What is the classic triad of RCC? What are other clinical findings?

A

Triad: hematuria, palpable mass, flank pain; may also see secondary polycythemia, fever, and weight loss

52
Q

What are common sites of metastasis in RCC?

A

Lung and bone

53
Q

What is the epidemiology of RCC? What is the genetic defect?

A

Males 50-70 years, increased incidence with smoking and obesity. Sporadic gene deletion on chromosome 3 or inherited (VHL syndrome). May also be associated with paraneoplastic syndromes.

54
Q

What are the features of Wilms’ tumor?

A

Contains embryonic glomerular structures. Presents with huge, palpable flank mass and/or hematuria.

55
Q

What is the epidemiology of Wilms’ tumor?

A

Most common renal malignancy of early childhood (ages 2-4)
Caused by deletion of tumor suppressor gene WT1 on chromosome 11.
May be part of Beckwith-Wiedemann syndrome (WT2) or WAGR complex (Wilms’ tumor, aniridia, genitourinary malformation, mental retardation)

56
Q

What are the features of transitional cell carcinoma?

A

Most common tumor of the urinary tract (renal calyces, renal pelvis, ureters, bladder). Presents with painless hematuria.

57
Q

What are the features of acute pyelonephritis?

A

Affects the cortex with relative sparing of glomeruli/vessels. Presents with fever, CVA tenderness, n/v.
WBC casts in urine are classic.

58
Q

What are the histological findings in acute pyelonephritis?

A

Neutrophilic infiltration into renal interstitium.

59
Q

What are the causes/predisposing factors of chronic pyelonephritis?

A

Result of recurrent episodes of acute pyelonephritis. Typically requires predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones

60
Q

What are the histologic findings in chronic pyelonephritis?

A

Coarse, asymmetric corticomedullary scarring with lymphocytic infiltration and fibrosis, blunted calyx, tubules can contain eosinophilic casts (thyroidization)

61
Q

What are the features of drug-induced interstitial nephritis?

A

Acute interstitial renal inflammation. Pyuria (eosinophils) and azotemia occurring after administration of drugs that act as haptens, including HSR –>fever, rash, hematuria, CVA tenderness OR asymptomatic

62
Q

What are the types of drugs implicated in interstitial nephritis?

A

Typically occurs 1-2 weeks after use of diuretics, penicillin derivatives, sulfonamides, rifampin or months after starting NSAIDs

63
Q

What are the features of diffuse cortical necrosis?

A

Acute generalized cortical infarction of both kidney. Likely due to combination of vasospasm and DIC

64
Q

What is the epidemiology of diffuse cortical necrosis?

A

Associated with obstetric catastrophes (e.g. abruptio placentae) and septic shock

65
Q

What are the features of acute tubular necrosis?

A

Most common cause of intrinsic renal failure.
3 stages: Inciting event, maintenance phase (oliguria, lasts 1-3 weeks with risk of hyperkalemia, highest risk of death), recovery phase (polyuric, BUN/Cr fall, risk of hypokalemia). Hallmark muddy brown casts.

66
Q

What are possible causes of ATN?

A

Renal ischemia (shock, sepsis), crush injury (myoglobinuria), drugs (sulfonamides, MTX, IV acyclovir, triamterene), toxins

67
Q

What are the features of renal papillary necrosis?

A

Sloughing of renal papillae –>gross hematuria and proteinuria. May be triggered by recent infection or immune stimulus.

68
Q

What are common associations in renal papillary necrosis?

A

Diabetes mellitus, acute pyelonephritis, chronic phenacetin use, sickle cell anemia and trait

69
Q

What is the definition of ARF/AKI?

A

Acute renal failure is defined as an abrupt decline in renal function with increased Cr and BUN over a period of several days

70
Q

What defines prerenal azotemia?

A

As a result of decreased RBF –>decreased GFR. Na+/H2O and urea retained by kidney in an attempt to conserve volume so BUN/Cr ratio increases

71
Q

What defines intrinsic renal failure?

A

Generally due to ATN or ischemia/toxins; less commonly due to acute glomerulonephritis.
Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule –>dec. GFR
Impaired BUN reabsorption –>decreased BUN/Cr ratio

72
Q

What defines postrenal azotemia?

A

Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction

73
Q

What is the Uosm, UNa, FeNa, and serum BUN:Cr in prerenal azotemia?

A

Uosm >500, UNa 20

74
Q

What is the Uosm, UNa, FeNa, and serum BUN:Cr in intrinsic renal failure?

A

Uosm 40, FeNa >2%, serum BUN:Cr <15

75
Q

What is the Uosm, UNa, FeNa, and serum BUN:Cr in postrenal azotemia?

A

Uosm 40, FeNa >2%, serum BUN:Cr >15

76
Q

What are some cardiovascular consequences of renal failure?

A

Na+/H2O retention –>CHF, pulmonary edema, HTN

77
Q

What are some metabolic consequences of renal failure?

A

Hyperkalemia, metabolic acidosis, dyslipidemia, uremia (elevated BUN:Cr, nausea and anorexia, asterixis, encephalopathy, platelet dysfunction)

78
Q

What are some hematological consequences of renal failure?

A

Anemia (failure of Epo production)

79
Q

What are some pediatric complications of renal failure?

A

Growth retardation and developmental delay

80
Q

What are some renal complications of renal failure?

A

Renal osteodystrophy –>failure of Vit D hydroxylation, hypocalcemia, hyperphosphatemia (secondary hyperparathyroidism) –>subperiosteal thinning of bones

81
Q

What defines ADPKD?

A

Multiple, large, bilateral cysts that ultimately destroy the kidney parenchyma. Presents with flank pain, hematuria, HTN, UTI, progressive renal failure. Malignant potential.

82
Q

What is the epidemiology of ADPKD?

A

AD mutation in PKD1 or PKD2. Death from complications of CKD or HTN (caused by increased renin production). Syndrome presents in middle age.

83
Q

What are common associations of ADPKD?

A

Berry aneurysms, MVP, benign hepatic cysts

84
Q

What defines ARPKD?

A

Infantile, parenchymal presentation (radial formation). Significant renal failure in utero can lead to Potter’s syndrome. Concerns beyond neonatal period include HTN, portal HTN, progressive renal insufficiency

85
Q

What defines medullary cystic disease (cystic renal dysplasia)?

A

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; shrunken kidneys on ultrasound. Poor prognosis.

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