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Managing cardiovascular risk in people with chronic kidney disease: a review of the evidence from randomized controlled trials.

ABSTRACT: Cardiovascular disease is the leading cause of death and morbidity in people with chronic kidney disease (CKD) making measures to modify cardiovascular risk a clinical priority. The relationship between risk factors and cardiovascular outcomes is often substantially different in people with CKD compared with the general population, leading to uncertainty around pathophysiological mechanisms and the validity of generalizations from the general population. Furthermore, published reports of subgroup analyses from clinical trials have suggested that a range of interventions may have different effects in people with kidney disease compared with those with normal kidney function. There is a relative scarcity of randomized controlled trials (RCTs) conducted in CKD populations, and most such trials are small and underpowered. As a result, evidence to support cardiovascular risk modification measures for people with CKD is largely derived from small trials and post hoc analyses of RCTs conducted in the general population. In this review, we examine the available RCT evidence on interventions aimed at preventing cardiovascular events in people with kidney disease to identify beneficial treatments as well as current gaps in knowledge that should be a priority for future research.

SUBMITTER: Jun M

PROVIDER: S-EPMC3513885 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature

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Managing cardiovascular risk in people with chronic kidney disease: a review of the evidence from randomized controlled trials.

Jun Min M Lv Jicheng J Perkovic Vlado V Jardine Meg J MJ

Therapeutic advances in chronic disease 20110701 4

Cardiovascular disease is the leading cause of death and morbidity in people with chronic kidney disease (CKD) making measures to modify cardiovascular risk a clinical priority. The relationship between risk factors and cardiovascular outcomes is often substantially different in people with CKD compared with the general population, leading to uncertainty around pathophysiological mechanisms and the validity of generalizations from the general population. Furthermore, published reports of subgrou ...[more]

PMID: 23251754

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Project description:ObjectiveTo define the cardiovascular effects of lowering blood pressure in people with chronic kidney disease.DesignCollaborative prospective meta-analysis of randomised trials.Data sources and eligibilityParticipating randomised trials of drugs to lower blood pressure compared with placebo or each other or that compare different blood pressure targets, with at least 1000 patient years of follow-up per arm.Main outcome measuresMajor cardiovascular events (stroke, myocardial infarction, heart failure, or cardiovascular death) in composite and individually and all cause death.Participants26 trials (152,290 participants), including 30,295 individuals with reduced estimated glomerular filtration rate (eGFR), which was defined as eGFR <60 mL/min/1.73 m(2).Data extractionIndividual participant data were available for 23 trials, with summary data from another three. Meta-analysis according to baseline kidney function was performed. Pooled hazard ratios per 5 mm Hg lower blood pressure were estimated with a random effects model.ResultsCompared with placebo, blood pressure lowering regimens reduced the risk of major cardiovascular events by about a sixth per 5 mm Hg reduction in systolic blood pressure in individuals with (hazard ratio 0.83, 95% confidence interval 0.76 to 0.90) and without reduced eGFR (0.83, 0.79 to 0.88), with no evidence for any difference in effect (P=1.00 for homogeneity). The results were similar irrespective of whether blood pressure was reduced by regimens based on angiotensin converting enzyme inhibitors, calcium antagonists, or diuretics/β blockers. There was no evidence that the effects of different drug classes on major cardiovascular events varied between patients with different eGFR (all P>0.60 for homogeneity).ConclusionsBlood pressure lowering is an effective strategy for preventing cardiovascular events among people with moderately reduced eGFR. There is little evidence from these overviews to support the preferential choice of particular drug classes for the prevention of cardiovascular events in chronic kidney disease.

Project description:BackgroundDiverticular disease treatment is limited to fibres, antibiotics, and surgery. There is conflicting evidence on mesalazine benefits and harms.AimWe systematically reviewed current evidence on benefits and harms of mesalazine versus all other treatments in people with diverticular disease.MethodsWe searched MEDLINE, EMBASE, CENTRAL, ClinicalTrials.gov for studies published to July 2018. We estimated risk ratios (RR) for dichotomous outcomes (disease remission/recurrence, acute diverticulitis in symptomatic uncomplicated diverticular disease, need for surgery/hospitalization, all-cause/disease-related mortality, adverse events), mean differences (MD) or standardized MD (SMD) for continuous outcomes (quality of life, symptoms score, time to recurrence/remission), and their 95% confidence intervals (CI) using random-effects models. We quantified heterogeneity by Chi2 and I2 tests. We performed subgroup analyses by disease subtype, comparator, follow-up duration, mesalazine dose, and mode of administration.ResultsWe identified 13 randomized trials (n=3028 participants). There was a higher likelihood of disease remission with mesalazine than controls in acute uncomplicated diverticulitis (1 trial, 81 participants, RR=2.67, 95%CI=1.05-6.79), but not in symptomatic uncomplicated diverticular disease (1 trial, 123 participants, RR=1.04, 95%CI=0.81-1.34). There was a lower likelihood of disease recurrence with mesalazine than controls in symptomatic uncomplicated diverticular disease (2 trials, 216 participants, RR=0.52, 95%CI=0.28-0.97), but not in acute uncomplicated diverticulitis (7 trials, 2196 participants, RR=0.90, 95%CI=0.61-1.33). There was no difference in the likelihood of developing acute diverticulitis in symptomatic uncomplicated diverticular disease between the two groups (3 trials, 484 participants, RR=0.26, 95%CI=0.06-1.20). There was a higher global symptoms score reduction with mesalazine than controls in symptomatic uncomplicated diverticular disease (2 trials, 326 participants, SMD=-1.01, 95%CI=-1.51,-0.52) and acute uncomplicated diverticulitis (2 trials, 153 participants, SMD=-0.56, 95%CI=-0.88,-0.24).ConclusionsMesalazine may reduce recurrences in symptomatic uncomplicated diverticular disease. There is uncertainty on the effect of mesalazine in achieving diverticular disease remission. Mesalazine may not prevent acute diverticulitis in symptomatic uncomplicated diverticular disease.

Project description:ObjectiveGut flora imbalance characterizes patients with chronic kidney disease (CKD). Although biotic supplementation has been proposed to lessen inflammation and oxidative stress and, thus, reduce the risk of progressive kidney damage and cardiovascular disease, the effects remain controversial. We conducted a meta-analysis to assess the therapeutic benefits of biotics in CKD.MethodsPubMed, Embase, and Cochrane databases were systematically searched for randomized controlled trials that evaluated any biotic (prebiotic, probiotic, synbiotics) supplements in patients with CKD (CKD, stage 3-4 to end-stage renal disease). Primary endpoints included changes in renal function, markers of inflammation, and oxidative stress. Secondary endpoints included changes in levels of uremic toxins and variations in lipid metabolism.ResultsTwenty-three eligible studies included 842 participants. In a pooled-analysis, biotics did not change estimated glomerular filtration rate (mean difference [MD] = 0.08, P = .92) or serum albumin (MD = -0.01, P = .86), although prebiotics reduced serum creatinine (standardized mean difference [SMD] = -0.23, P = .009) and blood urea nitrogen (MD = -6.05, P < .00001). Biotics improved total antioxidative capacity (SMD = 0.37, P = .007) and malondialdehyde (SMD = -0.96, P = .006) and reduced the inflammatory marker interleukin-6 (SMD = -0.30, P = .01) although not C-reactive protein (SMD = -0.22, P = .20). Biotic intervention reduced some uremic toxins, including p-cresol sulfate (SMD = -2.18, P < .0001) and indoxyl sulfate (MD = -5.14, P = .0009), which decreased in dialysis-dependent patients. Another toxin, indole-3-acetic acid (MD = -0.22, P = .63), did not change. Lipids were unaffected by biotic intervention (total cholesterol: SMD = -0.01, P = .89; high-density lipoprotein: SMD = -0.08, P = .76; low-density lipoprotein: MD = 3.54, P = .28; triglyceride: MD = -2.26, P = .58).ConclusionThe results highlight the favorable influence of biotics on circulating markers of creatinine, oxidant stress (malondialdehyde, total antioxidative capacity), inflammation (interleukin-6), and uremic toxins (p-cresol sulfate) in patients with CKD. Biotics did not affect estimated glomerular filtration rate, albumin, indole-3-acetic acid, or lipids in either predialysis or dialysis patients.

Project description:BackgroundChronic pain and depression are common comorbid conditions, but there is limited evidence-based guidance for management of the two conditions together. In recent years, there has been an increase in the number of chronic pain randomized controlled trials that collect depression outcomes, but it is unknown how often these trials include people with depression or significant depressive symptoms. If trials do not include participants representative of real-world populations, evidence and guidance generated from these trials risk being inapplicable for large proportions of the target population, or worse, risk harm. Thus, in order to identify pathways to improve the conduct of clinical trials, the aims of this study were to (1) estimate the proportion of randomized controlled trials evaluating chronic pain interventions and reporting depression outcomes that include participants with significant depressive symptoms; and (2) assess the variability of inclusion proportions by pain type, intervention type, gender, country of origin, and publication year.MethodsStudies were extracted from an umbrella review of interventions for chronic pain that reported depression outcomes. Screening and data extraction were completed in duplicate and conflicts were resolved by a third author. Randomized controlled trials with at least 50% adult participants and validated depression scales were included, and randomized controlled trials with populations whose mean scores were at or above depression thresholds at baseline were considered to have included participants with depression.ResultsOf the 346 randomized controlled trials analyzed, 142 (41%) included participants with depression. Eight pain-type groups and nine intervention types were identified. Randomized controlled trials investigating fibromyalgia and mixed chronic pain had the highest proportion of participants with depression, whereas studies of arthritis and axial pain had among the lowest. Randomized controlled trials from the United States had a significantly lower inclusion proportion compared with non-US studies, especially for studies on arthritis. The increase in inclusion proportion by publication year was driven by the increase in fibromyalgia studies.Discussion and conclusionThis study highlights opportunities to improve the conduct of chronic pain clinical trials. The majority of randomized controlled trials s analyzed evaluated participants without significant depressive symptoms at baseline, thus the findings synthesized in systematic reviews and subsequent guidelines are most applicable to the subset of real-world populations that do not have significant depressive symptoms. As well, systemic biases around psychological conditions and gender may be important contributors to differences in the study of depression in fibromyalgia compared with common conditions such as arthritis and axial pain. In order to better inform clinical practice, future research must intentionally include individuals with comorbid depression in trials of common chronic pain conditions, and consider methods to mitigate biases that may distort study design.

Project description:ObjectiveThis systematic review aims to investigate the efficacy and safety of moxibustion for chronic kidney disease (CKD).MethodsNine databases were searched to identify relevant evidence up to March 8, 2020. Randomized controlled trials (RCTs) that tested moxibustion + basic treatments versus basic treatments alone for patients with CKD and reported, at least, one of the outcomes of interest were included. In the meta-analyses, the mean differences (MDs) and 95% confidence intervals (CIs) were used to measure the effect size.ResultsTwenty-three RCTs (n = 1571) with a moderate to high risk of bias were included. The pooled estimates showed that compared with the controls, patients after moxibustion had a significant reduction in serum creatinine (MD -17.34 μmol/L, 95% CI -28.44 to -6.23; I 2 = 87%), 24-hour urine protein excretion (MD -0.75 g/h, 95% CI -1.07 to -0.42; I 2 = 84%), and blood urea nitrogen (MD -0.63 mmol/L, 95% CI -1.09 to -0.18; I 2 = 37%) and a significant improvement in the quality of life (MD 10.18, 95% CI 3.67 to 16.69; I 2 = 57%). Moxibustion did not show a significant effect on the estimated glomerular filtration rate (eGFR), creatinine clearance, or hemoglobin. The subgroup analyses showed that a longer course of moxibustion (>8 weeks) and indirect moxibustion had a greater effect on reducing serum creatinine. The effect of moxibustion on blood urea nitrogen changed to be nonsignificant after excluding RCTs with a high risk of bias (MD -0.96 mmol/L, 95% CI -2.96 to 1.03). Only one adverse event of burn was reported.ConclusionsThis systematic review suggests that, as an adjuvant therapy, moxibustion may improve serum creatinine, urinary protein excretion, blood urea nitrogen, and quality of life in patients with CKD. Moxibustion may not have effects on eGFR, creatinine clearance, or hemoglobin. The quality of evidence is weakened by the limitations of risk of bias, heterogeneity, and imprecision.

Project description:Vitamin D receptor agonists (VDRAs) are commonly prescribed in chronic kidney disease (CKD). However, their protective effects on bone remain controversial. We performed a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the effect of VDRAs on fracture risk and bone mineral density (BMD) in adult patients with CKD. We searched MEDLINE, EMBASE, CENTRAL, ClinicalTrials.gov, and the WHO's International Clinical Trials Registry Platform databases from inception to June 19, 2021. We included RCTs comparing VDRAs, to placebo or another medication, in adults with CKD requiring or not dialysis. Conference abstracts and trials involving kidney transplant recipients and/or comparing VDRAs to antiresorptive or anabolic bone therapy were excluded. Primary outcome was fracture at any anatomical site. Secondary outcomes were BMD at femoral neck, lumbar spine, and/or total hip. Prespecified subgroup analyses were conducted according to baseline demographics, overall risk of bias, and follow-up time. From 6868 references retrieved, eight RCTs were eligible: five reported fracture, two reported BMD, and one reported both outcomes. As comparator, one study used no VDRAs, one used nutritional intervention and no medication, and six used placebo. In meta-analysis, VDRAs were not associated with a significant reduction in total fractures in overall (risk ratio = 0.79, 95% confidence interval 0.38-1.65, I2 = 0%, six trials, 1507 participants, 27 fractures) or in prespecified subgroup analyses. Three trials reported BMD at different sites and with different BMD measurements; thus, a meta-analysis could not be performed. Two RCTs were at high risk of bias, notably because of deviations from the intended interventions. As limitation, we have to mention the low total number of fractures included in our meta-analysis. In conclusion, current evidence from RCTs is insufficient to associate VDRAs with bone protection in CKD. Further large and long-term studies specifically designed to evaluate the efficacy of VDRAs on bone outcomes are thus required. © 2022 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

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Managing cardiovascular risk in people with chronic kidney disease: a review of the evidence from randomized controlled trials.

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Managing cardiovascular risk in people with chronic kidney disease: a review of the evidence from randomized controlled trials.

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