Effect of Mineralocorticoid on Serum Potassium Regulation and Urine Ammonium Excretion in Chronic Renal Patients.
- Author:
Seo Jin LEE
1
;
Un Sil JEON
;
Ho Jun CHIN
;
Woo Seong HUH
;
Yun Suk CHO
;
Kang Seock KIM
;
Kwon Wook JOO
;
Jin Suk HAN
;
Suhng Gwon KIM
;
Jung Sang LEE
Author Information
1. Department of Internal Medicine, College of Medicine, Seoul National University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Mineralocorticoid;
Urine ammonium excretion;
Hyperkalemia;
Chronic renal failure
- MeSH:
Acid-Base Equilibrium;
Aldosterone;
Ammonium Compounds*;
Blood Pressure;
Body Weight;
Homeostasis;
Humans;
Hydrogen-Ion Concentration;
Hyperkalemia;
Kidney Failure, Chronic;
Mineralocorticoids;
Potassium*;
Protons
- From:Korean Journal of Nephrology
2000;19(2):278-284
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Mineralocorticoids influences on acid-base homeostasis by the regulation of urine acidification. But its mechanism of acion is not well known in human. This study compared the acid-base status and the indices of urine acidification before and after mineralocorticoid administration in human, and analyzed the effect of mineralocorticoids on human acid-base homeostasis. We administered 9a-fludrocortisone in 6 chronic renal failure patients and 6 normal controls 0.5mg daily for 7 days. The results were as following: 1) After administration of 9a-fludrocortisone in patients group, serum aldosterone level changed from 120.2+/-71.0pg/mL to 44.8+/-32.2pg/mL(mean+/-SD, p< 0.05). Serum HCO- level was not changed. Urine ammonium excretion was incresed from 24.6+/-12.3 mmol/day to 43.7+/-19.0 (p<0.05), but there were no change in urine pH and urine anion gap, Serum potassium level decreased from 5.5+/-0.7mBq/L to 4.1+/-0.5mEq/L (p<0.05), and TTKG increased from 3.9 to 8.9(p<0.05). 2) After administration of 9a-fludrocortisone in control group, serum aldosterone level changed from 99.7+/-44.5pg/mL to 25.1+/-3 mL(p<0.05). Serum HCO- level was not changed. Urine ammonium excretion was incresed from 44.3+/-21.6mmoVday to 76.3+/-19.6(p<0.05), but there were no change in urine pH and urine anion gap. Serum potassium level decreased from 4.8+/-0.5mEq/L to 3.9+/-0.2mHq/L(p< 0.05), but there was no change in TTKG. 3) No patient or control showed any discomfort after 9-fludrocortisone administration, and there was no elevation in diastolic blood pressure, increase in body weight, electrolyte abnormality. In summary, after 9alpha-fludrocortisane administration, urinary ammonium excretion increased in both patients and control group, and this phenomenon occured with correction of hyperkalemia without urine pH change. This result implies urinary ammonium excretion increase by mineralocorticoid. In human increase in renal distal acidification by mineralocorticoid is due to increase in renal ammoniagenesis rather than stimulation on proton excretion.
