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Angiotensin-converting enzyme inhibitor withdrawal and ACE gene polymorphism
H Nonoguchi1, S Kiyama, H Inoue
1Third Department of Internal Medicine, Kumamoto University School of Medicine, Japan. nono@kaiju.medic.kumamoto-u.ac.jp
Clinical Nephrology
|October 29, 2003
Summary
Stopping angiotensin-converting enzyme (ACE) inhibitors can worsen kidney function in patients with specific ACE gene variations (II or DI genotypes), particularly those with high proteinuria.
Area of Science:
- Nephrology
- Genetics
- Pharmacology
Background:
- Angiotensin-converting enzyme (ACE) inhibitors are crucial in managing chronic renal failure.
- The ACE gene's insertion/deletion (I/D) polymorphism may impact ACE inhibitor efficacy and chronic renal failure progression.
Purpose of the Study:
- To investigate the impact of ACE inhibitor withdrawal on renal function decline.
- To evaluate the influence of ACE gene polymorphism, blood pressure, and proteinuria on renal function after ACE inhibitor discontinuation.
Main Methods:
- Retrospective collection of patients with chronic glomerulonephritis and benign nephrosclerosis who ceased ACE inhibitor therapy.
- Multiple regression analysis to assess the relationship between renal function decline and influencing factors.
Main Results:
- Forty-two patients discontinued ACE inhibitors; renal function deterioration was observed in those with II or DI ACE gene genotypes starting two months post-withdrawal.
- Proteinuria levels, ACE gene insertion presence, and baseline serum creatinine were significant predictors of renal function decline (adjusted R2 = 0.48).
Conclusions:
- ACE inhibitor withdrawal leads to renal function deterioration in patients with II or DI genotypes, high proteinuria, and elevated serum creatinine.
- This deterioration may be linked to a rebound increase in serum ACE activity.