Pascale Khairallah1, Julia J Scialla2,3. 1. Department of Medicine, Duke University School of Medicine, Durham, NC, USA. 2. Duke Clinical Research Institute, Duke University School of Medicine, Durham, NC, USA. Julia.scialla@duke.edu. 3. Department of Medicine, Durham Veterans Affairs Medical Center, Durham, NC, USA. Julia.scialla@duke.edu.
Abstract
PURPOSE OF REVIEW: Acid-base homeostasis is impaired in chronic kidney disease (CKD) and may contribute to disease progression. Diabetes, a major cause of CKD worldwide, may exacerbate acidosis further due to differences in acid production and excretion. Here, we review the role of abnormal acid-base homeostasis in the pathogenesis and progression of diabetes and diabetic kidney disease. RECENT FINDINGS: Acidosis and dietary acid loading may contribute to the development and worsening of insulin resistance and hypertension, thereby promoting diabetes and diabetic CKD. However, although metabolic acidosis associates with progression of CKD generally, the results in diabetic CKD are mixed. Data suggests that metabolic acid production in diabetes may be higher than would be predicted based on dietary intake alone, and new observational data suggests that this higher diet-independent acid production could potentially be protective. The role of acid-base homeostasis in diabetic CKD progression is complex and must consider differences in endogenous acid production and excretion in diabetes. Ongoing observational and interventional studies in this field should consider the unique physiology of diabetes.
PURPOSE OF REVIEW: Acid-base homeostasis is impaired in chronic kidney disease (CKD) and may contribute to disease progression. Diabetes, a major cause of CKD worldwide, may exacerbate acidosis further due to differences in acid production and excretion. Here, we review the role of abnormal acid-base homeostasis in the pathogenesis and progression of diabetes and diabetic kidney disease. RECENT FINDINGS:Acidosis and dietary acid loading may contribute to the development and worsening of insulin resistance and hypertension, thereby promoting diabetes and diabetic CKD. However, although metabolic acidosis associates with progression of CKD generally, the results in diabetic CKD are mixed. Data suggests that metabolic acid production in diabetes may be higher than would be predicted based on dietary intake alone, and new observational data suggests that this higher diet-independent acid production could potentially be protective. The role of acid-base homeostasis in diabetic CKD progression is complex and must consider differences in endogenous acid production and excretion in diabetes. Ongoing observational and interventional studies in this field should consider the unique physiology of diabetes.
Authors: Jessica C Kiefte-de Jong; Yanping Li; Mu Chen; Gary C Curhan; Josiemer Mattei; Vasanti S Malik; John P Forman; Oscar H Franco; Frank B Hu Journal: Diabetologia Date: 2016-11-17 Impact factor: 10.122
Authors: Julia J Scialla; Landon Brown; Susan Gurley; David L Corcoran; James R Bain; Michael J Muehlbauer; Sara K O'Neal; Thomas M O'Connell; Myles Wolf; Michal L Melamed; Thomas H Hostetter; Matthew K Abramowitz Journal: Clin J Am Soc Nephrol Date: 2018-06-22 Impact factor: 8.237
Authors: Landon Brown; Alison Luciano; Jane Pendergast; Pascale Khairallah; Cheryl A M Anderson; James Sondheimer; L Lee Hamm; Ana C Ricardo; Panduranga Rao; Mahboob Rahman; Edgar R Miller; Daohang Sha; Dawei Xie; Harold I Feldman; John Asplin; Myles Wolf; Julia J Scialla Journal: Am J Kidney Dis Date: 2019-03-22 Impact factor: 8.860