ArticleJournal of nephrology2018
Acute and chronic effects of metabolic acidosis on renal function and structure.
Article in Journal of nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 15 citations in OpenAlex.
- Metabolic acidosis in anaesthesia and critical care.BJA education · 2024Review
- Metabolic Acidosis in Patients with CKD: Epidemiology, Pathogenesis, and Treatment.Kidney diseases (Basel, Switzerland) · 2021Review
- Acute acid load in chronic kidney disease increases plasma potassium, plasma aldosterone and urinary renin.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020Article
- Rutin ameliorates metabolic acidosis and fibrosis in alloxan induced diabetic nephropathy and cardiomyopathy in experimental rats.Molecular and cellular biochemistry · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEmerging evidence suggests that chronic metabolic acidosis (CMA) may have significant implications in terms of worsening renal disease in CKD patients, but the effect of CMA on renal function and structure has not been fully elucidated.
methodWe studied the acute and chronic consequences of an acid load (AL) on glomerular filtration rate (GFR) and renal histology in C57BL/6 mice. FITC-inulin clearance was performed at several time points; markers of renal fibrosis were studied at mRNA and protein levels; finally, kidney expression of candidate molecules triggering changes in renal function was studied.
resultsGlomerular hyperfiltration occurred within 1-3 days from AL; after 1 week, the GFR returned to baseline and then declined progressively within 15-21 days. The GFR decline was accompanied by the onset of renal fibrosis, as shown by Masson trichrome staining. Markers of renal fibrosis, namely α-smooth muscle actin and collagen-1, increased after 1 day of acid loading in both mRNA and protein levels and remained higher than baseline for up to 21 days. Well-known mediators of renal fibrosis, including transforming growth factor (TGF)-β and the intrarenal renin-angiotensin system (RAS) axis, were increased even before the decline of the GFR.
conclusionAcid load caused hyperfiltration acutely and a progressive decline of the GFR chronically; the evidence of renal fibrosis indicates that structural and not only functional renal changes occurred. The concomitant upregulation of TGF-β and intrarenal RAS axis indicates that those factors may be potentially involved in the progression of kidney disease in this setting.
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Registered trials
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