Renal First Aid Pathology II Flashcards
Oxalate crystals
ethylene glycol (antifreeze) or vitamin C abuse.
Conditions that cause hypercalcemia (cancer,
t PTH) can -+ hypercalciuria and
radioopaque stones (calcium oxalate, calcium phosphate, or both).
Most common kidney stone presentation:
calcium oxalate stone in a patient with hypercalciuria and normocalcemia.
Can lead to severe complications, such as hydronephrosis and pyelonephritis. Treat and prevent by encouraging fluid intake.
kidney stones
Treatments for recurrent calcium oxalate/phosphate stones
thiazides and citrate
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.
Ammonium magnesium phosphate (“struvite”)
three urease positive bugs that can cause struvite stones
(Proteus mirabilis, Staphylococcus, Klebsiella)
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.
uric acid stone
Most often 2ndary to cystinuria. Hexagonal crystals. Treat with alkalinization of urine.
Cystine stones
kidney stones on xray
calcium + struvite + cystine = radioopaque
Uric acid = radiolUcent
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.
hydronephrosis
RCC originates from
proximal tubule cells
Most common renal malignancy.
Renal cell carcinoma
RCC originates from proximal tubule cells
-+ polygonal clear cells filled with accumulated
lipids and carbohydrates.
RCC risk factors
Most common in men 50-70 years of age. t incidence with smoking and obesity.
Manifests clinically with hematuria, palpable mass, 2° polycythemia, flank pain, fever, and weight loss.
RCC
hematagenous spread of rcc
Invades renal vein then IVC and spreads hematogenously; metastasizes to lung and bone.
Associated with gene deletion on chromosome
WHAT (deletion may be sporadic or inherited as von Hippel-Lindau syndrome).
3
3 paraneoplastic syndromes w. wh/ Rcc is associated
ectopic EPO,
ACTH,
PTHrP
Why is RCC “silent?”
in retroperitoneum, commonly presents as a metastatic neoplasm.
Treatment of RCC:
resection if localized disease.
Resistant to conventional chemotherapy and radiation therapy.
Most common renal malignancy of early childhood (ages 2-4). Contains embryonic glomerular structures. Presents with huge, palpable flank mass and/or hematuria.
WIlms’ tumor (nephroblastoma)
With what gene deletion is Wilms’ tumor associated?
tumor suppressor gene WTl on chromosome ll.
Syndromes with which Wilm’s tumor is associated
Beckwith Wiedemann syndrome or WAGR complex : Wilms’ tumor, Aniridia, Genitourinary malformation, and mental Retardation.
WAGR complex is: : Wilms’ tumor, Aniridia, Genitourinary malformation, and mental Retardation.
: Wilms’ tumor, Aniridia, Genitourinary malformation, and mental Retardation.
Most common tumor of urinary tract system (can occur in renal calyces, renal pelvis, ureters, and bladder)
Transitional cell carcinoma
Presentation of transitional cell carcionma
painless hematuria with no casts
Transitional cell carcinoma is associated with problems in your Pee SAC:
Phenacetin,
Smoking,
Aniline dyes, and
Cyclophosphamide.
White blood cell casts in urine
acute pyelonephritis
presentation of acute pyelonephritis
fever, CVA tenderness, nausea, vomiting
what part of kidney is most affected with acute pyelonephritis?
affects cortex with relative sparing of glomeruli/vessels
Coarse, asymmetric corticomedullary scarring, blunted calyx
chronic pyelonephritis
Presentation of drug-induced interstitial nephritis
pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as HAPTENS, inducing hypersensitivity
drugs that may cause interstitial nephritis
1-2 wks later: diuretics, PCN derivatives, sulfonamides, rifampin;
months later: NSAIDs
Acute generalized cortical infarction of both kidneys. Likely due to a combination of vasospasm and DIC.
Diffuse cortical necrosis
Associated with obstetric catastrophes (e.g., abruptio placentae) and septic shock.
Diffuse cortical necrosis
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.
Acute tubular necrosis
describe three stages of ATN
- Inciting event
- Maintenance phase-oliguric; lasts 1-3 weeks; risk of hyperkalemia
- Recovery phase-polyuric; BUN and serum creatinine fall; risk of hypokalemia
risk in maintenance phase of ATN
hyperkalemia
risk in recovery phase of ATN
hypokalemia
Sloughing of renal papillae –> gross hematuria and proteinuria. May be triggered by a recent infection or immune stimulus.
Renal papillary necrosis
Renal papillary necrosis is associated with four things:
- Diabetes mellitus
- Acute pyelonephritis
- Chronic phenacetin use (acetaminophen is phenacetin derivative)
- Sickle cell anemia and trait
In normal nephron, BUN is reabsorbed (WHY?!), but creatinine is not.
for countercurrent multiplication
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.
prerenal azotemia
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.
Intrinsic renal failure
Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction.
Post renal azotemia
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.
Renal osteodystophy
Na+, H2O retention Hyperkalemia Metabolic acidosis Uremia Anemia Renal osteodystrophy, Dyslipidemia Growth retardation and developmental delay
consequences of renal failure
Multiple, large, bilateral cysts that ultimately destroy the kidney parenchyma. Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure.
ADPKD
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.
ADPKD
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.
ARPKD
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.
Medullary cystic kidney disease
