Renal First Aid Pathology II

Question 1

Oxalate crystals

Answer 1

ethylene glycol (antifreeze) or vitamin C abuse.

Question 2

Conditions that cause hypercalcemia (cancer,

t PTH) can -+ hypercalciuria and

Answer 2

radioopaque stones (calcium oxalate, calcium phosphate, or both).

Question 3

Most common kidney stone presentation:

Answer 3

calcium oxalate stone in a patient with hypercalciuria and normocalcemia.

Question 4

Can lead to severe complications, such as hydronephrosis and pyelonephritis. Treat and prevent by encouraging fluid intake.

Answer 4

kidney stones

Question 5

Treatments for recurrent calcium oxalate/phosphate stones

Answer 5

thiazides and citrate

Question 6

Caused by infection with urease-positive bugs
(Proteus mirabilis, Staphylococcus, Klebsiella)
that hydrolyze urea to ammonia -+ urine alkalinization. Can form staghorn calculi that can be a nidus for UTis.

Answer 6

Ammonium magnesium phosphate (“struvite”)

Question 7

three urease positive bugs that can cause struvite stones

Answer 7

(Proteus mirabilis, Staphylococcus, Klebsiella)

Question 8

Visible on CT and ultrasound but not x-ray.
Strong association with hyperuricemia
(e.g., gout). Often seen in diseases with
t cell turnover, such as leukemia. Treat with alkalinization of urine.

Answer 8

uric acid stone

Question 9

Most often 2ndary to cystinuria. Hexagonal crystals. Treat with alkalinization of urine.

Answer 9

Cystine stones

Question 10

kidney stones on xray

Answer 10

calcium + struvite + cystine = radioopaque

Uric acid = radiolUcent

Question 11

Back-up of urine into the kidney. Can be caused by urinary tract obstruction or vesicoureteral reAux. Causes dilation of renal pelvis and calyces proximal to obstruction. May result in parenchymal thinning in chronic, severe cases.

Answer 11

hydronephrosis

Question 12

RCC originates from

Answer 12

proximal tubule cells

Question 13

Most common renal malignancy.

Answer 13

Renal cell carcinoma

Question 14

RCC originates from proximal tubule cells

-+ polygonal clear cells filled with accumulated

Answer 14

lipids and carbohydrates.

Question 15

RCC risk factors

Answer 15

Most common in men 50-70 years of age. t incidence with smoking and obesity.

Question 16

Manifests clinically with hematuria, palpable mass, 2° polycythemia, flank pain, fever, and weight loss.

Answer 16

RCC

Question 17

hematagenous spread of rcc

Answer 17

Invades renal vein then IVC and spreads hematogenously; metastasizes to lung and bone.

Question 18

Associated with gene deletion on chromosome

WHAT (deletion may be sporadic or inherited as von Hippel-Lindau syndrome).

Answer 18

3

Question 19

3 paraneoplastic syndromes w. wh/ Rcc is associated

Answer 19

ectopic EPO,
ACTH,
PTHrP

Question 20

Why is RCC “silent?”

Answer 20

in retroperitoneum, commonly presents as a metastatic neoplasm.

Question 21

Treatment of RCC:

Answer 21

resection if localized disease.

Resistant to conventional chemotherapy and radiation therapy.

Question 22

Most common renal malignancy of early childhood (ages 2-4). Contains embryonic glomerular structures. Presents with huge, palpable flank mass and/or hematuria.

Answer 22

WIlms’ tumor (nephroblastoma)

Question 23

With what gene deletion is Wilms’ tumor associated?

Answer 23

tumor suppressor gene WTl on chromosome ll.

Question 24

Syndromes with which Wilm’s tumor is associated

Answer 24

Beckwith­ Wiedemann syndrome or WAGR complex : Wilms’ tumor, Aniridia, Genitourinary malformation, and mental Retardation.

Question 25

WAGR complex is: : Wilms' tumor, Aniridia, Genitourinary malformation, and mental Retardation.

Answer 25

: Wilms' tumor, Aniridia, Genitourinary malformation, and mental Retardation.

Question 26

Most common tumor of urinary tract system (can occur in renal calyces, renal pelvis, ureters, and bladder)

Answer 26

Transitional cell carcinoma

Question 27

Presentation of transitional cell carcionma

Answer 27

painless hematuria with no casts

Question 28

Transitional cell carcinoma is associated with problems in your Pee SAC:

Answer 28

Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide.

Question 29

White blood cell casts in urine

Answer 29

acute pyelonephritis

Question 30

presentation of acute pyelonephritis

Answer 30

fever, CVA tenderness, nausea, vomiting

Question 31

what part of kidney is most affected with acute pyelonephritis?

Answer 31

affects cortex with relative sparing of glomeruli/vessels

Question 32

Coarse, asymmetric corticomedullary scarring, blunted calyx

Answer 32

chronic pyelonephritis

Question 33

Presentation of drug-induced interstitial nephritis

Answer 33

pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as HAPTENS, inducing hypersensitivity

Question 34

drugs that may cause interstitial nephritis

Answer 34

1-2 wks later: diuretics, PCN derivatives, sulfonamides, rifampin; months later: NSAIDs

Question 35

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

Answer 35

Diffuse cortical necrosis

Question 36

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

Answer 36

Diffuse cortical necrosis

Question 37

Most common cause of intrinsic renal failure. Self-reversible in some cases, but can be fatal if left untreated. Death most often occurs during initial oliguric phase.

Answer 37

Acute tubular necrosis

Question 38

describe three stages of ATN

Answer 38

1. Inciting event 2. Maintenance phase-oliguric; lasts 1-3 weeks; risk of hyperkalemia 3. Recovery phase-polyuric; BUN and serum creatinine fall; risk of hypokalemia

Question 39

risk in maintenance phase of ATN

Answer 39

hyperkalemia

Question 40

risk in recovery phase of ATN

Answer 40

hypokalemia

Question 41

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

Answer 41

Renal papillary necrosis

Question 42

Renal papillary necrosis is associated with four things:

Answer 42

* Diabetes mellitus * Acute pyelonephritis * Chronic phenacetin use (acetaminophen is phenacetin derivative) * Sickle cell anemia and trait

Question 43

In normal nephron, BUN is reabsorbed (WHY?!), but creatinine is not.

Answer 43

for countercurrent multiplication

Question 44

As a result of decrease RBF (e.g., hypotension) --> decreased GFR, Na+fH20 and urea retained by kidney in an attempt to conserve volume, so BUN/creatinine ratio t.

Answer 44

prerenal azotemia

Question 45

Generally due to ATN or ischemia/toxins and less commonly to acute glomerulonephritis (e.g., RPGN). Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule --> dec GFR. Urine has epithelial/granular casts. BUN reabsorption is impaired --> BUN/creatinine ratio.

Answer 45

Intrinsic renal failure

Question 46

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

Answer 46

Post renal azotemia

Question 47

Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia --> 2° hyperparathyroidism. Hyperphosphatemia also independently decreases serum Ca2+ by causing tissue calcifications, whereas decreased 1,25-(0H)z vitamin D --> decreased intestinal Ca2+ absorption. Causes subperiosteal thinning of bones.

Answer 47

Renal osteodystophy

Question 48

``` Na+, H2O retention Hyperkalemia Metabolic acidosis Uremia Anemia Renal osteodystrophy, Dyslipidemia Growth retardation and developmental delay ```

Answer 48

consequences of renal failure

Question 49

Multiple, large, bilateral cysts that ultimately destroy the kidney parenchyma. Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure.

Answer 49

ADPKD

Question 50

Autosomal-Dominant mutation in PKDl or PKD2 . Death from complications of chronic kidney disease or hypertension (caused by inc renin production). Associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts.

Answer 50

ADPKD

Question 51

Infantile presentation in parenchyma. AR. Associated with congenital hepatic fibrosis. Significant renal failure in utero can lead to Potter's syndrome. Concerns beyond neonatal period include hypertension, portal hypertension, and progressive renal insufficiency.

Answer 51

ARPKD

Question 52

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.

Answer 52

Medullary cystic kidney disease