Renal - Diseases Flashcards
Acute post-streptococcal glomerulonephritis
Most commonly seen in children ~2 wks after GAS infection of pharynx/skin; Type III hypersensitivity reaction, self-limiting
Presents with hypertension, periorbital/peripheral edema, dark colored urine
Alport Syndrome
X-linked mutation of type IV collagen leading to thinning and splitting of GBM; presents with glomerulonephritis (nephritic syndrome) + deafness
IgA Nephropathy (Berger Disease)
Caused by IgA immune deposition in the glomerulus
Presents as episodic hematuria flares following URI or acute gastroenteritis + Henloch-Schonlein purpura
IM shows IgA immune complex deposition in the mesangium
Pre-renal azotemia
Caused by decreased renal blood flow due to hypotension, shock, sepsis, cirrhosis, CHF
Kidney retains Na, H2O, and urea in an effort to conserve volume
Intrinsic renal failure
Usually caused by acute tubular necrosis due to ischemic or toxic damage to tubular epithelial cells, which slough into the lumen causing obstruction, fluid back-flow, and decreased GFR
Toxic agents include aminoglycosides, lead, cisplatin, radiocontrast, myoglobin/hemoglobinuria
Risk of hyperkalemia, metabolic acidosis
Post-renal azotemia
Caused by bilateral outflow obstruction (stones, BPH, neoplasia, congenital) causing fluid backflow and decreased GFR
Consequences of acute renal failure
MADHUNGER
Metabolic acidosis Dyslipidemia (elevated triglycerides) Hyperkalemia Uremia Na/H2O retention Growth retardation / developmental delay (kids) Erythropoietin failure (anemia) Renal osteodystrophy
Renal osteodystrophy
Thinning of bones seen in renal disease
Failure of kidney to hydroxylate Vitamin D causes hypocalcemia and hyperphosphatemia, which stimulates secondary hyperparathyroidism with subsequent bone resorption
Uremia - Clinical signs
Elevated serum BUN / Creatinine Nausea / anorexia Pericarditis / pleuritis Asterixis Encephalopathy Skin findings - pruritis Platelet dysfunction
Rapidly Progressive Glomerulonephritis (RPGN)
A pattern of nephritic kidney inflammation that can be caused by a variety of disease processes, including:
Goodpasture’s Disease
Granulomatosis with polyangiitis (Wegener’s)
Microscopic polyangiitis
Minimal Change Disease
Most common cause of nephrotic syndrome in children
Excellent response to steroid therapy
Nephrogenic Diabetes Insipidus
Inability of the AVP receptor on the kidney to respond to vasopressin; may be hereditary, or secondary to hypercalcemia, Lithium, demeclocycline (ADH antagonist)
Characterized by polyuria and polydipsia in the setting of elevated serum osmolarity; reflects an inability of the kidney to concentrate urine
Labs: Low urine specific gravity, serum osmolarity > 290, hypernatremia
Diagnosis: Water restriction test causes no change in urine osmolarity
Treatment: Hydrochlorothiazide, amiloride
Common side effect of Lithium therapy
Treated with Amiloride,
Central Diabetes Insipidus
Primary deficiency of ADH caused by dysfunction of the posterior pituitary - tumor, autoimmune destruction, trauma, surgery
Labs: Low urine specific gravity in the setting of high serum osmolarity (>290)
Diagnosis: Water restriction test results in > 50% increase in urine osmolarity
Treatment: Intranasal DDAVP
Gouty Nephropathy
Most common extra-articular manifestation of chronic gout, caused by deposition of urate crystals in the renal medulla where they can form intratubular precipitates or uric acid renal stones
Tubular obstruction leads to cortical atrophy and scarring; 20% fatality due to renal failure
Diffuse corticol necrosis
Generalized infarctions of the renal cortices; commonly seen as a complication of DIC, often in the setting of obstetric complication
Presents with obrupt onset of anuria, gross hematuria, and flank pain
Diagnosed by US demonstrating hypodensities in the renal cortex
