Therapeutic uses of aspirin in renal diseases

Winchester, James F.

doi:10.1016/s0272-6386(96)90564-8

Cited by 19 publications

(8 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The evidence for a profibrotic role of platelets in diseases affecting the glomerular capillaries (i.e., glomerulonephritis and glomerulosclerosis) has mainly been indirect (for reviews see [15,27]): (1) platelets and their degranulation products have been documented in both experimental and human glomerulopathies, such as mesangioproliferative glomerulonephritis, membranous glomerulonephritis, and lupus nephritis; (2) shortened biological half-life of platelets, indicating increased platelet consumption, has been demonstrated in patients with various glomerular diseases; and (3) platelets contain a number of vasoactive, chemotactic, and profibrotic substances, which, when released within the glomerulus, are likely to amplify the tissue repair process. These substances include platelet-activating factor, platelet secretary products, polycationic macromolecules, platelet factor-4, b-thromboglobulin, various growth factors, and, important in the context of this study, high concentrations the profibrotic cytokine TGF-b.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Platelet inhibition limits TGF-β overexpression and matrix expansion after induction of anti-thy1 glomerulonephritis

Peters

Eisenberg

Daig

et al. 2004

Kidney International

View full text Add to dashboard Cite

The present study shows that platelets play a significant role in the sequence from mesangial cell injury to renal matrix expansion in anti-thy1 glomerulonephritis. The results, directly comparing renin-angiotensin-system and platelet inhibition, suggest that platelets contribute less than angiotensin II to TGF-beta overexpression and matrix accumulation in this model of acute glomerular wound repair.

show abstract

Section: Discussionmentioning

confidence: 99%

“…At present, platelet function in human disease may be inhibited by a number of pharmacologic approaches [11,15,27]. We chose clopidogrel instead of the clinically more widely used aspirin because its mode of action is more specifically directed toward platelet inhibition.…”

Section: Discussionmentioning

confidence: 99%

Platelet inhibition limits TGF-β overexpression and matrix expansion after induction of anti-thy1 glomerulonephritis

Peters

Eisenberg

Daig

et al. 2004

Kidney International

View full text Add to dashboard Cite

show abstract

“…Earlier studies reported amelioration of proteinuria by the TPr antagonists Bay U3405 (10) and S-1452 (14) in diabetic rats, suggesting that endogenous TPr agonists stimulate the development of diabetic nephropathy. In addition, some studies indicate a benefit of inhibiting TXA 2 synthase (10) or COX with aspirin, suggesting that COX-derived TXA 2 may be involved to some extent (15,16).…”

Section: Staining For the Nadph Oxidase Subunit P47mentioning

confidence: 99%

The Thromboxane Receptor Antagonist S18886 Attenuates Renal Oxidant Stress and Proteinuria in Diabetic Apolipoprotein E-Deficient Mice

Xu¹

2006

Diabetes

View full text Add to dashboard Cite

Arachidonic acid metabolites, some of which may activate thromboxane A 2 receptors (TPr) and contribute to the development of diabetes complications, including nephropathy, are elevated in diabetes. This study determined the effect of blocking TPr with S18886 or inhibiting cyclooxygenase with aspirin on oxidative stress and the early stages of nephropathy in streptozotocin-induced diabetic apolipoprotein E ؊/؊ mice. Diabetic mice were treated with S18886 (5 mg ⅐ kg ؊1 ⅐ day ؊1 ) or aspirin (30 mg ⅐ kg ؊1 ⅐ day ؊1 ) for 6 weeks. Neither S18886 nor aspirin affected hyperglycemia or hypercholesterolemia. There was intense immunohistochemical staining for nitrotyrosine in diabetic mouse kidney. In addition, a decrease in manganese superoxide dismutase (MnSOD) activity was associated with an increase in MnSOD tyrosine-34 nitration. Tyrosine nitration was significantly reduced by S18886 but not by aspirin. Staining for the NADPH oxidase subunit p47phox , inducible nitric oxide synthase, and 12-lipoxygenase was increased in diabetic mouse kidney, as were urine levels of 12-hydroxyeicosatetraenoic acid and 8-iso-prostaglandin F 2␣ . S18886 attenuated all of these markers of oxidant stress and inflammation. Furthermore, S18886 significantly attenuated microalbuminuria in diabetic mice and ameliorated histological evidence of diabetic nephropathy, including transforming growth factor-␤ and extracellular matrix expression. Thus, in contrast to inhibiting cyclooxygenase, blockade of TPr may have therapeutic potential in diabetic nephropathy, in part by attenuating oxidative stress. Diabetes 55:110 -119, 2006

show abstract

“…Low-dose aspirin (81 mg daily) has been associated with a 20% to 30% reduction in the risk of stroke, AMI, and CVD death across many populations [34]. The effect of aspirin on renal end points is unknown; however, given its CVD protective effect, it is recommended for adult patients with ESRD [35]. For those who are aspirin intolerant, general cardiology guidelines recommend the use of clopidogrel, although there are no published studies of clopidogrel on cardiovascular outcomes in the setting of ESRD.…”

Section: Antiplatelet Agentsmentioning

confidence: 99%

Evaluation and treatment of coronary artery disease in patients with end-stage renal disease

McCullough

2005

Kidney International

View full text Add to dashboard Cite

Evaluation and treatment of coronary artery disease in patients with end-stage renal disease. Patients with end-stage renal disease (ESRD) are at increased risk of death from coronary artery disease (CAD). The metabolic milieu that results from renal dysfunction appears to accelerate the atherosclerotic process by decades in patients with ESRD. The extremely high prevalence of atherosclerosis in patients with ESRD mandates risk factor identification and treatment. Traditionally, CAD in this patient population has been treated conservatively. Analysis of large databases has highlighted the scope and complexity of this problem; nonetheless, there is a paucity of randomized, controlled trials of CAD in patients with ESRD. In this paper the following issues related to evaluation and treatment of patients with chronic kidney disease are addressed: (1) optimal CAD risk management; (2) evaluation for CAD in patients with ESRD, including the identification of coronary calcification; (3) treatment of CAD with medical therapy and revascularization; (4) relative merits of percutaneous coronary intervention versus bypass surgery. In general, an aggressive approach to medical management of CAD is warranted, even in the setting of subclinical CAD. A low threshold for diagnostic testing should be employed in patients with ESRD. When significant CAD is identified, ESRD patients appear to benefit more from revascularization compared to conservative medical management. Thus, if clinically reasonable, patients with ESRD and CAD should be managed aggressively to improve survival and reduce the incidence of future cardiac events.

show abstract

Therapeutic uses of aspirin in renal diseases

Cited by 19 publications

References 39 publications

Platelet inhibition limits TGF-β overexpression and matrix expansion after induction of anti-thy1 glomerulonephritis

Platelet inhibition limits TGF-β overexpression and matrix expansion after induction of anti-thy1 glomerulonephritis

The Thromboxane Receptor Antagonist S18886 Attenuates Renal Oxidant Stress and Proteinuria in Diabetic Apolipoprotein E-Deficient Mice

Evaluation and treatment of coronary artery disease in patients with end-stage renal disease

Contact Info

Product

Resources

About