Effects of Nonsteroidal Anti-Inflammatory Drugs on Prostaglandins and Renal Function

Carmichael, Jan M.; Shankel, Stewart W.

doi:10.1016/s0022-5347(17)47625-7

Cited by 12 publications

(21 citation statements)

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“…In addition, non-steroidal anti-inflammatory analgesics can cause tubulo-interstitial damage, the nephrotic syndrome and renal papillary necrosis (analgesic nephropathy) (Blackshear et al, 1985;Carmichael & Shankel, 1985;Levin, 1988).…”

Section: Introductionmentioning

confidence: 99%

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Prescott

Mattison

Menzies

et al. 1990

Brit J Clinical Pharma

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1 Renal function was assessed in 10 healthy female volunteers during administration of placebo, paracetamol (acetaminophen) (4.0 g daily) and indomethacin (150 mg daily) for 3 days under conditions of controlled sodium and fluid intake. 2 Paracetamol and indomethacin had no significant effect on the glomerular filtration rate and effective renal plasma flow as measured by the renal clearances of inulin, creatinine and p-aminohippurate (PAH). 3 Compared with placebo, paracetamol reduced the mean urinary excretion of prostaglandin E2 by 43% on the second day and 58% on the third treatment day (P < 0.01). With indomethacin the corresponding reductions were 73 and 80%. Paracetamol and indomethacin had much less effect on the excretion of prostaglandin 6-keto Fia, and a significant decrease was observed only on the third day. 4 The decreased urinary excretion of prostaglandin E2, produced by paracetamol was associated with a reduction in sodium excretion of more than 50% (P < 0.01) and delay in the onset of diuresis following an acute water load. 5 The renal effects of paracetamol and indomethacin appear to differ. Although indomethacin reduced prostaglandin excretion more than paracetamol it had a similar effect on sodium excretion and less initial antidiuretic action. Unlike paracetamol, indomethacin also reduced basal plasma renin activity. 6 Paracetamol reduced the total body clearance of PAH and increased its plasma halflife. This effect could be attributed to inhibition of the acetylation of PAH by paracetamol. 7 In normal use paracetamol does not appear to have the adverse renal effects associated with the non-steroidal anti-inflammatory analgesics and further studies are required to establish the clinical significance of these findings.

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Section: Introductionmentioning

confidence: 99%

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Prescott

Mattison

Menzies

et al. 1990

Brit J Clinical Pharma

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“…More recently, two other groups of drugs that cause functional renal insufficiency under certain conditions have been identified. Nonsteroidal antiinflammatory drugs that act by inhibiting prostaglandin synthesis have been associated with several renal syndromes [90][91][92].…”

Section: Acute Renal Failure From Radiologic Contrastmentioning

confidence: 99%

“…However, when stimuli for volume retention, such as sodium depletion, congestive heart failure, nephrosis, cirrhosis, or renal artery stenosis, are present, these drugs can block compensatory increases in vasodilatory prostaglandins and cause rapid reversible decreases in GFR [33,[90][91][92]. All nonsteroidal antiinflammatory drugs probably have the potential to alter GFR but sulindac, which may not reduce renal prostaglandin synthesis as much as other agents, seems to have a smaller effect on renal function than others.…”

Section: Acute Renal Failure From Radiologic Contrastmentioning

confidence: 99%

“…Hence, sulindac may be the drug of choice when nonsteroidal antiinflammatory drugs must be used in a high-risk patient [90][91][92]. ' Vasodilators, often used in the ICU to reduce cardiac afterload, may also reduce renal perfusion and GFR, if increases in cardiac output do not compensate for the vasodilatory effects.…”

Section: Acute Renal Failure From Radiologic Contrastmentioning

confidence: 99%

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Acute Renal Failure in Critically Ill Patients

Ellison¹,

Bia

1987

J Intensive Care Med

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Ellison DH, Bia MJ. Acute renal failure in critically ill patients. J Intensive Care Med 1987;2:8-24.Acute renal failure is an important cause of morbidity in critically ill patients. Acute renal failure results from prerenal and postrenal causes and, most importantly, acute tubular necrosis (ATN). Although it is known that renal toxins and renal ischemia are the most common causes of ATN in hospitalized patients, the exact pathogenesis of this entity is still not fully understood. Patients in the intensive care unit are at high risk for ATN because of hemodynamic instability, the administration of nephrotoxic antibiotics or chemotherapeutic agents, and exposure to radiographic contrast agents. The acquired immunodeficiency syndrome is also associated with an increased risk of renal failure development, either from complications of the disease itself or from its treatment. Many consequences of acute renal failure such as volume overload, acidosis, hyperkalemia, and serositis can be managed adequately with peritoneal dialysis, hemodialysis, or a newer technique, continuous arteriovenous hemofiltration. Despite improvements in treatment, however, the mortality of ATN remains high. In this review, we recommend measures to prevent ATN in certain clinical situations that commonly occur among critically ill patients. We also review therapeutic options for treating patients in whom acute renal failure develops and discuss newer developments that may begin to reduce the excessive morbidity associated with ATN.In its broadest sense acute renal failure refers to an abrupt (days to weeks) decrement in glomerular filtration rate (GFR) from any cause. Acute renal failure occurs in approximately 5% of all admissions to medical and. surgical wards in general hospitals [1]. The frequency of this complication is even higher, between 10 and 20%, in critically ill patients and in those admitted to intensive care units (ICUs) [2][3][4][5]. The most common causes of acute renal failure in a modern hospital setting include prerenal azotemia and acute tubular necrosis (ATN) resulting from decreases in renal perfusion or administration of nephrotoxic drugs. Renal ischemia may occur because of shock, operation, sepsis, burns, or decreased true or effective intravascular volume. Although hypotension is common in these settings, operation, sepsis, and burns may cause renal ischemic damage even without a measurable lowering of systemic blood pressure [1]. The leading causes of nephrotoxin-induced acute renal failure include the administration of radiographic contrast media and antibiotics, especially the aminoglycosides. In one study of 129 patients [1], renal ischemia and nephrotoxin administration caused 79% of hospital acquired acute renal failure. Iatrogenic factors, broadly defined as surgery, volume contraction, or the administration of nephrotoxins, accounted for over half (55%) of all episodes. For patients in an ICU, shock, sepsis, and operation, especially for abdominal aortic aneurysms, constitute the most common precipitating fa...

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“…Plasma concentrations of sodium were 133 mmol/l, potassium [2][3][4][5][6][7][8] mmolIl, and urea 4-1 mmol/l. Liver function was substantially altered: serum aspartate transaminase activity was 319 IU/l (normal range 12-42 IU/1) and alanine transferase activity was 660 IU/I (normal range 10-50 IU/A); alkaline phosphatase activity was 493 IU/l (normal range 90-300 IU/1); and serum total bilirubin concentration was 59 p.molIl (normal range < 17 imol/l) and albumin concentration 32 g/l (normal range 36-52 g/l).…”

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confidence: 99%

Toxic interaction of lithium carbonate and mefenamic acid.

Macdonald¹,

Neale²

1988

BMJ

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Probable fatal interaction between ciprofloxacin and theophylline Dr R HOLDEN (Edinburgh) writes: Thomson et al recently reported theophylline toxicity in an elderly patient concurrently taking ciprofloxacin.' The Committee on Safety of Medicines has been notified of several other cases (R D Mann, personal communication). We report a further probable interaction with a fatal outcome.A 65 year old woman with a history of a left hemiplegia, atrial fibrillation, congestive cardiac failure, and inoperable carcinoma of the breast was admitted after collapsing. Five days before admission she had been prescribed ciprofloxacin 250 mg twice daily and slow release theophylline (Uniphyllin Continus) 600 mg daily for a chest infection. Her condition had been stable until the time of collapse. She had been taking digoxin 0 25 mg, bumetanide 1 mg, and tamoxifen 40 mg daily for more than a year.On examination she was conscious but unable to communicate and had frequent epileptic seizures, involving the non-hemiplegic side. She had developed fast atrial fibrillation with a ventricular rate of 160 beats/minute and blood pressure of 120/60 mm Hg, but cardiovascular examination gave otherwise unremarkable results. Neurological examination showed features of a previous left hemiplegia and an equivocal right plantar response.Radiography of the chest showed slight cardiomegaly, and electrocardiography showed atrial fibrillation with a heart rate of 160 beats/minute and widespread ST segment depression. Plasma concentrations of sodium were 133 mmol/l, potassium [2][3][4][5][6][7][8] mmolIl, and urea 4-1 mmol/l. Liver function was substantially altered: serum aspartate transaminase activity was 319 IU/l (normal range 12-42 IU/1) and alanine transferase activity was 660 IU/I (normal range 10-50 IU/A); alkaline phosphatase activity was 493 IU/l (normal range 90-300 IU/1); and serum total bilirubin concentration was 59 p.molIl (normal range < 17 imol/l) and albumin concentration 32 g/l (normal range 36-52 g/l). Haemoglobin concentration was 118 g/l and white cell count 17 6x 109/l with moderate neutrophilia. Serum concentration of digoxin was 1-3 nmol/l (reference range 1-3-2-5 nmol/l) and theophylline 188 [smol/l (55-110 tmol/l).The patient was treated with intravenous digoxin 0-5 mg and subcutaneous diazepam 10 mg, but one hour later her heart rate was still the same, she continued to have frequent seizures, and she had become unconscious. Phenytoin 250 mg was given intravenously, abolishing the seizures. Over the next six hours the patient remained deeply unconscious, her heart rate remaining between 140 Twice an 18 year old girl used a popular proprietary preparation containing methyl nicotinate 1%, capsicin BPC 0-12% w/w, and preservatives in a cream base. She was otherwise fit, taking only a combined oral contraceptive, being a non-smoker, and having been discharged as fit after investigation for a symptomless systolic murmur, with electrocardiogram, chest x ray film, echocardiogram, and Doppler ultrasound all normal. On the first...

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Effects of Nonsteroidal Anti-Inflammatory Drugs on Prostaglandins and Renal Function

Cited by 12 publications

References 0 publications

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Acute Renal Failure in Critically Ill Patients

Toxic interaction of lithium carbonate and mefenamic acid.

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