Urine pH < 5.5. Hypoaldosteronism hyperkalemia NH3 synthesis in PCT NH4+ excretion.
Causes: aldosterone production (eg, diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (eg, K+-sparing diuretics, nephropathy due to obstruction, TMP/SMX).
LM—diffuse capillary and GBM thickening C . IF—granular as a result of immune complex deposition. Nephrotic presentation of SLE.
EM—"spike and dome" appearance with subepithelial deposits.
Most common cause of 1° nephrotic syndrome in Caucasian adults. Can be 1° (eg, antibodies to phospholipase A2 receptor) or 2° to drugs (eg, NSAIDs, penicillamine, gold), infections (eg, HBV, HCV, syphilis), SLE, or solid tumors.
1° disease has poor response to steroids. May progress to chronic renal disease.
Originates from PCT cells polygonal clear cells A filled with accumulated lipids and carbohydrates.
Often golden-yellow B due to lipid content. Most common in men 50-70 years old. incidence with smoking and obesity.
Manifests clinically with hematuria, palpable mass, 2° polycythemia, flank pain, fever, weight loss. Invades renal vein (may develop varicocele if left sided) then IVC and spreads hematogenously; metastasizes to lung and bone.
Treatment: surgery/ablation for localized disease. Immunotherapy (eg, aldesleukin) or targeted therapy for metastatic disease, rarely curative.
Resistant to chemotherapy and radiation therapy.
Most common 1° renal malignancy. Associated with gene deletion on chromosome
3 (sporadic or inherited as von Hippel-Lindau
syndrome). RCC = 3 letters = chromosome 3. Associated with paraneoplastic syndromes (eg,
ectopic EPO, ACTH, PTHrP, renin).
Most common renal malignancy of early childhood (ages 2-4). Contains embryonic glomerular structures. Presents with large, palpable, unilateral flank mass A and/or hematuria.
"Loss of function" mutations of tumor suppressor genes WT1 or WT2 on chromosome 11. May be a part of several syndromes:
WAGR complex: Wilms tumor, Aniridia (absence of iris), Genitourinary malformations, mental Retardation/intellectual disability (WT1 deletion)
Denys-Drash: Wilms tumor, early-onset nephrotic syndrome, male pseudohermaphroditism (WT1 mutation)
Beckwith-Wiedemann: Wilms tumor, macroglossia, organomegaly, hemihyperplasia (WT2 mutation)
Neutrophils infiltrate renal interstitium A . Affects cortex with relative sparing of glomeruli/vessels. Presents with fevers, flank pain (costovertebral angle tenderness), nausea/vomiting, chills.
Causes include ascending UTI (E coli is most common), hematogenous spread to kidney. Presents with WBCs in urine +/− WBC casts. CT would show striated parenchymal enhancement B .
Risk factors include indwelling urinary catheter, urinary tract obstruction, vesicoureteral reflux, diabetes mellitus, pregnancy.
Complications include chronic pyelonephritis, renal papillary necrosis, perinephric abscess, urosepsis.
Acute interstitial renal inflammation. Pyuria (classically eosinophils) and azotemia occurring after administration of drugs that
act as haptens, inducing hypersensitivity (eg, diuretics, penicillin derivatives, proton pump inhibitors, sulfonamides, rifampin, NSAIDs).
Less commonly may be 2° to other processes such as systemic infections (eg, mycoplasma) or autoimmune diseases (eg, Sjögren syndrome, SLE, sarcoidosis).
Associated with fever, rash, hematuria, and costovertebral angle tenderness, but can be asymptomatic.
Remember these P's:
Penicillins and cephalosporins Proton pump inhibitors
Most common cause of acute kidney injury in hospitalized patients. Spontaneously resolves in many cases.
Can be fatal, especially during initial oliguric phase. FENa.
Key finding: granular ("muddy brown") casts A . 3 stages:
1. Inciting event
2. Maintenance phase—oliguric; lasts 1-3 weeks; risk of hyperkalemia, metabolic acidosis,
3. Recovery phase—polyuric; BUN and serum creatinine fall; risk of hypokalemia
Can be caused by ischemic or nephrotoxic injury:
Ischemic—2° to renal blood flow (eg, hypotension, shock, sepsis, hemorrhage, HF). Results
in death of tubular cells that may slough into tubular lumen B (PCT and thick ascending limb
are highly susceptible to injury).
Nephrotoxic—2° to injury resulting from toxic substances (eg, aminoglycosides, radiocontrast
agents, lead, cisplatin, ethylene glycol), crush injury (myoglobinuria), hemoglobinuria. PCT is particularly susceptible to injury.