Match each clinical scenario describing a medication-induced renal, electrolyte, or acid-b… — USMLE Step 2 CK

Match each clinical scenario describing a medication-induced renal, electrolyte, or acid-base abnormality to the corresponding causative pharmacological agent.

During the course of antimicrobial therapy for a skin and soft tissue infection, a patient demonstrates an isolated rise in serum creatinine from $0.9 \text{ mg/dL}$ to $1.6 \text{ mg/dL}$ . Concurrent laboratory testing reveals a serum potassium of $5.4 \text{ mEq/L}$ , though the estimated glomerular filtration rate remains strictly within normal limits.Trimethoprim-sulfamethoxazole
Following initiation of intravenous antifungal therapy for an invasive mycosis, a patient develops profound lower extremity cramping. Biochemical evaluation shows a serum potassium of $2.8 \text{ mEq/L}$ , a non-anion gap metabolic acidosis, and an inappropriately elevated urine pH of $6.8$ .Amphotericin B
A patient managed pharmacologically for idiopathic intracranial hypertension reports progressive fatigue. A basic metabolic panel confirms a non-anion gap metabolic acidosis with a serum bicarbonate of $17 \text{ mEq/L}$ , while urinalysis demonstrates an appropriately acidic urine pH of $5.2$ .Acetazolamide
While receiving long-term maintenance therapy for a mood disorder, a patient complains of unremitting thirst and excessive urination. Serum sodium is elevated at $152 \text{ mEq/L}$ , and urine osmolality is $115 \text{ mOsm/kg}$ , which fails to increase significantly following the administration of exogenous desmopressin.Lithium carbonate

Cevap

The correct pairings identify Trimethoprim-sulfamethoxazole for the isolated creatinine elevation with hyperkalemia, Amphotericin B for the Type 1 RTA presentation, Acetazolamide for the Type 2 RTA presentation, and Lithium carbonate for the nephrogenic diabetes insipidus presentation.

Each pharmacological agent possesses a distinct pathophysiological mechanism affecting the renal tubules: Trimethoprim blocks both creatinine secretion and ENaC channels; Amphotericin B creates pores in the distal tubule causing a Type 1 RTA; Acetazolamide inhibits proximal carbonic anhydrase causing a Type 2 RTA; and Lithium induces ADH resistance at the collecting duct, causing nephrogenic DI.

Adım Adım Çözüm

Analyze the scenario with isolated creatinine rise and hyperkalemia but normal eGFR.

Identifies tubular secretion blockade and distal ENaC inhibition, consistent with trimethoprim-sulfamethoxazole use.

Differentiating pseudo-renal failure from true acute kidney injury is essential when managing patients on specific antimicrobials.

Evaluate the non-anion gap metabolic acidosis accompanied by severe hypokalemia and a high urine pH (> 5.5).

Classifies the disorder as Type 1 (distal) renal tubular acidosis, a known toxicity of amphotericin B.

The inability to excrete hydrogen ions distally results in an inappropriately alkaline urine despite systemic acidosis.

Evaluate the non-anion gap metabolic acidosis with intact distal acidification (urine pH < 5.5).

Identifies Type 2 (proximal) renal tubular acidosis, an expected effect of acetazolamide therapy.

Acetazolamide wastes bicarbonate proximally, but because the distal tubule is unharmed, the urine can eventually be acidified.

Analyze the ADH-resistant polyuria and hypernatremia.

Confirms a diagnosis of nephrogenic diabetes insipidus, which is a classic adverse effect of chronic lithium therapy.

The lack of response to exogenous desmopressin localizes the defect to the renal collecting duct rather than central ADH release.

Anahtar Kavram

Pathophysiology and identification of drug-induced nephrotoxicity and distinct acid-base/electrolyte derangements.

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