A Cochrane review [Abstract] 1 included 63 studies with a total of 50 725 subjects. 53 studies (n= 42 752) compared statins with placebo or no treatment. In people with chronic kidney disease not requiring dialysis, statins consistently decreased major cardiovascular events (RR 0.72, 95% CI 0.66 to 0.79; 14 studies, n=36 156), all-cause mortality (RR 0.83, 95% CI 0.73 to 0.96, statistical heterogeneity I2 =53%; 13 studies, n=34 978), cardiovascular deaths (RR 0.77, 95% CI 0.69 to 0.87; 8 studies, n=19 112), and myocardial infarction (RR 0.55, 95% CI 0.42 to 0.73; 10 studies, n=9 475). Statins had uncertain effects on stroke (RR 0.64, 95% CI 0.37 to 1.08; 7 studies, n=9 115). No difference in kidney failure (RR 0.98, 95% CI 0.91 to 1.05; 3 studies, n=6 704) was observed. Statins seemed to improve kidney function (CrCl or eGFR: MD 1.83, 95% CI 0.27 to 3.39 mL/min; 18 studies, n=4 213). The incidence of elevated liver enzymes, cancer and withdrawal rates due to adverse events were not significantly different between patients when reported. Few studies reported rhabdomyolysis or elevated CK, thus the effect of statins on these outcomes remained unclear.
A systematic review and meta-analysis 2 assessing the efficacy of statins on kidney outcomes included 57 studies with a total of 143 888 participants. Statin treatment did not produce an apparent beneficial effect for kidney failure events (OR 0.98, 95% CI 0.87 to1.10; P=0.7) or end-stage renal disease events (OR 0.98, 95% CI 0.90 to1.07; P=0.7). However, compared with control or placebo, it slowed down the rate of decline in eGFR (MD 0.41, 95% CI 0.11 to 0.70 mL/min/1.73m per year) and the change in proteinuria or albuminuria (MD -0.65, 95% CI -0.94 to -0.37). In addition, statin therapy significantly reduced the risk for cardiovascular events (OR, 0.69, 95% CI 0.61 to 0.79; P<0.001).
A systematic review 3 included 27 studies with a total of 39 704 subjects. Studies included patients with cardiovascular disease (CVD), glomerulonephritis, diabetes, hypertension, hyperlipidaemia and general patients. Studies of patients with end-stage renal disease were excluded. The included studies evaluated atorvastatin, pravastatin, fluvastatin, simvastatin, lovastatin and cerivastatin. Overall, the change in the weighted mean differences for eGFR was statistically significant (1.22 ml/min per yr slower in statin recipients; 95% CI 0.44 to 2.00). There was substantial heterogeneity (I-squared 96%). The effect of statins remained statistically significant with a smaller treatment effect when only higher quality studies were analysed. In subgroup analysis, the benefit of statin therapy was statistically significant in studies of participants with CVD (0.93 ml/min per yr slower than control subjects; 95% CI 0.10 to 1.76) but was non-significant for studies of participants with diabetic or hypertensive kidney disease or glomerulonephritis. There were no significant differences between statins and control in the rate of change in proteinuria (reduction in WMD 0.37 g/24 hours, 95% CI -0.75 to 0.02) or albuminuria (reduction in WMD -0.02 g/24 hours, 95% CI -0.06 to 0.02); substantial heterogeneity was found (I-squared 83% and 92%, respectively).
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