Key result
Enalapril and hyponatremia are independently linked to worsening renal function during ACE inhibition in severe HF.
Why the study?
Identifying which patients with severe chronic heart failure are at greatest risk of developing functional renal insufficiency during converting enzyme inhibition was needed.
Does hyponatremia or enalapril therapy increase the risk of developing functional renal insufficiency (decline in creatinine clearance) in patients with severe chronic heart failure receiving converting enzyme inhibition?
Observational (n=59)
Does hyponatremia or enalapril therapy increase the risk of developing functional renal insufficiency (decline in creatinine clearance) in patients with severe chronic heart failure receiving converting enzyme inhibition?
In patients with severe chronic heart failure, pre-existing hyponatremia (or elevated plasma renin activity) and the use of enalapril rather than captopril independently predict a decline in renal function during ACE inhibitor therapy.
Answers are grounded in this paper and cite their sources.
Hyponatremia and enalapril may flag renal risk on ACE inhibitors in severe HF; hypothesis-generating for differential effects versus captopril.
To identify patients with severe chronic heart failure who are at greatest risk of developing functional renal insufficiency during converting enzyme inhibition, creatinine clearance was measured in 59 patients before and after long-term therapy with captopril (39 patients) or enalapril (20 patients), while digitalis and diuretic therapy was kept constant. Creatinine clearance increased or remained constant in 33 of the 59 patients (Group I), but declined in the remaining 26 patients (Group II). The two groups were similar with respect to the cause of heart failure, pretreatment renal function and all pretreatment hemodynamic variables. Patients in Group II, however, had lower values for serum sodium concentration (134.8 +/- 1.0 versus 137.0 +/- 0.6 mmol/liter) and higher values for plasma renin activity (10.6 +/- 3.4 versus 3.0 +/- 0.5 ng/ml per hour), received larger doses of furosemide (108 +/- 11 versus 84 +/- 6 mg/day), were more frequently diabetic (42 versus 15%) and were more frequently treated with enalapril (50 versus 21%) than were patients in Group I (all p less than 0.05). By stepwise logistic analysis, only hyponatremia (or an elevated plasma renin activity) and enalapril therapy independently predicted the decline in creatinine clearance during converting enzyme inhibition. These observations could not be explained by changes in systemic blood pressure. In patients with a normal serum sodium concentration (greater than or equal to 137 mmol/liter), creatinine clearance increased with captopril (+21%, p less than 0.05), but not with enalapril (-6%, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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Packer et al. (1987) conducted an observational in Severe chronic heart failure (n=59). Hyponatremia and enalapril therapy during ACE inhibition vs. Normal serum sodium concentration and captopril therapy was evaluated on Decline in creatinine clearance (functional renal insufficiency) (p=<0.05). Hyponatremia (134.8 vs 137.0 mmol/L) and enalapril vs captopril use (50% vs 21% of decline group; p<0.05) independently predicted declining creatinine clearance during ACE inhibition in severe HF.
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