Abstract
The aim of this study was to determine the effects of renin-angiotensin system (RAS) blockade maintenance on renal protection in chronic kidney disease (CKD) patients with hyperkalemia occurring during treatment with RAS blockade. CKD III or IV patients, who were prescribed with RAS blockers and also had hyperkalemia, were included. The study population was divided into two groups based on maintenance or withdrawal of RAS blocker. Renal outcomes (doubling of creatinine or end-stage renal disease) and incidence of hyperkalemia were compared between the two groups. Out of 258 subjects who developed hyperkalemia during treatment with RAS blockers, 150 (58.1%) patients continued on RAS blockades, while RAS blockades were discontinued for more than 3 months in the remaining 108 patients. Renal event-free survival was significantly higher in the maintenance group compared with the withdrawal group. Cox proportional hazard ratio for renal outcomes was 1.35 (95% CI: 1.08-1.92, p=0.04) in the withdrawal group compared with the maintenance group. However, the incidence of hyperkalemia and hyperkalemia-related hospitalization or mortality did not differ between the two groups. This study demonstrated that the maintenance of RAS blockade is beneficial for the preservation of renal function and relatively tolerable in patients with CKD and hyperkalemia occurring during treatment with RAS blockade.
Highlights
The renin–angiotensin system (RAS) plays an important role in the pathogenesis and progression of chronic kidney disease (CKD)
Most of the patients in the maintenance group were maintained on the previous dose of RAS blockers, and the dose of RAS blockers was reduced in 41/150 patients (27.3%)
There were no significant differences in underlying renal diseases, serum potassium levels, estimated glomerular filtration (eGFR), or urinary protein-tocreatinine ratio (UPCR) ratio at baseline between the two groups
Summary
The renin–angiotensin system (RAS) plays an important role in the pathogenesis and progression of chronic kidney disease (CKD). Numerous studies have reported that activation of the intra-renal RAS contributes to glomerular hypertrophy, mesangial expansion and glomerulosclerosis in various renal diseases.[1] Previous clinical and experimental studies have demonstrated that inhibition of the RAS using angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) results in the reduction of proteinuria and retards progression of renal disease in addition to lowering blood pressure. If the serum potassium level increases above 5.5 mmol/l during use of RAS blockade, discontinuation of RAS blockade should be considered,[11,12] with hyperkalemia managed by, for example, prescription of a Journal of the Renin-Angiotensin-Aldosterone System 15(4)
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