ReviewMetabolic Acidosis of CKD: Diagnosis, Clinical Characteristics, and Treatment
Section snippets
Prevalence of metabolic acidosis in patients with CKD
The exact prevalence of metabolic acidosis in patients with CKD is unknown. Early studies indicated that hypobicarbonatemia caused by metabolic acidosis only developed when GFR decreased to less than 25% of normal.3 The recent analysis of the third annual National Health and Nutrition Examination Survey (NHANES III; 1988 to 1994)16 found that a detectable decrease in plasma bicarbonate concentration was not seen until GFR was less than 20 mL/min (<0.33 mL/s). Based on estimates of the number of
Onset, Severity, and Stability of Metabolic Acidosis
Clinical characteristics of metabolic acidosis in patients with CKD are listed in Table 1. A detectable decrease in plasma bicarbonate concentration initially appears when GFR decreases to less than 20% to 25% of normal.3, 20, 21, 22 At this level of GFR, it is likely that approximately 80% of patients will manifest some degree of hypobicarbonatemia.7, 8, 22 The metabolic acidosis and accompanying acidemia generally are mild to moderate in degree, with plasma bicarbonate concentrations ranging
Clinical characteristics of acid-base parameters in dialysis patients
This topic recently was reviewed by us and others.15, 45 As noted, after patients develop end-stage renal failure, the majority will have metabolic acidosis.7 Theoretically, after maintenance hemodialysis therapy has been established and bicarbonate stores have been repleted, delivery of base during the usual thrice-weekly dialysis procedure would be anticipated to return predialysis plasma bicarbonate concentrations to normal values of 24 to 25 mEq/L (mmol/L). However, with a dialysate
Clinical effects of metabolic acidosis in patients with CKD
Experimental studies in animals and clinical studies of humans have shown that chronic metabolic acidosis can have diverse deleterious effects on organ function (Table 2).
Some experimental studies examining the impact of metabolic acidosis on organ function were performed in individuals with completely normal renal function,54, 55, 56 and these findings have been inferred to also apply to patients with CKD because this disorder is the most common cause of metabolic acidosis lasting for more
Treatment of metabolic acidosis in patients with CKD
Because metabolic acidosis in patients with CKD appears to be associated with significant clinical abnormalities, several investigators examined the impact of treating the metabolic acidosis. Studies were performed in patients with CKD before and after the initiation of long-term maintenance dialysis therapy. Metabolic acidosis was corrected by the administration of base, alteration in dialysate base concentration, or both. In some studies, metabolic acidosis was completely normalized, whereas
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Cited by (234)
Serum Chloride and Mortality in patients on continuous ambulatory peritoneal dialysis: A multi-center retrospective study
2021, eClinicalMedicineCitation Excerpt :The kidney is the primary regulator of homeostasis of chloride, and renal tubular reabsorption of chloride is essential for maintaining the volume of extracellular fluid [12–14]. Multiple electrolyte disorders and metabolic acidosis, which have diverse deleterious effects on organ function, are common in patients with chronic kidney disease (CKD) when the estimated glomerular filtration rate (eGFR) declines to less than 20% to 25% of normal [15,16]. A multicenter, prospective, observational study with 923 Japanese pre-dialysis CKD patients reported that low serum chloride was associated with an increased risk of 3-year cardiovascular disease (CVD) events and mortality [17].
Chronic kidney disease
2021, The LancetAcidosis induces significant changes to the murine supraspinatus enthesis organic matrix
2024, Connective Tissue ResearchEffects of correcting metabolic acidosis on muscle mass and functionality in chronic kidney disease: a systematic review and meta-analysis
2023, Journal of Cachexia, Sarcopenia and Muscle
Supported in part by the Veterans Administration (J.A.K.); Max Factor Family Foundation; the Richard and Hinda Rosenthal Foundation, and the Fredericka Taublitz Fund (I.K.).
Originally published online as doi:10.1053/j.ajkd.2005.03.003 on April 29, 2005.