Endocrine Abstracts

Introduction: Hyperprolactinaemia may occur in 30% of adults with chronic kidney disease (CKD), although rare in paediatrics. The pathophysiology might be further complicated by pre-existing pituitary abnormalities.

Case: Symptomatic hyperprolactinaemia developed in this adolescent girl with CKD and hypopituitarism. History involved neonatal hypoxic ischaemic encephalopathy (HIE) and renal cortical necrosis. CKD Stage 3 ensued. Growth declined by 2.3 years (height −4.78 SDS) and GH therapy for CKD commenced aged 4.3 years. By 8 years, without dose increase, she maintained height velocity >97th centile. GH deficiency seemed a possible alternative (due to pituitary vasculature compromise during HIE). We identified additional anterior pituitary hormone deficiencies requiring replacement: TSH, ACTH, gonadotrophins, (TSH 2.5 mU/l, freeT4 8.8 pmol/l, synacthen peak cortisol 220 nmol/l and prepubertal by 13 years).

Aged 15 years, she developed galactorrhoea. Investigation showed prolactin 7530 mIU/l (normal<600 mIU/l). Over preceding months, renal failure had progressed to CKD5 (GFR 15 ml/min per 1.73 m²) with peritoneal dialysis initiation, alongside ethinylestradiol dose increase from 10 to 20 μg daily. There were no further medications implicated in hyperprolactinaemia. Pituitary MRI excluded prolactinoma. The prolactin level remains unchanged by dialysis.

Discussion: Hyperprolactinaemia in CKD is predominantly a direct uraemic toxin effect on hypothalamic function (reducing inhibitory dopaminergic tonus increasing prolactin secretion). Reduced clearance provides a lesser contribution to elevated prolactin levels. Neither peritoneal nor haemodialysis correct hyperprolactinaemia. Ultimately, renal transplantation normalises prolactin. CKD progression is likely the main contributor to hyperprolactinaemia, although the pubertal oestrogen rise may amplify hyperprolactinaemia. Our patient’s increase may have been more dramatic due to exogenous oestrogen requirement.

Prevalence of galactorrhoea (symptomatic hyperprolactinaemia) is unknown in the CKD population. This is the only known case of galactorrhoea in an adolescent with CKD and hypopituitarism. This case is more unusual as accompanied by other anterior pituitary hormone deficiencies. We can speculate whether the hypopituitarism contributed to altered prolactin inhibition, although the hyperprolactinaemia was a recent development.