A Cochrane review [Abstract] 1 included 22 studies with a total of 3 465 subjects; 17 studies (n=3 282) compared statin with placebo or no treatment, and 5 studies (n=183) compared two different statin regimens.
Statins seemed to reduce statistically non-significantly major cardiovascular events, cardiovascular mortality (table T1), and fatal or non-fatal myocardial infarction (RR 0.70, 95% CI 0.48 to 1.01; 1 study, n=2 102).
| Outcome | Relative effect (95% CI) | Assumed risk (placebo or no treatment) | Corresponding risk (statin) | Participants (studies) |
|---|---|---|---|---|
| Major cardiovascular events | RR 0.84(0.66 to 1.06) | 20 per 1000 | 17 per 1000 (13 to 21) | 2 102 (1) |
| All-cause mortality | RR 1.08(0.63 to 1.83) | 20 per 1000 | 22 per 1000 (12 to 37) | 2 760 (6) |
| Cardiovascular mortality | RR 0.68(0.45 to 1.01) | 5 per 1000 | 3 per 1000 (2 to 5) | 2 322 (4) |
Statins had uncertain effects on all-cause mortality (table T1), fatal or non-fatal stroke (RR 1.18, 95% CI 0.85 to 1.63; 1 study, n=2 102), creatine kinase elevation (RR 0.86, 95% CI 0.39 to 1.89; 3 studies, n=2 233); liver enzyme elevation (RR 0.62, 95% CI 0.33 to 1.19; 4 studies, n=608), withdrawal due to adverse events (RR 0.89, 95% CI 0.74 to 1.06; 9 studies, n=2 810), and cancer (RR 0.94, 95% CI 0.82 to 1.07; 1 study, n=2 094).
Statins significantly reduced serum total cholesterol (MD -42.43 mg/dL (=1.1 mmol/L), 95% CI -51.22 to -33.65; 12 studies, n=3 070); low-density lipoprotein cholesterol (MD -43.19 mg/dL, 95% CI -52.59 to -33.78; 11 studies, n=3 004); serum triglycerides (MD -27.28 mg/dL, 95% CI -34.29 to -20.27; 11 studies, n=3 012); and lowered high-density lipoprotein cholesterol (MD -5.69 mg/dL, 95% CI -10.35 to -1.03; 11 studies, n=3 005). There was marked heterogeneity in the analyses for total cholesterol, LDL cholesterol and HDL cholesterol levels.
Statins had uncertain effects on kidney function: ESKD (RR 1.14, 95% CI 0.94 to 1.37; 6 studies, n=2 740); proteinuria (MD -0.04 g/24 h, 95% CI -0.17 to 0.25; 2 studies, n=136); acute allograft rejection (RR 0.88, 95% CI 0.61 to 1.28; 4 studies, n=582); and GFR (MD -1.00 mL/min, 95% CI -9.96 to 7.96; 1 study, n=62).
Data directly comparing differing statin regimens could not be meta-analysed.
Another meta-analysis 2 included 7 sudies (2 RCTs and 5 cohort studies) with a total of 1870 kidney transplant patients that received statins and 3339 kidney transplant patients as the control group. Statins had no protective effect on transplant rejection, graft survival or patient survival after kidney transplantation. The effect of statins on graft survival, however, was significant when adjusted for factors such as age, sex, and serum creatinine level (HR, 0.80; 95% CI 0.69 to 0.92; P = .003). Similarly, patient survival was significantly better with statin use (adjusted HR, 0.75; 95% CI 0.63 to 0.88; P = .003).
An observational cohort study 3 included 165 adult patients with kidney transplantation and tacrolimus treatment. Compared with the control group (n=73), the statin-users (n=92) had a significantly reduced risk of major cardiovascular event (MACE) (adjusted HR, 0.31; 95% CI 0.13 to 0.74). In the Cox regression analysis, old age, history of CVD, and comorbid hypertension were identified as independent factors associated with increased MACE. The total cholesterol levels were not significantly different between the two groups. Subjects with higher cumulative defined daily dose of statins had significantly lower risks of MACE.
Comment: The quality of evidence is downgraded by study quality (inadequate or unclear allocation concealment and lack of blinding) and imprecise results.
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