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Regulation of Acid-Base Balance in Chronic Kidney Disease.
Adv Chronic Kidney Dis. 2017 09; 24(5):274-279.AC

Abstract

The kidneys play a major role in the regulation of acid-base balance by reabsorbing bicarbonate filtered by the glomeruli and excreting titratable acids and ammonia into the urine. In CKD, with declining kidney function, acid retention and metabolic acidosis occur, but the extent of acid retention depends not only on the degree of kidney impairment but also on the dietary acid load. Acid retention can occur even when the serum bicarbonate level is apparently normal. With reduced kidney function, acid transport processes in the surviving nephrons are augmented but as disease progresses ammonia excretion and, in some individuals, the ability to reabsorb bicarbonate falls, whereas titratable acid excretion is preserved until kidney function is severely impaired. Urinary ammonia levels are used to gauge the renal response to acid loads and are best assessed by direct measurement of urinary ammonia levels rather than by indirect assessments. In individuals with acidosis from CKD, an inappropriately low degree of ammonia excretion points to the pathogenic role of impaired urinary acid excretion. The presence of a normal bicarbonate level in CKD complicates the interpretation of the urinary ammonia excretion as such individuals could be in acid-base balance or could be retaining acid without manifesting a low bicarbonate level. At this time, the decision to give bicarbonate supplementation in CKD is reserved for those with a bicarbonate level of 22 mEq/L, but because of potential harm of overtreatment, supplementation should be adjusted to maintain a bicarbonate level of <26 mEq/L.

Authors+Show Affiliations

Nephrology Section 111L, VA Greater Los Angeles Healthcare System, David Geffen School of Medicine at UCLA, Los Angeles, CA; and Tulane University School of Medicine, New Orleans, LA. Electronic address: Glenn.Nagami@va.gov.Nephrology Section 111L, VA Greater Los Angeles Healthcare System, David Geffen School of Medicine at UCLA, Los Angeles, CA; and Tulane University School of Medicine, New Orleans, LA.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

29031353

Citation

Nagami, Glenn T., and L Lee Hamm. "Regulation of Acid-Base Balance in Chronic Kidney Disease." Advances in Chronic Kidney Disease, vol. 24, no. 5, 2017, pp. 274-279.
Nagami GT, Hamm LL. Regulation of Acid-Base Balance in Chronic Kidney Disease. Adv Chronic Kidney Dis. 2017;24(5):274-279.
Nagami, G. T., & Hamm, L. L. (2017). Regulation of Acid-Base Balance in Chronic Kidney Disease. Advances in Chronic Kidney Disease, 24(5), 274-279. https://doi.org/10.1053/j.ackd.2017.07.004
Nagami GT, Hamm LL. Regulation of Acid-Base Balance in Chronic Kidney Disease. Adv Chronic Kidney Dis. 2017;24(5):274-279. PubMed PMID: 29031353.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of Acid-Base Balance in Chronic Kidney Disease. AU - Nagami,Glenn T, AU - Hamm,L Lee, PY - 2017/07/03/received PY - 2017/07/28/accepted PY - 2017/10/17/entrez PY - 2017/10/17/pubmed PY - 2018/6/16/medline KW - Acid-base equilibrium KW - Acidosis KW - Ammonia metabolism KW - Bicarbonates KW - Renal insufficiency SP - 274 EP - 279 JF - Advances in chronic kidney disease JO - Adv Chronic Kidney Dis VL - 24 IS - 5 N2 - The kidneys play a major role in the regulation of acid-base balance by reabsorbing bicarbonate filtered by the glomeruli and excreting titratable acids and ammonia into the urine. In CKD, with declining kidney function, acid retention and metabolic acidosis occur, but the extent of acid retention depends not only on the degree of kidney impairment but also on the dietary acid load. Acid retention can occur even when the serum bicarbonate level is apparently normal. With reduced kidney function, acid transport processes in the surviving nephrons are augmented but as disease progresses ammonia excretion and, in some individuals, the ability to reabsorb bicarbonate falls, whereas titratable acid excretion is preserved until kidney function is severely impaired. Urinary ammonia levels are used to gauge the renal response to acid loads and are best assessed by direct measurement of urinary ammonia levels rather than by indirect assessments. In individuals with acidosis from CKD, an inappropriately low degree of ammonia excretion points to the pathogenic role of impaired urinary acid excretion. The presence of a normal bicarbonate level in CKD complicates the interpretation of the urinary ammonia excretion as such individuals could be in acid-base balance or could be retaining acid without manifesting a low bicarbonate level. At this time, the decision to give bicarbonate supplementation in CKD is reserved for those with a bicarbonate level of 22 mEq/L, but because of potential harm of overtreatment, supplementation should be adjusted to maintain a bicarbonate level of <26 mEq/L. SN - 1548-5609 UR - https://www.unboundmedicine.com/medline/citation/29031353/Regulation_of_Acid_Base_Balance_in_Chronic_Kidney_Disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1548-5595(17)30121-0 DB - PRIME DP - Unbound Medicine ER -