ACE I/D polymorphism and short-term renal response to ACE inhibition; Role of sodium status
ASN 30th Annual Meeting, San Antonio
J Am Soc Nephrol (Sep) 8:78A 1997
0376 In experimental and human renal disease, ACE inhibitors appear to retard renal function loss. Subjects with varying ACE genotypes may respond differently to ACE inhibitors in both their reno-protective and anti-proteinuric effects. Sodium restriction which activates the renin-angiotensin system augments the short term lowering of proteinuria seen with ACE inhibitors. The present study was designed to evaluate the influence of ACE genotype on this augmentation by sodium restriction.
Eighty-eight non-diabetic proteinuric ( >1 gm) patients were studied. The ACE genotype was distributed as follows: DD (25), ID (40) and II (23). Baseline MAP and extent of proteinuria were similar across the three groups. Treatment with an ACE inhibitor reduced BP and proteinuria to a similar extent in the three groups. A correlation was found between the response in BP and proteinuria and urinary sodium excretion in the DD group only. Those subjects with higher sodium excretion showed little response to ACE inhibition.
Comment: These results are cross-sectional and short term. It is likely that the genotype has a modifying influence on the response to ACE therapy. This study implies that sodium restriction may be a useful strategy for all patients since genotyping of ACE is not routinely available. (George Mansoor, M.D., University of Connecticut)
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ASN 30th Annual Meeting, San Antonio
H: Drug therapy : ACE inhibitors
H: Pathophysiology : Salt (sodium, chloride) sensitivity