Hyperchloremic acidosis develops at the stage G4 and shifts to high anion gap acidosis at the stage G5 in chronic kidney disease.

BACKGROUND: Amelioration of hyperchloremic acidosis (Cl-Ac), a common complication in chronic kidney disease (CKD), could preserve renal function in chronic kidney disease (CKD). However, the development of Cl-Ac in CKD has not been clarified yet. METHODS: The degree of Cl-Ac, which is indicated as the bicarbonate concentration decrease with serum chloride concentration increase (∆[HCO3-]Cl), was compared with the estimated glomerular filtration rate (eGFR) by using CKD patient records. RESULTS: In 307 records with metabolic acidosis, a spline curve obtained from the plot comparing ∆[HCO3-]Cl with eGFR showed that ∆[HCO3-]Cl did not change, increased, and decreased during eGFR decrease until 27, from 27 to 17.5, and from 17.5 mL/min/1.73 m2, respectively. CONCLUSION: By CKD progression, Cl-Ac progressed and regressed at the CKD stages G4 and G5, respectively. The regression would have reflected the shift of Cl-Ac to high anion gap acidosis.

Salvation of peritoneal dialysis catheter potency by using an angiographic guidewire.

Catheter obstruction is a major cause of dialysate flow problems in peritoneal dialysis (PD). It will lead to PD technique failure, when its conservative management such as vigorous instillation of dialysate occasionally fails to salvage the catheter potency. In this report, we present two cases of catheter obstruction caused by intraluminal clots of PD catheter. The clots, which could not be removed by the conservative management, were removed by a new technique using an angiographic guidewire. The technique could be an option to resolve PD catheter obstruction.

Misdiagnosis of high anion gap acidosis owing to instrument error of a device.

The anion gap (AG) is a tool to diagnose metabolic acid-base disorders in the physiological approach to acid-base assessment. It is used to detect high AG acidosis, a type of metabolic acidosis caused by serum concentration increase in usually unmeasured anions; AG larger than the reference for it indicates the presence of high AG acidosis. This report presents a case of hyperlactatemia which was not detected as high AG acidosis possibly because of instrument error of a device in measurement of serum sodium and chloride concentrations. The case indicates that the error will make AG unable to detect high AG acidosis of any cause. Hence, upon suspicion of high AG acidosis caused by measurable anions such as lactate and ketones, it is recommended to measure their serum concentration.

Functions of the D-ribosyl moiety and the lower axial ligand of the nucleotide loop of coenzyme B(12) in diol dehydratase and ethanolamine ammonia-lyase reactions.

The roles of the D-ribosyl moiety and the bulky axial ligand of the nucleotide loop of adenosylcobalamin in coenzymic function have been investigated using two series of coenzyme analogs bearing various artificial bases. The 2-methylbenzimidazolyl trimethylene analog that exists exclusively in the base-off form was a totally inactive coenzyme for diol dehydratase and served as a competitive inhibitor. The benzimidazolyl trimethylene analog and the benzimidazolylcobamide coenzyme were highly active for diol dehydratase and ethanolamine ammonia-lyase. The imidazolylcobamide coenzyme was 59 and 9% as active as the normal coenzyme for diol dehydratase and ethanolamine ammonia-lyase, respectively. The latter analog served as an effective suicide coenzyme for both enzymes, although the partition ratio (k(cat)/k(inact)) of 630 for ethanolamine ammonia-lyase is much lower than that for diol dehydratase. Suicide inactivation was accompanied by the accumulation of a cob(II)amide species, indicating irreversible cleavage of the coenzyme Co-C bond during the inactivation. It was thus concluded that the bulkiness of a Co-coordinating base of the nucleotide loop is essential for both the initial activity and continuous catalytic turnovers. Since the k(cat)/k(inact) value for the imidazolylcobamide in diol dehydratase was 27-times higher than that for the imidazolyl trimethylene analog, it is clear that the ribosyl moiety protects the reaction intermediates from suicide inactivation. Stopped-flow measurements indicated that the rate of Co-C bond homolysis is essentially unaffected by the bulkiness of the Co-coordinating base for diol dehydratase. Thus, it seems unlikely that the Co-C bond is labilized through a ground state mechanochemical triggering mechanism in diol dehydratase.