2010/07/21 by Walter H. Hörl · 1 citation
Biochemistry, Genetics and Molecular Biology · Medicine · Pharmacology, Toxicology and Pharmaceutics · #Acute kidney injury #Adverse effect #Cirrhosis #Cyclooxygenase #Drug #Eicosanoids and Hypertension Pharmacology #Enzyme #Heart failure #Inflammatory mediators and NSAID effects #Internal medicine #Kidney #Kidney disease #Medicine #Pharmacogenetics and Drug Metabolism #Pharmacology #Renal function #Urology
paper · pdf · doi:10.3390/ph3072291
openalex publication_date 2010/07/21 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/23
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the isoenzymes COX-1 and COX-2 of cyclooxygenase (COX). Renal side effects (e.g., kidney function, fluid and urinary electrolyte excretion) vary with the extent of COX-2-COX-1 selectivity and the administered dose of these compounds. While young healthy subjects will rarely experience adverse renal effects with the use of NSAIDs, elderly patients and those with co-morbibity (e.g., congestive heart failure, liver cirrhosis or chronic kidney disease) and drug combinations (e.g., renin-angiotensin blockers, diuretics plus NSAIDs) may develop acute renal failure. This review summarizes our present knowledge how traditional NSAIDs and selective COX-2 inhibitors may affect the kidney under various experimental and clinical conditions, and how these drugs may influence renal inflammation, water transport, sodium and potassium balance and how renal dysfunction or hypertension may result.