Cyclooxygenase-2 Inhibition and Renal Function

Pfister, Alfred K.; Crisalli, Robert J.; Carter, William H.

doi:10.7326/0003-4819-134-11-200106050-00017

Cited by 17 publications

(6 citation statements)

References 2 publications

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“…Up‐regulation of COX‐2 has been observed in renal biopsies from patients with renal arterial stenosis, diabetic nephropathy, lupus nephritis, hypertension, congestive heart failure, and children with Bartter syndrome [6,7,10,13,16–18]. The impact of blocking COX‐2‐derived prostaglandins for the development of acute renal failure has been shown in several reports [5,19,20].…”

Section: Introductionmentioning

confidence: 99%

Expression of cyclooxygenase-1 and cyclooxygenase-2 in human renal allograft rejection - a prospective study

et al. 2006

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Summary Cyclooxygenases (COX) are known to be involved in inflammatory kidney diseases. However, there are no data available about the expression of COX‐1 and only preliminary reports about the expression of COX‐2 in biopsies of patients undergoing acute renal allograft rejection. We conducted this prospective study to analyze the expression, distribution, and cellular localization of COX‐1 and ‐2 and thus to elucidate the role of COX in human kidney transplantation. One hundred forty‐four biopsies were included from patients without rejection and unaltered morphology (n = 60), with acute interstitial rejection (n = 7), with acute vascular rejection (n = 21), with chronic allograft nephropathy (n = 16), without rejection but with various other lesions (n = 40). COX‐1 and ‐2 expression was localized in each biopsy by immunohistochemistry. We found a highly significant up‐regulation of COX‐1 in vessels and in infiltrating interstitial cells of patients with acute allograft rejection compared with biopsies with well‐preserved tissue. Also, COX‐2 expression was significantly elevated in infiltrating interstitial cells of biopsies with acute rejection. This is the first prospective study demonstrating a significant induction of both COX‐1 and ‐2 in human allograft biopsies with acute rejection after renal transplantation.

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Section: Introductionmentioning

confidence: 99%

Expression of cyclooxygenase-1 and cyclooxygenase-2 in human renal allograft rejection - a prospective study

et al. 2006

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“…Furthermore, also a patient after renal transplantation had reversible acute renal failure after use of 50 mg of rofecoxib for 4 weeks (maximum serum creatinine concentration of 4.0 mg/dl; recovery to 1.2 mg/dl within 3 days) [146]. In another case report dealing with a 55-year-old woman with idiopathic pleural effusions treated with a diuretic combination therapy, 200 mg of celecoxib caused a weight gain of 4.54 kg over 2 weeks without an increase in serum creatinine [147]. Finally, we have observed a patient with heart failure that suffered from oliguria and acute renal failure after a single dose of 25 mg of rofecoxib [148].…”

Section: Acute Renal Failurementioning

confidence: 99%

Renal Cyclooxygenase-2 (Cox-2)

Krämer

Kammerl

Kömhoff

2004

Kidney Blood Press Res

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Background/Aims: The role of COX-2 for renal function during renal development, for physiology and pathophysiology of renal diseases and the side effects of available COX-2 inhibitors, has gained increasing interest. We aimed therefore to review the respective role of renal COX-2. Methods: Review of relevant recent publications in the field, and in addition of in part unpublished data obtained in our laboratories. Results: COX-2 is ‘constitutively’ localized in the kidney i.e. in macula densa, TALH, interstitial cells, and is of utmost importance for normal renal development. Renal COX-2 is regulated by for example sodium and volume intake, angiotensin II, glucocorticoids often involving specific COX-2 promotor response elements. COX-2 derived prostanoids are required for preservation of renal blood flow and glomerular filtration especially in states of fluid deficit, they promote natriuresis, and furthermore may stimulate renin secretion during low-sodium intake/loop diuretic use. Conversely, COX-2 inhibitors decrease glomerular filtration, and renal perfusion, sometimes even causing acute renal failure. In addition, COX-2 inhibitors cause sodium retention, edema formation, cardiac failure and hypertension. The role of COX-2 derived prostanoids in renal inflammation or failure including diabetic nephropathy and renal transplantation remains at present controversial. Conclusion: COX-2 is one of the major players in renal physiology and pathophysiology. One focus of future work should be placed on COX-2 in primary renal diseases.

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“…68 Animal models show that rofecoxib interferes with diuretic efficacy, 69 and published case reports suggest that this is also true of celecoxib. 64 In a study of elderly hypertensives, 9.5% of rofecoxib-recipients vs. 4.9% of celecoxib-recipients developed edema, 60 but the significance of this difference is unclear since more celecoxib patients were on concurrent ACE-inhibitor therapy, which may have been protective. In summary, the limited data available to date suggest that COX-2 inhibitors are as likely as traditional NSAIDs to cause CHF.…”

Section: Heart Failure Exacerbationsmentioning

confidence: 99%

“…Case reports have documented episodes of acute renal failure, hyperkalemia, metabolic acidosis, hyponatremia, heart failure and tubulo-interstitial nephritis in patients taking celecoxib or rofecoxib, [61][62][63][64] although these events occurred mostly in patients with risk factors for nephrotoxicity. In patients with chronic renal insufficiency or renal allografts, celecoxib and rofecoxib have been reported to cause acute renal failure with accompanying congestive heart failure (CHF) and hyperkalemia.…”

mentioning

confidence: 99%

Review of the selective COX-2 inhibitors celecoxib and rofecoxib: focus on clinical aspects

Loewen

2002

CJEM

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The selective cyclooxygenase-2 (COX-2) inhibitors celecoxib and rofecoxib were designed to have similar efficacy but less gastrointestinal toxicity than traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Their efficacy has been demonstrated in the treatment of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, postoperative dental pain and dysmenorrhea. These agents produce fewer endoscopic ulcers, symptomatic ulcers and gastrointestinal bleeds than traditional NSAIDs; although the absolute benefit is small and the gastropreserving effect is negated by concurrent use of low-dose aspirin for cardiovascular risk reduction. Nephrotoxicity and hyptertension remain concerns with COX-2 inhibitors, as they are with traditional NSAIDs. COX-2 inhibitors may be safe alternatives to traditional NSAIDs for patients with aspirin-sensitive asthma. RÉSUMÉLes inhibiteurs sélectifs de la cyclo-oxygénase-2 (COX-2) célécoxib et rofécoxib ont été conçus pour agir de manière aussi efficace que les anti-inflammatoires non stéroïdiens (AINS) traditionnels, mais avec moins de toxicité gastro-intestinale. Ils se sont révélés efficaces dans le traitement de l'arthrose, de l'arthrite rhumatoïde, de la spondylarthrite ankylosante, de la dentalgie post-chirurgicale et de la dysménorrhée. Ces agents provoquent moins d'ulcères endoscopiques, d'ulcères symptomatiques et de saignements gastro-intestinaux que les AINS traditionnels; cependant, le bienfait absolu est faible et l'effet de gastro-préservation est annulé par le recours concomitant à de l'aspirine à faible dose pour la réduction du risque cardiovasculaire. La néphrotoxicité et l'hypertension demeurent une préoccupation avec les inhibiteurs de la COX-2, tout comme avec les AINS traditionnels. Les inhibiteurs de la COX-2 peuvent se révéler une solution de rechange sécuri-taire aux AINS traditionnels chez les patients atteints d'asthme hypersensible à l'aspirine.

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Cyclooxygenase-2 Inhibition and Renal Function

Cited by 17 publications

References 2 publications

Expression of cyclooxygenase-1 and cyclooxygenase-2 in human renal allograft rejection - a prospective study

Expression of cyclooxygenase-1 and cyclooxygenase-2 in human renal allograft rejection - a prospective study

Renal Cyclooxygenase-2 (Cox-2)

Review of the selective COX-2 inhibitors celecoxib and rofecoxib: focus on clinical aspects

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