Renal impairment enzyme inhibitors

Angiotensin-converting enzyme inhibitors should be used with caution in patients taking diuretics because of an enhanced hypotensive effect. Angiotensin-converting enzyme inhibitors should also be used with caution in patients with renal impairment. Renal function needs to be monitored in patients with renovascular disease. 

Because indomethacin may increase serum potassium concentrations, indomethacin and spironolactone should be administered concomitantly with caution. Potassium-sparing diuretics should be used with caution, and serum potassium should be determined frequently in patients receiving an angiotensin-converting enzyme (ACE) inhibitor (e.g., captopril). Concomitant administration with an ACE inhibitor may increase the risk of hyperkalemia. The dosage of spironolactone should be reduced, or the drug discontinued, as necessary. Patients with renal impairment may be at increased risk of hyperkalemia [65]. 

The oral dose of voriconazole does not have to be adjusted in patients who have renal impairment. However, intravenous administration of voriconazole should be avoided in these patients as the carrier vehicle sulfobu-tyl ether P-cyclodextrin sodium can accumulate in these patients. Dosage adjustment is required in patients who have chronic hepatic impairment. As voriconazole is a substrate for a number of cytochrome P450 enzymes, a number of clinically important dmg interactions occur with dmgs including ciclospotin, tacrolimus, phenytoin, warfarin, HIV protease inhibitors and non-nucleoside reverse transcriptase inhibitors. 

Proton pump inhibitors undergo rapid first-pass and systemic hepatic metabolism and have negligible renal clearance. Dose reduction is not needed for patients with renal insufficiency or mild to moderate liver disease but should be considered in patients with severe liver impairment. Although other proton pumps exist in the body, the H+,K+ ATPase appears to exist only in the parietal cell and is distinct structurally and functionally from other H+ -transporting enzymes. 

ACE inhibitors prevent the formation of angiotensin II by angiotensin-converting enzyme (ACE) and thereby reduce peripheral vascular resistance and blood pressure. In addition, ACE inhibitors prevent the effect of angiotensin II on protein synthesis in myocardial and vascular muscle cells, and thus diminish ventricular hypertrophy. As adverse effects, ACE inhibitors may provoke dry cough, impaired renal function, and hyperkalemia. When ACE inhibitors are poorly tolerated, an ATq-receptor antagonist can be given. 

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