Distal renal tubular acidosis in a patient with Hashimoto’s thyroiditis: a case report

Renal tubular acidosis (RTA) is a rare disorder that can be inherited or acquired, and results in an inability of the kidneys to maintain normal acid-base balance. We present a case of recurrent, severe hypokalaemia and rhabdomyolysis in a young woman who had an associated normal anion gap metabolic acidosis and was subsequently diagnosed with distal RTA associated with Hashimoto’s thyroiditis. Distal RTA associated with Hashimoto’s thyroiditis is rare and probably develops because of autoimmune-mediated mechanisms, causing an inability of the H+-ATPase pump in alpha-intercalated cells of the cortical collecting duct to secrete H+, with subsequent failure of urinary acidification. In this case, this hypothesis was supported by the exclusion of common genetic mutations associated with distal RTA. We illustrate that utilizing a systematic, physiology-based approach for challenging electrolyte and acid-base disorders enables identification of the root cause and underlying disease mechanisms

The agreement between fasting glucose and markers of chronic glycaemic exposure in individuals with and without chronic kidney disease: a cross-sectional study

Abstract Background To assess whether the agreement between fasting glucose and glycated proteins is affected by chronic kidney disease (CKD) in a community-based sample of 1621 mixed-ancestry South Africans. Methods CKD was defined as an estimated glomerular filtration rate < 60 ml/min/1.73 m2. Fasting plasma glucose and haemoglobin A1c (HbA1c) concentrations were measured by enzymatic hexokinase method and high-performance liquid chromatography, respectively, with fructosamine and glycated albumin measured by immunoturbidimetry and enzymatic method, respectively. Results Of those with CKD (n = 96), 79, 16 and 5% where in stages 3, 4 and 5, respectively. Those with CKD had higher levels of HbA1c (6.2 vs. 5.7%; p < 0.0001), glycated albumin (15.0 vs. 13.0%; p < 0.0001) and fructosamine levels (269.7 vs. 236.4 μmol/l; p < 0.0001), compared to those without CKD. Higher fasting glucose levels were associated with higher HbA1c, glycated albumin and fructosamine, independent of age, gender, and CKD. However, the association with HbA1c and glycated albumin differed by CKD status, at the upper concentrations of the respective markers (interaction term for both: p ≤ 0.095). Conclusion Our results suggest that although HbA1c and glycated albumin perform acceptably under conditions of normoglycaemia, these markers correlate less well with blood glucose levels in people with CKD who are not on dialysis