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Article: Direct Renin Inhibition in Non-diabetic chronic Kidney disease (DRINK): a prospective randomized trial

TitleDirect Renin Inhibition in Non-diabetic chronic Kidney disease (DRINK): a prospective randomized trial
Authors
Keywordschronic renal disease
outcomes
renin inhibitor
Issue Date2021
PublisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/
Citation
Nephrology Dialysis Transplantation, 2021, v. 36 n. 9, p. 1648–1656 How to Cite?
AbstractBackground: The potential long-term safety and efficacy of aliskiren in nondiabetic chronic kidney disease (CKD) are unknown. We sought to investigate the renoprotective effect of aliskiren on nondiabetic CKD patients. Methods: In this open-label, parallel, randomized controlled trial, nondiabetic CKD Stages 3–4 patients were randomized to receive aliskiren added to an angiotensin II receptor blocker (ARB) at the maximal tolerated dose, or ARB alone. Primary outcome was the rate of change in estimated glomerular filtration rate (eGFR). Secondary endpoints included rate of change in urine protein-to-creatinine ratio (UPCR), cardiovascular events and hyperkalemia. Composite renal outcomes of doubling of baseline serum creatinine or a 40% reduction in eGFR or incident end-stage renal disease or death were analyzed as post hoc analysis. Results: Seventy-six patients were randomized: 37 to aliskiren (mean age 55.1 ± 11.1 years) and 39 to control (mean age 55.0 ± 9.4 years). Their baseline demographics were comparable to eGFR (31.9 ± 9.0 versus 27.7 ± 9.0 mL/min/1.73 m2, P = 0.05) and UPCR (30.7 ± 12.6 versus 47.8 ± 2.8 mg/mmol, P = 0.33) for treatment versus control subjects. After 144 weeks of follow-up, there was no difference in the rate of eGFR change between groups. Six patients in the aliskiren group and seven in the control group reached the renal composite endpoint (16.2% versus 17.9%, P = 0.84). The cardiovascular event rate was 10.8% versus 2.6% (P = 0.217). The hyperkalemia rate was 18.9% versus 5.1% with an adjusted hazard ratio of 7.71 (95% confidence interval 1.14 to 52.3, P = 0.04) for the aliskiren arm. Conclusion: Aliskiren neither conferred additional renoprotective benefit nor increased adverse events, except for more hyperkalemia in nondiabetic CKD patients.
Persistent Identifierhttp://hdl.handle.net/10722/283982
ISSN
2023 Impact Factor: 4.8
2023 SCImago Journal Rankings: 1.414
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTang, SCW-
dc.contributor.authorChan, KW-
dc.contributor.authorIp, DKM-
dc.contributor.authorYap, DYH-
dc.contributor.authorMa, MKM-
dc.contributor.authorMok, MMY-
dc.contributor.authorChan, GCW-
dc.contributor.authorTam, S-
dc.contributor.authorLai, KN-
dc.date.accessioned2020-07-20T05:55:05Z-
dc.date.available2020-07-20T05:55:05Z-
dc.date.issued2021-
dc.identifier.citationNephrology Dialysis Transplantation, 2021, v. 36 n. 9, p. 1648–1656-
dc.identifier.issn0931-0509-
dc.identifier.urihttp://hdl.handle.net/10722/283982-
dc.description.abstractBackground: The potential long-term safety and efficacy of aliskiren in nondiabetic chronic kidney disease (CKD) are unknown. We sought to investigate the renoprotective effect of aliskiren on nondiabetic CKD patients. Methods: In this open-label, parallel, randomized controlled trial, nondiabetic CKD Stages 3–4 patients were randomized to receive aliskiren added to an angiotensin II receptor blocker (ARB) at the maximal tolerated dose, or ARB alone. Primary outcome was the rate of change in estimated glomerular filtration rate (eGFR). Secondary endpoints included rate of change in urine protein-to-creatinine ratio (UPCR), cardiovascular events and hyperkalemia. Composite renal outcomes of doubling of baseline serum creatinine or a 40% reduction in eGFR or incident end-stage renal disease or death were analyzed as post hoc analysis. Results: Seventy-six patients were randomized: 37 to aliskiren (mean age 55.1 ± 11.1 years) and 39 to control (mean age 55.0 ± 9.4 years). Their baseline demographics were comparable to eGFR (31.9 ± 9.0 versus 27.7 ± 9.0 mL/min/1.73 m2, P = 0.05) and UPCR (30.7 ± 12.6 versus 47.8 ± 2.8 mg/mmol, P = 0.33) for treatment versus control subjects. After 144 weeks of follow-up, there was no difference in the rate of eGFR change between groups. Six patients in the aliskiren group and seven in the control group reached the renal composite endpoint (16.2% versus 17.9%, P = 0.84). The cardiovascular event rate was 10.8% versus 2.6% (P = 0.217). The hyperkalemia rate was 18.9% versus 5.1% with an adjusted hazard ratio of 7.71 (95% confidence interval 1.14 to 52.3, P = 0.04) for the aliskiren arm. Conclusion: Aliskiren neither conferred additional renoprotective benefit nor increased adverse events, except for more hyperkalemia in nondiabetic CKD patients.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/-
dc.relation.ispartofNephrology Dialysis Transplantation-
dc.rightsThis is a pre-copy-editing, author-produced PDF of an article accepted for publication in Nephrology Dialysis Transplantation following peer review. The definitive publisher-authenticated version Nephrology Dialysis Transplantation, 2021, v. 36 n. 9, p. 1648–1656 is available online at: https://academic.oup.com/ndt/article-abstract/36/9/1648/5866683?redirectedFrom=fulltext-
dc.subjectchronic renal disease-
dc.subjectoutcomes-
dc.subjectrenin inhibitor-
dc.titleDirect Renin Inhibition in Non-diabetic chronic Kidney disease (DRINK): a prospective randomized trial-
dc.typeArticle-
dc.identifier.emailTang, SCW: scwtang@hku.hk-
dc.identifier.emailChan, KW: chriskwc@hku.hk-
dc.identifier.emailIp, DKM: dkmip@hku.hk-
dc.identifier.emailYap, DYH: desmondy@hku.hk-
dc.identifier.emailMa, MKM: h9914584@graduate.hku.hk-
dc.identifier.emailMok, MMY: mmymok@hku.hk-
dc.identifier.emailChan, GCW: gcwchan1@hku.hk-
dc.identifier.emailTam, S: stam@hkucc.hku.hk-
dc.identifier.emailLai, KN: knlai@hku.hk-
dc.identifier.authorityTang, SCW=rp00480-
dc.identifier.authorityIp, DKM=rp00256-
dc.identifier.authorityYap, DYH=rp01607-
dc.identifier.authorityLai, KN=rp00324-
dc.description.naturepostprint-
dc.identifier.doi10.1093/ndt/gfaa085-
dc.identifier.scopuseid_2-s2.0-85115440534-
dc.identifier.hkuros310828-
dc.identifier.volume36-
dc.identifier.issue9-
dc.identifier.spage1648-
dc.identifier.epage1656-
dc.identifier.isiWOS:000715360600014-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl0931-0509-

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