Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney Disease
| Autor: | Jerry M. Buysse, Donald E. Wesson, David A. Bushinsky |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Renal function Risk Assessment Severity of Illness Index chemistry.chemical_compound Fibrosis Internal medicine Up Front Matters medicine Humans Prospective Studies Renal Insufficiency Chronic Aldosterone Retrospective Studies Acid-Base Equilibrium Kidney Endothelin-1 business.industry Angiotensin II Chronic metabolic acidosis Metabolic acidosis General Medicine medicine.disease Adaptation Physiological Endocrinology medicine.anatomical_structure Treatment Outcome chemistry Nephrology Disease Progression Kidney Failure Chronic Female business Acidosis Biomarkers Kidney disease Follow-Up Studies Glomerular Filtration Rate |
| Zdroj: | J Am Soc Nephrol |
| ISSN: | 1533-3450 |
| Popis: | Retrospective analyses and single-center prospective studies identify chronic metabolic acidosis as an independent and modifiable risk factor for progression of CKD. In patients with CKD, untreated chronic metabolic acidosis often leads to an accelerated reduction in GFR. Mechanisms responsible for this reduction include adaptive responses that increase acid excretion but lead to a decline in kidney function. Metabolic acidosis in CKD stimulates production of intrakidney paracrine hormones including angiotensin II, aldosterone, and endothelin-1 (ET-1) that mediate the immediate benefit of increased kidney acid excretion, but their chronic upregulation promotes inflammation and fibrosis. Chronic metabolic acidosis also stimulates ammoniagenesis that increases acid excretion but also leads to ammonia-induced complement activation and deposition of C3 and C5b-9 that can cause tubule-interstitial damage, further worsening disease progression. These effects, along with acid accumulation in kidney tissue, combine to accelerate progression of kidney disease. Treatment of chronic metabolic acidosis attenuates these adaptive responses; reduces levels of angiotensin II, aldosterone, and ET-1; reduces ammoniagenesis; and diminishes inflammation and fibrosis that may lead to slowing of CKD progression. |
| Databáze: | OpenAIRE |
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