Lisinopril in the treatment of hypertensive patients with renal impairment

Donohoe, J.; Kelly, John G.; Laher, M; Doyle, Gerald D.

doi:10.1016/0002-9343(88)90347-6

Cited by 14 publications

(5 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1-1 was seen. Similar observations in patients with impaired renal function and prolonged lisinopril therapy were also reported by Jackson et al [28] and Donohoe et al [29].…”

Section: Discussionsupporting

confidence: 86%

Pharmacokinetics and pharmacodynamics of lisinopril in advanced renal failure

Neubeck

Fliser²,

Pritsch³

et al. 1994

Eur J Clin Pharmacol

View full text Add to dashboard Cite

To prevent drug accumulation and adverse effects the dose of hydrophilic angiotensin-converting enzyme (ACE) inhibitors, e.g. lisinopril, must be reduced in patients with renal failure. To obtain a rational basis for dose recommendations, we undertook a prospective clinical trial. After 15 days of lisinopril treatment pharmacokinetic and pharmacodynamic parameters were determined in patients with advanced renal failure (n = 8; endogenous creatinine clearance [CLCR]: 18 ml.min-1.1.73 m-2) and in healthy subjects with normal renal function (n = 16; CLCR: 107 ml.min-1.1.73 m-2). The volunteers received 10 mg lisinopril once daily, the daily dose in patients (1.1-2.2 mg) was adjusted to the individual CLCR according to the method of Dettli [13]. After 15 days of lisinopril treatment the mean maximal serum concentration (Cmax) in patients was lower than in volunteers (30.7 vs 40.7 ng.ml-1, while the mean area under the concentration-time curve (AUC0-24 h) was higher (525 vs 473 ng.h-1.ml-1). ACE activity on day 15 was almost completely inhibited in both groups. Plasma renin activity, angiotensin I and angiotensin II levels documented marked inhibition of converting enzyme in volunteers and patients. Furthermore, average mean arterial blood pressure in patients decreased by 5 mmHg and proteinuria from 3.9-2.7 g per 24 h after 15 days of treatment with the reduced dose of lisinopril. Adjustment of the dose of lisinopril prevents significant accumulation of the drug in patients with advanced renal failure during chronic therapy. Mean serum levels did not exceed this in subjects with normal renal function receiving a standard dose.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…1-1 was seen. Similar observations in patients with impaired renal function and prolonged lisinopril therapy were also reported by Jackson et al [28] and Donohoe et al [29].…”

Section: Discussionsupporting

confidence: 86%

Pharmacokinetics and pharmacodynamics of lisinopril in advanced renal failure

Neubeck

Fliser²,

Pritsch³

et al. 1994

Eur J Clin Pharmacol

View full text Add to dashboard Cite

show abstract

“…Van Schaik et al (1988) found that adverse events associated with lisinopril were more common in patients with renal impairment than in those with normal renal function and suggested that dosage be reduced when GFR falls below 30 ml/min. Because of the risk of drug accumulation in other clinical studies with lisinopril (Donohue et al 1988) and enalapril (Abraham et al 1988), in the present study half the recommended dose was administered to patients with CLcR below 30 mlfmin.…”

mentioning

confidence: 99%

Comparison of the Steady-State Pharmacokinetics of Fosinopril, Lisinopril and Enalapril in Patients with Chronic Renal Insufficiency

Sica

Cutler

Parmer

et al. 1991

Clinical Pharmacokinetics

View full text Add to dashboard Cite

The phosphinyl ester prodrug fosinopril, a new angiotensin converting enzyme (ACE) inhibitor, is fully hydrolysed after oral administration to the pharmacologically active diacid, fosinoprilat. This metabolite is cleared by both hepatic and renal routes, while most other ACE inhibitors are cleared exclusively by the kidney. In the present study, after administration of multiple fixed oral doses the accumulation of the active moieties of fosinopril, enalapril and lisinopril was compared in patients with renal insufficiency. 29 patients with creatinine clearances (CLCR) less than 30 ml/min received either fosinopril 10mg (n = 9), enalapril 2.5mg (n = 10) or lisinopril 5mg (n = 10) once daily for 10 days in a nonblind (open-label) parallel study. Pharmacokinetic parameters including area under the serum concentration-time curve (AUC), peak serum concentration (Cmax) and time to peak concentration (tmax), as well as renal function, blood pressure, and plasma renin activity (PRA) and aldosterone levels, were determined on the first and last days of the study. The percentage (+/- SEM) increases in AUC from day 1 to day 10 for fosinoprilat, enalaprilat and lisinopril were 26.8 +/- 9.9 (nonsignificant), 76.6 +/- 16.6 (p less than 0.001) and 161.7 +/- 31.8% (p less than 0.001), respectively. These results indicate that there was significantly less accumulation of fosinoprilat, based on accumulation indices, relative to either enalaprilat (p less than 0.05) or lisinopril (p less than 0.001) during the study. The Cmax of fosinopril increased significantly less than that of lisinopril (21.1 vs 123.6%; p less than 0.01). Renal function was not altered in any group, and blood pressure changed modestly.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…The presence of an elevated filtration fraction in hypertensive patients with CRF could reflect an elevation in the glomerular capillary pressure. Mathematical modeling of determinants of [34] aCreatinine or isotope clearance (ml/min). bNo 9 in incidence of l)roteinuria.…”

Section: Crf: Humansmentioning

confidence: 99%

“…However, several studies have reported a 5-26% increase in serum ereatinine concentrations with chronic ACE inhibitor therapy. When the effect of ACE inhibition on the progression of renal disease has been studied, variable responses have been observed [24, 34,35,38,391. In one retrospective study, 12 months of enalapril therapy in patients with CRF (despite decreased but poorly controlled blood pressure) was associated with stable renal function compared with a group of non-ACE-inhibitor-treated patients who had a slow decline in renal function [39].…”

Section: Ace Inhibition In Chronic Renal Disease: Humansmentioning

confidence: 99%

See 1 more Smart Citation

Renal effects of angiotensin converting enzyme inhibitors: Nondiabetic chronic renal disease

Opsahl

Abraham

Keane

1990

Cardiovasc Drug Ther

View full text Add to dashboard Cite

Based on studies in the rat remnant kidney model, it has been proposed that glomerular hypertension is responsible for the progressive nature of chronic renal disease. In that model, therapy with angiotensin converting enzyme (ACE) inhibitors reduced glomerular pressures. As a result, glomerular injury was reduced and the rate of progression of renal disease was slowed. Thus, alterations in hemodynamics may play an important role in glomerular injury. However, it is now evident that a variety of metabolic and other factors affect the progression of renal disease. Moreover, recent studies suggest that ACE inhibitors may also have beneficial effects that are independent of alterations in glomerular pressure. In humans, the glomerular hemodynamic response to renal disease cannot be measured, and it is not known whether or under which conditions glomerular capillary pressure might be elevated. Treatment with ACE inhibitors safely lowers blood pressure without adversely affecting renal function in most patients with nondiabetic chronic renal failure. Although proteinuria and the rate of progression of renal disease may decrease in some patients, these effects are inconsistently seen. Identification of the factors that modulate this variability in response to ACE inhibition may provide new insight into the pathogenesis and treatment of progressive renal disease in humans.

show abstract

Lisinopril in the treatment of hypertensive patients with renal impairment

Cited by 14 publications

References 4 publications

Pharmacokinetics and pharmacodynamics of lisinopril in advanced renal failure

Pharmacokinetics and pharmacodynamics of lisinopril in advanced renal failure

Comparison of the Steady-State Pharmacokinetics of Fosinopril, Lisinopril and Enalapril in Patients with Chronic Renal Insufficiency

Renal effects of angiotensin converting enzyme inhibitors: Nondiabetic chronic renal disease

Contact Info

Product

Resources

About