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Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter?
Am J Kidney Dis. 2019 06; 73(6):858-865.AJ

Abstract

Patients with chronic kidney disease (CKD) continue to produce endogenous acids but have a reduction in net acid excretion, resulting in a primary decrease in serum bicarbonate concentration, which is termed chronic metabolic acidosis. Recent prospective studies, along with retrospective cohort analyses, demonstrate a higher risk for CKD progression with untreated metabolic acidosis. To normalize serum bicarbonate levels, acidemic patients are often treated with sodium bicarbonate (NaHCO3) or sodium citrate, which have been shown to slow the progression of CKD. However, studies using this approach have routinely excluded patients with common sodium-sensitive comorbid conditions, such as poorly controlled hypertension, congestive heart failure, volume overload, or edema. This article examines the effect of the anion that accompanies sodium delivered with these therapies. Do the negative effects on blood pressure (BP) and sodium retention, as measured by an increase in edema, weight gain, and congestive heart failure, observed with oral administration of sodium chloride (NaCl) differ when a similar amount of sodium is given with bicarbonate or citrate in this patient population? A review of the literature suggests that NaHCO3 does not increase BP or sodium retention when administered to patients with CKD during a concurrent severe NaCl dietary restriction (∼10 mEq/d). However, this degree of NaCl restriction is feasible only under strict control in clinical research environments. In contrast, when NaHCO3 is given to patients without severe dietary NaCl restriction, there is an increase in BP and sodium retention. Thus, unless patients with CKD can tolerate a diet virtually devoid of NaCl, additional sodium, regardless of the accompanying anion, appears to increase BP and sodium retention.

Authors+Show Affiliations

University of Rochester School of Medicine and Dentistry, Rochester, NY. Electronic address: david_bushinsky@urmc.rochester.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

30518477

Citation

Bushinsky, David A.. "Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter?" American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation, vol. 73, no. 6, 2019, pp. 858-865.
Bushinsky DA. Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter? Am J Kidney Dis. 2019;73(6):858-865.
Bushinsky, D. A. (2019). Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter? American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation, 73(6), 858-865. https://doi.org/10.1053/j.ajkd.2018.09.004
Bushinsky DA. Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter. Am J Kidney Dis. 2019;73(6):858-865. PubMed PMID: 30518477.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter? A1 - Bushinsky,David A, Y1 - 2018/12/03/ PY - 2018/04/05/received PY - 2018/09/07/accepted PY - 2018/12/7/pubmed PY - 2020/3/12/medline PY - 2018/12/7/entrez KW - CKD progression KW - Chronic kidney disease (CKD) KW - anion KW - blood pressure KW - edema KW - metabolic acidosis KW - oral base supplementation KW - review KW - sodium KW - sodium bicarbonate KW - sodium chloride KW - sodium citrate KW - sodium retention KW - sodium-sensitive comorbidities KW - weight gain SP - 858 EP - 865 JF - American journal of kidney diseases : the official journal of the National Kidney Foundation JO - Am J Kidney Dis VL - 73 IS - 6 N2 - Patients with chronic kidney disease (CKD) continue to produce endogenous acids but have a reduction in net acid excretion, resulting in a primary decrease in serum bicarbonate concentration, which is termed chronic metabolic acidosis. Recent prospective studies, along with retrospective cohort analyses, demonstrate a higher risk for CKD progression with untreated metabolic acidosis. To normalize serum bicarbonate levels, acidemic patients are often treated with sodium bicarbonate (NaHCO3) or sodium citrate, which have been shown to slow the progression of CKD. However, studies using this approach have routinely excluded patients with common sodium-sensitive comorbid conditions, such as poorly controlled hypertension, congestive heart failure, volume overload, or edema. This article examines the effect of the anion that accompanies sodium delivered with these therapies. Do the negative effects on blood pressure (BP) and sodium retention, as measured by an increase in edema, weight gain, and congestive heart failure, observed with oral administration of sodium chloride (NaCl) differ when a similar amount of sodium is given with bicarbonate or citrate in this patient population? A review of the literature suggests that NaHCO3 does not increase BP or sodium retention when administered to patients with CKD during a concurrent severe NaCl dietary restriction (∼10 mEq/d). However, this degree of NaCl restriction is feasible only under strict control in clinical research environments. In contrast, when NaHCO3 is given to patients without severe dietary NaCl restriction, there is an increase in BP and sodium retention. Thus, unless patients with CKD can tolerate a diet virtually devoid of NaCl, additional sodium, regardless of the accompanying anion, appears to increase BP and sodium retention. SN - 1523-6838 UR - https://www.unboundmedicine.com/medline/citation/30518477/Tolerance_to_Sodium_in_Patients_With_CKD_Induced_Metabolic_Acidosis:_Does_the_Accompanying_Anion_Matter L2 - https://linkinghub.elsevier.com/retrieve/pii/S0272-6386(18)31009-6 DB - PRIME DP - Unbound Medicine ER -