Masayuki Tanemoto1,2. 1. Division of Nephrology, Department of Internal Medicine, Shin-Kuki General Hospital, Saitama, Japan. mtanemoto-tky@umin.ac.jp. 2. Division of Nephrology, Department of Internal Medicine, International University of Health and Welfare School of Medicine, 13-1 Higashi-Kaigan-Cho, Atami, 413-8790, Shizuoka, Japan. mtanemoto-tky@umin.ac.jp.
Abstract
BACKGROUND: Gap acidosis, a type of metabolic acidosis caused by titratable acid accumulation, participates in CKD progression. It was found at all the stages of chronic kidney disease (CKD), whereas the kidney was believed to preserve its ability to excrete titratable acid until renal function is impaired severely. METHODS: Serum concentrations of lactate (Lac) and the other usually unmeasured anions (OUA) were separately examined using 420 records of blood gas analysis performed simultaneously with serum chemistry at a general hospital. RESULTS: Between the records grouped by the CKD stage, Lac was generally higher in the early stages than the late stages (2.2 ± 1.1, 1.9 ± 1.7, 1.5 ± 1.3, and 1.2 ± 0.6 mmol/L in G1-2, G3, G4, and G5, respectively). While OUA was not significantly different between G1-2, G3, and G4 (1.3 ± 2.0, 2.5 ± 2.7, and 2.6 ± 2.2 mEq/L, respectively), it was higher in G5 (4.7 ± 2.3 mEq/L) than in G1-4 (P < 0.001). In G5, OUA generally increased as eGFR decreased, and OUA was 6.6 ± 1.9, 4.7 ± 2.1 and 3.6 ± 2.0 mEq/L in subgroups of eGFR < 5, 5-10, and 10-15 mL/min/1.73 m2, respectively (P ≤ 0.001). CONCLUSIONS: Gap acidosis except lactic acidosis developed and progressed during the CKD stage G5, while lactic acidosis developed in the CKD stages G1-4. Prevention of lactic acidosis by preserving peripheral perfusion in the early CKD stages could slow CKD progression.
BACKGROUND: Gap acidosis, a type of metabolic acidosis caused by titratable acid accumulation, participates in CKD progression. It was found at all the stages of chronic kidney disease (CKD), whereas the kidney was believed to preserve its ability to excrete titratable acid until renal function is impaired severely. METHODS: Serum concentrations of lactate (Lac) and the other usually unmeasured anions (OUA) were separately examined using 420 records of blood gas analysis performed simultaneously with serum chemistry at a general hospital. RESULTS: Between the records grouped by the CKD stage, Lac was generally higher in the early stages than the late stages (2.2 ± 1.1, 1.9 ± 1.7, 1.5 ± 1.3, and 1.2 ± 0.6 mmol/L in G1-2, G3, G4, and G5, respectively). While OUA was not significantly different between G1-2, G3, and G4 (1.3 ± 2.0, 2.5 ± 2.7, and 2.6 ± 2.2 mEq/L, respectively), it was higher in G5 (4.7 ± 2.3 mEq/L) than in G1-4 (P < 0.001). In G5, OUA generally increased as eGFR decreased, and OUA was 6.6 ± 1.9, 4.7 ± 2.1 and 3.6 ± 2.0 mEq/L in subgroups of eGFR < 5, 5-10, and 10-15 mL/min/1.73 m2, respectively (P ≤ 0.001). CONCLUSIONS: Gap acidosis except lactic acidosis developed and progressed during the CKD stage G5, while lactic acidosis developed in the CKD stages G1-4. Prevention of lactic acidosis by preserving peripheral perfusion in the early CKD stages could slow CKD progression.
Entities:
Keywords:
Acid–base; Chronic kidney disease; Gap acidosis; Lactic acidosis
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