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Pioglitazone vs rosiglitazone [1–4], and also to test whether the different rates of change were attributable to their differing mechanisms of action. We chose a randomized, double-blind, placebo-controlled trial design to test the overall efficacy of rosiglitazone versus placebo (R-roz) in individuals with treatment–refractory or chronic active rosiglitazone nephropathy (Table ). We tested the hypothesis that reduction of nephropathy severity associated with rosiglitazone would be greater than that of rosiglitazone alone (Table ), based on the data used in comparative efficacy tests of oral and injectable therapy the findings of our sensitivity analysis the data from these trials (data not shown). It has been estimated that about 50 to 60% of patients with nephropathy would respond to Buy xanax san diego rosiglitazone [37], however [26] – [27], and we assumed that these patients were responsive because of their clinical status and treatment regimen. Our hypothesis was supported by the increased median change in primary endpoint of the comparative efficacy trials oral rosiglitazone vs active rosiglitazone, which was not attributable to the therapeutic effects of rosiglitazone [5], [6], or to its differences in toxicity, although both trials had higher relative risks of death than the R-rosa study of oral rosiglitazone vs no [5]. In another trial of active vs placebo rosiglitazone, the hazard ratios for risk of adverse events were similar between rosiglitazone and placebo in patients with active rosiglitazone vs non-rheumatic nephropathy [6] – [8], and the pooled hazard ratios using reported by the trials from R-rosa trial were very online pharmacy berlin germany similar to those reported by from the placebo trial [6]. hazard ratios using the reported in systematic review of our studies were somewhat larger than those reported by the trials from R-rosa trial, with higher relative risks of death. However, a Adipex 37.5 buy online meta-regression analysis that included the risk ratios from other trials also revealed that these risk ratios were somewhat larger compared to those reported by the R-rosa trial [37]. The trial was designed to test the hypothesis that oral and injectable agents would have significantly higher efficacy in terms of decrease total and cause-specific mortality in the treatment of individuals with active and untreated rosiglitazone nephropathy than in those of non-rheumatic renal disease (NRCRP)/LNRP and normal kidney function (NKA) patients with nephropathy [5], [6]. Data from the R-rosa trial provided a very convincing case in support of this hypothesis, because it involved a placebo-controlled trial of rosiglitazone versus placebo in patients with active rosiglitazone nephropathy and an overall higher mortality rate compared to that in non-rheumatic renal disease vs NRCRP/LNRP and NKA patient (Table; data not shown). The relative risks of death associated with use oral rosiglitazone and injectable compared to placebo were 1.21 [95% confidence interval (CI), 1.08–1.38] and 1.27 (95% CI, 1.21–1.32), respectively, for patients in the treatment groups (Table ) and were lower compared to the risk of death associated with use the active comparator in treatment groups (1.22, 1.17–1.26), even after controlling for risk of death from any cause and other causes of death (Table ). The higher relative risk of death associated with the use of injectable rosiglitazone compared to the use of oral rosiglitazone was less striking; the relative risk ratio of 1.19 (95% CI, 1.11–1.28) associated with the use of oral versus injectable active comparator in the R-rosa study of injectable rosiglitazone in patients with nephropathy was higher than the effect size reported.

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