Renal Flashcards
What effect do atrial natriuretic peptide and brain natriuretic peptide have on kidneys?
ANP (stretch on atria) and BNP (stretch on ventricles) are released due to volume expansion. These act on the kidney to increase GFR, natriuresis, and diuresis.
What drugs can cause drug-induced acute interstitial nephritis (AIN)?
Beta-lactam antibiotics, NSAIDs, solfonamides, rifampin, and diuretics. Patients often present with fever, rash, and acute renal failure. AIN is thought to be mediated by IgE-mediated hypersensitivity or cell-mediated (type IV) reactions, depending on the drug. It primarily involves the renal interstitium, causing interstitial edema and leukocyte infiltration (lymphocytes, macrophages, and eosinophils). RBCs, WBCs, and eosinophils may be seen in urine.
What are features of acute tubular necrosis?
Proximal tubular cell ballooning and vacuolar degeneration.
What is the filtration fraction of a healthy individual?
20%
What is the most common site of obstruction in unilateral fetal hydronephrosis?
Narrowing or kinking of the proximal ureter at the ureteropelvic junction (UPJ).
What is the histologic appearance of nodular glomerulosclerosis?
Kimmelstiel-Wilson nodules (located in the peripheral mesangium, ovoid or spherical in shape, lamellated appearance, eosinophilc on H and E stain, periodic acid-Schiff +). The most common cause is diabetic nephropathy. Can eventually progress to nephrotic syndrome.
Compare and contrast autosomal dominant from autosomal recessive polycystic kidney disease?
AD: Bilateral enlarged kidneys due to numerous cysts in the cortex and medulla. Presents with flank pain, hematuria, hypertension, urinary infection, and progressive renal failure in ~50% of patients. Mutations to PKD1 (~85%) or PKD2 (~15%). Associated with berry aneurysms, mitral valve prolapse and benign hepatic cysts.
AR: Cystic dilation of collecting ducts. Presents in infancy. Can lead to Potter sequence if significant oliguria occurs. Associated with congenital hepatic fibrosis. After the neonatal period, infants can get systemic hypertension, progressive renal insufficiency, and portal hypertension (fibrotic liver). Mutation in PKHD1 gene.
What is the treatment for primary (psychogenic) polydipsia?
Water restriction.
These patients have hyponatremia with a low initial urine osmolality. PP is characterized by pathological water drinking and is most common in middle-aged women and patients with underlying psychiatric disease. Can test by injecting with vasopressin. If there is no change in serum osmolality, then it is most likely PP as opposed to DI.
What type of kidney stone a patients with Crohn’s disease at risk for?
Oxalate stones. Patients get impaired reabsorption of bile acids in the terminal ileum. This leads to impaired fat absorption. The excess lipids in the bowel lumen bind to calcium ions, and these soap complexes are then excreted in the feces. This leads to increased oxalate absorption. In the healthy bowel, dietary calcium binds to dietary oxalate, producing insoluble calcium oxalate salts that promote oxalate excretion in feces.
What is renal osteodystrophy?
A bone disease that occurs when your kidneys fail to maintain proper levels of calcium and phosphorus in the blood. It’s common in people with kidney disease and affects most dialysis patients.
How does paroxysmal nocturnal hemoglobinuria (PNH) cause damage to the kidneys?
Chronic hemolysis will lead to iron deposition in the kidney (hemosiderosis), which can interfere with proximal tubule function and cause interstitial scarring and cortical infarcts. PNH is due to a mutated phosphatidylinositol glycan class A (PIGA) gene, which helps synthesize the glycosylphosphatidylinositol (GPI) anchor protein. GPI helps attache several cell surface proteins (e.g. CD55 decay accelerating factor, CD59 MAC inhibitory factor) that inhibit complement, and thus inhibit RBC hemolysis due to complement activation.
What portion of the nephron does uric acid precipitate out in in the setting of tumor lysis syndrome?
The collecting ducts due to low urine pH (uric acid is soluble at physiologic pH but precipitates in an acidic environment). This can be reduced with urine arlkalinization, hydration, and allopurinol.
What is the effect of increased urinary citrate on the formation of renal calculi?
Increased citrate in the urine can prevent calculi formation, because citrate binds free (ionized) calcium, thus preventing calcium precipitation. Potassium citrate is often prescribed to prevent recurrent stones in adults when dietary modifications are unsuccessful.
What renal structure does renal cell carcinoma arise from?
Proximal renal tubules
What are the three phases of acute tubular necrosis (ATN)?
Initiation phase: slight decrease in urine output for ~36 hrs as a result of the original ischemic or toxic insult.
Maintenance phase: lasts 1-2 wks, oliguria, fluid overload, electrolyte abnormalities (hyperkalemia, metabolic acidosis). Low GFR and elevated serum creatinine. Light microscopy shows tubular epithelial necrosis, denudation of the tubular basement membrane, and casts containing cellular debris.
Recovery phase: re-epithelization of tubules. GFR recovers faster than tubular cells leading to transient polyuria and loss of electrolytes. Majority of patients eventually experience complete restoration of renal function.
