当前位置： SCI文献检索 > DIABETES RESEARCH AND CLINICAL PRACTICE期刊下所有文献 > Nitric oxide system is involved in glomerular hyperfiltration in Japanese normo- and micro-albuminuric patients with type 2 diabetes.

Nitric oxide system is involved in glomerular hyperfiltration in Japanese normo- and micro-albuminuric patients with type 2 diabetes.

Abstract：

:Glomerular hyperfiltration plays a pathogenic role in the early stages of diabetic nephropathy. Experimental studies in laboratory animals suggest that nitric oxide (NO) might be involved in the pathogenesis of glomerular hyperfiltration. We performed a cross-sectional study to determine the relationship between diabetic glomerular hyperfiltration and the NO system. Normoalbuminuric (n=41), microalbuminuric (n=25), and macroalbuminuric (n=16) patients with type 2 diabetes were recruited in this study and compared with age-matched 84 non-diabetic control subjects. Creatinine clearance and urinary NO(2)(-)/NO(3)(-) excretion (urinary NOx) were measured, and the expression of endothelial cell nitric oxide synthase (ecNOS) was evaluated in human renal tissues. Glomerular hyperfiltration was present in 19 (37.5%) and nine (36.6%) of normoalbuminuric and microalbuminuric type 2 diabetic patients, respectively. The urinary NOx was significantly higher in normoalbuminuric patients compared with normal subjects. Creatinine clearance correlated significantly with urinary NOx in normoalbuminuric and microalbuminuric patients. Immunohistochemical staining intensities for ecNOS were significantly increased in glomerular endothelial cells of microalbuminuric type 2 diabetic patients as compared with the control subjects. These results suggest that NO may contribute to the pathogenesis of glomerular hyperfiltration in Japanese type 2 diabetic patients.

journal_name

Diabetes Res Clin Pract

journal_title

Diabetes research and clinical practice

authors

Hiragushi K,Sugimoto H,Shikata K,Yamashita T,Miyatake N,Shikata Y,Wada J,Kumagai I,Fukushima M,Makino H

doi

10.1016/s0168-8227(01)00260-1

subject

Has Abstract

pub_date

2001-09-01 00:00:00

pages

149-59

issue

3

eissn

0168-8227

issn

1872-8227

pii

S0168822701002601

journal_volume

53

pub_type

杂志文章,多中心研究

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