Meta-Analysis of the Effect of Statins on Renal Function

Qiang Geng, PhD, Jingyi Ren, MD, Junxian Song, PhD, Sufang Li, PhD, and Hong Chen, MD*

Statins can signicantly improve the lipid prole and reduce cardiovascular events. How-
ever, benecial effects of statins on renal function are still controversial. PubMed, the
Cochrane Central Register of Controlled Trials, Web of Knowledge, and ClinicalTrials.gov
Web sites were searched for randomized controlled trials. The selected studies reported
renal function during treatment with statins and control. Forty-one studies with a total of
88,523 participants were included in this analysis. Compared with statins, placebo group
had signicantly decreased estimated glomerular ltration rate (eGFR): the standardized
mean difference (SMD) of eGFR in change from baseline was 0.15 (95% condence interval
[CI] 0.07 to 0.23, p [ 0.0004) in patients with eGFR >60 ml/min and 0.09 (95% CI 0.01 to
0.17, p [ 0.02) in patients with eGFR 30 to 60 ml/min. Compared with placebo, statin
group had signicantly greater reduction of proteinuria: the SMD of proteinuria in change
from baseline was L1.12 (95% CI L1.95 to L0.30, p [ 0.008) in patients with urinary
protein excretion 30 to 300 mg/day and L0.77 (95% CI L1.35 to L0.18, p [ 0.01) in
patients with urinary protein excretion > 300 mg/day. eGFR was signicantly greater with
high-intensity statins than with moderate-intensity statins (SMD 0.12, 95% CI 0.08 to 0.16,
p [ 0.00001). Placebo group had signicantly decreased eGFR for 1 to 3 years (SMD 0.05,
95% CI 0.02 to 0.08, p [ 0.003) and >3 years (SMD 0.14, 95% CI 0.04 to 0.25, p [ 0.007)
of statin therapy. The benecial effect of statins on renal function may be dosage related
and duration dependent. In conclusion, statins appear to decrease the rate of reduction of
eGFR and slow the progression of pathologic proteinuria moderately. 2014 Elsevier
Inc. All rights reserved. (Am J Cardiol 2014;114:562e570)

Statins are the most widely prescribed drugs for the treat-
ment of atherosclerosis, and they substantially reduce cardio-
vascular disease morbidity and mortality in prevention.
However, it has not been established whether statins provide
similar benecial effects on the kidney. There is a growing
afrmation that statins may offer renoprotective effects as
illustrated in a number of cohort studies, other meta-analyses,
and statements by professional organizations.1e4 In contrast,
some studies failed to demonstrate renoprotection from statins.5
Concerns about these conicting results make physicians
reluctant to prescribe statins in patients with chronic kidney
disease (CKD). To assess whether statins had benecial effects
on kidney, we performed this meta-analysis to investigate the
effects of statins on estimated glomerular ltration rate (eGFR)
and urinary protein excretion between statin and control groups.
Methods
Our meta-analysis was performed according to the
Preferred Reporting Items for Systematic Reviews and
Department of Cardiology, Peking University Peoples Hospital,
Beijing, China. Manuscript received March 27, 2014; revised manuscript
received and accepted May 27, 2014.
Drs. Geng and Ren contributed equally to this work.
This work was supported by the National Natural Science Foundation
grant 30570712 and 81070179 funded by the national natural science fund
committee (China).
See page 570 for disclosure information.
*Corresponding author: Tel: (86) 10 88325339; fax: (86)
10 88325339.
E-mail address: chenhongbj@medmail.com.cn (H. Chen).
Meta-Analyses reporting guidelines.6 We searched the
PubMed, the Cochrane Central Register of Controlled Tri-
als, Web of Knowledge, and ClinicalTrials.gov Web sites to
identify the published or unpublished randomized controlled
trials (RCTs) in any language from 1987 to 2013. The
following terms were used: hydroxymethylglutaryl-CoA
reductase inhibitors, atorvastatin, simvastatin, rosuvastatin,
pravastatin, lovastatin, uvastatin, pitavastatin, statin, kid-
ney, renal, glomerular ltration rate, nephropathy, albu-
minuria, and proteinuria.
Two investigators independently identied reports ac-
cording to the inclusion criteria. Disagreements were
resolved by discussion and consensus. Study quality was
estimated using the Cochrane classication for assessing the
risk of bias (sequence generation, allocation concealment,
blinding, selective reporting, and intention-to-treat
analysis).7
The inclusion criteria were (1) RCTs of statins versus
control (placebo, another statin, or usual care); (2) partici-
pants aged >18 years; (3) report of baseline and at end of
follow-up data on kidney function (eGFR, creatinine clear-
ance, or urinary protein excretion); and (4) report of change
from baseline on renal function and damage (eGFR, creat-
inine clearance, or urinary protein excretion). The exclusion
criteria were (1) participants aged <18 years; (2) studies
without kidney function; (3) participants with contrast-
induced nephropathy or dialysis; and (4) reviews,
nonhuman studies, case reports, and abstracts.
The characteristics of the study were extracted from the
included studies: author, year, sample size, age, design,
follow-up duration, statin and dosage, type of renal disease,
eGFR, and urinary protein excretion.

0002-9149/14/$ - see front matter 2014 Elsevier Inc. All rights reserved. www.ajconline.org
http://dx.doi.org/10.1016/j.amjcard.2014.05.033
 Preventive Cardiology/The Effect of Statins on Renal Function
Figure 1. Study selection ow diagram. Initially, 8,660 studies were
identied; of these, 8,626 studies failed to meet the inclusion criteria and 41
studies were included in this meta-analysis.
The change from baseline in eGFR in milliliters per
minute per year was calculated in this analysis. In our
meta-analysis, creatinine clearance is regarded as an
eGFR.8,9 Twenty-ve studies (Supplementary References
3,5,6,9,11e14,16e22,24,27,28,30e35,37) enrolled pa-
tients with eGFR >60 ml/min/1.73 m2. Nine studies
(Supplementary References 1,4,6,7,10,25,26,29,38)
enrolled patients with eGFR <60 ml/min/1.73 m2.
In our analysis, albuminuria and proteinuria were
considered together. Three studies (Supplementary
References 2,22,36) enrolled patients with urinary protein
(or albumin) excretion <30 mg/day. Six studies (Supple
mentary References 8,9,15,23,33,35) enrolled patients with
urinary protein (or albumin) excretion 30 to 300 mg/day.
Thirteen studies (Supplementary References 1,7,9e13,19,
20,21,25,32,34) enrolled patients with urinary protein (or
albumin) excretion >300 mg/day.
High-intensity, moderate-intensity, and low-in-
tensity statin therapy denitions were derived from the recent
American College of Cardiology/American Heart Association
guidelines.10 We analyzed our data by comparing high-
intensity statins versus moderate-intensity statins. We also
investigated the effect of high-intensity, moderate-intensity,
and low-intensity statins on eGFR and urinary protein
excretion. Eight studies (Supplementary References 1,6,27,
28,30,39e41) adopted high-intensity statins. Twenty-ve
studies (Supplementary References 2e5,7,9,11,12,16e18,
22e24,26,27,29,31,34,35,37e41) adopted moderate-
intensity statins. Twelve studies (Supplementary
References 8,10,13e15,19e21,25,32,33,36) adopted low-
intensity statins.
Nikolic et al11 found that the benet of statins may
depend on the duration of treatment. So we investigated the
relation between the duration of treatment (<1 year, 1 to
563
3 years, and >3 years) and the effect of statins on renal
function. The duration of statin therapy in 15 studies
(Supplementary References 4,8,9,12,15,19e21,26,27,
31e34,38) was <1 year. The duration of statin therapy in
11 studies (Supplementary References 1,2,10,13,23,25,
28e30,35,36) was from 1 to 3 years. The duration of
statin therapy in 12 studies (Supplementary References
3,5,6,7,11,14,16e18,22,24,37) was >3 years.
The I2 statistic was used to assess heterogeneity. I2
>50% and p <0.10 indicated statistically signicant het-
erogeneity. A funnel plot was used to assess publication
bias. In the present study, 2-sided p <0.05 was considered
signicant.
The change from baseline in eGFR in milliliters per
minute per year and in urinary protein excretion was
calculated using the standardized mean difference (SMD).
Missing mean was replaced with median. Missing SD was
imputed using the width of interquartile ranges divided by
1.35 or on the basis of p values.7 The meta-analysis was
performed using Review Manager software (version 5.0;
Cochrane Collaboration, Oxford, United Kingdom).
Results
Initially, 8,660 studies were searched, consisting of 366
potentially relevant studies and 8,294 studies that were
removed after reading titles and abstracts. Of 366 poten-
tially relevant studies, 325 failed to match the inclusion
criteria. Finally, 41 studies with a total of 88,523 partici-
pants were included in this meta-analysis. Flowchart for
identication of studies is presented in Figure 1. The
baseline characteristics of studies in the meta-analysis are
given in Table 1.
AURORA (an assessment of survival and cardiovascular
events) and 4D (Deutsche Diabetes Dialyse Studie) studies
had evaluated the use of statins in patients on regular he-
modialysis. In our meta-analysis, dialysis was one of the
exclusion criteria. We could not get the eGFR data of
SHARP (study of heart and renal protection) study. We had
sent an e-mail to the corresponding author, but the author
did not reply to us. So, AURORA, 4D, and SHARP trials
were excluded in our meta-analysis.
The risk of bias in the selected studies is presented in
Supplementary Table 1. All the studies selected in our meta-
analysis were RCTs and had adequate random sequence
generation. Twenty-ve studies used allocation concealment
methods. Twenty-four studies reported that patients were
blinded to treatment, and 23 studies reported that the
outcome assessors were blinded to the patient groups.
Fifteen studies had intention-to-treat analysis. No studies
had selective outcome reporting.
To investigate the effects of statins versus placebo on
eGFR, 24 studies (Supplementary References 5,6,9,11e14,
16e22,24,27,28,30e35,37) enrolled 75,723 participants
with eGFR >60 ml/min/1.73 m2, and 9 studies
(Supplementary References 1,4,6,7,10,25,26,29,38) enrolled
2,222 participants with eGFR <60 ml/min/1.73 m2.
The SMD of eGFR in change from baseline was stratied
by baseline eGFR. In patients with eGFR >60 ml/min/
1.73 m2, the SMD of eGFR was 0.15 (95% condence in-
terval [CI] 0.07 to 0.23, p 0.0004; Figure 2). In patients
 564
Table 1
Characteristics of studies included in the meta-analysis
Studies Treatment Control No. of Patients Mean Age (Years) Baseline eGFR (ml/min/1.73 m2) Baseline Urinary Protein Excretion (mg/d) Follow up
(Months)
Treatment Control Treatment Control Treatment Control Treatment Control

BianchiS1 A 40 mg Placebo 28 28 56.5 56.8 50.8  9.5 50.0  10.1 2500  1900 1900  1400 12
Dalla NoraS2 A 10 mg Placebo 12 13 66 63 NR NR 5.76  16 7.2  12 12
AthyrosS3 A 24 mg Placebo 800 800 58 59 76  13 77  12 NR NR 36
GoicoecheaS4 A 20 mg Placebo 44 19 66.2 70 42.8  24.9 44.2  25.9 NR NR 6
ColhounS5 A 10 mg Placebo 447 437 61.5 61.8 64.5  10.0 64.9  10.0 NR NR 46.8
KorenS6 A 40.5 mg Placebo 235 158 65.6 64.8 51.3  7.8 51.1  8.5 NR NR 54.3
A 40.5 mg Placebo 811 564 59.8 60.2 79.4  15.2 79.1  15.6 NR NR 54.3
FassettS7 A 10 mg Placebo 58 65 60 60.3 31.9  11.0 29.1  12.8 1430  2280 1180  1610 36
LintottS8 F 40 mg Placebo 32 10 57 63 NR NR 200  537 297  403 3
BuemiS9 F 40 mg Placebo 8 13 36 38 90  44 90  40 Proteinuria 845  699 Proteinuria 837  523 6
Albuminuria 296  244 Albuminuria 293  183

The American Journal of Cardiology (www.ajconline.org)

YasudaS10 F 20 mg Placebo 39 41 57 58 59  31 60  26 800  1248 700  640 12
FellstromS11 F 40e80 mg Placebo 1050 1052 49.5 50 60.2  20.8 60.3  20.7 500  1400 400  700 60
RuggenentiS12 F 40e80 mg Placebo 83 88 51.4 51.4 67.7  45.2 59.4  34.0 1200  1200 1500  1400 6
LamS13 L 30 mg Placebo 16 18 58.9 53.9 83.1  38 84.3  21.6 810  680 1140  1273 24
KendrickS14 L 20 mg Placebo 3303 3301 58e62 58e62 >60 >60 NR NR 63.6
ZhangS15 P 20 mg Placebo 10 10 43 43 NR NR 93.6  53 93.6  53 3
ShepherdS16 P 40 mg Placebo 3302 3293 55.3 55.1 >60 >60 NR NR 58.8
SacksS17 P 40 mg Placebo 2081 2078 59 59 >60 >60 NR NR 60
LIPIDS18 P 40 mg Placebo 4512 4502 62 62 >60 >60 NR NR 73.2
ImaiS19 P 5e10 mg Placebo 32 25 58.5 49.5 64.4  30.5 54.4  30.5 1100  1358 1400  1450 6
LeeS20 P 10 mg Placebo 31 32 50 47 85  16 90  19 1234  490 1193  507 6
LeeS21 P 10 mg Placebo 42 40 50 48 85  16 90  19 1323  592 1207  531 6
AtthobariS22 P 40 mg Placebo 400 388 52.1 50.9 75.7  12.1 75.5  12.0 NR NR 48
NanayakkaraS23 P 40 mg Placebo 47 46 54 52 NR NR 45  854 71  650 24
RahmanS24 P 40 mg Placebo 1342 1298 63.3 63.1 101.8  12.9 102.4  12.3 NR NR 57.6
P 40 mg Placebo 2903 2960 67 67 75.3  8.0 75.2  8.1 NR NR 57.6
P 40 mg Placebo 779 778 70.7 70.6 50.8  8.2 50.6  8.4 NR NR 57.6
FassettS25 P 20 mg Placebo 29 20 53 49 58.5  18.2 49.9  23.2 370  490 220  230 24
VermaS26 R 10 mg Placebo 44 39 73 74 42.3  11.1 49.4  11.9 NR NR 5
KostapanosS27 R 10 mg Placebo 45 40 51.7 52.2 83.4  15.4 82.9  13.2 NR NR 3
R 20 mg Placebo 45 40 52.4 52.2 82.3  12.5 82.9  13.2 NR NR 3
CrouseS28 R 40 mg Placebo 702 282 57 57 >60 >60 NR NR 24
SawaraS29 R 2.5 mg Placebo 22 16 63.8 67.0 50.7  18.7 57.3  16.2 NR NR 12
VidtS30 R 20 mg Placebo 8143 8136 66 66 75.4  17.5 75.4  17.1 NR NR 27.6
AbeS31 R 2.5e10 mg Placebo 52 52 64.5 64.9 70.4  11.9 69.3  9.5 69.3  9.5 69.3  9.5 6
HommelS32 S 10e20 mg Placebo 12 9 41 35 64  30 72  23 698  1313 755  1290 3
NielsenS33 S 10e20 mg Placebo 8 10 65 65 96.6  22.6 97.1  21.2 28  18 49  40 9
ThomasS34 S 10e40 mg Placebo 15 15 52 49 76.5  36.5 75.4  40.2 5290  3490 4400  2680 6
TonoloS35 S 20 mg Placebo 10 9 60 62 101  8 97  7 73  50.4 70  45.9 12
FriedS36 S 10e20 mg Placebo 19 20 33.3 31.0 NR NR 11  8 15  10 24
CollinsS37 S 40 mg Placebo 7999 7697 40e80 40e80 >60 >60 NR NR 60
 Preventive Cardiology/The Effect of Statins on Renal Function 565

with eGFR <60 ml/min/1.73 m2, the SMD of eGFR was

0.09 (95% CI 0.01 to 0.17, p 0.02; Figure 2).
13
13
13
13
60
6

Twenty-one studies with a total of 3,933 participants

reported effects of statins on urinary protein excretion. The
SMD of urinary protein excretion in change from baseline
was stratied by baseline data. In patients with urinary
protein excretion <30 mg/day, the SMD of urinary protein
excretion was 0.29 (95% CI 0.94 to 0.37, p 0.39;
NR
NR
NR
NR
NR
NR

Figure 3). In patients with urinary protein excretion 30 to

300 mg/day, the SMD of urinary protein excretion
was 1.12 (95% CI 1.95 to 0.30, p 0.008; Figure 3).
In patients with urinary protein excretion >300 mg/day, the
SMD of urinary protein excretion was 0.77 (95%
CI 1.35 to 0.18, p 0.01; Figure 3).
eGFR was signicantly greater with high-intensity statins
than with moderate-intensity statins (SMD 0.12, 95% CI 0.08
NR
NR
NR
NR
NR
NR

to 0.16, p <0.00001; Figure 4). Compared with placebo, statin

group had signicantly increased eGFR: the SMD of eGFR
was 0.1 (95% CI 0.01 to 0.19, p 0.03; Figure 4) in patients
with high-intensity statin therapy and 0.15 (95% CI 0.05 to
0.26, p 0.004; Figure 4) in patients with moderate-intensity
24.1
24.1
28.1
28.1
11.4

statin therapy. No statistically signicant difference in eGFR

13

was found between low-intensity statin therapy and placebo








(Figure 4). A statistically signicant reduction of urinary

68.8
68.8
78.3
78.3
65.6
32

protein excretion was found for low-intensity statins

compared with placebo (SMD 1.06, 95% CI 1.76
to 0.36, p 0.003; Supplementary Figure 1). The difference
24.9
25.8
30.0
30.4
11.2

of reduction of urinary protein excretion was nonsignicant

12

between moderate-intensity statins and placebo








(Supplementary Figure 1). Because of insufcient data, the

72.1
72.6
71.5
76.8
65.0
40

A atorvastatin; F uvastatin; L lovastatin; P Pravastatin; R rosuvastatin; S simvastatin.

effect of high-intensity statins on urinary protein excretion

could not be investigated.
Placebo group had signicantly decreased eGFR for
60.9

<1 year (SMD 0.14, 95% CI 0.01 to 0.27, p 0.04), 1 to

55
NR
NR
NR
NR

3 years (SMD 0.05, 95% CI 0.02 to 0.08, p 0.003),

and >3 years (SMD 0.14, 95% CI 0.04 to 0.25, p 0.007)
of statin therapy (Figure 5). A signicant decrease of pro-
61.2
60
NR
NR
NR
NR

teinuria was observed for 1 to 3 years of statin therapy

(SMD 0.19, 95% CI 1.54 to 0.27, p 0.005), with no
signicant decrease for both <1 and >3 years of statin
therapy (Supplementary Figure 2).
4829
118
118
27

70
70

Discussion
4827
111
124
28

80
87

In our analysis, we identied 41 RCTs that assessed the

effect of statins on kidney function and urinary protein
excretion. In good agreement with previous ndings,1,4,9
statins could reduce the decrease in eGFR for patients
A 10 mg
R 10 mg
R 10 mg
R 10 mg
R 10 mg
Placebo

with stages 1 to 3 of CKD and decrease pathologic pro-

teinuria moderately.
Most patients with CKD had mixed dyslipidemia, and
mixed dyslipidemia could accelerate kidney function loss.12
A 80 mg

A 80 mg

A 80 mg
R 40 mg

R 40 mg
S 40 mg

The National Kidney Foundation regarded CKD as a car-

diovascular disease risk equivalent.12 The ndings of this
analysis were not unexpected, because statins had pleio-
tropic effects. Statins, independently of their cholesterol-
lowering effect, could ameliorate endothelial function and
PLANETIIS40

reduce inammatory and brogenic processes in the renal

PLANETIS39

ShepherdS41
PanichiS38

interstitium13; this might explain why statins could improve

kidney function and reduce pathologic urinary protein
excretion.
566 The American Journal of Cardiology (www.ajconline.org)

Figure 2. Forest plots of eGFR for statins versus placebo in patients with (A) eGFR >60 ml/min/1.73 m2 (SMD 0.15, 95% CI 0.07 to 0.23, p 0.0004) and (B)
eGFR <60 ml/min/1.73 m2 (SMD 0.09, 95% CI 0.01 to 0.17, p 0.02). IV inverse variance; LIPID the Long-Term Intervention with Pravastatin in
Ischaemic Disease; Std. standardized.

However, trials about the effect of statins on kidney
function and protein excretion yielded controversial results,
some trials conrming renoprotective effect and proteinuria
reduction,4,9 others showing no effect.5 One meta-analysis
by Sandhu et al9 involving 39,704 patients demonstrated
that statins could slow the rate of reduction in eGFR by a
mean of 1.22 ml/min/year. Another meta-analysis by
Douglas et al4 including 1,384 patients showed that statins
may decrease pathologic urinary protein excretion. In
contrast, in a large-scale RCT,5 no renoprotective effects
were found.
According to the recent American College of Cardiology/
American Heart Association guidelines, we also investigated
the effect of high-, moderate-, and low-intensity statins on
eGFR and urinary protein excretion. High-intensity statin
therapy resulted in signicantly greater eGFR than moderate-
intensity statins. Compared with placebo, high- and
moderate-intensity statins could signicantly decrease the
 Preventive Cardiology/The Effect of Statins on Renal Function 567

Figure 3. Forest plots of urinary protein excretion for statins versus placebo in patients with (A) urinary protein excretion <30 mg/day (SMD 0.29, 95%
CI 0.94 to 0.37, p 0.39), (B) urinary protein excretion 30 to 300 mg/day (SMD 1.12, 95% CI 1.95 to 0.30, p 0.008), and (C) urinary protein
excretion >300 mg/day (SMD 0.77, 95% CI 1.35 to 0.18, p 0.01). IV inverse variance; Std. standardized.

rate of reduction of eGFR. In contrast, the difference in eGFR
was nonsignicant between low-intensity statins and placebo.
The effect of statins on eGFR may be dosage related. The
reasons might be that high- and moderate-intensity statins
could provide more signicant clinical benet compared with
low-intensity ones. In our analysis, we found that low-
intensity statin therapy could signicantly reduce the uri-
nary protein excretion compared with placebo. In contrast,
the difference in urinary protein excretion was nonsignicant
between moderate-intensity statin therapy and placebo.
Because of insufcient data, we could not investigate the
effect of high-intensity statin therapy on urinary protein
excretion. Sidaway et al14 determined that statins could
inhibit reabsorption of protein. And this effect is apparently
dose related. However, our ndings about the effect of statins
on urinary protein excretion were inconsistent with those by
Sidaway et al.14 However, this needs to be further validated in
large-scale and long follow-up period RCTs.
Nikolic et al11 found that the benet of statins may depend
on the duration of treatment. According to Nikolic et al, we
also divided our studies into 3 groups: <1 year, from 1 to
3 years, and >3 years. For <1 year, from 1 to 3 years, and
>3 years of statin therapy, placebo group had signicantly
decreased eGFR. A signicant decrease of proteinuria was
observed for 1 to 3 years of statin therapy, with no signicant
decrease for both <1 and >3 years of statin therapy. We
568 The American Journal of Cardiology (www.ajconline.org)

Figure 4. Forest plots of eGFR for (A) moderate- versus high-intensity statins (SMD 0.12, 95% CI 0.08 to 0.16, p <0.00001), (B) high-intensity statins versus
placebo (SMD 0.10, 95% CI 0.01 to 0.19, p 0.03), (C) moderate-intensity statins versus placebo (SMD 0.15, 95% CI 0.05 to 0.26, p 0.004), and (D)
low-intensity statins versus placebo (SMD 0.03, 95% CI 0.01 to 0.08, p 0.16). IV inverse variance; LIPID the Long-Term Intervention with
Pravastatin in Ischaemic Disease; PLANET I Prospective evaluation of proteinuria and renal function in diabetic patients with progressive renal disease;
PLANET II Prospective evaluation of proteinuria and renal function in non-diabetic patients with progressive renal disease; Std. standardized.
 Preventive Cardiology/The Effect of Statins on Renal Function 569

Figure 5. Forest plots of eGFR for statins versus placebo in patients with treatment duration (A) <1 year (SMD 0.14, 95% CI 0.01 to 0.27, p 0.04), (B) from 1
to 3 years (SMD 0.05, 95% CI 0.02 to 0.08, p 0.003), and (C) >3 years (SMD 0.14, 95% CI 0.04 to 0.25, p 0.007). IV inverse variance; LIPID the
Long-Term Intervention with Pravastatin in Ischaemic Disease; Std. standardized.
570 The American Journal of Cardiology (www.ajconline.org)
believed that the benecial effect of statins on eGFR and
urinary protein excretion may depend on the duration of
statin treatment. Notably, our ndings are consistent with the
meta-analysis performed by Nikolic et al.11
In our analysis, we also found that statins could signi-
cantly reduce total cholesterol, triglycerides, and low-
density lipoprotein cholesterol in patients with CKD.
Statins could improve the lipid prole in patients with CKD.
Generally speaking, statins are well tolerated in patients with
stages 1 to 3 CKD. However, the effects of statins on renal
function are still controversial in 4 and 5 stages of CKD.15
Hopefully, this meta-analysis will provide evidence that
treatment with statins may have benecial effects on kidney.
As with any study, our meta-analysis had several limi-
tations. First, the numbers of patients in many positive
studies were relatively small. The results of this analysis
need to be conrmed. Second, the designs and the methods
used in trials were different. Not all studies were double-
blinded. Third, because of insufcient data, we could not
investigate the effect of statins on eGFR and urinary protein
excretion in patients with stages 4 and 5 CKD. Fourth, there
were different ways of calculating eGFR in our analysis.
Acknowledgment: All authors had access to the data and
participated in writing this manuscript.
Disclosures
The authors have no conicts of interest to disclose.
Supplementary Data
Supplementary data associated with this article can be
found, in the online version, at http://dx.doi.org/10.1016/j.
amjcard.2014.05.033.
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