Iatrogenic iodine as a cause of hypothyroidism in infants with end-stage renal failure

Between 1996 and 2005, two of seven infants in our unit on overnight continuous-cycle peritoneal dialysis (CCPD) acquired hypothyroidism following normal thyroid function on neonatal screening. Case 1 had posterior urethral valves, commenced CCPD at day 29, and developed hypothyroidism requiring treatment at 3 months: TSH 258 mu/l (ref.: 0.3–3.8), total thyroxine 74 nmol/l (ref.: 77–159). Plasma iodine concentration was 7.44 µmol/l (ref.: 0.23–0.68). Iodine concentrations in peritoneal dialysis (PD) fluid were found to be higher at the end of the first cycle (11.4 µmol/l) than at the end of the twelfth cycle (1.55 µmol/l). Case 2 had posterior urethral valves, commenced CCPD on day 4 and was diagnosed with hypothyroidism following a prolonged jaundice screen. Thyroxine replacement was stopped 2 months after a renal transplant. A third child commenced CCPD on day 2 and had high plasma iodine concentrations at 8 weeks (5.79 µmol/l). He had borderline thyroid function, not requiring replacement. Our hypothesis is that these infants developed hypothyroidism as a consequence of iodine exposure via the Wolff–Chaikoff effect. Iodine levels were higher in the PD fluid than in plasma. This suggests that povidine-iodine 10% in the PD cap may be the source of the high plasma iodine levels.