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
- Medicine, Biology
- 1994
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.
- Biology, MedicineJournal of the American Society of Nephrology : JASN
- 2018
Hyperkalemia decreases proximal tubule ammonia generation and collecting duct ammonia transport, leading to impaired ammonia excretion that causes metabolic acidosis.