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Acid retention accompanies reduced GFR in humans and increases plasma levels of endothelin and aldosterone.
Am J Physiol Renal Physiol. 2011 Apr; 300(4):F830-7.AJ

Abstract

Dietary alkali slows GFR decline in humans with a moderately reduced glomerular filtration rate (GFR) despite the absence of metabolic acidosis. Similarly, dietary alkali slows GFR decline in animals with 2/3 nephrectomy (Nx), a chronic kidney disease (CKD) model without metabolic acidosis in which GFR decline is mediated by acid (H(+)) retention through endothelin (ET) and mineralocorticoid receptors. To gain insight as to whether this mechanism might mediate GFR decline in humans, we explored whether macroalbuminuric subjects with moderately reduced (CKD stage 2 = 60-90 ml/min; CKD 2) compared with normal estimated GFR (> 90 ml/min; CKD 1), each without metabolic acidosis, have H(+) retention that increases plasma levels of ET-1 and aldosterone. Baseline plasma ET and aldosterone concentrations were each higher in CKD 2 than CKD 1. Baseline dietary H(+) and urine net acid excretion (NAE) were not different between groups, but an acute oral NaHCO₃ bolus reduced urine NAE less (i.e., postbolus urine NAE was higher) in CKD 2 than CKD 1, consistent with greater H(+) retention in CKD 2 subjects. Thirty days of oral NaHCO₃ reduced H(+) retention in CKD 2 but not CKD 1 subjects and reduced plasma ET and aldosterone in both groups but to levels that remained higher in CKD 2 for each. Subjects with CKD stage 2 eGFR and no metabolic acidosis nevertheless have H(+) retention that increases plasma ET and aldosterone levels, factors that might mediate subsequent GFR decline and other untoward vascular effects.

Authors+Show Affiliations

Department of Internal Medicine, Texas A&M College of Medicine, St., Temple, TX, USA. dwesson@swmail.sw.orgNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21270096

Citation

Wesson, Donald E., et al. "Acid Retention Accompanies Reduced GFR in Humans and Increases Plasma Levels of Endothelin and Aldosterone." American Journal of Physiology. Renal Physiology, vol. 300, no. 4, 2011, pp. F830-7.
Wesson DE, Simoni J, Broglio K, et al. Acid retention accompanies reduced GFR in humans and increases plasma levels of endothelin and aldosterone. Am J Physiol Renal Physiol. 2011;300(4):F830-7.
Wesson, D. E., Simoni, J., Broglio, K., & Sheather, S. (2011). Acid retention accompanies reduced GFR in humans and increases plasma levels of endothelin and aldosterone. American Journal of Physiology. Renal Physiology, 300(4), F830-7. https://doi.org/10.1152/ajprenal.00587.2010
Wesson DE, et al. Acid Retention Accompanies Reduced GFR in Humans and Increases Plasma Levels of Endothelin and Aldosterone. Am J Physiol Renal Physiol. 2011;300(4):F830-7. PubMed PMID: 21270096.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acid retention accompanies reduced GFR in humans and increases plasma levels of endothelin and aldosterone. AU - Wesson,Donald E, AU - Simoni,Jan, AU - Broglio,Kristine, AU - Sheather,Simon, Y1 - 2011/01/26/ PY - 2011/1/29/entrez PY - 2011/1/29/pubmed PY - 2011/7/2/medline SP - F830 EP - 7 JF - American journal of physiology. Renal physiology JO - Am J Physiol Renal Physiol VL - 300 IS - 4 N2 - Dietary alkali slows GFR decline in humans with a moderately reduced glomerular filtration rate (GFR) despite the absence of metabolic acidosis. Similarly, dietary alkali slows GFR decline in animals with 2/3 nephrectomy (Nx), a chronic kidney disease (CKD) model without metabolic acidosis in which GFR decline is mediated by acid (H(+)) retention through endothelin (ET) and mineralocorticoid receptors. To gain insight as to whether this mechanism might mediate GFR decline in humans, we explored whether macroalbuminuric subjects with moderately reduced (CKD stage 2 = 60-90 ml/min; CKD 2) compared with normal estimated GFR (> 90 ml/min; CKD 1), each without metabolic acidosis, have H(+) retention that increases plasma levels of ET-1 and aldosterone. Baseline plasma ET and aldosterone concentrations were each higher in CKD 2 than CKD 1. Baseline dietary H(+) and urine net acid excretion (NAE) were not different between groups, but an acute oral NaHCO₃ bolus reduced urine NAE less (i.e., postbolus urine NAE was higher) in CKD 2 than CKD 1, consistent with greater H(+) retention in CKD 2 subjects. Thirty days of oral NaHCO₃ reduced H(+) retention in CKD 2 but not CKD 1 subjects and reduced plasma ET and aldosterone in both groups but to levels that remained higher in CKD 2 for each. Subjects with CKD stage 2 eGFR and no metabolic acidosis nevertheless have H(+) retention that increases plasma ET and aldosterone levels, factors that might mediate subsequent GFR decline and other untoward vascular effects. SN - 1522-1466 UR - https://www.unboundmedicine.com/medline/citation/21270096/Acid_retention_accompanies_reduced_GFR_in_humans_and_increases_plasma_levels_of_endothelin_and_aldosterone_ L2 - https://journals.physiology.org/doi/10.1152/ajprenal.00587.2010?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -