2019 Volume 62 Issue 7 Pages 383-388
A 38-year-old man was admitted to our hospital to undergo treatment for diabetes, nephrotic syndrome, hypokalemia and hypertension. He had been diagnosed with type 2 diabetes 11 years previously, and his glucose control had been poor. Four years previously, he was normotensive and showed trace levels of urinary albumin excretion and a normal serum potassium concentration. On admission, he showed metabolic alkalosis, low plasma renin activity, and low a plasma aldosterone concentration with hypertension. Because we suspected Liddle syndrome, triamterene was administered, and his hypertension and hypokalemia both improved. Our patient had no family history of hypertension, and no mutation of ENaC (amyloid-sensitive epithelial sodium channel) gene exon 13, but showed increased urinary excretion of serine protease. These findings suggested that the increased serine protease level had a similar effect to the high activation of ENaC. This case showed a similar presentation to Liddle syndrome due to nephrotic syndrome caused by diabetic nephropathy.