Endocrine Abstracts

A 44-year-old gentleman known to have adult polycystic kidney disease with chronic renal failure was found to be profoundly hypothyroid in predialysis assessments in the renal clinic. He was symptomatic feeling tired and generally unwell with multiple problems, which were initially all attributed to his renal failure. Investigations of his thyroid by ultrasound revealed two nodules in the left lobe and one nodule in the right lobe of the thyroid. FNAC failed to differentiate between a colloid nodule, follicular adenoma or follicular carcinoma and hence in November 2005 he underwent a left thyroid lobectomy which was histologically confirmed as Hashimoto’s thyroiditis.

He was commenced on Thyroxine 50 mcg and the dose titrated to 100 mcg. The thyroid functions normalised and his TSH declined to 1.66 μ/l. However since commencing peritoneal dialysis in August 2006, the TSH crept up to 46 μ/l and his Thyroxine requirement kept increasing.

From 150 mcg thyroxine daily he has needed to increase to the dose to 225 mcg od, bringing the TSH to 8.84 μ/l and free-thyroxine (T4) to 20.3 pmol/l. He was advised to increase the dose in steps of 25 mcg with repeat thyroid function tests to assess.Thyroxine can be filtered across the peritoneum and is lost in the dialysate fluid. This results in increasing requirement of thyroxine dose as illustrated here. Measuring the free thyroxine levels in the peritoneal dialysate fluid is not yet validated. In our patient, unvalidated peritoneal fluid free thyroxine level was measured at 1.51 pmol/l with serum free thyroxine of 22.4 pmol/l in October 2007. The thyroxine filtered into the dialysate fluid (12.3 l/24 h) is lost, necessitating additional replacement. Patients on peritoneal dialysis but normal thyroid tissue can compensate for this loss by increasing the endogenous production. In patients with thyroidectomy or Hashimotos disease the replacement will need to be monitored more regularly and dose up-titrated.