2026-06-25T02:47:50Z https://repub.eur.nl/oai

oai:repub.eur.nl:133062 2023-11-26T18:51:45Z

urn:NBN:nl:ui:15-1765/133062 2023-11-26T18:51:45 mods http://hdl.handle.net/1765/133062 hdl:1765/133062 urn:NBN:nl:ui:15-1765/133062 doi:10.1007/s40620-020-00944-5 http://hdl.handle.net/1765/133062 https://repub.eur.nl/pub/133062/Repub_133062_O-A.pdf application/pdf Filesize: 1084764 bytes born digital D.M. Bovée (Dominique) Bovée Dominique aut author L.C.W. Roksnoer (Lodi) Roksnoer Lodi aut author C. van Kooten (Cees) Kooten Cees aut author J.I. Rotmans (Joris) Rotmans Joris aut author L. Vogt (Liffert) Vogt Liffert aut author de Borst, M.H. (Martin H.) de Borst M.H. (Martin H.) aut author R. Zietse (Bob) Zietse Bob aut author A.H.J. Danser (Jan) Danser Jan aut author E.J. Hoorn (Ewout) Hoorn Ewout aut author Background: Acidosis-induced kidney injury is mediated by the intrarenal renin-angiotensin system, for which urinary renin is a potential marker. Therefore, we hypothesized that sodium bicarbonate supplementation reduces urinary renin excretion in patients with chronic kidney disease (CKD) and metabolic acidosis. Methods: Patients with CKD stage G4 and plasma bicarbonate 15–24 mmol/l were randomized to receive sodium bicarbonate (3 × 1000 mg/day, ~ 0.5 mEq/kg), sodium chloride (2 × 1,00 mg/day), or no treatment for 4 weeks (n = 15/arm). The effects on urinary renin excretion (primary outcome), other plasma and urine parameters of the renin-angiotensin system, endothelin-1, and proteinuria were analyzed. Results: Forty-five patients were included (62 ± 15 years, eGFR 21 ± 5 ml/min/1.73m2, plasma bicarbonate 21.7 ± 3.3 mmol/l). Sodium bicarbonate supplementation increased plasma bicarbonate (20.8 to 23.8 mmol/l) and reduced urinary ammonium excretion (15 to 8 mmol/day, both P < 0.05). Furthermore, a trend towards lower plasma aldosterone (291 to 204 ng/L, P = 0.07) and potassium (5.1 to 4.8 mmol/l, P = 0.06) was observed in patients receiving sodium bicarbonate. Sodium bicarbonate did not significantly change the urinary excretion of renin, angiotensinogen, aldosterone, endothelin-1, albumin, or α1-microglobulin. Sodium chloride supplementation reduced plasma renin (166 to 122 ng/L), and increased the urinary excretions of angiotensinogen, albumin, and α1-microglobulin (all P < 0.05). Conclusions: Despite correction of acidosis and reduction in urinary ammonium excretion, sodium bicarbonate supplementation did not improve urinary markers of the renin-angiotensin system, endothelin-1, or proteinuria. Possible explanations include bicarbonate dose, short treatment time, or the inability of urinary renin to reflect intrarenal renin-angiotensin system activity. Graphic abstract: [Figure not available: see fulltext.] Journal of Nephrology 21365 11218428 2020-12-31 en English Aldosterone Clinical trial Proteinuria Renin Effect of sodium bicarbonate supplementation on the renin-angiotensin system in patients with chronic kidney disease and acidosis: a randomized clinical trial text info:eu-repo/semantics/article 13654956X 093068468 http://purl.org/eprint/accessRights/OpenAccess