Drug-induced acute renal failure: recognizing and treating prerenal, postrenal, and pseudorenal injury.
Female; Male; Aged; Risk Factors; Hemodynamics; Physical Examination; Inpatients; Middle Age; Kidney Function Tests; Kidney Failure; Nephrotoxicity; Antiinflammatory Agents; Acute – Etiology; Angiotensin-Converting Enzyme Inhibitors – Adverse Effects; Antineoplastic Agents – Adverse Effects; Non-Steroidal – Adverse Effects; Acute – Chemically Induced; Acute – Diagnosis; Acute – Therapy; Enzyme Inhibitors – Adverse Effects; Renal Circulation – Drug Effects
Angiotensin-converting enzyme (ACE) inhibitors and NSAIDs are among the drugs most commonly associated with acute renal failure (ARF). Patients at risk for ACE inhibitor-induced ARF include those with congestive heart failure (CHF) or compromised left ventricular (IV) function and those receiving diuretics. In these settings, discontinue the ACE inhibitor and direct therapy toward correcting volume or improving the ineffective circulation (by appropriately reducing afterload, by ensuring adequate IV filling pressures, and by treating ischemia). Risk factors for NSAID-included ARF include CHI, poor renal perfusion, and recent hospitalization. Postrenal ARF may be precipitated by drugs that are highly insoluble in addic urine, such as antineoplastic agents and HmG-CoA reductase inhibitors. Alkalinization of urine and hydration are the cornerstones of management of this type of ARF.
Frazee L A; Rutecki G W; Whittier F C
Consultant (00107069)
1997
1997-05
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Drug-induced acute renal failure: keys to recognizing and treating intrarenal toxicity.
Adult; Female; Male; Aged; Risk Factors; Kidney Function Tests; Kidney Failure; Physiologic; Monitoring; Nephrotoxicity; Antiinflammatory Agents; Non-Steroidal – Adverse Effects; Acute – Chemically Induced; Acute – Diagnosis; Acute – Therapy; Aminoglycosides – Adverse Effects; Amphotericin B – Adverse Effects; Contrast Media – Adverse Effects; Drugs – Adverse Effects; Nephrotoxicity – Prevention and Control
Drug-induced acute tubular necrosis is a primary cause of acute renal failure (ARF); it may result from the use of such agents as aminoglycosides, amphotericin B, and radilocontrast media. To reduce the risk of aminoglycoside toxicity, prescribe the shortest course possible, use once-daily dosing, monitor serum concentrations, and avoid using these agents altogether in patients with known risk factors. Radiocontrast media-associated ARF is most likely to occur with preexisting renal damage, especially in a patient with diabetes mellitus. Since sodium depletion is the most important risk factor for nephrotoxic injury with amphotericin B use, saline loading is recommended both before and during drug administration. Drug-induced acute interstitial nephritis, another important cause of ARF, has been associated with a number of antibiotics, especially penicillin and ampicillin; many patients recover with the removal of the offending agent.
Frazee L A; Rutecki G W; Whittier F C
Consultant (00107069)
1997
1997-06
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Cardiovascular and gastrointestinal risks of nonsteroidal antiinflammatory drugs revisited: Comment on the article by the American College of rheumatology Ad Hoc group on use of selective and nonselective nonsteroidal antiinflammatory drugs...Arthritis Rheum. 2008 Aug 15;59(8):1058-73
Drug Interactions; Practice Guidelines; Drug Therapy; Combination; Medical Practice; Evidence-Based; Antiinflammatory Agents; Cox-2 Inhibitors – Adverse Effects; Non-Steroidal – Adverse Effects; Rheumatic Diseases – Drug Therapy
Rothschild B
Arthritis & Rheumatism: Arthritis Care & Research
2009
2009-02-15
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/art.24159" target="_blank" rel="noreferrer noopener">10.1002/art.24159</a>