1 Department of Nephrology, Endocrinology and Metabolic Diseases in Katowice and 2 Department of Surgery in Bytom, Silesian University Medical School, Poland, and 3 Laboratory of Molecular Oncology, Department of Urology, Ruprecht-Karls University, Heidelberg, Germany
Correspondence and offprint requests to: Prof. dr hab. n. med. F. Kokot, Department of Nephrology, Endocrinology and Metabolic Diseases, Silesian University School of Medicine, Francuska Str. 20/24, 40-027 Katowice, Poland.
Keywords: apoptosis; loss of heterozygosity; tertiary hyperparathyroidism
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Introduction |
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Case |
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She received a kidney from a cadaver donor. The initial immunosuppressive treatment consisted of prednisolone, azathioprin and cyclosporin. A week later an episode of acute graft rejection prompted us to intensify the immunosuppressive therapy (steroid bolus). After this treatment, a systematic improvement in renal excretory function was noticed (decrease in serum creatinine to 2 mg/dl). In parallel to the normalization of graft function hypercalcaemia (S-Ca 3.3 mmol/l), hypophosphataemia (S-iP 0.8 mmol/l) and an elevated activity of serum total alkaline phosphatases (2500 nmol/l/s) were observed. The serum iPTH level at that time was 500 pg/ml. Ultrasonography of the neck revealed an enlargement of all four parathyroid glands, which was most marked for the right lower gland (1.6 cm in diameter). The patient decided to delay the proposed surgical procedure as long as possible. Based on the preliminary report of Kitaoka et al. [1] we performed a direct, ultrasonography-guided injection of 1 ml of calcitriol solution (1 µg/ml Calcijex, Abbott GmbH) into the largest parathyroid gland. Calcitriol was injected twice at a 1-month interval. We did not observe any suppression of parathyroid function. Serum calcium even increased up to 3.5 mmol/l and iPTH was between 500 and 700 pg/ml.
Two months after kidney transplantation the patient was referred to the surgical department (on the seventh day after the second intraparathyroid calcitriol injection). Total parathyroidectomy with intramuscular transplantation of the parathyroid tissue into the forearm was performed. Parathyroids were markedly enlarged (size 415 mm) with a histological pattern of nodular hyperplasia. After surgery a rapid decrease in serum calcium and iPTH (20 pg/ml) was observed.
Several nodules were found in both lower parathyroid glands. For further genetic analyses we used four nodules from the right lower gland (injected) and one from the left lower one (not injected). No apoptotic fragmentation of DNA was observed in either the injected or uninjected parathyroid gland (Figure 1). The microsatellite analysis for markers localized to chromosome 1p, 1q, 2p, 2q, 3p, 3q, 4p, 5q, 6q, 7p, 8p, 9p, 10q, 11p, 11q, 12q, 13q, 14q, 15q, 16q, 17p, 17q, 20q regions did not show any alteration.
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Discussion |
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Direct injection of calcitriol into an enlarged parathyroid gland provides the highest possible local concentration of this hormone. In contrast to the report by Kitaoka et al. [1] such treatment was ineffective in our case. Furthermore, we failed to observe apoptotic DNA fragmentation by agarose gel electrophorens both in the injected and an uninjected parathyroid gland.
In the majority of kidney transplant patients in parallel to the restoration of renal function, normalization of serum calcium and PTH and involution of parathyroid hyperplasia can be noticed, although sometimes not earlier than 12 years after successful kidney transplantation. As shown in our case, lack of marked apoptosis of the hyperplastic parathyroid cells after local calcitriol injection is in line with Parfitt's suggestion [5], that involution due to apoptosis is sometimes too slow to be of clinical relevance.
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References |
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