scholarly journals Comparing the Efficacy of Angiotensin Converting Enzyme In-hibitors with Calcium Channel Blockers on the Treatment of Di-abetic Nephropathy: A Meta-Analysis

Author(s):  
Zhaowei ZHANG ◽  
Chunlin CHEN ◽  
Shiwen LV ◽  
Yalan ZHU ◽  
Tianzi FANG

Background: The angiotensin-converting enzyme inhibitors (ACEIs) could improve the symptoms of diabetic nephropathy. Whether the calcium channel blockers (CCBs) could be as effective as ACEIs on treating diabetic nephropathy is controversial. Here, we aimed to compare the efficacy of ACEIs with CCBs on the treatment of diabetic nephropathy by performing a meta-analysis of randomized controlled trials (RCTs). Methods: The Pubmed, Medline, Embase and The Cochrane Database were searched up to July 2017 for eligible randomized clinical trials studies. Effect sizes were summarized as mean difference (MD) or standardized mean difference (SMD) with 95% confidence intervals (P-value<0.05). Results: Seven RCTs involving 430 participants comparing ACEIs with CCBs were included. No benefit was seen in comparative group of ACEIs on systolic blood pressure(SBP) (MD=1.05 mmHg; 95% CI: -0.97 to 3.08, P=0.31), diastolic blood pressure (DBP) (MD= -0.34 mmHg; 95% CI: -1.2 to 0.51, P=0.43), urinary albumin excretion rates (UAER) (MD=1.91μg/min; 95% CI: -10.3 to 14.12, P=0.76), 24-h urine protein (24-UP) (SMD=-0.26; 95%CI: -0.55 to 0.03, P=0.08), glomerular filtration rate (GFR) (SMD=0.01; 95% CI: -0.38 to 0.41, P=0.95). On safety aspect, the risk of adverse reactions between ACEIs group and CCBs group are similar (RR=1.18; 95% CI: 0.61 to 2.28; P=0.61). Conclusion: Both ACEIs and CCBs could improve the BP, UAER, 24h-UP, and GFR of diabetic nephropathy to a similar extent

1998 ◽  
Vol 9 (11) ◽  
pp. 2096-2101 ◽  
Author(s):  
P Ruggenenti ◽  
A Perna ◽  
R Benini ◽  
G Remuzzi

Dihydropyridine-type calcium channel blockers (dihydropyridine CCB) adversely affect renal function in diabetes. The effects of dihydropyridine CCB on 24-h urinary protein excretion rate and GFR decline (deltaGFR) were prospectively evaluated in 117 nondiabetic patients with chronic, proteinuric nephropathies enrolled in the Ramipril Efficacy in Nephropathy study and randomized to angiotensin-converting enzyme inhibition (ACEI) or placebo plus conventional antihypertensive therapy. Sixty-three percent of patients were treated with dihydropyridine CCB. During follow-up, CCB-treated compared with no CCB patients had higher proteinuria (mean+/-SEM: 4.8+/-0.2 g/24 h versus 4.2+/-0.2 g/24 h, respectively, P = 0.015) and mean arterial BP (MAP). The difference in proteinuria was significant in the placebo group (5.1+/-0.2 g/24 h versus 4.3+/-0.3 g/24 h, P = 0.02), but not in the ACEI group (4.4+/-0.2 g/24 h versus 4.1+/-0.2 g/24 h). Of note, CCB-treated patients had significantly less proteinuria (P = 0.028) in the ACEI group compared with placebo. CCB-treated versus no CCB patients had a faster deltaGFR in the overall study population and in the placebo group, but not in the Ramipril group. Proteinuria was comparable in CCBtreated and no CCB patients for MAP < or = 100 mmHg, but was higher in CCB-treated patients for MAP >100 mmHg. Similarly, proteinuria was comparable in the placebo and in the ACEI group for MAP < or = 100 mmHg, but was higher in the placebo group for MAP >100 mmHg. In CCB- and placebo-treated patients, a linear correlation (P = 0.006 for both groups) was found between proteinuria and MAP values. MAP, proteinuria, and deltaGFR in patients given nifedipine versus those given other dihydropyridine CCB were comparable. Thus, in nondiabetic proteinuric nephropathies, dihydropyridine CCB may have an adverse effect on renal protein handling that depends on the severity of hypertension and is minimized by ACEI therapy or tight BP control. ACE inhibitors may electively limit proteinuria in patients on dihydropyridine CCB treatment and/or with uncontrolled hypertension.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M L Krogager ◽  
R N Mortensen ◽  
P E Lund ◽  
H Boeggild ◽  
S M Hansen ◽  
...  

Abstract Aims Little is known about the occurrence of potassium disturbances in relation to combination therapy in hypertension. Using data from Danish electronic registries, we investigated the association between different combinations of antihypertensive therapy and potassium imbalances, in 22,060 individuals, between 1995–2012. Methods Using incidence density matching, two comparison patients without hypokalemia were matched to each corresponding patient with hypokalemia on age, gender, renal function, time from HTN date to date of potassium measurement. The same approach was applied to identify matches for patients with hyperkalemia. The ten most common antihypertensive drug combinations in our population were: (1) Beta-blockers + Angiotensin converting enzyme inhibitors, (2) Angiotensin converting enzyme inhibitors + Thiazides, (3) Angiotensin converting enzyme inhibitors + Thiazides + Potassium supplement, (4) Angiotensin receptor blockers + Other diuretics, (5) Beta-blockers + Angiotensin converting enzyme inhibitors + Potassium supplement (ATC: A12B), (6) Beta-blockers + Calcium channel blockers, (7) Beta-blockers + Thiazides + Potassium supplement, (8) Calcium channel blockers + Angiotensin converting enzyme inhibitors, (9) Calcium channel blockers + Thiazides + Potassium supplement, (10) Other antihypertensive drug combinations. We used conditional logistic regression analysis to examine the risk of developing hypo- and hyperkalemia in relation to different combinations of antihypertensive drugs within one year. The multivariable model was adjusted for serum sodium, malignancy, inflammatory bowel disease, diabetes, alcoholism and beta2-agonists. Results The multivariable analysis showed 10.5 times increased odds for developing hypokalemia if administered Calcium channel blockers + Thiazides + Potassium supplement (95% CI 4.97–22.06) compared to Angiotensin converting enzyme inhibitors + Beta blockers. Other drug combinations significantly associated with increased hypokalemia risk were: Angiotensin converting enzyme inhibitors + Thiazides (OR 5.01, 95% CI 2.32–10.79), Angiotensin converting enzyme inhibitors + Loop + Potassium supplement (A12B) (OR 4.03, 95% CI 1.69–9.62), Angiotensin converting enzyme inhibitors + Thiazides + Potassium supplement (OR 4.16, 95% CI 2.01–8.64) and Calcium channel blockers + Angiotensin converting enzyme inhibitors (OR 4.04, 95% CI 1.72–9.50). None of the ten groups were associated with increased odds for developing hyperkalemia in the multivariable analysis. Cumulative incidence curves for hypokale Conclusion Thiazide diuretics in combination with angiotensin converting enzyme inhibitors or calcium channel blockers were strongly associated with hypokalemia risk within one year from treatment initiation. Acknowledgement/Funding None


Sign in / Sign up

Export Citation Format

Share Document