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Effects of T-type calcium channel blockers on renal function and aldosterone in patients with hypertension: a systematic review and meta-analysis.

Li X, Yang MS - PLoS ONE (2014)

Bottom Line: High blood pressure can cause kidney damage, which can increase blood pressure, leading to a vicious cycle.Compared with L-type CCBs, T-type CCBs resulted in a significant decline in aldosterone (mean difference = -15.19, 95% CI -19.65 - -10.72, p<1×10(-5)), proteinuria (mean difference = -0.73, 95% CI -0.88 - -0.57, p<1×10(-5)), protein to creatinine ratio (mean difference = -0.22, 95% CI -0.41 - -0.03, p = 0.02), and urinary albumin to creatinine ratio (mean difference = -55.38, 95% CI -86.67 - -24.09, p = 0.0005); no significant difference was noted for systolic blood pressure (SBP) (p = 0.76) and diastolic blood pressure (DBP) (p = 0.16).The effects of T-type CCBs did not significantly differ from those of RAS antagonists for SBP (p = 0.98), DBP (p = 0.86), glomerular filtration rate (p = 0.93), albuminuria (p = 0.97), creatinine clearance rate (p = 0.24), and serum creatinine (p = 0.27) in patients with hypertension.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, College of Pharmacy, Chongqing Medical University, Chongqing, People's Republic of China.

ABSTRACT

Background: High blood pressure can cause kidney damage, which can increase blood pressure, leading to a vicious cycle. It is not clear whether the protective effects of T-type calcium channel blockers (T-type CCBs) on renal function are better than those of L-type CCBs or renin-angiotensin system (RAS) antagonists in patients with hypertension.

Methods and findings: PUBMED, MEDLINE, EMBASE, OVID, Web of Science, Cochrane, CNKI, MEDCH, VIP, and WANFANG databases were searched for clinical trials published in English or Chinese from January 1, 1990, to December 31, 2013. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated and reported. A total of 1494 reports were collected, of which 24 studies with 1,696 participants (including 809 reports comparing T-type CCBs versus L-type CCBs and 887 reports comparing T-type CCB versus RAS antagonists) met the inclusion criteria. Compared with L-type CCBs, T-type CCBs resulted in a significant decline in aldosterone (mean difference = -15.19, 95% CI -19.65 - -10.72, p<1×10(-5)), proteinuria (mean difference = -0.73, 95% CI -0.88 - -0.57, p<1×10(-5)), protein to creatinine ratio (mean difference = -0.22, 95% CI -0.41 - -0.03, p = 0.02), and urinary albumin to creatinine ratio (mean difference = -55.38, 95% CI -86.67 - -24.09, p = 0.0005); no significant difference was noted for systolic blood pressure (SBP) (p = 0.76) and diastolic blood pressure (DBP) (p = 0.16). The effects of T-type CCBs did not significantly differ from those of RAS antagonists for SBP (p = 0.98), DBP (p = 0.86), glomerular filtration rate (p = 0.93), albuminuria (p = 0.97), creatinine clearance rate (p = 0.24), and serum creatinine (p = 0.27) in patients with hypertension.

Conclusion: In a pooled analysis of data from 24 studies measuring the effects of T-type CCBs on renal function and aldosterone, the protective effects of T-type CCBs on renal function were enhanced compared with L-type CCBs but did not differ from RAS antagonists. Their protective effects on renal function were independent of blood pressure.

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Mean differences and 95% CIs of included studies and pooled data for T-type CCBs versus L-type CCBs.(A) Systolic blood pressure (SBP). (B) Diastolic blood pressure (DBP). (C) Glomerular filtration rate (GFR). (D) Serum creatinine (SCr). (E) Aldosterone. (F) Proteinuria in hypertensive patients with CKD. (G) The urinary protein to creatinine ratio in hypertensive patients with CKD. (H) The urinary albumin to creatinine ratio in hypertensive patients with diabetic nephropathy.
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pone-0109834-g002: Mean differences and 95% CIs of included studies and pooled data for T-type CCBs versus L-type CCBs.(A) Systolic blood pressure (SBP). (B) Diastolic blood pressure (DBP). (C) Glomerular filtration rate (GFR). (D) Serum creatinine (SCr). (E) Aldosterone. (F) Proteinuria in hypertensive patients with CKD. (G) The urinary protein to creatinine ratio in hypertensive patients with CKD. (H) The urinary albumin to creatinine ratio in hypertensive patients with diabetic nephropathy.

Mentions: Seventeen independent reports with 534 experimental subjects and 502 controls were included [12]–[28]. No significant difference was noted for SBP (MD = 0.16, 95% CI −0.87–1.20, p = 0.76) between T-type CCBs and L-type CCBs (see Figure 2-A).


Effects of T-type calcium channel blockers on renal function and aldosterone in patients with hypertension: a systematic review and meta-analysis.

Li X, Yang MS - PLoS ONE (2014)

Mean differences and 95% CIs of included studies and pooled data for T-type CCBs versus L-type CCBs.(A) Systolic blood pressure (SBP). (B) Diastolic blood pressure (DBP). (C) Glomerular filtration rate (GFR). (D) Serum creatinine (SCr). (E) Aldosterone. (F) Proteinuria in hypertensive patients with CKD. (G) The urinary protein to creatinine ratio in hypertensive patients with CKD. (H) The urinary albumin to creatinine ratio in hypertensive patients with diabetic nephropathy.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4201480&req=5

pone-0109834-g002: Mean differences and 95% CIs of included studies and pooled data for T-type CCBs versus L-type CCBs.(A) Systolic blood pressure (SBP). (B) Diastolic blood pressure (DBP). (C) Glomerular filtration rate (GFR). (D) Serum creatinine (SCr). (E) Aldosterone. (F) Proteinuria in hypertensive patients with CKD. (G) The urinary protein to creatinine ratio in hypertensive patients with CKD. (H) The urinary albumin to creatinine ratio in hypertensive patients with diabetic nephropathy.
Mentions: Seventeen independent reports with 534 experimental subjects and 502 controls were included [12]–[28]. No significant difference was noted for SBP (MD = 0.16, 95% CI −0.87–1.20, p = 0.76) between T-type CCBs and L-type CCBs (see Figure 2-A).

Bottom Line: High blood pressure can cause kidney damage, which can increase blood pressure, leading to a vicious cycle.Compared with L-type CCBs, T-type CCBs resulted in a significant decline in aldosterone (mean difference = -15.19, 95% CI -19.65 - -10.72, p<1×10(-5)), proteinuria (mean difference = -0.73, 95% CI -0.88 - -0.57, p<1×10(-5)), protein to creatinine ratio (mean difference = -0.22, 95% CI -0.41 - -0.03, p = 0.02), and urinary albumin to creatinine ratio (mean difference = -55.38, 95% CI -86.67 - -24.09, p = 0.0005); no significant difference was noted for systolic blood pressure (SBP) (p = 0.76) and diastolic blood pressure (DBP) (p = 0.16).The effects of T-type CCBs did not significantly differ from those of RAS antagonists for SBP (p = 0.98), DBP (p = 0.86), glomerular filtration rate (p = 0.93), albuminuria (p = 0.97), creatinine clearance rate (p = 0.24), and serum creatinine (p = 0.27) in patients with hypertension.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, College of Pharmacy, Chongqing Medical University, Chongqing, People's Republic of China.

ABSTRACT

Background: High blood pressure can cause kidney damage, which can increase blood pressure, leading to a vicious cycle. It is not clear whether the protective effects of T-type calcium channel blockers (T-type CCBs) on renal function are better than those of L-type CCBs or renin-angiotensin system (RAS) antagonists in patients with hypertension.

Methods and findings: PUBMED, MEDLINE, EMBASE, OVID, Web of Science, Cochrane, CNKI, MEDCH, VIP, and WANFANG databases were searched for clinical trials published in English or Chinese from January 1, 1990, to December 31, 2013. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated and reported. A total of 1494 reports were collected, of which 24 studies with 1,696 participants (including 809 reports comparing T-type CCBs versus L-type CCBs and 887 reports comparing T-type CCB versus RAS antagonists) met the inclusion criteria. Compared with L-type CCBs, T-type CCBs resulted in a significant decline in aldosterone (mean difference = -15.19, 95% CI -19.65 - -10.72, p<1×10(-5)), proteinuria (mean difference = -0.73, 95% CI -0.88 - -0.57, p<1×10(-5)), protein to creatinine ratio (mean difference = -0.22, 95% CI -0.41 - -0.03, p = 0.02), and urinary albumin to creatinine ratio (mean difference = -55.38, 95% CI -86.67 - -24.09, p = 0.0005); no significant difference was noted for systolic blood pressure (SBP) (p = 0.76) and diastolic blood pressure (DBP) (p = 0.16). The effects of T-type CCBs did not significantly differ from those of RAS antagonists for SBP (p = 0.98), DBP (p = 0.86), glomerular filtration rate (p = 0.93), albuminuria (p = 0.97), creatinine clearance rate (p = 0.24), and serum creatinine (p = 0.27) in patients with hypertension.

Conclusion: In a pooled analysis of data from 24 studies measuring the effects of T-type CCBs on renal function and aldosterone, the protective effects of T-type CCBs on renal function were enhanced compared with L-type CCBs but did not differ from RAS antagonists. Their protective effects on renal function were independent of blood pressure.

Show MeSH
Related in: MedlinePlus