Impaired renal tubular potassium secretion in systemic lupus erythematosus

Ann Intern Med. 1977 Mar;86(3):268-71. doi: 10.7326/0003-4819-86-3-268.


Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.

Publication types

  • Case Reports
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetazolamide / pharmacology
  • Adult
  • Aldosterone / metabolism
  • Female
  • Fludrocortisone / pharmacology
  • Furosemide / pharmacology
  • Humans
  • Hyperkalemia / etiology
  • Kidney Tubules / metabolism*
  • Lupus Erythematosus, Systemic / complications
  • Lupus Erythematosus, Systemic / metabolism*
  • Natriuresis
  • Potassium / metabolism*
  • Renin / blood
  • Sodium / metabolism


  • Aldosterone
  • Furosemide
  • Sodium
  • Renin
  • Acetazolamide
  • Potassium
  • Fludrocortisone