ABIM Nephrology common mistakes
ABIM Nephrology · Understand the traps and how to avoid them.
Calculating the serum anion gap without correcting for hypoalbuminemia, then labeling a high-gap acidosis as normal or vice versa.
The standard Na - (Cl + HCO3) formula assumes a normal albumin of ~4 g/dL; in hypoalbuminemic patients (nephrotic syndrome, cirrhosis, critical illness) the uncorrected gap underestimates the true gap and masks an osmolar or organic acidosis.
What to do instead
Apply the albumin correction (add ~2.5 to the measured gap for every 1 g/dL albumin below 4), state the corrected value in your reasoning, and pair it with the delta-delta to check for a mixed disorder.
Treating a high anion gap metabolic acidosis with bicarbonate before identifying and addressing the underlying cause (e.g., missed methanol, ethylene glycol, or ketoacidosis).
Pattern recognition pushes candidates toward symptomatic correction; the gap itself is a clue to a toxin or substrate problem that requires specific therapy (fomepizole, insulin, etc.), and bicarbonate has narrow indications.
What to do instead
Always derive a differential for the elevated gap (MUDPILES/KULT), compute the osmolar gap when toxins are possible, and reserve bicarbonate for severe acidemia (pH <7.1) or specific conditions; document the cause-directed plan.
Using the serum creatinine alone to estimate GFR in a patient with low muscle mass, amputation, or advanced cirrhosis, and then dosing drugs or staging CKD on that number.
Creatinine-based eGFR equations are calibrated to average muscle mass; sarcopenia makes creatinine falsely low and eGFR falsely reassuring, while creatinine rise lags injury in AKI.
What to do instead
Cross-check with cystatin C-based eGFR when muscle mass is atypical, trend creatinine over time, and use measured clearance or explicit caveats for drug dosing in extremes of body composition.
Attributing AKI to acute tubular necrosis by default without systematically excluding prerenal, obstructive, and glomerular/interstitial causes first.
ATN is the most common hospital-acquired AKI, so it becomes a default label; candidates skip the urinalysis with microscopy, fractional excretion indices, and bladder scan that separate the categories.
What to do instead
Run a fixed checklist before committing: volume status and response to fluids, post-void residual or renal ultrasound for obstruction, urine sediment for casts/eosinophils/RBCs, and FeNa/FeUrea interpreted in context (diuretics invalidate FeNa).
Interpreting a fractional excretion of sodium in a patient on loop diuretics or with CKD as if it reliably distinguishes prerenal from intrinsic disease.
The test is taught as a clean discriminator, but diuretics, contrast, and chronic kidney disease distort tubular sodium handling, producing misleading values.
What to do instead
Use FEUrea (or a fluid challenge with careful monitoring) when diuretics are on board, recognize that CKD raises baseline FeNa, and integrate the index with the clinical volume assessment rather than treating it as definitive.
Managing hyperkalemia with calcium, insulin, and albuterol and then discharging without addressing total body potassium and the ongoing source.
Emergent therapy shifts potassium intracellularly and looks effective on the repeat lab, so the transient nature of the effect and the need for removal (diuretics, binders, dialysis) are forgotten.
What to do instead
After temporizing measures, explicitly plan potassium elimination (loop diuretic, GI binder, dialysis if indicated), recheck potassium within hours, and remove offending drugs (RAAS inhibitors, potassium-sparing agents, NSAIDs) with a documented follow-up level.
Diagnosing hypertensive emergency and lowering blood pressure aggressively in the first hour in a patient without end-organ damage, or conversely under-treating true end-organ injury.
Candidates conflate severe hypertension with emergency; the presence or absence of acute target-organ injury (encephalopathy, aortic dissection, pulmonary edema, AKI, retinal hemorrhage) drives the rate of reduction, and misclassification causes either cerebral hypoperfusion or delayed treatment.
What to do instead
State explicitly whether acute end-organ damage is present; if not, use oral agents and outpatient escalation. If present, reduce mean arterial pressure by no more than ~20-25% in the first hour (except aortic dissection, where rapid control is required), using titratable IV agents.
Choosing a dialyzer, modality, or prescription without matching it to the clinical indication (e.g., using conventional hemodialysis for a toxin with high protein binding or small volume of distribution).
Candidates default to intermittent hemodialysis for all poisonings and to standard prescriptions for all AKI, ignoring clearance kinetics, hemodynamic stability, and the specific solute to be removed.
What to do instead
Match therapy to the indication: intermittent HD for small, water-soluble, low-Vd toxins; CRRT for hemodynamically unstable patients; and know that protein-bound or large-Vd toxins are poorly dialyzed. State the clearance rationale.
Working up hematuria or proteinuria with imaging or a repeat urinalysis alone and omitting quantification and serologic/microscopic assessment before labeling it benign.
Asymptomatic findings are often dismissed; candidates skip 24-hour or spot protein-to-creatinine quantification, urine microscopy for dysmorphic RBCs and casts, and complement/serologies that separate glomerular from urologic disease.
What to do instead
For glomerular-pattern hematuria or any significant proteinuria, quantify protein (UPCR/ACR), examine sediment for acanthocytes and RBC casts, check complement and relevant serologies, and refer for biopsy when indicated rather than repeating a dipstick.
Adjusting renally cleared drug doses only by serum creatinine level and ignoring the actual eGFR, loading-dose requirements, and dialysis-related removal.
Candidates memorize a few dose cutoffs but miss that loading doses are usually unchanged, that some drugs require post-dialysis supplementation, and that creatinine-based estimates mislead in AKI and low muscle mass.
What to do instead
For each renally cleared drug, state the eGFR used, keep the loading dose full, adjust maintenance dosing to the estimate, and specify whether the drug is dialyzable and needs re-dosing after a session.