Serum homocysteine level and protein intake are related to risk of microalbuminuria: The Hoorn study

Ellen K. Hoogeveen*, Pieter J. Kostense, Agnes Jager, Robert J. Heine, Cornelis Jakobs, Lex M. Bouter, Ab J.M. Donker, Coen D.A. Stehouwer

*Corresponding author for this work

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Abstract

Background. Microalbuminuria (MA) is a strong predictor of cardiovascular disease, but its causes are incompletely understood. Hyperhomocysteinemia is a recently recognized risk factor for cardiovascular disease independent of established risk factors. It is not known whether hyperhomocysteinemia is associated with MA, and thus could be a possible cause of microalbuminuria. Methods. We studied an age-, sex- and glucose- tolerance-stratified random sample of a 50- to 75-year-old general Caucasian population (N = 680). The urinary albumin-to-creatinine ratio (ACR) was measured in an early morning spot urine sample. MA was defined as an ACR > 3.0 mg/mmol. Results. The prevalence of MA was 4.3% (13 of 304) in subjects with normal glucose tolerance, 9.2% (1.7 of 185) in impaired glucose tolerance and 18.3% (30 of 164) in non-insulin-dependent diabetes mellitus (NIDDM); it was 3.7% (15 of 402) in subjects without hypertension and 17.9% (45 of 251) in those with hypertension. After adjusting for age, sex, glucose tolerance category, hypertension, dyslipidemia and smoking, the odds ratio [OR; 95% confidence interval (95%CI)] for MA per 5 μmol/liter total homocysteine increment was 1.33 (1.08 to 1.63). Additional adjustment for HbA(1c), waist-hip ratio, protein intake and serum creatinine did not attenuate the association between MA and total homocysteine. A 0.1 g/kg · day increment of protein intake was also associated with an increased risk for MA after adjustment for age, sex, classical risk factors and serum total homocysteine [OR (95% CI); 1.20 (1.08 to 1.32)]. Conclusion. Both hyperhomocysteinemia and protein intake are related to microalbuminuria independent of NIDDM and hypertension. Hyperhomocysteinemia may partly explain the link between MA and increased risk of cardiovascular disease.

Original languageEnglish
Pages (from-to)203-209
Number of pages7
JournalKidney International
Volume54
Issue number1
DOIs
Publication statusPublished - Jul 1998
Externally publishedYes

Bibliographical note

ACKNOWLEDGMENTS:
This study was supported by a Clinical Research Fellowship from the Diabetes Fonds Nederland and the Netherlands Organization for Scientific Research (NWO) to C.D.A.S. The authors are indebted to Ms. Monique Meijers-Kuperus, Ms. Petra van de Weg-Raaphorst and Ms. Wendy Guérand for their excellent laboratory assistance.

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