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Impaired regulation of calcium excretion in kidney transplant recipients

Gestörte Regulation der Calcium Ausscheidung bei Nierentransplantierten

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Zusammenfassung

Störungen des Mineralstoffwechsels und Hyperkalzämie sind bei Nierentransplantierten häufig. Der Quotient der Calcium/Kreatinin (Ca/Kr) Clearance wurde als Kriterium zur Unterscheidung von verschiedenen Erkrankungen des Calciumstoffwechsels verwendet. Wir untersuchten 91 Nierentransplantierte (davon 53 Männer) im Alter von 23–70 Jahren mit einer Kr. Clearance von >60 ml/min. Folgende mit dem Mineralstoffwechsel im Zusammenhang stehende Parameter wurden im Serum gemessen: iPTH (Parathormon), gesamte alkalische Phosphatase (tALP), Telopeptid (ein Marker des Knochenabbaus, CTX), 25-OH-Vitamin D3, gesamtes und ionisiertes Calcium, anorganisches Phosphat, Kreatinin. Kr und Ca wurden auch im Harn, ebenso wie der Quotient der Ca/Kr Clearance, bestimmt. Die Patienten wurden entsprechend ihres Ca/Kr Clearance Quotienten in folgende 3 Gruppen geteilt: 1) <0,01: Erkrankungen, die durch gestörten Ca-sensitiven Rezeptor verursacht sind (N = 30); 2) 0,01–0,02: Normale (N = 45); und 3) >0,02: Hyperparathyreoidismus (N = 16). In der Gruppe 1 hatten 7 Patienten eine Hypercalzämie und 4 Patienten eine Hyperkalzämie mit erhöhten PTH Werten. Eine Verschlechterung der renalen Ca Ausscheidung scheint bei Nierentransplantierten auch bei guter Nierenfunktion auftreten zu können. Unverhältnismäßig geringe Calciurie und gestörte Sensitivität des Ca-sensitiven Rezeptors könnten pathogenetische Faktoren für die Hypercalcaämie bei Nierentransplantierten sein.

Summary

Disorders of mineral metabolism and hypercalcemia are frequent in kidney transplant recipients. Calcium to creatinine (Ca/Cr) clearance ratio was used as a criterion to distinguish between different calcium metabolism disorders. The study comprised 91 (53 men, 38 women) kidney recipients aged 23–70 years, with creatinine clearance (CrCl) >60 ml/min. The following parameters related to mineral metabolism were measured in serum: iPTH, total alkaline phosphatase (tALP), telopeptide (bone degradation marker, CTX), 25(OH)D3, total and ionized calcium, Ca++ , Pi, creatinine (Cr). Creatinine and Ca were also determined in urine, as well as Ca/Cr clearance ratio. According to the Ca/Cr clearance ratio, patients were divided into three groups as follows: <0.01 (found in disorders caused by reduced calcium-sensing receptor sensitivity, N = 30), 0.01–0.02 (normal value, N = 45), and >0.02 (found in hyperparathyroidism, N = 16). In the group of patients with Ca/Cr clearance ratio <0.01, seven patients had hypercalcemia, and four patients had hypercalcemia and elevated iPTH. It seems that impairment of renal calcium excretion may occur in kidney transplant recipients with good kidney function. Inappropriately low calciuria and impaired sensitivity of calcium-sensing receptor may be pathogenetic factors causing hypercalcemia in kidney transplant recipients.

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References

  • Torres A, Lorenzo V, Salido E. Calcium metabolism and skeletal problems after transplantation. J Am Soc Nephrol 2002;13:551–8

    PubMed  Google Scholar 

  • Weisinger JR, Carlini RG, Rojas E, Bellorin-Font E. Bone disease after renal transplantation. Clin Am J Soc Nephrol 2006;1:1300–13

    Article  CAS  Google Scholar 

  • Reinhardt W, Bartelworth H, Jockenhoevel F, Schmidt-Gayk H, Witzke O, Wagner K, et al. Sequential changes of biochemical bone parameters after kidney transplantation. Nephrol Dial Transplant 1998;13:432–42

    Article  Google Scholar 

  • Šmalcelj R, Kušec V, Puretić M, Mareković Z. Biochemical parameters of bone turnover in kidney transplant recipients. Wien Klin Wochenschrift 1998;10:326–30

    Google Scholar 

  • Serra LA, Savoca R, Huber AR, Hepp U, Delsignore A, Hersberger M, et al. Effective control of persistent hyperparathyroidism with cinacalcet in renal allograft recipients. Nephrol Dial Transplant 2007;22:577–83

    Article  CAS  PubMed  Google Scholar 

  • Borchardt K, Sulzbacher I, Benesch T, Fodinger M, Sunder-Plassmann G, Haas M. Low-turnover bone disease in hypercalcemic hyperparathyroidism after kidney transplantation. Am J Transplant 2007;7:2515–21

    Article  Google Scholar 

  • Rosenbaum RW, Hruska KA, Korkor A, Andeson C, Slatopolsky E. Decreased phosphate reabsorption after renal transplantation: Evidence for a mechanism independent of calcium and parathyroid hormone. Kidney Int 1981;19:568–78

    Article  CAS  PubMed  Google Scholar 

  • Evenpoel P, Claes K, Kuypers D, Maes B, Bammens B, Vanrenterghem Y. Natural history of parathyroid function and calcium metabolism after kidney transplantation: a single centre study. Nephrol Dial Transplant 2004;19:1281–7

    Article  Google Scholar 

  • Julian BA, Quarles LD, Nieman KM. Musculoskeletal complications after renal transplantaion: pathogenesis and treatment. Am J Kidney Dis 1992;19:99–120

    Article  CAS  PubMed  Google Scholar 

  • Massari P. Disorders of bone and mineral metabolism after renal transplantation. Kidney Int 1997;52:1419–21

    Article  Google Scholar 

  • Reynolds JL, Joannides AJ, Skepper JN, Mc-Nair R, Schurgers LJ, Proudfoot D, et al. Human vascular smooth muscle cells undergo vesicle-mediated calcification in response to changes in extracellular calcium and phosphate concentrations: a potential mechanism for accelerated vascular calcification in ESRD. J Am Soc Nephrol 2004;15:2857–67

    Article  CAS  PubMed  Google Scholar 

  • Gwiner W, Suppe S, Mengel M, Holy L, Kreipe HH, Haller H, Schwarz A. Early calcification of renal allografts detected by protocol biopsies. Causes and clinical implications. Am J Transplant 2005;5:1934–41

    Article  Google Scholar 

  • Brown EM, Herbert SC. A cloned extracellular Ca(2+)-sensing receptor: molecular mediator of the actions of extracellular Ca2+ on parathyroid and kidney cells. Kidney Int 1996;49:1042–6

    Article  CAS  PubMed  Google Scholar 

  • Marx SJ, Stock JL, Attie MF, Downs RW Jr, Gardner DG, Brown EM, et al. Familial hypocalciuric hypercalcaemia; recognition among patients referred after unsuccessful parathyroid exploration. Ann Intern Med 1980;92:351–6

    Article  CAS  PubMed  Google Scholar 

  • Caskey FJ, Pickett TM. Disturbed calcium metabolism in a patient with bipolar disorder and impaired renal function. Nephrol Dial Transplant 2005;20:1752–5

    Article  PubMed  Google Scholar 

  • Boudville NC, Hodsman AB. Renal function and 25-hydroxy vitamin D concentrations predict parathyroid hormone levels in renal transplant patients. Nephrol Dial Transplant 2006;21:2621–4

    Article  CAS  PubMed  Google Scholar 

  • Green J, Debby H, Lederer E, Levi M, Zajicek HK, Bick T. Evidence for a PTH-independent humoral mechanism in post-transplant hypophosphatemia and phosphaturia. Kidney Int 2001;60:1182–96

    Article  CAS  PubMed  Google Scholar 

  • Bhan I, Shah A, Holmes J, Isakova T, Gutierrez O, Burnett S-A, Jueppner H, et al. Post-transplant hypophosphatemia: Tertiary "Hyper-Phosphatoninism"? Kidney Int 2006;70:1486–94

    Article  CAS  PubMed  Google Scholar 

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Authors and Affiliations

  1. Department of Dialysis, Zagreb University Hospital Center Zagreb, Zagreb, Croatia

    Ruzica Smalcelj

  2. Department of Laboratory Diagnostics, Zagreb University Hospital Center Zagreb, Zagreb, Croatia

    Vesna Kusec

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  1. Ruzica Smalcelj
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  2. Vesna Kusec
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Correspondence to Ruzica Smalcelj.

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Smalcelj, R., Kusec, V. Impaired regulation of calcium excretion in kidney transplant recipients. Wien Klin Wochenschr 123, 334–339 (2011). https://doi.org/10.1007/s00508-011-1575-6

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  • DOI: https://doi.org/10.1007/s00508-011-1575-6

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