Laboratory evaluation is performed during a routine follow-up visit for a 64-year-old man … — USMLE Step 2 CK

Laboratory evaluation is performed during a routine follow-up visit for a 64-year-old man with a 15-year history of type 2 diabetes mellitus and hypertension. The patient reports feeling generally well and explicitly denies any recent nausea, vomiting, or diarrhea. His current medication regimen consists of metformin, lisinopril, amlodipine, and atorvastatin. Blood pressure is $134/82 \text{ mmHg}$ and pulse is $72/\text{min}$ .

Laboratory results are as follows:

Test	Result
Serum sodium	$137 \text{ mEq/L}$
Serum potassium	$5.9 \text{ mEq/L}$
Serum chloride	$110 \text{ mEq/L}$
Serum bicarbonate	$15 \text{ mEq/L}$
Blood urea nitrogen	$34 \text{ mg/dL}$
Serum creatinine	$1.8 \text{ mg/dL}$
Blood glucose	$142 \text{ mg/dL}$

Urinalysis reveals a pH of $5.2$ and is negative for glucose, ketones, and cellular casts.

Which of the following pathophysiologic mechanisms best explains this patient's current laboratory findings?

Reduced production of and distal tubular responsiveness to aldosteroneAnswer
B
Failure of alpha-intercalated cells to secrete hydrogen ions
C
Impaired bicarbonate reabsorption in the proximal convoluted tubule
D
Accumulation of unmeasured endogenous acidic organic anions
E
Significant gastrointestinal loss of bicarbonate-rich secretions

Answer

Reduced production of and distal tubular responsiveness to aldosterone

This patient has a normal anion gap metabolic acidosis (Anion Gap = 137 - (110 + 15) = 12 mEq/L) accompanied by hyperkalemia. This pattern is pathognomonic for Type 4 Renal Tubular Acidosis (RTA). The most common etiology for Type 4 RTA in adults is hyporeninemic hypoaldosteronism due to diabetic nephropathy. Aldosterone normally functions to reabsorb sodium in exchange for potassium and hydrogen ion secretion in the distal tubule and collecting duct. A lack of aldosterone (or resistance to it) leads to retention of both potassium and hydrogen, causing hyperkalemic metabolic acidosis. The patient's use of lisinopril (an ACE inhibitor) further suppresses aldosterone synthesis, exacerbating the condition.

Step-by-Step Solution

Calculate the serum anion gap.

Na^+ - (Cl^- + HCO_3^-) = 137 - (110 + 15) = 12 \text{ mEq/L}

To classify the metabolic acidosis as either normal anion gap or high anion gap. A gap of 12 is within the normal range.

Assess the serum potassium level in the context of the acid-base disorder.

The patient has hyperkalemia (

5.9 \text{ mEq/L}

) along with a normal anion gap metabolic acidosis (NAGMA).

Potassium levels help differentiate the causes of NAGMA. Diarrhea and Type 1/2 RTA present with hypokalemia, whereas Type 4 RTA presents with hyperkalemia.

Synthesize the clinical history and medication list.

The patient has longstanding diabetes mellitus and is taking lisinopril (an ACE inhibitor).

Diabetic nephropathy classically damages the juxtaglomerular apparatus, reducing renin secretion (hyporeninemic hypoaldosteronism). ACE inhibitors further decrease aldosterone levels, fully explaining the Type 4 RTA presentation.

Key Concept

Hyperkalemic normal anion gap metabolic acidosis (Type 4 RTA) is commonly caused by hyporeninemic hypoaldosteronism due to diabetic nephropathy and exacerbated by ACE inhibitors.

Estimated Time:1m 30s

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