Hypothesis: A simple algorithm to distinguish between hypoaldosteronism and renal aldosterone resistance in patients with persistent hyperkalemia

Abstract

In hyperkalemic patients a plasma aldosterone to potassium algorithm may help distinguish HA from RAR, thereby guiding therapy.

Transient type 1 pseudo-hypoaldosteronism: report on an eight-patient series and literature review

“…The very high ratios of plasma aldosterone to potassium, together with the diminished urinary K/Na values, strongly support the conclusion that hyponatremia and hyperkalemia result from a lack of response of the renal tubule to endogenous mineralocorticoids [8,12,13,40]. Because of the retrospective nature of the study, we could not calculate fractional excretion of sodium (FENa) or fractional excretion of potassium (FEK), or the transtubular potassium concentration gradient (TTKG), but previous studies demonstrated that FENa was significantly increased and both FEK and TTKG were significantly decreased, sustaining the distal tubular unresponsiveness to aldosterone [6,19,41,42].…”

Relative hypoaldosteronism in a patient with Wolcott‐Rallison syndrome

“…In patients with non‐urgent hyperkalaemia with renal impairment, given that 75% will have hypoaldosteronism, a trial of fludrocortisone seems justifiable . The potential adverse effect of steroids on glycaemic control was not observed in our patient, supporting the physiological need for mineralocorticoid replacement.…”

Fludrocortisone for Heparin-Induced Hyperkalemia

“…The diagnosis was further supported by the calculation of plasma aldosterone/(plasma potassium -4.2), which was less than 280 (patient data: 96/[5.5 -4.2]). 4 The serum renin concentration was only slightly elevated (0.35 ng/L/s; normal value for patient in the supine position < 0.28 ng/L/s), and the serum cortisol level was normal (436 nmol/L; normal range 175-685 nmol/L). To overcome the heparin-induced hypoaldosterone state, fludrocortisone 0.1 mg once daily was given orally on days 15, 16, and 17.…”