Type 4 renal tubular acidosis in a kidney transplant recipient.

We report a case of a 66-year-old diabetic patient who presented with muscle weakness 2 weeks after kidney transplantation. Her immunosuppressive regimen included tacrolimus, mycophenolate mofetil, and steroids. She was found to have hyperkalemia and normal anion gap metabolic acidosis. Tacrolimus levels were in therapeutic range. All other drugs such as beta blockers and trimethoprim - sulfamethoxazole were stopped. She did not respond to routine antikalemic measures. Further evaluation revealed type 4 renal tubular acidosis. Serum potassium levels returned to normal after starting sodium bicarbonate and fludrocortisone therapy. Though hyperkalemia is common in kidney transplant recipients, determining exact cause can guide specific treatment.

Incidence of hyperkalemia in kidney transplant recipients who receive calcineurin inhibitors is about 44% [1]. Ischemia, tubular necrosis, rejection, and drugs are some of the common causes of hyperkalemia. Determining exact cause can guide specific treatment. We describe a case of kidney transplant recipient who had persistent hyperkalemia due to type 4 renal tubular acidosis (RTA) and was treated with fludrocortisone and sodium bicarbonate therapy.

A 66-year-old female diabetic patient presented 2 weeks after kidney transplantation with muscle weakness. Her medications included tacrolimus, mycophenolate mofetil, prednisolone, trimethoprim-sulfamethoxazole, and carvedilol. Her laboratory reports showed serum creatinine 0.6 mg/dl, serum sodium 135 mEq/L, serum potassium 6.5 mEq/L, serum chloride 110 mEq/L, and serum bicarbonate 18 mEq/L.

We stopped co-trimoxazole and carvedilol. She was started on frusemide, oral potassium binding resins, and oral sodium bicarbonate. Serum tacrolimus levels were 7.1 ng/L. Repeat serum potassium reading was 7 mEq/L. Further evaluation showed urine pH 5.1, urine sodium 40 mEq/L, urine potassium 30 mEq/L, and urine chloride 50 mEq/L. The serum anion gap was 7 mEq/L and urinary anion gap was 20 mEq/L. Hyperkalemia distal RTA was ruled out as urinary pH was <5.5. A normal anion gap metabolic acidosis, positive urinary anion gap with a urine pH of <5.5 was suggestive of type 4 RTA. We started the patient on fludrocortisone 0.1 mg/day. Serum potassium levels on consecutive days were 5.8 mEq/L, 5.1 mEq/L, and 4.5 mEq/L. Fludrocortisone was gradually tapered after 10 days and stopped. Patient remained normokalemic at follow-up.

Though there are a few case reports, exact prevalence of type 4 RTA in kidney transplant recipients in early posttransplant period is not known [2], [3]. In one study of 109 kidney transplant recipients, RTA was seen in 36 patients and only 3 of these patients had type 4 RTA. Late after transplant, incidence of type 4 RTA in late transplant period can be as high as 28% [4], [5].

In this case, type 4 RTA was probably a result of tacrolimus-induced aldosterone resistance of renal tubules. Finding the etiology of hyperkalemia will make specific treatment possible.

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Nil.

Conflicts of interest

None declared.