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J Am Soc Nephrol 10:1916-1920, 1999
© 1999 American Society of Nephrology


REGULAR ARTICLES

The Angiotensin-Converting Enzyme Genotype and Microalbuminuria in Autosomal Dominant Polycystic Kidney Disease

MARJAN A. VAN DIJK*, DORIEN J.M. PETERS{ddagger}, MARTIJN H. BREUNING{dagger} and PETER C. CHANG*

* Department of Nephrology, Leiden University Medical Centre, Leiden University, The Netherlands
{dagger} Clinical Genetic Centre, Leiden University Medical Centre, Leiden University, The Netherlands
{ddagger} Department of Human Genetics, Sylvius Laboratories, Leiden University, The Netherlands

Correspondence to Dr. Marjan A. van Dijk, Leiden University Medical Centre, Department of Nephrology, C3-P, P. O. Box 9600, 2300 RC Leiden, The Netherlands. Phone: +31 71 5262218/1924; Fax: +31 71 5248118; E-mail: MEAvdHulst{at}nephrology.azl.nl

Abstract

Abstract. Autosomal dominant polycystic kidney disease (ADPKD) has a variable clinical course. Clinical parameters associated with a worse prognosis are hypertension and proteinuria or microalbuminuria (MA). Because chronic stimulation of the renin-angiotensin system is likely to be present in ADPKD patients, the effect of the angiotensin-converting enzyme insertion/deletion (ACE I/D) genotype on the variability of these clinical parameters was examined in untreated ADPKD patients. Proteinuria and MA were determined in 24-h urine collections. BP measurements were performed with an ambulatory monitor, over 24 h. With analysis of covariance, the ACE genotype was found to be significantly associated with MA, corrected for age, gender, GFR, mean arterial pressure, body surface area, and urinary Na+ excretion (P < 0.05). The patients homozygous for the deletion (DD) had the highest rate of MA (P < 0.05) compared to the patients homozygous for the insertion (II). There was no relationship between the ACE genotype and BP or renal function. A significant positive correlation was found between MA and mean arterial pressure (r = 0.31, P < 0.05), whereas a significant negative correlation was found between MA and renal function (r = -0.28, P < 0.05). In conclusion, in ADPKD patients, MA is partly determined by the ACE I/D polymorphism. Because MA is associated with an enhanced progression toward renal failure, the ACE genotype could help in identifying patients at risk for a worse prognosis.




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