ABIM Nephrology cheat sheet

Nephrotic syndrome: proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia; complications include thrombosis (especially membranous) and infection.

Minimal change disease: most common nephrotic syndrome in children; selective proteinuria; responsive to corticosteroids; podocyte foot process effacement on EM.

Focal segmental glomerulosclerosis: often corticosteroid-resistant; associated with HIV, heroin, obesity, and APOL1 risk alleles; poor prognosis without remission.

Membranous nephropathy: anti-PLA2R antibodies in 70-80% of primary cases; secondary causes include malignancy, hepatitis B, SLE, and medications (NSAIDs, penicillamine).

IgA nephropathy: most common primary glomerulonephritis worldwide; mesangial IgA deposits; presents with synpharyngitic gross hematuria; elevated serum IgA in 50%.

Rapidly progressive glomerulonephritis: crescents on biopsy; anti-GBM (linear IgG), ANCA (pauci-immune), or immune complex-mediated; treat with pulse steroids and cyclophosphamide or rituximab.

Post-streptococcal glomerulonephritis: low C3, subepithelial humps on EM; presents 1-3 weeks after pharyngitis or 3-6 weeks after impetigo; supportive care.

Membranoproliferative glomerulonephritis: low C3; patterns include C3 glomerulopathy (dense deposit disease) and immune complex-mediated; associated with hepatitis C and cryoglobulinemia.

Acute interstitial nephritis: triad of rash, fever, eosinophilia in <30%; most common causes are antibiotics (beta-lactams, rifampin), NSAIDs, and PPIs; urinalysis shows sterile pyuria and WBC casts.

Drug-induced AIN treatment: discontinue offending agent; corticosteroids may hasten recovery if given early, but evidence is limited.

Analgesic nephropathy: chronic interstitial nephritis and papillary necrosis from prolonged combination analgesic use; associated with transitional cell carcinoma.

Renal artery stenosis: atherosclerotic (older, smoker, extrarenal atherosclerosis) or fibromuscular dysplasia (young women, string-of-beads on angiography); ACEi/ARB can precipitate AKI.

Thrombotic microangiopathy: schistocytes, thrombocytopenia, elevated LDH, AKI; causes include TTP (ADAMTS13 deficiency), HUS (Shiga toxin), and complement-mediated (atypical HUS).

Cholesterol atheroembolism: post-catheterization or anticoagulation; livedo reticularis, eosinophilia, eosinophiluria, progressive renal failure over weeks; no specific therapy.

Scleroderma renal crisis: abrupt hypertension, AKI, microangiopathic hemolysis; treat with ACE inhibitors (captopril); avoid steroids.

Renal papillary necrosis: causes include diabetes, sickle cell disease, analgesic abuse, pyelonephritis, and obstruction; sloughed papillae may cause hematuria or obstruction.

KDIGO AKI definition: increase in serum creatinine ≥0.3 mg/dL within 48 hours, or ≥1.5 times baseline within 7 days, or urine volume <0.5 mL/kg/h for 6 hours.

Prerenal AKI: FENa <1%, BUN/creatinine ratio >20, bland urine sediment; responds to volume repletion. FENa unreliable with diuretics (use FEUrea <35%).

Acute tubular necrosis: muddy brown casts, FENa >2%; common causes are ischemia and nephrotoxins (aminoglycosides, contrast, cisplatin).

Hepatorenal syndrome: functional renal failure in advanced liver disease; diagnostic criteria include ascites, creatinine >1.5 mg/dL, no response to volume, absence of shock, and proteinuria <500 mg/day; treat with terlipressin plus albumin.

Contrast-induced AKI: prevention with IV isotonic saline; N-acetylcysteine not proven; avoid repeat contrast for 48-72 hours.

Rhabdomyolysis: CK >5,000 U/L, pigmented granular casts, hyperkalemia, hyperphosphatemia, hypocalcemia; treat with aggressive IV fluids.

Renal replacement therapy indications in AKI: refractory hyperkalemia, severe acidosis, volume overload, uremic complications (pericarditis, encephalopathy), and certain poisonings.

Urinary indices: prerenal FENa <1%, ATN FENa >2%; FENa = (UNa × PCr) / (PNa × UCr) × 100.

CKD definition: GFR <60 mL/min/1.73 m² or markers of kidney damage (albuminuria, hematuria, structural abnormalities) for >3 months.

CKD staging by GFR: G1 ≥90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15 (mL/min/1.73 m²).

Albuminuria categories: A1 <30 mg/g, A2 30-300 mg/g, A3 >300 mg/g; higher category predicts faster progression and cardiovascular risk.

Slowing progression: ACE inhibitors or ARBs for albuminuria; SGLT2 inhibitors for CKD with albuminuria or heart failure; blood pressure target <120 mmHg systolic (SPRINT) if tolerated.

Metabolic acidosis in CKD: serum bicarbonate <22 mEq/L associated with protein catabolism and bone disease; treat with oral sodium bicarbonate to maintain ≥22 mEq/L.

Anemia of CKD: normocytic normochromic; due to erythropoietin deficiency; treat with iron repletion and ESA when Hb <10 g/dL; target 10-11 g/dL.

CKD-MBD: hyperphosphatemia, hypocalcemia, elevated PTH, and FGF23; treat with dietary phosphate restriction, phosphate binders, and active vitamin D analogs.

Uremic bleeding: platelet dysfunction from uremia; treat with desmopressin (DDAVP) or conjugated estrogens; dialysis improves platelet function.

Hyponatremia: assess volume status and urine osmolality; SIADH has urine osmolality >100 mOsm/kg, urine Na >40 mEq/L, euvolemia; treat with fluid restriction, vaptans, or urea.

Hyperkalemia: ECG changes (peaked T waves, widened QRS, sine wave); treat with IV calcium gluconate for cardiac stabilization, insulin/glucose, beta-agonists, and potassium removal (diuretics, binders, dialysis).

Metabolic acidosis: anion gap = Na - (Cl + HCO3); normal 8-12 mEq/L; elevated gap causes include ketoacidosis, lactic acidosis, renal failure, and toxins (methanol, ethylene glycol, salicylates).

Metabolic alkalosis: associated with hypokalemia, hypochloremia, and volume depletion; urine chloride <20 mEq/L suggests saline-responsive; >20 mEq/L suggests mineralocorticoid excess or diuretics.

Hypocalcemia: corrected calcium = measured Ca + 0.8 × (4.0 - albumin); symptoms include tetany, Chvostek and Trousseau signs, QT prolongation; treat with IV calcium gluconate.

Hyperphosphatemia: causes include CKD, tumor lysis, rhabdomyolysis, and hypoparathyroidism; treat with phosphate binders and dialysis.

Hypokalemia: ECG changes (U waves, flattened T waves, ST depression); replace with oral or IV potassium; check magnesium because hypomagnesemia causes refractory hypokalemia.

Osmolal gap = measured osmolality - calculated osmolality (2Na + glucose/18 + BUN/2.8); gap >10 suggests ingestion of methanol, ethylene glycol, or isopropanol.

Primary aldosteronism: hypertension with hypokalemia, elevated aldosterone, suppressed renin; screen with aldosterone-to-renin ratio; confirm with saline suppression or captopril challenge.

Renovascular hypertension: ACE inhibitors can cause acute kidney injury and are relatively contraindicated in bilateral renal artery stenosis or stenosis in a solitary kidney.

Malignant hypertension: severe hypertension with target organ damage (retinopathy, encephalopathy, AKI, heart failure); treat with IV medications and lower mean arterial pressure by ≤25% in the first hour.

Hypertensive emergency vs urgency: emergency has acute target organ damage and requires IV therapy; urgency has no end-organ damage and uses oral agents.

Pheochromocytoma: episodic hypertension, headache, sweating, palpitations; diagnose with plasma free metanephrines; treat with alpha blockade before beta blockade.

Fibromuscular dysplasia: non-atherosclerotic stenosis, typically in young women; string-of-beads appearance; treatment with angioplasty without stent.

Drug-resistant hypertension: failure to reach goal on 3 agents including a diuretic; common causes include nonadherence, sleep apnea, CKD, and primary aldosteronism.

Hemodialysis adequacy: Kt/V ≥1.2 per session (three times weekly) or urea reduction ratio ≥65%.

Peritoneal dialysis: Kt/V ≥1.7 per week; peritonitis presents with abdominal pain, cloudy effluent, and effluent WBC >100/mm³ with >50% neutrophils; treat with intraperitoneal antibiotics.

Vascular access: arteriovenous fistula preferred (lowest infection and thrombosis rates), then arteriovenous graft, then tunneled catheter; catheter use has highest infection risk.

Dialysis disequilibrium syndrome: cerebral edema from rapid osmolar shifts; prevent with slower initial dialysis and lower blood flow; symptoms include headache, nausea, confusion, seizures.

Hypotension during hemodialysis: common causes include excessive ultrafiltration, vasodilation, and autonomic dysfunction; treat by reducing ultrafiltration and administering saline.

Continuous renal replacement therapy: preferred in hemodynamically unstable ICU patients; modalities include CVVH (convection), CVHD (diffusion), and CVVHDF.

Dialysis in poisoning: effective for low-molecular-weight, low-protein-bound, low-volume-of-distribution toxins (e.g., methanol, ethylene glycol, lithium, salicylates).

Hyperacute rejection: occurs minutes to hours after transplant; caused by preformed antibodies; treatment is immediate nephrectomy.

Acute cellular rejection: occurs days to months; presents with rising creatinine; biopsy shows interstitial lymphocytic infiltrate and tubulitis; treat with pulse corticosteroids.

Antibody-mediated rejection: donor-specific antibodies, capillary margination, C4d deposition; treat with plasmapheresis, IVIG, and rituximab.

Calcineurin inhibitor toxicity: tacrolimus and cyclosporine cause nephrotoxicity, hypertension, hyperkalemia, and tremor; monitor levels.

Post-transplant lymphoproliferative disorder: associated with Epstein-Barr virus and immunosuppression; reduce immunosuppression and treat with rituximab.

BK virus nephropathy: presents with rising creatinine and BK viremia; biopsy shows viral cytopathic changes; reduce immunosuppression.

Opportunistic infections: Pneumocystis jirovecii pneumonia (trimethoprim-sulfamethoxazole prophylaxis), cytomegalovirus (ganciclovir), and cryptococcosis.

Calcium oxalate stones: most common; associated with hypercalciuria, hyperoxaluria, hypocitraturia, and low urine volume; treat with hydration and thiazides for hypercalciuria.

Uric acid stones: radiolucent on plain radiograph; associated with low urine pH; treat with alkalinization (potassium citrate) and allopurinol.

Struvite stones: associated with urease-producing bacteria (Proteus); staghorn calculi; require complete stone removal and eradication of infection.

Cystine stones: hexagonal crystals; caused by cystinuria; treat with high fluid intake and urinary alkalinization.

Autosomal dominant polycystic kidney disease: bilateral cysts, hypertension, hematuria, and risk of intracranial aneurysms; treat with tolvaptan to slow cyst growth.

Autosomal recessive polycystic kidney disease: presents in infancy with enlarged cystic kidneys and congenital hepatic fibrosis; associated with PKHD1 mutations.

Nephrolithiasis prevention: increase fluid intake to achieve urine output >2.5 L/day; reduce sodium and animal protein; thiazides for hypercalciuria.

Alport syndrome: X-linked (COL4A5) in 80%; presents with hematuria, progressive renal failure, sensorineural hearing loss, and anterior lenticonus.

Fabry disease: X-linked deficiency of alpha-galactosidase A; presents with proteinuria, angiokeratomas, acroparesthesias, and corneal verticillata; treat with enzyme replacement.

Autosomal dominant tubulointerstitial kidney disease: mutations in UMOD (uromodulin), MUC1, or HNF1B; presents with gout and progressive CKD.

Nail-patella syndrome: LMX1B mutation; presents with nail dysplasia, absent patellae, and proteinuria from podocyte injury.

Congenital nephrotic syndrome: Finnish type from NPHS1 mutations; presents with massive proteinuria in infancy; treat with albumin infusions and nephrectomy.

Primary hyperoxaluria: enzyme deficiencies (AGXT, GRHPR, HOGA1) causing recurrent calcium oxalate stones and systemic oxalosis; treat with pyridoxine and liver-kidney transplant.

Aminoglycosides: cause acute tubular necrosis; risk factors include prolonged use, elevated trough levels, and concurrent nephrotoxins; monitor levels.

NSAIDs: cause hemodynamically mediated AKI (especially with ACE inhibitors and diuretics), acute interstitial nephritis, and papillary necrosis.

ACE inhibitors/ARBs: cause hyperkalemia, AKI in renal artery stenosis, and angioedema; avoid in pregnancy (fetotoxicity).

Calcineurin inhibitors: tacrolimus and cyclosporine cause vasoconstriction, hypertension, hyperkalemia, and chronic nephrotoxicity.

Cisplatin: causes acute kidney injury and chronic tubulointerstitial fibrosis; prevent with saline hydration and mannitol.

Lithium: causes nephrogenic diabetes insipidus and chronic tubulointerstitial nephritis; monitor levels and avoid NSAIDs.

Vancomycin: associated with acute interstitial nephritis, especially with piperacillin-tazobactam; monitor levels and renal function.

Perioperative AKI: risk factors include hypotension, hypovolemia, sepsis, and nephrotoxins; maintain adequate perfusion and avoid nephrotoxins.

Cardiac surgery-associated AKI: occurs in up to 30%; risk factors include cardiopulmonary bypass time, low ejection fraction, and diabetes.

Sepsis-associated AKI: often multifactorial; maintain mean arterial pressure ≥65 mmHg with vasopressors if needed; avoid nephrotoxins.

Abdominal compartment syndrome: intra-abdominal pressure >20 mmHg with new organ dysfunction; causes oliguric AKI; treat with decompression.

Contrast-induced AKI: prevention with IV isotonic saline; use lowest volume of contrast; avoid repeat contrast for 48-72 hours.

Fluid resuscitation in critically ill: balanced crystalloids may be preferred over normal saline; avoid starch solutions.

Renal replacement therapy in ICU: continuous modalities preferred for hemodynamic instability; indications include refractory hyperkalemia, acidosis, and volume overload.