Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.

Chronic stable diabetic patients (n = 6) were compared with healthy control subjects (n = 5) after acute oral intake of 50 mEq of potassium chloride (KCl) to investigate for possible derangements of homeostatic responses for acute term (3 hrs) to acute potassium load. Plasma renin activity (PRA), pl...

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Main Authors:	Kim, H. J., Ahn, Y. H., Park, C. H., Kang, C. M., Park, H. C., Bae, H. Y., Choi, S. D.
Format:	Online
Language:	English
Published:	Korean Academy of Medical Sciences 1993
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3053855/

id	pubmed-3053855
recordtype	oai_dc
spelling	pubmed-30538552011-03-16 Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus. Kim, H. J. Ahn, Y. H. Park, C. H. Kang, C. M. Park, H. C. Bae, H. Y. Choi, S. D. Research Article Chronic stable diabetic patients (n = 6) were compared with healthy control subjects (n = 5) after acute oral intake of 50 mEq of potassium chloride (KCl) to investigate for possible derangements of homeostatic responses for acute term (3 hrs) to acute potassium load. Plasma renin activity (PRA), plasma aldosterone (PA), and transtubular potassium concentration gradient (TTKG) known as a useful semiquantative index of distal nephron potassium secretion were measured. All the baseline parameters were comparable between diabetic and non-diabetic subjects except for significantly reduced creatinine clearance in diabetics (mean +/- SEM, 105 +/- 4 vs. 85 +/- 5 ml/min, p < 0.05). Following acute oral KCl load, the peak increases of serum potassium changes from basal levels were noted at 2 hours in both groups, but were higher in diabetic subjects (mean +/- SEM, 0.42 +/- 0.06 vs. 0.62 +/- 0.09 mEq/L). Also, 4 out of 6 diabetic subjects but none of the control subjects at 2 hours after oral KCl load became hyperkalemic ( > 5.0 mEq/L). PRA did not show any significant changes, whereas PA was increased simultaneously with increments in serum potassium in both groups, with blunted increases in the diabetics. However, TTKG was increased prominently in control subjects (8.18 from 4.98), but only slightly in diabetic subjects (4.55 from 4.18), with statistical difference between the two groups (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) Korean Academy of Medical Sciences 1993-02 /pmc/articles/PMC3053855/ /pubmed/8343217 Text en
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Kim, H. J. Ahn, Y. H. Park, C. H. Kang, C. M. Park, H. C. Bae, H. Y. Choi, S. D.
spellingShingle	Kim, H. J. Ahn, Y. H. Park, C. H. Kang, C. M. Park, H. C. Bae, H. Y. Choi, S. D. Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.
author_facet	Kim, H. J. Ahn, Y. H. Park, C. H. Kang, C. M. Park, H. C. Bae, H. Y. Choi, S. D.
author_sort	Kim, H. J.
title	Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.
title_short	Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.
title_full	Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.
title_fullStr	Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.
title_full_unstemmed	Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.
title_sort	impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.
description	Chronic stable diabetic patients (n = 6) were compared with healthy control subjects (n = 5) after acute oral intake of 50 mEq of potassium chloride (KCl) to investigate for possible derangements of homeostatic responses for acute term (3 hrs) to acute potassium load. Plasma renin activity (PRA), plasma aldosterone (PA), and transtubular potassium concentration gradient (TTKG) known as a useful semiquantative index of distal nephron potassium secretion were measured. All the baseline parameters were comparable between diabetic and non-diabetic subjects except for significantly reduced creatinine clearance in diabetics (mean +/- SEM, 105 +/- 4 vs. 85 +/- 5 ml/min, p < 0.05). Following acute oral KCl load, the peak increases of serum potassium changes from basal levels were noted at 2 hours in both groups, but were higher in diabetic subjects (mean +/- SEM, 0.42 +/- 0.06 vs. 0.62 +/- 0.09 mEq/L). Also, 4 out of 6 diabetic subjects but none of the control subjects at 2 hours after oral KCl load became hyperkalemic ( > 5.0 mEq/L). PRA did not show any significant changes, whereas PA was increased simultaneously with increments in serum potassium in both groups, with blunted increases in the diabetics. However, TTKG was increased prominently in control subjects (8.18 from 4.98), but only slightly in diabetic subjects (4.55 from 4.18), with statistical difference between the two groups (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
publisher	Korean Academy of Medical Sciences
publishDate	1993
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3053855/
_version_	1611444430905016320

Impaired homeostatic mechanism of potassium handling after acute oral potassium load in diabetes mellitus.

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