title: Reduction of erythrocyte (Na(+)-K+)ATPase activity in type 2 (non-insulin-dependent) diabetic patients with microalbuminuria.
abstract: In order to elucidate the causal relationship between (Na(+)-K+)ATPase and diabetic nephropathy, we studied the erythrocyte (Na(+)-K+)ATPase activity in Type 2 diabetic patients, 20 with microalbuminuria and 27 without microalbuminuria and in 16 control subjects. (Na(+)-K+)ATPase activities in microalbuminuric patients (0.273 +/- 0.012 mumol Pi/mg protein/h, mean +/- SE) were significantly reduced compared with those without microalbuminuric patients (0.308 +/- 0.011 mumol Pi/mg protein/h, p < 0.05) and control subjects (0.330 +/- 0.011 mumol Pi/mg protein/h, p < 0.01). Microalbuminuric patients had higher systolic blood pressure (133 +/- 3 vs 124 +/- 3 mmHg, p < 0.05) and greater frequency of parental hypertension (50% vs 19%, p < 0.05) than those without microalbuminuria. (Na(+)-K+)ATPase activities in diabetic patients with hypertension were significantly reduced compared with those in diabetic patients without hypertension. Moreover, (Na(+)-K+)ATPase activities in diabetic patients with parental hypertension were significantly reduced compared with those in patients without parental hypertension. There was no difference in erythrocyte Na+ content between with and without microalbuminuria or hypertension or parental hypertension in diabetic patients. Erythrocyte Na+ content was significantly negatively correlated with (Na(+)-K+)ATPase activity in control subjects (r = -0.619, p < 0.05), but not in diabetic patients (r = -0.194). Plasma digitalis-like substances showed no correlation with (Na(+)-K+)ATPase activities in diabetic patients with microalbuminuria or hypertension or parental hypertension. We concluded that the reduction of erythrocyte (Na(+)-K+)ATPase activity may be related to a familial predisposition to arterial hypertension and may partly be responsible for the development of diabetic nephropathy in Type 2 diabetic patients.
authors.affiliation: Second Department of Internal Medicine, Chiba University, School of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Mimura
authors.forename: H
authors.initials: H
authors.lastname: Makino
authors.forename: A
authors.initials: A
authors.lastname: Kanatsuka
authors.forename: T
authors.initials: T
authors.lastname: Asai
authors.forename: S
authors.initials: S
authors.lastname: Yoshida
mesh_terms: D000328:Adult; D000419:Albuminuria / Q000201:enzymology*; D001798:Blood Proteins / Q000378:metabolism; D002298:Cardenolides; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000201:enzymology*; D003928:Diabetic Nephropathies / Q000097:blood / Q000201:enzymology*; D004077:Digoxin; D004912:Erythrocytes / Q000201:enzymology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000201:enzymology / Q000235:genetics; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D012503:Saponins; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood*
chemical_list: D001798:Blood Proteins; D002298:Cardenolides; D012503:Saponins; C034504:digoxin-like factors; D004077:Digoxin; D000254:Sodium-Potassium-Exchanging ATPase