Pathology - renal

Question 1

RBC casts

Answer 1

glomerulonephritis, malignant hypertension

Question 2

WBC casts

Answer 2

tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

Question 3

fatty casts

Answer 3

Nephrotic syndrome

Question 4

granular casts

Answer 4

acute tubular necrosis

Question 5

Waxy casts

Answer 5

end-stage renal failure

Question 6

Nephritic syndrome

Answer 6

sign of GBM disruption

incr. BUN/Cr, oliguria, hematuria, RBC casts

Causes: acute post-streptococcal, rapidly progressive glomerulonephritis, IgA nephropathy, Alport syndrome, membranoproliferative glomerulonephritis

Question 7

Nephrotic syndrome

Answer 7

podocyte disruption –> charge barrier impaired

Massive proteinuria w/ low serum albumin, incr. lipids, edema, can lead to hyperthrombotic state (loss of antithrombin-3)

primary podocyte damage: PSGS, MCD, membranous nephropathy

secondary podocyte damage: amyloidosis, diabetic glomerulonephropathy

Question 8

Peripheral/periorbital edema 2 weeks after GABHS infection, cola-colored urine, hypertension

Hypercellular glomeruli
IgG/IgM/C3 deposition along GBM and mesangium

Answer 8

Acute post-streptococcal glomerulonephritis

Subepithelial immune complex humps (Type III reaction!)

Question 9

Rapidly deteriorating renal function, hematuria

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

Answer 9

RPGN (incl Goodpasture’s, Wegener’s c-ANCA, microscopic polyangiitis p-ANCA)

Question 10

SLE, presents often as nephrotic and nephritic syndromes concurrently

wire looping of capillaries
immune complex deposition
granular appearance on IF

Answer 10

Diffuse proliferative glomerulonephritis

**most common cause of death in SLE

Question 11

Renal insufficiency and gasteoenteritis (Henoch-Schonlein Purpura)
Episodic hematuria

mesangial proliferation

Answer 11

IgA nephropathy

mesangial IgA-based IC deposits in mesangium

Question 12

Eye problems, glomerulonephritis, sensorineural deafness

thinning of GBM

Answer 12

Alport syndrome

Type IV collagen defect

X-linked

Question 13

Copresentation of nephritic and nephrotic syndrome

Answer 13

Membranoproliferative glomerulonephritis

Type 1: subendothelial IC deposits, tram-track appearance (GBM splitting)
Type 2: intramembranous IC deposits, C3 nephritic factor

Question 14

Most common cause of nephrotic syndrome in AAs/Hispanics, secondary to sickle cell/HIV/heroin abuse/obesity

Answer 14

FSGS

segmental sclerosis, effacement of podocyte foot processes

inconsistent response to steroids

Question 15

Most common cause of nephrotic syndrome in children, lots of triggers

Answer 15

MCD

normal glomeruli but podocyte effacement

may be secondary to lymphoma, excellent response to steroids

Question 16

Most common cause of nephrotic syndrome in Caucasian adults, lots of triggers, assoc w/ SLE and solid tumors (lung, colon)

Diffuse granular capillary and GBM thickening, spike and dome appearance with subepithelial deposits, can have antibodies to podocyte transmembrane proteins

Answer 16

Membranous nephropathy

nephrotic presentation of SLE, poor response to steroids

Question 17

Congo red stain shows apple green bifringence

Answer 17

Amyloidosis

Nephrotic syndrome

Question 18

Diabetic glomerulonephropathy

Answer 18

Mesangial expansion, GBM thickening, esoinophilic nodular glomerulosclerosis

Glycosylation of GBM –> incr. permeability and thickening

Glycosylation of efferent arterioles –> incr. GFR –> mesangial expansion

Question 19

Kidney stones seen in pt w/ hypercalciuria and normocalcemia

Envelope or dumbbell-shaped calcium oxalate stones

Answer 19

Calcium stones

Oxalate: ethylene glycol poisoning, Vit. C abuse, malabsorption, precipitate at low pH

tx: hydration, thiazides, citrate, pyridoxine, low protein diet

Question 20

Kidney stones seen in pt w/ infection by urease + bugs (proteus, klebsiella, staph sapro)

Coffin lid-shaped stones

Answer 20

Struvite (ammonium magnesium phosphate)

Commonly form staghorn calculi

Question 21

Kidney stones seen in pt w/ dehydration or incr. cell turnover

Rhomboid-shaped or rosettes

Answer 21

Uric acid

tx: allopurinol, alkalinization of urine, low protein diet

Question 22

Kidney stones in pt w/ loss of cystine-reabsorbing PCT transporter

Hexagonal shaped

Answer 22

Cystine stones

Hexagonal shaped

Mostly seen in children, with positive sodium cyanide nitroprusside test, and they also have aminoaciduria

tx: alkalinization of urine

Question 23

Renal cell carcinoma pathology

Answer 23

PCT cells, polygonal clear cells filled with accumulated lipids and carbs/glycogen

invades renal vein then IVC and spreads hematogenously

gene deletion on Ch.3 (sporadic or von Hippel Landau)

assoc. with lots of paraneoplastic syndromes

Question 24

Renal oncocytoma

Answer 24

Benign epithelial cell tumor

Large eosinophilic cells with abundant mitochondria without perinuclear clearing

Question 25

Wilms tumor

Answer 25

large, palpable, unilateral flank mass loss of function of tumor suppressors WT1/WT2 May be part of Beckwith-Wiedemann or WAGR (wilms, aniridia - absence of iris, GU malformation, mental retardation)

Question 26

SCC of bladder

Answer 26

chronic irritation of bladder (Schistosoma haematobium infection) presents with painless hematuria

Question 27

Causes of UTIs

Answer 27

E. coli Staph sapro Klebsiella Proteus - ammonia scent nitrites in gram negatives (E. coli) negative cultures suggest urethritis

Question 28

Pyelonephritis

Answer 28

neutrophils infiltrate renal interstitium striated parenchymal enhancement on CT complications: renal papillary necrosis, perinephric abscess, urosepsis

Question 29

Chronic pyelonephritis

Answer 29

vesicoureteral reflux or chronic kidney stones asymmetric corticomedullary scarring, blunted calyx tubular can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney)

Question 30

Signs of drug-induced interstitial nephritis

Answer 30

Pyuria and azotemia Drugs act as haptens, inducing hypersensitivity

Question 31

Muddy brown granular casts

Answer 31

Acute tubular necrosis 3 stages: inciting phase, maintenance phase, recovery phase ischemic - decr. renal blood flow (hypovolemia, shock) nephrotoxic - toxins, crush injury, hemoglobin, most common in PCT

Question 32

Gross hematuria and proteinuria

Answer 32

Renal papillary necrosis Seen in SAND... sickle cell, acute pyelonephritis, NSAIDs, diabetes

Question 33

incr. Cr and incr. BUN

Answer 33

acute kidney injury

Question 34

FENa values for AKI

Answer 34

2% = intrinsic renal, postrenal

Question 35

Low Vit. D, low serum Ca, high serum PO4

Answer 35

renal osteodystrophy

Question 36

ADPKD

Answer 36

autosomal dominant, mutation in PKD1 assoc. w/ berry aneurysms, mitral valve prolapse, benign hepatic cysts

Question 37

ARPKD

Answer 37

infantile polycystic kidney disease congenital hepatic fibrosis, can lead to Potter sequence

Question 38

Progressive renal insufficiency with inability to concentrate urine

Answer 38

Medullary cystic disease not visualized, but shrunken kidneys on ultrasound

Question 39

Anechoic cysts vs. solid components

Answer 39

Simple vs. complex renal cysts Simple are filled w/ ultrafiltrate Complex are septated, enhanced or solid, and must be removed due to incr. risk of RCC

Question 40

Evaluating metabolic alkalosis

Answer 40

First, assess urine chloride (low = vomiting), then volume status Three most common causes: vomiting/NG suction, thiazide/loop diuretic use, mineralocorticoid use

Question 41

Hemolytic uremic syndrome (HUS)

Answer 41

s/p E.coli (O157:H7) or Shigella infection toxins injure endothelium of preglomerular arterioles, leading to platelet aggregation and formation of microthrombi (shear stress --> hemolysis) Look for thrombocytopenia, anemia and AKI