CAQ-Nephrology common mistakes
CAQ-Nephrology · Understand the traps and how to avoid them.
Classifies a normal-anion-gap metabolic acidosis with the urine anion gap without first documenting urine sodium >20 mEq/L.
The urine anion gap assumes urine sodium approximates urine chloride and that ammonium is the only unmeasured cation; in low-sodium urine or with ammonium-containing toxins (e.g., glue, toluene) the gap is positive despite appropriate ammonium excretion.
What to do instead
Check urine sodium, urine pH, and urine osmolal gap; use the urine osmolar gap when urine sodium is low, and interpret the result with the clinical ingestant history.
Uses a sodium-deficit formula to set the entire correction rate for chronic hyponatremia and does not recheck sodium after the first liters.
Deficit formulas assume a closed system and ignore ongoing hypotonic losses, desmopressin effect, and the nonlinear relationship between sodium and tonicity; overcorrection causes osmotic demyelination.
What to do instead
Estimate the effect of 1 L of fluid with Adrogué-Madias, limit correction to 8-10 mmol/L in 24 h (lower in high-risk patients), recheck every 4 h, and use DDAVP plus free water to re-lower if overcorrected.
Calls hematuria 'glomerular' based on dipstick alone, without urine microscopy for dysmorphic RBCs/RBC casts and without complement C3/C4.
Dipstick detects heme, not RBC morphology; isolated hematuria often has a urologic cause, and complement patterns narrow the glomerular differential.
What to do instead
Perform microscopy on a fresh sample, document RBC casts/dysmorphic RBCs, check complement, and pursue urologic evaluation when the sediment is nondiagnostic.
In an older adult with nephrotic syndrome, proceeds directly to kidney biopsy without SPEP/serum free light chain ratio, hepatitis B/C, HIV, and a drug/NSAID history.
Primary podocytopathies are less likely with age; paraprotein-associated disease, viral glomerulonephritis, and drug-induced membranous nephropathy or FSGS change management and biopsy timing.
What to do instead
Order paraprotein studies, viral serologies, complement, and a careful medication review before or alongside biopsy; interpret biopsy with these results.
Attributes unexplained AKI to prerenal disease and gives a fluid bolus without a bladder scan or renal ultrasound.
Obstructive uropathy is reversible and can be silent; anchoring on volume depletion and responding to a small urine output can delay decompression.
What to do instead
Obtain a bladder scan and renal ultrasound early in unexplained AKI, especially with stones, prostate disease, malignancy, or a single kidney; assess volume tolerance before fluids.
Uses fractional excretion of sodium (FENa) to separate prerenal AKI from ATN in a patient receiving furosemide or after contrast.
Loop diuretics increase sodium excretion and can make FENa >1% in prerenal states; contrast and CKD alter the interpretation.
What to do instead
Use FEUrea when diuretics are active, interpret FENa with urine microscopy and clinical volume status, and avoid treating a single index as diagnostic.
Accepts a Kt/V or urea reduction ratio at target without verifying delivered treatment time, blood flow, dialyzer clearance, and residual kidney function.
Prescribed Kt/V is not delivered Kt/V; early termination, access recirculation, and residual function alter adequacy, and a target value can mask underdialysis.
What to do instead
Review dialysis run sheets, access function, and residual urea clearance; calculate delivered Kt/V and adjust the prescription before labeling adequacy.
In a kidney transplant recipient with rising creatinine, attributes the change to rejection and increases immunosuppression without checking tacrolimus trough and interacting medications.
Calcineurin inhibitor toxicity, drug interactions (azoles, macrolides, diltiazem), BK nephropathy, and obstruction mimic rejection; empiric intensification can worsen nephrotoxicity.
What to do instead
Check trough level, review interacting drugs, obtain BK viral load and ultrasound, and biopsy before changing immunosuppression when the cause is unclear.
Does not consider renovascular disease in resistant hypertension with flash pulmonary edema or in a young woman with abdominal bruit and worsening creatinine after ACE inhibitor.
Renovascular hypertension is a secondary cause that changes therapy; ACE inhibitor-induced creatinine rise can be the clue, but fear of the drug leads to avoidance of the diagnosis.
What to do instead
Screen with renal artery duplex, CTA, or MRA when clinical features suggest fibromuscular dysplasia or atherosclerotic renal artery stenosis; review medication chronology.
In scleroderma renal crisis, withholds ACE inhibitor because creatinine is rising and treats with high-dose steroids while waiting for biopsy.
Scleroderma renal crisis is a thrombotic microangiopathy driven by hyperreninemia; ACE inhibitors are first-line and steroids can precipitate or worsen the crisis.
What to do instead
Start captopril immediately (short-acting ACE inhibitor), titrate to blood pressure and creatinine, avoid steroids, and involve nephrology for dialysis if needed.