Abstract: TH-PO1099

Transient Hyporeninemic Hypoaldosteronism with Renal Salt Wasting: An Unusual Presentation

Session Information

Category: Fluid, Electrolytes, and Acid-Base

  • 704 Fluid, Electrolyte, Acid-Base Disorders

Authors

  • Arif, Huda, Loyola University, Chicago, Illinois, United States
  • Leehey, David J., Loyola University Medical Center, Oak Park, Illinois, United States
Background

We are presenting a case of transient hypoaldosteronism with hyporeninemia presenting with orthostatic hypotension and renal salt wasting without cerebral disease. Adrenal insufficiency was ruled out by normal ACTH and cortisol levels

Methods

A 61-year-old gentleman with no significant medical history except for mild essential hypertension was referred to the renal clinic after multiple visits to the emergency room for symptomatic orthostatic hypotension requiring isotonic saline infusion. Evaluation in clinic showed orthostatic hypotension with an intact autonomic response. He reported polyuria with approximately 3-4L daily urine output. Laboratory evaluation revealed persistent hypoaldosteronism with plasma aldosterone levels <1 ng/dL, low plasma renin activity (0.23-1.10 ng/mL/h), and normal ACTH and cortisol levels. He had normal renal function and normal plasma potassium and total carbon dioxide levels. His plasma sodium levels were generally normal with occasional mild hyponatremia noted. He had persistently elevated urinary sodium concentrations (> 20 mmol/L) in the face of hypotension, and 24h urine sodium and aldosterone excretions were 164 mg and < 1 mcg, respectively. He was treated with fludrocortisone 0.1 mg daily with marked improvement in orthostatic symptoms. Over the course of years, his renin and aldosterone normalized and fludrocortisone was tapered to minimal dose. Attempts to stop fludrocortisone resulted in recurrence of symptoms.

Conclusion

Aldosterone causes reabsorption of sodium and chloride and excretion of potassium and hydrogen ions in the distal convulated tubule. Selective or isolated aldosterone deficiency can result from a deficiency in renin secretion or decreased adrenal synthesis. Hyporeninemic hypoaldosteronism is most common in patient with mild to moderate renal insufficiency due to diabetic nephropathy or chronic interstitial nephritis. It can also occur with acute GN and in patients taking NSAID and CNI. The characteristic electrolyte findings of this disorder are hyperkalemic hyperchloremic acidosis and occasionally mild hyponatremia, usually in the setting of impaired renal function.
This case illustrates the importance of considering the diagnosis of hypoaldosteronism in adult patients with symptoms and signs of renal salt wasting in the absence of hyperkalemic hyperchloremic acidosis.