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{{Infobox medical condition (new)
| name
| synonyms
| image
| caption
| pronounce
| field
| types
Chronic Metabolic Acidosis
| symptoms
| complications = '''Acute:''' poor morbidity and mortality outcomes;<br>
'''Chronic:''' adverse outcomes on kidney function, musculoskeletal system, possible cardiovascular effects
| onset
| duration
| causes
'''Chronic:''' Impaired kidney function
| risks
| diagnosis
| differential
| prevention
| treatment
'''Chronic:''' Diet rich in fruits and vegetables, oral alkali therapy<ref>{{cite journal |last1=Navaneethan |first1=Sankar D. |last2=Shao |first2=Jun |last3=Buysse |first3=Jerry |last4=Bushinsky |first4=David A. |title=Effects of Treatment of Metabolic Acidosis in CKD: A Systematic Review and Meta-Analysis |journal=Clinical Journal of the American Society of Nephrology |volume=14 |issue=7 |pages=1011–1020 |language=en |doi=10.2215/CJN.13091118 |pmid=31196951 |pmc=6625635 |date=5 July 2019}}</ref>
| medication
| prognosis
| frequency
'''Chronic:''' Highly prevalent in people with Chronic Kidney Disease: 9.4% CKD Stage 3a; 18.1% CKD Stage 3b; 31.5% CKD Stage 4 and 5 <ref>{{cite journal |last1=Inker |first1=Lesley A. |last2=Coresh |first2=Josef |last3=Levey |first3=Andrew S. |last4=Tonelli |first4=Marcello |last5=Muntner |first5=Paul |title=Estimated GFR, Albuminuria, and Complications of Chronic Kidney Disease |journal=Journal of the American Society of Nephrology |volume=22 |issue=12 |pages=2322–2331 |language=en |doi=10.1681/ASN.2010111181 |pmid=21965377 |pmc=3279937 |date=1 December 2011}}</ref>
| deaths =
| }}
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=== Chronic metabolic acidosis ===
Chronic metabolic acidosis has non-specific clinical symptoms but can be readily diagnosed by testing serum bicarbonate levels in patients with
==Diagnostic approach and causes==
Metabolic acidosis results in a reduced serum pH that is due to metabolic and not respiratory dysfunction. Typically the serum bicarbonate concentration will be <22
=== Causes ===
Generally, metabolic acidosis occurs when the body produces too much acid (e.g., lactic acidosis, see below section), there is a loss of bicarbonate from the blood, or when the kidneys are not removing enough acid from the body.
Chronic metabolic acidosis is most often caused by a decreased capacity of the kidneys to excrete excess acids through renal ammoniagenesis. The typical Western diet generates
There are many causes of acute metabolic acidosis, and thus it is helpful to group them by the presence or absence of a normal anion gap.<ref>{{Cite book|title=Symptom to diagnosis: an evidence-based guide|url=https://accessmedicine.mhmedical.com/book.aspx?bookID=1088|url-access=subscription|last1=Stern|first1=Scott D. C.|last2=Cifu|first2=Adam S.|last3=Altkorn|first3=Diane|isbn=9780071803441|edition= 3rd|location=New York|publisher=[[McGraw-Hill Education]]|date=2015|oclc=896866189}}</ref>
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'''Normal anion gap'''{{Main|Normal anion gap acidosis}}
Causes of normal anion gap include:<ref>{{Cite book|title=The renal system: basic science and clinical conditions|date=2010|publisher=Churchill Livingstone/Elsevier|last1=Field|first1=Michael J.|last2=Pollock|first2=Carol A.|last3=Harris|first3=David C.|isbn=9780702033711|edition=2nd|location=Edinburgh|oclc=319855752|url-access=registration|url=https://archive.org/details/renalsystembasic0000fiel}}</ref>
* Inorganic acid addition
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Adjunctive tests are useful in determining the aetiology of a raised anion gap metabolic acidosis including detection of an osmolar gap indicative of the presence of a toxic alcohol, measurement of serum ketones indicative of ketoacidosis and renal function tests and urinanalysis to detect renal dysfunction.
Elevated protein (albumin, globulins) may theoretically increase the anion gap but high levels are not usually encountered clinically. Hypoalbuminaemia, which is frequently encountered clinically, will ''mask'' an anion gap. As a rule of thumb, a decrease in serum albumin by
==Pathophysiology==
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===Buffer===
The decreased bicarbonate that distinguishes metabolic acidosis is therefore due to two separate processes: the buffer (from water and carbon dioxide) and additional renal generation. The buffer reactions are: <chem display=block>H+ + HCO3- <=> H2CO3 <=> CO2 + H2O</chem>
The [[
For example, blood gas machines usually determine bicarbonate concentrations from measured ''p''H and {{math|''P''<sub>a{{CO2}}</sub>}} values. Mathematically, the algorithm [[substitution (algebra)|substitutes]] the Henry's law formula into the Henderson-Hasselbach equation and then rearranges: <math chem display=block>\left[\ce{HCO3^-}\right]=(0.03\text{ L}^{-1}/\text{mmHg})P_{\text{a}\ce{CO2}}\cdot 10^{p\ce{H}-pK_\text{a}}</math> At [[sea level]], normal numbers might be {{math|''p''H ≈ 7.4}} and {{math|''P''<sub>a{{CO2}}</sub> ≈ 40 mmHg}}; these then imply <math chem display=block>\begin{align}
▲The [[Henderson-Hasselbalch equation]] mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system: <math chem display=block>p\ce{H}=pK_\text{a}+\log_{10}\frac{\left[\ce{HCO3-}\right]}{\left[\ce{CO2}\right]}</math> where ''pK''<sub>a</sub> ≈ 6.1. In clinical practice, the concentration of {{CO2}} is usual estimated via [[Henry's law]]: [{{CO2}}] = 0.03 × P<sub>{{CO2}}</sub>, where P<sub>{{CO2}}</sub> is the [[partial pressure]] of {{CO2}} in arterial blood.
\left[\ce{HCO3^-}\right]&=(0.03\text{ L}^{-1}/\text{mmHg})(40\text{ mmHg})\cdot10^{7.4-6.1} \\
&=24\text{ L}^{-1}
\end{align}</math>
== Consequences ==
=== Acute metabolic acidosis ===
Acute
=== Chronic metabolic acidosis ===
Chronic metabolic acidosis commonly occurs in people with
The most adverse consequences of chronic metabolic acidosis in people with
==Treatment==
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=== Acute metabolic acidosis ===
Bicarbonate therapy is generally administered In patients with severe acute acidemia (pH < 7.11), or with less severe acidemia (pH 7.
=== Chronic metabolic acidosis ===
For people with
Currently, the most commonly used treatment for chronic metabolic acidosis is oral bicarbonate. The NKF/KDOQI guidelines recommend starting treatment when serum bicarbonate levels are <22 mEq/L, in order to maintain levels ≥ 22 mEq/L.<ref name=":4">{{Cite journal|title=National Kidney Foundation: K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease.|url=https://www.kidney.org/sites/default/files/docs/boneguidelines.pdf|journal=Am J Kidney Dis|volume=42 (Suppl 3)|pages=S1–S201}}</ref><ref name=":5">{{Cite web|url=https://kdigo.org/guidelines/ckd-evaluation-and-management/|title=CKD Evaluation and Management – KDIGO|website=kdigo.org|access-date=2019-12-31}}</ref> Studies investigating the effects of oral alkali therapy demonstrated improvements in serum bicarbonate levels, resulting in a slower decline in kidney function, and reduction in proteinuria – leading to a reduction in the risk of progressing to kidney failure. However, side effects of oral alkali therapy include gastrointestinal intolerance, worsening edema, and worsening hypertension. Furthermore, large doses of oral alkali are required to treat chronic metabolic acidosis, and the pill burden can limit adherence.<ref>{{Cite journal|last1=Chen|first1=Wei|last2=Abramowitz|first2=Matthew K.|title=Advances in management of chronic metabolic acidosis in chronic kidney disease|journal=Current Opinion in Nephrology and Hypertension|volume=28|issue=5|pages=409–416|doi=10.1097/MNH.0000000000000524|issn=1473-6543|pmc=6677263|pmid=31232712|year=2019}}</ref>
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