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Chronic metabolic acidosis commonly occurs in people with Chronic Kidney Disease with an eGFR of less than 45 ml/min/1.73m<sup>2</sup>, most often with mild to moderate severity; however, metabolic acidosis can manifest earlier on in the course of Chronic Kidney Disease. Multiple animal and human studies have shown that metabolic acidosis in Chronic Kidney Disease, given its chronic nature, has a profound adverse impact on cellular function, overall contributing to high morbidities in patients.
The most adverse consequences of chronic metabolic acidosis in people with Chronic Kidney Disease and in particular, for those who have [[Kidney failure|end-stage renal disease (ESRD)]], are detrimental changes to the bones and muscles.<ref name=":1">{{Cite journal|last1=Kraut|first1=Jeffrey A.|last2=Madias|first2=Nicolaos E.|title=Adverse Effects of the Metabolic Acidosis of Chronic Kidney Disease|journal=Advances in Chronic Kidney Disease|language=en|volume=24|issue=5|pages=289–297|doi=10.1053/j.ackd.2017.06.005|pmid=29031355|year=2017}}</ref> Acid buffering leads to loss of bone density, resulting in an increased risk of bone fractures,<ref>{{Cite journal|last1=Kato|first1=Akihiko|last2=Kido|first2=Ryo|last3=Onishi|first3=Yoshihiro|last4=Kurita|first4=Noriaki|last5=Fukagawa|first5=Masafumi|last6=Akizawa|first6=Tadao|last7=Fukuhara|first7=Shunichi|date=2014|title=Association of serum bicarbonate with bone fractures in hemodialysis patients: the mineral and bone disorder outcomes study for Japanese CKD stage 5D patients (MBD-5D)|journal=Nephron Clinical Practice|volume=128|issue=1–2|pages=79–87|doi=10.1159/000365089|issn=1660-2110|pmid=25378374|s2cid=20320396}}</ref> renal osteodystrophy,<ref>{{Cite journal|last1=Lefebvre|first1=A.|last2=de Vernejoul|first2=M. C.|last3=Gueris|first3=J.|last4=Goldfarb|first4=B.|last5=Graulet|first5=A. M.|last6=Morieux|first6=C.|title=Optimal correction of acidosis changes progression of dialysis osteodystrophy|journal=Kidney International|volume=36|issue=6|pages=1112–1118|doi=10.1038/ki.1989.309|issn=0085-2538|pmid=2557481|year=1989}}</ref> and bone disease;<ref name=":1" /> as well, increased protein catabolism leads to muscle wasting.<ref>{{Cite journal|last1=Hanna|first1=Ramy M.|last2=Ghobry|first2=Lena|last3=Wassef|first3=Olivia|last4=Rhee|first4=Connie M.|last5=Kalantar-Zadeh|first5=Kamyar|title=A Practical Approach to Nutrition, Protein-Energy Wasting, Sarcopenia, and Cachexia in Patients with Chronic Kidney Disease|journal=Blood Purification|volume=49|issue=1–2|language=english|pages=202–211|doi=10.1159/000504240|issn=0253-5068|pmid=31851983|year=2020|s2cid=209418220|doi-access=free}}</ref><ref>{{Cite journal|last1=Foley|first1=Robert N.|last2=Wang|first2=Changchun|last3=Ishani|first3=Areef|last4=Collins|first4=Allan J.|last5=Murray|first5=Anne M.|date=2007|title=Kidney Function and Sarcopenia in the United States General Population: NHANES III|journal=American Journal of Nephrology|language=english|volume=27|issue=3|pages=279–286|doi=10.1159/000101827|issn=0250-8095|pmid=17440263|s2cid=2847009}}</ref> Furthermore, metabolic acidosis in Chronic Kidney Disease is also associated with a reduction in [[Renal function|eGFR]]; it is both a complication of Chronic Kidney Disease, as well as an underlying cause of Chronic Kidney Disease progression.<ref>{{Cite journal|last1=Shah|first1=Samir N.|last2=Abramowitz|first2=Matthew|last3=Hostetter|first3=Thomas H.|last4=Melamed|first4=Michal L.|date=2009-08-01|title=Serum bicarbonate levels and the progression of kidney disease: a cohort study|url=https://www.ncbi.nlm.nih.gov/pubmed/?term=shah+Serum+Bicarbonate+Levels+and+the+Progression+of+Kidney+Disease:+A+Cohort+Study.|journal=American Journal of Kidney Diseases |volume=54|issue=2|pages=270–277|doi=10.1053/j.ajkd.2009.02.014|issn=1523-6838|pmc=4354889|pmid=19394734}}</ref><ref>{{Cite journal|last1=Dobre|first1=Mirela|last2=Yang|first2=Wei|last3=Chen|first3=Jing|last4=Drawz|first4=Paul|last5=Hamm|first5=L. Lee|last6=Horwitz|first6=Edward|last7=Hostetter|first7=Thomas|last8=Jaar|first8=Bernard|last9=Lora|first9=Claudia M.|last10=Nessel|first10=Lisa|last11=Ojo|first11=Akinlolu|date=2013-10-01|title=Association of Serum Bicarbonate With Risk of Renal and Cardiovascular Outcomes in CKD: A Report From the Chronic Renal Insufficiency Cohort (CRIC) Study|journal=American Journal of Kidney Diseases|volume=62|issue=4|pages=670–678|doi=10.1053/j.ajkd.2013.01.017|pmid=23489677|pmc=3701754|issn=0272-6386}}</ref><ref>{{Cite journal|last1=Menon|first1=Vandana|last2=Tighiouart|first2=Hocine|last3=Vaughn|first3=Nubia Smith|last4=Beck|first4=Gerald J.|last5=Kusek|first5=John W.|last6=Collins|first6=Allan J.|last7=Greene|first7=Tom|last8=Sarnak|first8=Mark J.|date=2010-11-01|title=Serum Bicarbonate and Long-term Outcomes in CKD|journal=American Journal of Kidney Diseases|volume=56|issue=5|pages=907–914|doi=10.1053/j.ajkd.2010.03.023|pmid=20605301|issn=0272-6386}}</ref><ref>{{Cite journal|last1=Raphael|first1=Kalani L.|last2=Wei|first2=Guo|last3=Baird|first3=Bradley C.|last4=Greene|first4=Tom|last5=Beddhu|first5=Srinivasan|date=2011-02-01|title=Higher serum bicarbonate levels within the normal range are associated with better survival and renal outcomes in African Americans|journal=Kidney International|volume=79|issue=3|pages=356–362|doi=10.1038/ki.2010.388|pmid=20962743|pmc=5241271|issn=0085-2538}}</ref>
==Treatment==
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