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• W3094119455 abstract "Treatment with angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB) is used to reduce proteinuria and retard the progression of chronic kidney disease (CKD). However, resolution of proteinuria may be incomplete with these therapies and the addition of an aldosterone antagonist may be added to further prevent progression of CKD. This is an update of a Cochrane review first published in 2009 and updated in 2014.To evaluate the effects of aldosterone antagonists (selective (eplerenone), non-selective (spironolactone or canrenone), or non-steroidal mineralocorticoid antagonists (finerenone)) in adults who have CKD with proteinuria (nephrotic and non-nephrotic range) on: patient-centred endpoints including kidney failure (previously know as end-stage kidney disease (ESKD)), major cardiovascular events, and death (any cause); kidney function (proteinuria, estimated glomerular filtration rate (eGFR), and doubling of serum creatinine); blood pressure; and adverse events (including hyperkalaemia, acute kidney injury, and gynaecomastia).We searched the Cochrane Kidney and Transplant Register of Studies up to 13 January 2020 through contact with the Information Specialist using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Register (ICTRP) Search Portal, and ClinicalTrials.gov.We included randomised controlled trials (RCTs) and quasi-RCTs that compared aldosterone antagonists in combination with ACEi or ARB (or both) to other anti-hypertensive strategies or placebo in participants with proteinuric CKD.Two authors independently assessed study quality and extracted data. Data were summarised using random effects meta-analysis. We expressed summary treatment estimates as a risk ratio (RR) for dichotomous outcomes and mean difference (MD) for continuous outcomes, or standardised mean difference (SMD) when different scales were used together with their 95% confidence interval (CI). Risk of bias were assessed using the Cochrane tool. Evidence certainty was evaluated using GRADE.Forty-four studies (5745 participants) were included. Risk of bias in the evaluated methodological domains were unclear or high risk in most studies. Adequate random sequence generation was present in 12 studies, allocation concealment in five studies, blinding of participant and investigators in 18 studies, blinding of outcome assessment in 15 studies, and complete outcome reporting in 24 studies. All studies comparing aldosterone antagonists to placebo or standard care were used in addition to an ACEi or ARB (or both). None of the studies were powered to detect differences in patient-level outcomes including kidney failure, major cardiovascular events or death. Aldosterone antagonists had uncertain effects on kidney failure (2 studies, 84 participants: RR 3.00, 95% CI 0.33 to 27.65, I² = 0%; very low certainty evidence), death (3 studies, 421 participants: RR 0.58, 95% CI 0.10 to 3.50, I² = 0%; low certainty evidence), and cardiovascular events (3 studies, 1067 participants: RR 0.95, 95% CI 0.26 to 3.56; I² = 42%; low certainty evidence) compared to placebo or standard care. Aldosterone antagonists may reduce protein excretion (14 studies, 1193 participants: SMD -0.51, 95% CI -0.82 to -0.20, I² = 82%; very low certainty evidence), eGFR (13 studies, 1165 participants, MD -3.00 mL/min/1.73 m², 95% CI -5.51 to -0.49, I² = 0%, low certainty evidence) and systolic blood pressure (14 studies, 911 participants: MD -4.98 mmHg, 95% CI -8.22 to -1.75, I² = 87%; very low certainty evidence) compared to placebo or standard care. Aldosterone antagonists probably increase the risk of hyperkalaemia (17 studies, 3001 participants: RR 2.17, 95% CI 1.47 to 3.22, I² = 0%; moderate certainty evidence), acute kidney injury (5 studies, 1446 participants: RR 2.04, 95% CI 1.05 to 3.97, I² = 0%; moderate certainty evidence), and gynaecomastia (4 studies, 281 participants: RR 5.14, 95% CI 1.14 to 23.23, I² = 0%; moderate certainty evidence) compared to placebo or standard care. Non-selective aldosterone antagonists plus ACEi or ARB had uncertain effects on protein excretion (2 studies, 139 participants: SMD -1.59, 95% CI -3.80 to 0.62, I² = 93%; very low certainty evidence) but may increase serum potassium (2 studies, 121 participants: MD 0.31 mEq/L, 95% CI 0.17 to 0.45, I² = 0%; low certainty evidence) compared to diuretics plus ACEi or ARB. Selective aldosterone antagonists may increase the risk of hyperkalaemia (2 studies, 500 participants: RR 1.62, 95% CI 0.66 to 3.95, I² = 0%; low certainty evidence) compared ACEi or ARB (or both). There were insufficient studies to perform meta-analyses for the comparison between non-selective aldosterone antagonists and calcium channel blockers, selective aldosterone antagonists plus ACEi or ARB (or both) and nitrate plus ACEi or ARB (or both), and non-steroidal mineralocorticoid antagonists and selective aldosterone antagonists.The effects of aldosterone antagonists when added to ACEi or ARB (or both) on the risks of death, major cardiovascular events, and kidney failure in people with proteinuric CKD are uncertain. Aldosterone antagonists may reduce proteinuria, eGFR, and systolic blood pressure in adults who have mild to moderate CKD but may increase the risk of hyperkalaemia, acute kidney injury and gynaecomastia when added to ACEi and/or ARB." @default.
• W3094119455 created "2020-10-29" @default.
• W3094119455 creator A5003005836 @default.
• W3094119455 creator A5018429053 @default.
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• W3094119455 creator A5088788555 @default.
• W3094119455 date "2020-10-27" @default.
• W3094119455 modified "2023-10-13" @default.
• W3094119455 title "Aldosterone antagonists in addition to renin angiotensin system antagonists for preventing the progression of chronic kidney disease" @default.
• W3094119455 cites W100402970 @default.
• W3094119455 cites W1021061058 @default.
• W3094119455 cites W1197812293 @default.
• W3094119455 cites W138298882 @default.
• W3094119455 cites W142863667 @default.
• W3094119455 cites W1491423257 @default.
• W3094119455 cites W1508407208 @default.
• W3094119455 cites W1524880665 @default.
• W3094119455 cites W1550649928 @default.
• W3094119455 cites W1652096387 @default.
• W3094119455 cites W1748340540 @default.
• W3094119455 cites W1830102405 @default.
• W3094119455 cites W1850056200 @default.
• W3094119455 cites W1930140912 @default.
• W3094119455 cites W1956799205 @default.
• W3094119455 cites W1963930171 @default.
• W3094119455 cites W1964566884 @default.
• W3094119455 cites W1965883240 @default.
• W3094119455 cites W1971680322 @default.
• W3094119455 cites W1977075739 @default.
• W3094119455 cites W1977308100 @default.
• W3094119455 cites W1985366214 @default.
• W3094119455 cites W2000060059 @default.
• W3094119455 cites W2002997638 @default.
• W3094119455 cites W2003508199 @default.
• W3094119455 cites W2009279666 @default.
• W3094119455 cites W2010799694 @default.
• W3094119455 cites W2012631324 @default.
• W3094119455 cites W2014415076 @default.
• W3094119455 cites W2017268330 @default.
• W3094119455 cites W2017884988 @default.
• W3094119455 cites W2019223575 @default.
• W3094119455 cites W2020260206 @default.
• W3094119455 cites W2020811647 @default.
• W3094119455 cites W2021988356 @default.
• W3094119455 cites W2032116194 @default.
• W3094119455 cites W2032328806 @default.
• W3094119455 cites W2034146561 @default.
• W3094119455 cites W2035810126 @default.
• W3094119455 cites W203796782 @default.
• W3094119455 cites W2039087665 @default.
• W3094119455 cites W2039893332 @default.
• W3094119455 cites W2039985181 @default.
• W3094119455 cites W2043527080 @default.
• W3094119455 cites W2044787154 @default.
• W3094119455 cites W2047610525 @default.
• W3094119455 cites W2051678468 @default.
• W3094119455 cites W2054064241 @default.
• W3094119455 cites W2056194572 @default.
• W3094119455 cites W2056385115 @default.
• W3094119455 cites W2056976690 @default.
• W3094119455 cites W2058889794 @default.
• W3094119455 cites W2061018844 @default.
• W3094119455 cites W2067121693 @default.
• W3094119455 cites W2070502107 @default.
• W3094119455 cites W2072124509 @default.
• W3094119455 cites W2073391577 @default.
• W3094119455 cites W2075429282 @default.
• W3094119455 cites W2077195725 @default.
• W3094119455 cites W2079169053 @default.
• W3094119455 cites W2080843755 @default.
• W3094119455 cites W2090015616 @default.
• W3094119455 cites W2090621492 @default.
• W3094119455 cites W2094672734 @default.
• W3094119455 cites W2104170721 @default.
• W3094119455 cites W2104209472 @default.
• W3094119455 cites W2104675861 @default.
• W3094119455 cites W2106493153 @default.
• W3094119455 cites W2106516266 @default.
• W3094119455 cites W2110007857 @default.
• W3094119455 cites W2110392728 @default.
• W3094119455 cites W2116888154 @default.
• W3094119455 cites W2118932957 @default.
• W3094119455 cites W2119958764 @default.
• W3094119455 cites W2120124567 @default.
• W3094119455 cites W2120235169 @default.
• W3094119455 cites W2120872039 @default.
• W3094119455 cites W2122084107 @default.
• W3094119455 cites W2123656765 @default.
• W3094119455 cites W2125435699 @default.
• W3094119455 cites W2128052055 @default.
• W3094119455 cites W2129313827 @default.
• W3094119455 cites W2130201362 @default.
• W3094119455 cites W2132715232 @default.
• W3094119455 cites W2133275623 @default.
• W3094119455 cites W2134928243 @default.
• W3094119455 cites W2137278841 @default.
• W3094119455 cites W2138612646 @default.

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