Since that patient was not otherwise ill – normal vital signs, no fever – we decided to treat his nausea and vomiting as an extension of his previous GI dysfunction. We started metoclopramide, which worked well. We also wondered if his poorly functioning indwelling catheter may have contributed to his symptoms.

In terms of his lab tests, we suspected a normal gap metabolic acidosis, therefore we obtained an ABG (to exclude compensation for a respiratory alkalosis), a urine pH, and urine electrolytes (to calculate the urine anion gap).

His urine pH was 6.5, and he did have infected urine.

His urine electrolytes showed Na 73/ K 27/ Cl 70 – this gives a positive urine anion gap, which supports a renal buffering cause rather than bicarbonate losses (diarrhea).

For those who want to read more about the urine anion gap try one of these references – Solution to “A 42-Year-Old Man With HIV” (one of my Medscape case solutions) or Urine Anion Gap

The urine anion gap confirmed our assumption of a renal buffering problem. The relatively high urine pH suggested a distal RTA. Most distal RTA patients have hypokalemia. Some experts now include Type IV RTA as a distal RTA.

We suspect that our patient had a very specific form of distal RTA secondary to obstructive uropathy. Hyperkalemic distal renal tubular acidosis associated with obstructive uropathy

We studied renal function in 13 patients with obstructive uropathy and hyperkalemic metabolic acidosis to characterize the pathogenesis of this disorder. Base-line fractional potassium excretion was lower in all patients than in controls with similar glomerular filtration rates. Acetazolamide was given to 11 patients but failed to increase fractional potassium excretion to normal. In five patients, impaired potassium excretion was associated with decreased ammonium excretion, a urinary pH below 5.5 (5.18 +/- 0.07, mean +/- S.E.M.), and aldosterone deficiency. In the remaining eight patients, the urinary pH did not fall below 5.5 (6.4 +/- 0.2) with acidosis, and we failed to lower the urinary pH and increase fractional potassium excretion to normal by administering a mineralocorticoid and sodium sulfate. A syndrome of hyperkalemic distal renal tubular acidosis may occur in patients with obstructive uropathy. In some patients, this syndrome results from a defect in hydrogen and potassium secretion in the distal nephron rather than from aldosterone deficiency. Obstructive uropathy should be included in the differential diagnosis of hyperkalemic acidosis and renal insufficiency.

We suspect that the vomiting prevented the development of the expected hyperkalemia. He certainly showed signs of defective hydrogen and potassium secretion with his urine pH and low urine potassium.

The patient’s renal function improve dramatically with a new indwelling catheter and antibiotic treatment of his urinary tract infection. We gave him IV bicarbonate to correct his serum bicarbonate to a desired level of approximately 22. On discharge, 3 days after admission his lab values had returned to his baseline, as had his tolerance for oral intake.

Admission labs recalled:

Discharge labs:

I do not remember previously seeing obstructive uropathy cause an acidosis, so I wanted to document this story for myself. I hope that some readers find this story instructive and potentially helpful.