Meta-analysis of antiplatelet therapy for IgA nephropathy

Taji, Yoshinori; Kubo, Takashi; Shikata, Satoru; Morimoto, Takeshi

doi:10.1007/s10157-006-0433-8

Cited by 40 publications

(25 citation statements)

References 27 publications

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“…Other therapeutic options have been tried, including steroids, cytotoxics, tonsillectomy, anti-platelet drugs, fish oil, and vitamin E in order to modulate the rate of progression [18][19][20]. Steroids, colchicine, cyclophosphamide, cyclosporine, azathioprine, and plasmapheresis have been used to treat glomerulonephritis with Behçet's disease [3], but more studies are needed to clarify their effects on the course of glomerular disease.…”

Section: Discussionmentioning

confidence: 99%

Behçet’s disease complicated by IgA nephropathy with nephrotic syndrome

et al. 2008

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A 65-year-old woman with a 48-year history of Behçet's disease associated with nephrotic syndrome is described. Immunofluorescence study revealed IgA nephropathy. Following treatment with an angiotensin II type-I receptor-blocker, an anti-platelet drug, and an HMG-CoA reductase inhibitor, accompanied by dietary restrictions of protein and sodium, proteinuria was markedly decreased. This report describes our experience with a rare entity of Behçet's disease complicated by nephrotic syndrome due to IgA nephropathy. Routine urine examination and renal biopsy are needed for the detection and diagnosis of renal problems with Behçet's disease.

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Section: Discussionmentioning

confidence: 99%

Behçet’s disease complicated by IgA nephropathy with nephrotic syndrome

et al. 2008

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“…Our analysis showed that urokinase was beneficial for proteinuria and renal function in moderate to severe stages of IgA nephropathy. Taji et al (31) reported that dipyridamole was beneficial for proteinuria and renal function in moderate to severe stages of IgA nephropathy. But, the studies included in their study were not good, two studies of Yagame et al (12) and Woo et al (15) were not randomized.…”

Section: Discussionmentioning

confidence: 99%

Antithrombotic Drug Therapy for IgA Nephropathy: A Meta Analysis of Randomized Controlled Trials

Liu

Geng

Xin³

et al. 2011

Intern. Med.

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Background Antithrombotic agents, including antiplatelet agents, anticoagulants and thrombolysis agents, have been widely used in the management of immunoglobulin A (IgA) nephropathy in Chinese and Japanese populations. To systematically evaluate the effects of antithrombotic agents for IgA nephropathy. Methods Data sources consisted of MEDLINE, EMBASE, the Cochrane Library, Chinese Biomedical Literature Database (CBM), Chinese Science and Technology Periodicals Databases (CNKI) and Japana Centra Revuo Medicina (http://www.jamas.gr.jp) up to April 5, 2011. The quality of the studies was evaluated from the intention to treat analysis and allocation concealment, as well as by the Jadad method. Meta-analyses were performed on the outcomes of proteinuria and renal function. Results Six articles met the predetermined inclusion criteria. Antithrombotic agents showed statistically significant effects on proteinuria (p<0.0001) but not on the protection of renal function (p=0.07). The pooled risk ratio for proteinuria was 0.53, [95% confidence intervals (CI): 0.41-0.68; I 2 =0%] and for renal function it was 0.42 (95% CI 0.17-1.06; I 2 =72%). Subgroup analysis showed that dipyridamole was beneficial for proteinuria (p=0.0003) but had no significant effects on protecting renal function. Urokinase had statistically significant effects both on the reduction of proteinuria (p=0.0005) and protecting renal function (p<0.00001) when compared with the control group. Conclusion Antithrombotic agents had statistically significant effects on the reduction of proteinuria but not on the protection of renal function in patients with IgAN. Urokinase had statistically significant effects both on the reduction of proteinuria and on protecting renal function. Urokinase was shown to be a promising medication and should be investigated further.

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“…Additionaly experimental studies observed that adenosine, as an endogenous signaling molecule, plays a critical role in attenuating renal inflammation and renoprotection from acute ischemic renal failure [31][32][33][34]. There are conflicting data about effects of dipyridamole on renal function but not proteinuria, as it was reported that dipyridamole was shown to decrease proteinuria and or risk for rapid renal and development of end stage renal disease especially in early chronic kidney disease patients with diabetic nephropathy and various primary glomerulonephropathies such as IgA nephropathy, and membranoproliferative glomerulonephritis [30,[35][36][37]. Although the underlying mechanism is exactly unknown, several mechanisms supposed to renoprotective effect of dipyridamole such as inhibition of platelet activation and aggregation by increasing adenosine level, vasodilation via enhancing the nitric oxide pathway, acting as a antioxidant and inhibiting cellular proliferation of mesengial cells and renal fibroblasts and extracellular matrix accumulation [35].…”

Section: Increasing In the Creatinin And Or Cystatin -C Level N (%) Amentioning

confidence: 97%

“…Although dipyridamole effects via increasing extracellular adenosine concentration by the reducing the uptake of adenosine, in the light of the literature, we think that dipyridamol may not effect renal function by itself without facilitating factors for development kidney injury such as hypotension, ischemia, nehrotoxic drugs, hypovolemia, administration contrast media leading to medullary hypoxia, tubular toxicity and oxidative damage as seen in the pathophysiology of contrast induced nephropathy [5,9,[35][36][37].…”

Section: Increasing In the Creatinin And Or Cystatin -C Level N (%) Amentioning

confidence: 99%

Does intravenous dipyridamole administration cause acute renal impairment?

Kalyoncuoğlu¹,

Başkurt²,

Gülşen³

2017

Blood Heart Circ

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Purpose: Dipyridamole increases extracellular adenosine concentrations, and may result a significant decrease on GFR. The aim of the study was detect whether any deterioration occurs in renal function in patients who were undergoing dipyridamole myocardial perfusion scintigraphy. Material and method:94 patients (64 women, 30 men, mean age; 69 ± 10) undergoing dipyridamole myocardial perfusion scintigraphy enrolled to our study. Blood samples were taken from all patients for serum creatinine and cystatin C before and at 4th and 48 hours after the test. The patients were divided into two groups as GFR value higher (group A) and equal or lower (group B) than 60 mL/dk/1.73m² according to GFR calculation modalities. The development and incidence of nephropathy (25% increase in serum creatinine or cystatin C level from the baseline value at 4th and 48th hours after administration of dipyridamole) was determined betweeen the two groups.Result: Group B were significantly elder and more hypertensive than group A. Serum creatinine levels did not exhibit any difference between the groups at 4th and 48th hours in all calculation modalities. Besides that, only 4th hours cystatin C level showed significantly increasing in in patients with MDRD-GFR < 60 mL/ dk/1.73m² whereas 48th hours cystatin C levels did not. Any change in cystatin C levels also were not observed between the groups in other calculation modalities. Conclusion:Dipyridamole myocardial perfusion scintigraphy can be used safely in patients with GFR ≤ 60 mL/dk/1.73m² except end stage renal disease.

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Meta-analysis of antiplatelet therapy for IgA nephropathy

Cited by 40 publications

References 27 publications

Behçet’s disease complicated by IgA nephropathy with nephrotic syndrome

Behçet’s disease complicated by IgA nephropathy with nephrotic syndrome

Antithrombotic Drug Therapy for IgA Nephropathy: A Meta Analysis of Randomized Controlled Trials

Does intravenous dipyridamole administration cause acute renal impairment?

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