Case Presentation:

A 42–year–old woman presented with three days of worsening left flank pain radiating to her groin. She experienced similar pain over the past year, but it had never been this severe. She now noted tingling in her fingers and a tremor. She was afebrile, orthostatic, tachycardic without a murmur, and tachypneic with clear lung sounds. There was left flank tenderness without ecchymosis, and left lower quadrant pain with light palpation. Her CBC was normal. The potassium of 3.1, the creatinine was 1.58, the bicarbonate was 7, and her anion gap was normal. The pH was 7.10, with a pCO2 of 16. She had a positive urine anion gap, and the urine pH was 6.5. An abdominal X–ray revealed no abnormalities, though an abdominal CT scan revealed multiple bilateral renal calculi with left proximal hydroureter and hydronephrosis. She was diagnosed with a Renal Tubular Acidosis Type 1 (RTA–1), which inspired subsequent questioning. Upon further questioning, she admitted to taking three to four grams of Muccinex D (guaifenesin–pseudoephedrine) per day over the course of the past year.

Discussion:

Acid–base disorders are commonly encountered by the hospitalist. It is important the hospitalist have a disciplined approach to reaching a timely diagnosis. With our patient, arriving at the diagnosis early inspired targeted questioning to reveal the underlying etiology. Renal tubular acidosis is the accumulation of acid in the body due to the failure of the kidneys to appropriately acidify the urine. RTA’s are typically diagnosed by identifying a nonanion gap metabolic acidosis with a positive urinary anion gap. Since one chloride ion is retained for every bicarbonate ion lost, the anion gap remains normal; since the urine chloride is thus very low, the urinary anion gap (UAG: UNa + UK – UCl) is positive. Type–1 (distal RTA) is caused by a dysfunction of H+/K+–ATPase exchange pump, and is thus characterized by a loss of potassium in the urine (hypokalemia) and the inability to acidify the urine (urinary pH > 5.5). Most common causes of RTA–1 are inadequate renal perfusion, hypercalcemia, autoimmune, chronic hydronephrosis, and toxic injury. Guaifenesin and ephedrine metabolites have been discovered as primary components of renal calculi from patients who abuse these medications on a daily basis for extended periods. Unlike more common calcium containing radio–opaque stones, these stones are radiolucent on plain film and require a CT scan to be identified. This distinguishing marker was present in our patient. Direct injury occurred to the distal nephron from excessive Guaifenesin and ephedrine metabolite. The chronic obstruction, as evidenced by hydroureter and hyrdonepheosis, resulted in toxin accumulation that damaged the distal nephron.

Conclusions:

When faced with common disorders such as kidney stones, it’s vital for the hospitalist to attain a history. Although stones occur frequently, their cause is not always clear, and the potential side effects can result in significant systemic disease.