• Corpus ID: 25471221

Mineralocorticoid-induced kaliuresis in type-II pseudohypoaldosteronism.

@article{Travis1986MineralocorticoidinducedKI,
  title={Mineralocorticoid-induced kaliuresis in type-II pseudohypoaldosteronism.},
  author={Phyllis Stowell Travis and Howard M. Cushner},
  journal={The American journal of the medical sciences},
  year={1986},
  volume={292 4},
  pages={
          235-40
        }
}
Type II pseudohypoaldosteronism is an uncommonly reported disorder. The authors recently evaluated a patient who in many respects appeared to have this syndrome. He had hyperkalemia, a normal glomerular filtration rate, "normal" serum and urinary aldosterone levels, and low plasma renin activity. In addition, he had a hyperchloremic metabolic acidosis and hypertension. Fractional excretion of potassium was reduced in response to sodium chloride loading. However, renal potassium excretion in… 
2 Citations
PSEUDOHYPOALDOSTERONISM: A CASE REPORT
TLDR
Serum aldosterone and plasma renin activity were elevated but serum cortisol, 17 -hydroxyprogesterone, ACTH, 24 hour urinary 17ketosteroid, pregnanetriol, renal function and sonogram were normal and pseudohypoaldosteronism type I (pHA 1) was differentiated from congenital adrenal hyperplasia (CAH) and other metabolic disorders.
Mechanism of Hyperkalemia-Induced Metabolic Acidosis.
TLDR
Hyperkalemia decreases proximal tubule ammonia generation and collecting duct ammonia transport, leading to impaired ammonia excretion that causes metabolic acidosis.