Clinical High-Yield · 10 min read · April 28, 2026
Nephrology is a section that rewards systematic preparation. The boards test a specific, predictable set of renal content: CKD staging and management, the three categories of acute kidney injury, and the electrolyte disorders that require immediate recognition and treatment. Here is the high-yield content organized for maximum board efficiency.
CKD is defined as kidney damage or GFR <60 mL/min/1.73m² for more than 3 months. The KDIGO staging system classifies CKD by GFR (G1–G5) and albuminuria (A1–A3). The boards test the GFR stages and the management milestones at each stage.
CKD Stages by GFR:
Management milestones by stage:
Medications to avoid or dose-adjust in CKD: The boards test this extensively. Avoid NSAIDs (reduce GFR, cause fluid retention). Avoid metformin when GFR <30 (lactic acidosis risk). Avoid direct oral anticoagulants (DOACs) at low GFR levels (varies by agent). Dose-adjust: digoxin, gabapentin, many antibiotics (aminoglycosides, vancomycin, fluoroquinolones).
Board Pearl: ACE inhibitors and ARBs are renoprotective in CKD with proteinuria — but they can cause an initial rise in creatinine (up to 30% increase is acceptable) and hyperkalemia. A creatinine rise >30% or new hyperkalemia requires dose reduction or discontinuation.
AKI is defined as an abrupt increase in serum creatinine ≥0.3 mg/dL within 48 hours, or ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/hour for ≥6 hours. The boards test the three categories and their distinguishing features.
Prerenal AKI: Caused by decreased renal perfusion — dehydration, hemorrhage, heart failure, sepsis, NSAIDs (reduce prostaglandin-mediated afferent arteriolar dilation). Urine findings: concentrated urine (specific gravity >1.020, osmolality >500 mOsm/kg), low urine sodium (<20 mEq/L), FENa <1%. Treatment: correct the underlying cause — IV fluids for hypovolemia, treat heart failure, discontinue nephrotoxins.
Intrinsic (intrarenal) AKI: Caused by direct kidney damage. The...