Pharmacokinetics of lisinopril in hypertensive patients with normal and impaired renal function

Schaik, B. A. M. Van; Geyskes, G. G.; Wouw, Poll A. van der; Rooij, H.H. van; Porsius, A. J.

doi:10.1007/bf01061419

Cited by 27 publications

(22 citation statements)

References 10 publications

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“…Fruncillo et al (1987) suggested that enalaprilat accumulation in patients with severe renal insufficiency could increase the incidence of clinically significant adverse events, and recommended that lower enalapril doses should be used in such patients. 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: 97%

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

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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)

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mentioning

confidence: 97%

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

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“…b Kelly et al (1986); Lowenthal et al (1985). c Jackson et al (1988); Kelly et al (1987); Kiintziger et al (1987);Van Schaik et al (1988). d Total captopril; Onoyama et al (1986).…”

Section: Moxonidinementioning

confidence: 96%

“…The elimination of lisinopril from plasma is polyphasic, with most being eliminated during the earlier phase (t'l2<' = 5 to 7h) which is followed at low concentrations by a prolonged terminal phase (t'l2!l) of about 30h (Lancaster & Todd 1988;VIm et al 1982;Kelly & O'Malley 1990). Impaired renal function was associated WIth 10-creased serum concentrations of lisinopril, prolonged tmax and decreased excretion rate and urinary recovery (Jackson et al 1988;Kelly et al 1987;Van Schaik et al 1988). Van Schaik et al (1988) found that during 8 days' treatment the accumulation of lisinopril in hypertensive patients with severe renal failure (CLcR = 5 to 30 ml/min) did not cause hypotension or toxic effects.…”

Section: Lisinoprilmentioning

confidence: 96%

“…Impaired renal function was associated WIth 10-creased serum concentrations of lisinopril, prolonged tmax and decreased excretion rate and urinary recovery (Jackson et al 1988;Kelly et al 1987;Van Schaik et al 1988). Van Schaik et al (1988) found that during 8 days' treatment the accumulation of lisinopril in hypertensive patients with severe renal failure (CLcR = 5 to 30 ml/min) did not cause hypotension or toxic effects. All authors proposed that the initial dosage should be reduced to 2.5mg once daily in hypertensive patients with severe renal impairment, and may be titrated up progressively according to patient response.…”

Section: Lisinoprilmentioning

confidence: 96%

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Pharmacokinetics of Newer Drugs in Patients with Renal Impairment (Part II)

Singlas

Fillastre

1991

Clinical Pharmacokinetics

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Cardiovascular diseases occur frequently in patients with renal failure. Any pharmacokinetic impairment in these diseases should be considered when individualizing drug therapy. The pharmacokinetics of new cardiovascular drugs in uraemic patients are reviewed: alpha- and beta-blocking agents, ACE inhibitors, centrally acting antihypertensive agents, calcium antagonists, antiarrhythmic agents and inotropic agents. Guidelines are proposed for adjustment of dosage regimens as a function of renal impairment. Renal or extrarenal elimination of drugs and their metabolites, and the activity of the latter, are taken into account. The disposition of new drugs such as flestolol, alacepril, delapril, propafenone, milrinone or enoximone, is not well documented in patients with renal failure. Further characterizations of the elimination of these compounds are needed and the potential therapeutic or toxic effects of the metabolites require evaluation to determine whether the dosage needs to be adjusted. Until such investigations are performed, those drugs should not be used in uraemic patients; if no therapeutic alternative is available, clinical controls are necessary at regular intervals. Relationships between pharmacological or therapeutic effects and drug plasma concentrations should be evaluated for such long term use drugs. The knowledge of a plasma concentration therapeutic window is important to provide information which will be useful in determining appropriate drug dosage in renal failure.

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“…However, in hypertensive patients with impaired renal function, lisinopril accumulates, the accumulation being inversely correlated with creatinine clearance [128]. However, in hypertensive patients with impaired renal function, lisinopril accumulates, the accumulation being inversely correlated with creatinine clearance [128].…”

Section: Lisinoprilmentioning

confidence: 99%

Effects of cardiovascular disease on pharmacokinetics

Rodighiero

1989

Cardiovasc Drug Ther

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The pathophysiologic changes occurring in cardiovascular disease can affect the kinetics of drugs in several different ways. The present review examines these modifications and the underlying mechanisms. The kinetics of specific agents, such as antiarrhythmic, antihypertensive, cardiotonic, and other drugs are considered, and the clinical implications are outlined. The clinician should be aware of these modifications, because they require an adjustment of the dosage regimen. A rational basis for a correct therapeutic choice can be provided by adequate knowledge of these modifications.

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Pharmacokinetics of lisinopril in hypertensive patients with normal and impaired renal function

Cited by 27 publications

References 10 publications

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

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

Pharmacokinetics of Newer Drugs in Patients with Renal Impairment (Part II)

Effects of cardiovascular disease on pharmacokinetics

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