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DOI: 10.1055/a-2563-4573
Endocrine Disorders Can Be Reversible After Renal Transplantation in Patients with Chronic Kidney Disease: A Case Report
Endokrine Störungen können nach einer Nierentransplantation bei Patienten mit chronischer Nierenerkrankung reversibel sein: Ein Fallbericht
Introduction
The gradual loss of kidney functions initiate an inflammatory state and endocrine alterations that affecting multiple systems in patients with chronic kidney disease (CKD) [Harambat J et al., Nephrol Ther 2021; 17(6):476–484]. Serum prolactin (PRL) levels can increase in patients with advanced CKD due to the reduced clearance and increased secretion. PRL secretion is generally impaired in end-stage renal disease, but not in transplant recipients. In previous reports including adult patients, circulating PRL concentrations were reported to decline or normalize after successful kidney transplantations [Lo JC et al., Hemodial Int 2017; 21(2):190–196]. Thyroid dysfunction is another and a common endocrine disorder in advanced CKD, mostly seen as hypothyroidism. However, hyperthyroidism is very rare in patients with advanced CKD, which may be caused by thyroiditis or unknown mechanisms. Not only the disease itself, but also the long-term immunosuppression may be responsible of a variety of complications in those patients, including the development of thyroid disease [Veroux M et al., Transplant Proc 2009; 41:1142–1144].
Herein, we presented an adolescent patient with treatment-responsive hyperprolactinemia and hyperthyroidism in advanced CKD, which were resolved spontaneously after renal transplantation.
Case Presentation
A 16 years and 8 months old girl, who was undertaking peritoneal dialysis due to terminal CKD, referred to the department of pediatric endocrinology because of amenorrhoea and galactorrhea lasting for more than two months. She was followed up in the pediatric nephrology unit due to nephronophthisis and CKD stage 5, and received peritoneal dialysis for 2 years and hemodialysis for 6 months. She was using sertraline, propronolol, and colchicine treatments in addition to the peritoneal dialysis. Sertraline treatment was initiated by the psychiatrist, and the PRL level checked before starting the treatment was high as 200 mcg/L [Reference range (RR): 4.8–23.3 mcg/L]. In her family history, her father had a history of gastric cancer.
She had galactorrhea upon stimulation in the physical examination and her puberty was compatible with Tanner stage 5. At the time of admission, her weight, height, and body mass index were 61.1 kg [0.6 standard deviation score (SDS)], 160.5 cm (−0.4 SDS), and 23.72 kg/m2 (0.9 SDS), respectively. In her laboratory tests, serum PRL level was found as 593.6 mcg/L. Other pituitary hormone levels including thyroid hormones were found in normal ranges. No adenoma was detected in her pituitary 1.5 Tesla magnetic resonance imaging. Cabergoline treatment was started with a dose of 1 mg/week. Three months after the initiation of treatment, her galactorrhea persisted with stimulation. PRL level was found as 712.6 mcg/L and cabergoline treatment dose was increased to 3 mg/week gradually during the follow-up. Regular menstrual cycles was achieved after six months of treatment. A suitable donor for kidney was found and her PRL level was detected as 2.11 mcg/L and cabergoline treatment was reduced to 2.5 mg/week before the renal transplatation.
When she was hospitalized for the transplantation, her thyroid function tests revealed an obvious hyperthyroidism. Thyroid stimulating hormone (TSH) level was found as<0.005 mIU/L (RR: 0.51 – 4.30 mIU/L), free T4 (fT4) was 3.40 ng/dL (RR: 0.93 – 1.77 ng/dL), and free T3 (fT3) was 7.08 ng/L (RR: 2.3 – 5 ng/L). Methimazole (MMI) treatment was started with a dose of 0.5 mg/kg/day. In her physical examination, she was normotensive, had no tachycardia and also had no goitre. TSH-receptor stimulating antibody was found negative. Anti-thyroglobulin and anti-thyroid peroxidase antibodies were also negative as 14.8 IU/ml (RR:<115) and 10.7 IU/ml (RR:<34), respectively. The level of thyroglobulin was not measured. In the thyroid ultrasonography, dimensions of the gland were normal for her age, and the gland vascularization was normal and there was no nodules on the gland. One month later, fT4 and fT3 levels were found in normal ranges as 1.52 ng/dl and 3.96 ng/L, respectively. MMI treatment was continued in the same dosage. PRL level was 0.514 mcg/L, and cabergoline treatment was reduced to 2 mg/week. Then she found suitable for the transplantation surgery. One week after the transplantation, PRL level was decreased to 0.357 mcg/L, TSH level was 1.08 mIU/L, sT4 was 0.664 ng/dL and sT3 was 1.72 ng/L. MMI treatment was rearranged as 0.25 mg/kg/day and cabergoline treatment was resumed with a dose of 1 mg/week.
Two months after the transplantation, her galactorrhea complaint was completely resolved, her menstruation was regular, and she had no other compliants. Cabergoline was discontinued as the control PRL level was 1.41 mcg/L ([Fig. 1]). Also, MMI treatment was discontinued at the same time because fT4 was at the lower limit (1.02 ng/dL) and TSH was normal (3.59 mIU/L) ([Fig. 2]).




At the follow-up, six months after the transplantation, PRL level was 27 mcg/L without any treatment. Thyroid hormone levels were also normal and she was euthyroid.
Publication History
Article published online:
06 May 2025
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