title: Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment.
abstract: Metabolic acidosis is noted in the majority of patients with chronic kidney disease (CKD) when glomerular filtration rate (GFR) decreases to less than 20% to 25% of normal, although as many as 20% of individuals can have acid-base parameters close to or within the normal range. Acidosis generally is mild to moderate in degree, with plasma bicarbonate concentrations ranging from 12 to 22 mEq/L (mmol/L), and it is rare to see values less than 12 mEq/L (mmol/L) in the absence of an increased acid load. Degree of acidosis approximately correlates with severity of renal failure and usually is more severe at a lower GFR. The metabolic acidosis can be of the high-anion-gap variety, although anion gap can be normal or only moderately increased even with stage 4 to 5 CKD. Several adverse consequences have been associated with metabolic acidosis, including muscle wasting, bone disease, impaired growth, abnormalities in growth hormone and thyroid hormone secretion, impaired insulin sensitivity, progression of renal failure, and exacerbation of beta 2 -microglobulin accumulation. Administration of base aimed at normalization of plasma bicarbonate concentration might be associated with certain complications, such as volume overload, exacerbation of hypertension, and facilitation of vascular calcifications. Whether normalization of plasma bicarbonate concentrations in all patients is desirable therefore requires additional study. In the present review, we describe clinical and laboratory characteristics of metabolic acidosis, discuss potential adverse effects, and address benefits and complications of therapy.
authors.affiliation: Division of Nephrology, Veterans Affairs Greater Los Angeles Health Care System, Los Angeles, CA 90073, USA. jkraut@ucla.edu
authors.forename: Jeffrey A
authors.initials: JA
authors.lastname: Kraut
authors.forename: Ira
authors.initials: I
authors.lastname: Kurtz
mesh_terms: D000138:Acidosis / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism / Q000628:therapy; D001639:Bicarbonates / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology; D002908:Chronic Disease; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000209:etiology; D004573:Electrolytes / Q000097:blood; D018149:Glucose Intolerance / Q000209:etiology; D006728:Hormones / Q000378:metabolism; D006801:Humans; D034141:Hypoalbuminemia / Q000209:etiology; D007249:Inflammation / Q000209:etiology; D007674:Kidney Diseases / Q000150:complications* / Q000378:metabolism / Q000628:therapy; D007676:Kidney Failure, Chronic / Q000209:etiology; D007684:Kidney Tubules / Q000378:metabolism; D009133:Muscular Atrophy / Q000209:etiology; D015995:Prevalence; D006435:Renal Dialysis; D001613:beta 2-Microglobulin / Q000378:metabolism
chemical_list: D001639:Bicarbonates; D004573:Electrolytes; D006728:Hormones; D001613:beta 2-Microglobulin