Effects of nonsteroidal anti-inflammatory drugs on prostaglandins and renal function

Carmichael, Jan M.; Shankel, Stewart W.

doi:10.1016/0002-9343(85)90223-2

Cited by 224 publications

(52 citation statements)

References 94 publications

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“…36,37 In surgical patients with normal renal function, a transient decrement in renal function is observed but considered to be clinically irrelevant, 38 but in the setting of stressed kidneys, continued NSAID administration should be avoided. 36,39 Nevertheless, it is unknown if withholding NSAIDS from patients at higher risk of injury would affect the rate or magnitude of AKI.…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury following total joint arthroplasty: retrospective analysis

Weingarten

Gurrieri

Jarett

et al. 2012

Can J Anesth/J Can Anesth

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Introduction Postoperative acute kidney injury (AKI) following arthroplasty has not been well studied. Our aim was to identify factors associated with increased risk of AKI. Methods The medical records for adult patients who underwent elective total joint arthroplasty during June 1, 2007 to May 31, 2010 at the Mayo Clinic were reviewed to identify patients with normal preoperative kidney function who experienced perioperative AKI, defined as an increase in serum creatinine (sCr) by 26.4 lmolÁL -1 . For each AKI case, two controls were identified and matched for age, sex, and type of operation. Medical records were abstracted for demographics, comorbid conditions, and preoperative, intraoperative, and postoperative variables. Conditional logistic regression analyses were performed to identify risk factors for AKI. Results Of the 9,171 patients who underwent joint replacement operations, 167 with normal preoperative renal function developed AKI with a median [25 th , 75 th ] increase in sCr of 35.4 [26.4, 44.2] lmolÁL -1 . No patient required dialysis. A higher than normal body mass index, diabetes mellitus, the number of baseline antihypertensive medications, cerebral or peripheral vascular disease, use of general anesthesia, and perioperative blood transfusions were independently associated with risk for AKI. Hospital length of stay and intensive care admissions were greater in AKI patients, and in 12.0% of patients, sCr remained at least 26.4 lmolÁL -1 higher than preoperative baseline at least three months after surgery. Conclusion In this case-control investigation, we identified several factors associated with the development of postoperative AKI. Recognition of these risk factors could allow for the adoption of perioperative renal protective strategies in patients undergoing arthroplasty.

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Section: Discussionmentioning

confidence: 99%

Acute kidney injury following total joint arthroplasty: retrospective analysis

Weingarten

Gurrieri

Jarett

et al. 2012

Can J Anesth/J Can Anesth

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“…This was associated with a significant decrease in sodium excretion "-. , -& +1 +1+1 -excretion, and reduces plasma renin activity (Carmichael & Shankel, 1985). This mechanism .…”

Section: Urine Volume and Osmolalitymentioning

confidence: 97%

“…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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“…This prostaglandin was selected because it is the stable metabolite of PGI2 (Schlondorff & Ardaillou, 1986), mainly synthesised by the kidney (Patrono et al, 1982), and because prostacyclins play a determinant role in renal blood flow regulation (Dunn, 1987). Predictably (Carmichael & Shankel, 1985), pretreatment by KP significantly reduced renal excretion of 6-keto-PGF,C. As MTX is mainly cleared by glomerular filtration (Huang et al, 1979), pretreatment by KP quite logically impairs renal elimination of the anti-metabolite.…”

Section: Discussionmentioning

confidence: 99%

Biochemical and pharmacological consequences of the interaction between methotrexate and ketoprofen in the rabbit

Perrin

Milano²,

Thyss³

et al. 1990

Br J Cancer

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Summary Severe methotrexate (MTX) toxicity is a proven complication of associations of MTX and non-steroidal anti-inflammatory drugs (NSAIDs). This study investigated the interaction between MTX (50 or 100 mg kg-') and ketoprofen (KP) (3 mg kg-' day-', pretreatment for 8 days) in the rabbit. The drug association induced a reversible increase in blood urea and creatinine. The severity degree of 7-OH-MTX was prepared in our laboratory according to a method previously published (Jacobs et al., 1976). Briefly, MTX was incubated on rabbit liver homogenate purified in aldehyde oxidase activity. Total recovery was 15% (10 mg of 7-OH-MTX recovered for 75 mg of MTX incubated). The purity of the 7-OH-MTX (96%) was checked by HPLC and by UV and IR spectral analysis (Jacobs et al., 1976) (valency vibration of the -OH radical absorbing at 3,460 cm-').A KP preparation for i.v. injections (Profenid i.m. 100 mg Specia-Rhone Poulenc) was given at 3 mg kg-'.A calcium folinate preparation for i.v. injections (Lederfoline 50 mg, Lederle) was diluted five times by NaCI 0.9% and given at 0.5 mgkg-'.Cartridges for ultrafiltration were Centrifree (Amicon, Grace). Cartridges for solid extraction before HPLC analysis were SepPak C18 (Millipore Waters).A commercial RIA (1251)

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Effects of nonsteroidal anti-inflammatory drugs on prostaglandins and renal function

Cited by 224 publications

References 94 publications

Acute kidney injury following total joint arthroplasty: retrospective analysis

Acute kidney injury following total joint arthroplasty: retrospective analysis

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

Biochemical and pharmacological consequences of the interaction between methotrexate and ketoprofen in the rabbit

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