Renal adverse effects of nonsteroidal anti-inflammatory drugs

According to the manufacturer, it is not known whether valsartan is excreted into human milk. Because of the potential for adverse effects on the nursing infant, a decision should be made to discontinue breast-feeding or discontinue valsartan therapy. Valsartan has not been evaluated by the American Academy of Pediatrics (AAP); however, the ACE inhibitors captopril and enalapril are classified by the AAP as usually compatible with breast-feeding and may represent preferable alternatives in some patients. In addition, benazepril and quinapril are excreted in human breast milk in very small quantities ; therefore, a clinically significant risk to a breast-feeding infant is not expected. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.

We have assessed the effects of acute and chronic administration of etodolac, ketoprofen, and indomethacin on renal function in patients with mild to moderate chronic renal insufficiency (CRI). We studied 18 normal volunteers and 24 patients with CRI due to hypertension and/or diabetes mellitus with creatinine clearances between 19 and 83 mL/min/ m2. Clearance studies were performed with the first dose of nonsteroidal antiinflammatory drug (NSAID) to compare acute effects of the agent with a no-drug control. Subjects then received the NSAID for three to five days and, on the last day of study, underwent another clearance study to assess the effects of a single dose of NSAID superimposed on chronic dosing. With each dose of each NSAID, inulin and paraaminohippurate (PAH) clearances and fractional excretion of NA+ decreased. However, the baseline control collections after chronic dosing did not differ from the no-drug control periods. Hence, the decline in renal function with each dose is transient, and no overall adverse effect on renal function occurred with chronic dosing. In five patients with cirrhosis, we assessed the renal sparing effects of sulindac. After equilibration on a fixed sodium intake, they received a 200-mg dose of sulindac. In one patient, no adverse effect occurred; the remaining patients suffered declines in creatinine clearance of 29%, 87%, 37%, and 37%, respectively. This effect was transient and returned to control values six to eight hours after sulindac administration. At the time of maximal depression of renal function, serum concentrations of sulindac sulfide were comparable to those in subjects with normal hepatic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Using a registry from a single urology office, Dr Traish and colleagues compared data from 230 men (aged 47 to 68) taking dutasteride ( mg/day) and 230 men (aged 52 to 72 years) taking the alpha blocker tamsulosin ( mg) for lower urinary tract symptoms (LUTS) related to benign prostatic hyperplasia (BPH). Dutasteride significantly improved LUTS over 36 to 42 months, according to results published in Hormones Molecular Biology and Clinical Investigations . It reduced prostate volume, International Prostate Symptom Score, and PSA. However, the 5-ARI also was associated with increased blood glucose, hemoglobin A1c, triglycerides, and low-density lipoprotein levels over the long term. In addition, dutasteride appeared to increase liver transaminase activity and Aging Male Symptom score, which indicates inflammation and reduced quality of life.

A study by the Agency for Healthcare Research and Quality (AHRQ) found that in 2011, sedatives and hypnotics were a leading source for adverse drug events seen in the hospital setting. Approximately % of all ADEs present on admission and % of ADEs that originated during a hospital stay were caused by a sedative or hypnotic drug. [20] A second study by AHRQ found that in 2011, the most common specifically identified causes of adverse drug events that originated during hospital stays in the . were steroids, antibiotics, opiates/narcotics, and anticoagulants. Patients treated in urban teaching hospitals had higher rates of ADEs involving antibiotics and opiates/narcotics compared to those treated in urban nonteaching hospitals. Those treated in private, nonprofit hospitals had higher rates of most ADE causes compared to patients treated in public or private, for-profit hospitals. [21]

Torsemide is administered orally and intravenously. It is metabolized by the hepatic cytochrome P450 enzyme system and is a substrate for CYP2C9. In humans, three metabolites, one of which is active, are produced. The active metabolite does not contribute significantly to clinical activity. In normal adults, about 80% is cleared through hepatic metabolism and 20% is cleared in the urine as unchanged drug. In healthy adults, the elimination half-life is about hours.
 
Affected cytochrome P450 isoenzymes and drug transporters: CYP2C9
Torsemide is a substrate for CYP2C9.[] Theoretically, metabolism may be affected by drugs that are inhibitors of inducers of CYP2C9.

Renal adverse effects of nonsteroidal anti-inflammatory drugs

renal adverse effects of nonsteroidal anti-inflammatory drugs

A study by the Agency for Healthcare Research and Quality (AHRQ) found that in 2011, sedatives and hypnotics were a leading source for adverse drug events seen in the hospital setting. Approximately % of all ADEs present on admission and % of ADEs that originated during a hospital stay were caused by a sedative or hypnotic drug. [20] A second study by AHRQ found that in 2011, the most common specifically identified causes of adverse drug events that originated during hospital stays in the . were steroids, antibiotics, opiates/narcotics, and anticoagulants. Patients treated in urban teaching hospitals had higher rates of ADEs involving antibiotics and opiates/narcotics compared to those treated in urban nonteaching hospitals. Those treated in private, nonprofit hospitals had higher rates of most ADE causes compared to patients treated in public or private, for-profit hospitals. [21]

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