American Board of Internal Medicine Certification (ABIM Board Certification) Nephrology & Electrolyte Disorders Syllabus

Name the treatment classes for secondary hyperparathyroidism in CKD.

Dietary phosphate restriction, phosphate binders (non-calcium: sevelamer, lanthanum; calcium-based), active vitamin D analogs (calcitriol, paricalcitol), and calcimimetics (cinacalcet, etelcalcetide).

What causes anemia of CKD and what are its characteristics?

Primarily reduced erythropoietin production by failing kidneys (plus iron deficiency, uremic RBC survival reduction). It is normocytic, normochromic with low reticulocyte count.

What iron and hemoglobin targets guide ESA therapy in CKD anemia?

Replete iron first (target transferrin saturation >30% and ferritin >500 may indicate adequate stores; treat if TSAT <30% and ferritin <500). Start ESA when Hb <10 g/dL; do not target normal Hb (>11.5 increases stroke/CV/thrombosis risk).

When should patients with CKD be referred for kidney transplant evaluation and dialysis access planning?

Refer for transplant evaluation when eGFR <=20 mL/min/1.73m2 (preemptive transplant possible); plan permanent dialysis access (AV fistula preferred) when eGFR ~15-20 or progression is anticipated within ~1 year.

What are the absolute contraindications to kidney transplantation?

Active malignancy, active uncontrolled infection, active substance abuse, severe irreversible non-renal organ disease, and inability to adhere to immunosuppression.

Compare hemodialysis and peritoneal dialysis on a key advantage and disadvantage each.

Hemodialysis: efficient clearance but requires vascular access and clinic visits, with hemodynamic instability. Peritoneal dialysis: home-based with steady clearance and preserved residual function but risks peritonitis and protein loss.

How is nephrotic syndrome defined?

Proteinuria >3.5 g/day, hypoalbuminemia (<3 g/dL), edema, and hyperlipidemia; often with lipiduria (oval fat bodies, 'maltese cross' under polarized light).

What is the most common cause of nephrotic syndrome in adults overall, and in children?

Adults: focal segmental glomerulosclerosis (FSGS) overall; membranous nephropathy is the most common primary cause in older White adults. Children: minimal change disease.

What antibody is associated with primary membranous nephropathy?

Anti-phospholipase A2 receptor (anti-PLA2R) antibodies (present in ~70-80%). Membranous carries the highest risk of renal vein thrombosis among nephrotic glomerulopathies.

What are the key secondary associations of membranous nephropathy, FSGS, and minimal change disease?

Membranous: solid tumors, hepatitis B, lupus (class V), NSAIDs. FSGS: HIV, obesity, heroin, reflux nephropathy. Minimal change: NSAIDs and Hodgkin lymphoma.

How is nephritic syndrome characterized?

Hematuria with dysmorphic RBCs and RBC casts, variable proteinuria (usually <3.5 g/day), hypertension, edema, and often reduced GFR (azotemia).

What is the complement and antibody pattern of post-streptococcal glomerulonephritis?

Low C3 (normalizes by 8 weeks), elevated ASO/anti-DNase B, nephritic syndrome 1-3 weeks after pharyngitis (or 3-6 weeks after skin infection); biopsy shows subepithelial 'humps'.

List the glomerulonephritides that cause LOW serum complement.

Post-streptococcal GN, infective endocarditis-associated GN, lupus nephritis, membranoproliferative GN (MPGN), and cryoglobulinemia (often hepatitis C related).

List the pauci-immune (normal complement, ANCA-associated) causes of rapidly progressive glomerulonephritis.

Granulomatosis with polyangiitis (c-ANCA/PR3), microscopic polyangiitis (p-ANCA/MPO), and eosinophilic granulomatosis with polyangiitis (Churg-Strauss).

What are the three immunofluorescence patterns of rapidly progressive (crescentic) GN?

1) Linear IgG = anti-GBM disease (Goodpasture). 2) Granular ('lumpy-bumpy') = immune-complex (lupus, post-strep, IgA). 3) Pauci-immune (negative/scant) = ANCA-associated vasculitis.

What is the most common glomerulonephritis worldwide, and its classic presentation?

IgA nephropathy (Berger disease). Classic: gross hematuria within 1-3 days of an upper respiratory infection ('synpharyngitic'); mesangial IgA deposits on biopsy.

What are the renal biopsy hallmarks of diabetic nephropathy?

Mesangial expansion, glomerular basement membrane thickening, and Kimmelstiel-Wilson nodules (nodular glomerulosclerosis). Clinically: long-standing diabetes, progressive albuminuria, often with retinopathy.

How does hypertensive nephrosclerosis appear clinically and histologically?

Clinically: long-standing hypertension, modest proteinuria, slowly progressive CKD. Histology: arteriolar hyalinosis, intimal thickening, and global glomerulosclerosis with tubular atrophy.

What are the genetics and key extrarenal manifestations of autosomal dominant polycystic kidney disease (ADPKD)?

Mutations in PKD1 (chromosome 16, more severe) or PKD2 (chromosome 4). Manifestations: hypertension, hematuria, kidney stones, hepatic cysts, and intracranial (berry) aneurysms; mitral valve prolapse.

What drug slows progression of ADPKD, and what is its mechanism?

Tolvaptan, a vasopressin V2-receptor antagonist, slows cyst growth and eGFR decline in rapidly progressive ADPKD; main risk is hepatotoxicity (requires liver monitoring).

What is Alport syndrome and its classic clinical triad?

Hereditary nephritis from type IV collagen mutations (usually X-linked, COL4A5). Triad: progressive hematuric nephritis, sensorineural hearing loss, and ocular abnormalities (anterior lenticonus). Biopsy shows 'basket-weave' GBM splitting.

How do you calculate corrected sodium in the setting of hyperglycemia?

Add ~1.6 mEq/L (some use 2.4) to measured sodium for every 100 mg/dL that glucose exceeds 100 mg/dL. This corrects translocational (hyperglycemic) hyponatremia.

What is the diagnostic approach to hyponatremia using serum and urine osmolality and urine sodium?

First check serum osm (rule out pseudo/hyperglycemic). For true hypotonic hyponatremia: urine osm <100 suggests primary polydipsia/low solute; urine osm >100 with urine Na <20 = hypovolemic/hypervolemic; urine Na >20 (euvolemic) = SIADH.

What is the maximum safe rate of sodium correction in chronic hyponatremia and the risk of overcorrection?

Limit correction to <=8 mEq/L per 24 hours (some use 6-8) to avoid osmotic demyelination syndrome (central pontine myelinolysis).

What are the diagnostic criteria for SIADH?

Euvolemic hypotonic hyponatremia (serum osm <275), inappropriately concentrated urine (urine osm >100), urine Na >30-40 mEq/L, normal thyroid/adrenal function, and no diuretic use.

How do central and nephrogenic diabetes insipidus differ on the desmopressin (DDAVP) test?

After DDAVP, central DI shows a >50% rise in urine osmolality (responds to ADH); nephrogenic DI shows little/no rise (kidneys resistant to ADH). Both present with hypotonic polyuria and hypernatremia if water access is limited.

What ECG changes occur with hyperkalemia, in order of progression?

Peaked T waves -> PR prolongation and flattened/lost P waves -> widened QRS -> sine wave -> ventricular fibrillation/asystole.

What is the acute treatment sequence for severe hyperkalemia?

1) IV calcium gluconate (membrane stabilization, does not lower K). 2) Shift K intracellularly: insulin+glucose, beta-agonist (albuterol), bicarbonate if acidotic. 3) Remove K: loop diuretics, GI binders (patiromer, SZC), and hemodialysis if refractory.

How do you use the transtubular potassium gradient/urine K to distinguish causes of hypokalemia, and what acid-base clue helps?

Low urine K (<20) = GI/transcellular losses (appropriate renal conservation). High urine K = renal wasting. With metabolic alkalosis + low urine chloride think vomiting; with high BP think hyperaldosteronism; normotensive renal wasting suggests Bartter/Gitelman.

What electrolyte must be corrected before potassium will normalize in refractory hypokalemia?

Magnesium. Hypomagnesemia increases renal potassium wasting (and causes refractory hypocalcemia), so magnesium must be repleted for potassium and calcium to correct.

How do you calculate the corrected calcium for hypoalbuminemia?

Corrected Ca = measured Ca + 0.8 x (4.0 - serum albumin in g/dL). Ionized calcium is the definitive measure when albumin is abnormal.

What is the anion gap formula, and what is the differential for a high anion gap metabolic acidosis?

Anion gap = Na - (Cl + HCO3) (normal 8-12). High AG causes (GOLD MARK): Glycols (ethylene/propylene), Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure (uremia), Ketoacidosis.

What is Winter's formula for expected respiratory compensation in metabolic acidosis?

Expected PaCO2 = 1.5 x [HCO3] + 8 +/- 2. If measured PaCO2 is higher, there is a concurrent respiratory acidosis; if lower, a concurrent respiratory alkalosis.

How are the three classic renal tubular acidoses (RTA) distinguished by serum potassium and urine pH?

Type 1 (distal): hypokalemia, urine pH >5.5, risk of stones. Type 2 (proximal): hypokalemia, urine pH variable (<5.5 when severe), with Fanconi syndrome. Type 4 (hypoaldosteronism): HYPERkalemia, urine pH <5.5. All are normal anion gap acidoses.

How are metabolic alkaloses classified using urine chloride?

Urine chloride <20 mEq/L = saline-responsive (vomiting/NG suction, diuretic use, contraction). Urine chloride >20 mEq/L = saline-resistant (hyperaldosteronism, Cushing, Bartter/Gitelman, severe hypokalemia).