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Tubulärer Phosphattransport nach erfolgreicher Nierentransplantation

Tubular phosphate-handling after successful kidney transplantation

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Summary

Disturbances in phosphate homeostasis are almost universally present in patients with chronic renal failure. They consist of phosphate-accumulation, hyperphosphatemia, extraosseous calcifications, hyperparathyroidism and disturbances in Vitamin-D metabolism. After successful transplantation these disturbances are believed to resolve quickly, but sometimes phosphate wasting occurs in the early post-transplant phase. This study was determined to investigate phosphate handling by the transplanted kidney in 42 patients with longterm good and stable transplant function (serum creatinine (Cr) <2,0 mg/100 ml, graft survival >6 months). Calcium (Ca), inorganic phosphorus (P), creatinine was measured in plasma and urine, maximal tubular reabsorption capacity for phosphorus (phosphate threshold, TmP/GFR) was calculated using Walton and Bijvoet's [21] nomogram; immunoreactive parathyroid hormone (iPTH) was determined using an antibody against the C-regional part of the PTH-molecule.

Only 8 patients (19%) showed normal renal phosphate handling as indicated by normal plasma-phosphate, normal TmP/GFR and normal iPTH. 34 patients (81%) had a decreased TmP/GFR. This phosphate leak was due to persistant hyperparathyroidism in 15 patients, 4 of them showing additionally hypophosphatemia and hypercalcemia. In the remaining 19 patients there was a PTH-independent phosphate leak as indicated by a decreased TmP/GFR despite normal iPTH values. In this group 9 patients had a decompensated phosphate leak leading to hypophosphatemia. The results show a high incidence of abnormalities in renal phosphate handling even after successful kidney transplantation with longterm surviving good and stable functioning allografts. To prevent osteomalacia and other symptomes of the phosphate depletion syndrome, means should be undertaken to increase plasma phosphate levels by lowering PTH-levels in the patients with the PTH-dependent phosphate leak (active Vitamin D analogues, parathyroidectomy) whereas sufficient phosphate suplementation (oral phosphate and/or also active Vitamin D analogues) is necessary in patients with PTH-independent decompensated phosphate leak.

Zusammenfassung

Störungen der Phosphathomöostase werden nahezu obligat bei Patienten mit chronischer Niereninsuffizienz beobachtet. Sie bestehen in einer Hyperphosphatämie, extraossären Verkalkungen, sekundärem Hyperparathyreoidismus und gestörtem Vitamin D-Metabolismus. Nach erfolgreicher Nierentransplantation soll es zu einer raschen Normalisierung des gestörten Phosphatstoffwechsels kommen. Trotzdem findet sich manchmal ein renaler Phosphatverlust in der frühen postoperativen Phase. Ziel dieser Untersuchung war es, den tubulären Phosphattransport der transplantierten Niere bei 42 Patienten mit guter und stabiler Transplantatfunktion zu untersuchen (Serum-Kreatinin (Cr) <2,0 mg/100 ml, ml, Transplantatüberlebensdauer >6 Monate). Calcium (Ca), anorganischer Phosphor (P) und Kreatinin wurden im Plasma und Harn gemessen, die maximale tubuläre Phosphatrückresorptionsrate (Phosphat-threshold, TmP/GFR) unter Verwendung von Walton und Bijvoet's Normogramm [21] errechnet; das immunreaktive Parathormon wurde mittels einem gegen das C-regionale Ende des Parathormonmoleküls reagierenden Antikörper bestimmt.

Nur 8 Patienten (19%) zeigten einen normalen renalen Phosphatstoffwechsel, definiert durch normalen Plasma-Phosphorspiegel, normale TmP/GFR und normales iPTH. 34 Patienten (81%) hatten eine erniedrigte TmP/GFR. Dieser renale Phosphatverlust war bei 15 Patienten mit einem persistierenden Hyperparathy-reoidismus vergesellschaftet, wobei bei 4 Patienten zusätzlich eine Hypophosphatämie und Hypercalcämie bestand. Die verbleibenden 19 Patienten wiesen einen von der Epithelkörperchenfunktion unabhängigen renalen Phosphatverlust auf, welcher durch eine verminderte TmP/GFR bei normaler Parathormonkonzentration definiert wurde. In dieser Patientengruppe wiesen 9 Patienten einen zur Hypophosphatämie führenden dekompensierten renalen Phosphatverlust auf.

Die Resultate zeigen einen hohen Prozentsatz von Störungen des Phosphatstoffwechsels nach erfolgreicher Nierentransplantation mit guter und stabiler Transplantatfunktion auf. Um der Entstehung einer Osteomalazie und anderen Zeichen des Phosphatdepletionssyndroms vorzubeugen, steht die Erhöhung des Plasma-Phosphats durch Supprimierung der Parathormonsekretion bei der Patientengruppe mit dem parathormonabhängigen renalen Phosphatverlust (aktive Vitamin-D-Metabolite, Parathyreoidektomie) bzw. ausreichende Phosphatsupplementation (Phosphor oral und/oder gleichfalls aktive Vitamin D-Metabolite) bei der anderen Patientengruppe im Mittelpunkt des therapeutischen Interesses.

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Kovarik, J., Graf, H., Stummvoll, H.K. et al. Tubulärer Phosphattransport nach erfolgreicher Nierentransplantation. Klin Wochenschr 58, 863–869 (1980). https://doi.org/10.1007/BF01476997

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