Advertisement

Parathyroid Hormone Resistance in Renal Allograft Recipients

  • M. Kleerekoper
  • R. S. Bernstein
  • C. Cruz
  • N. W. Levin
  • A. M. Parfitt
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 151)

Abstract

Hypophosphatemia is common after renal transplantation and has been variously ascribed to persistent hyperparathyroidism, to tubular damage from rejection, or to the effect of corticosteroid or immunosuppressive therapy (1–3). To learn more about the mechanisms, we measured TmP/GFR, nephrogenous cyclic AMP (NcAMP) and immunoreactive PTH in 25 renal transplant patients with stable renal function (Ccr≥70 ml/min/1.73 m2,≥6 months post-transplant), 21 healthy control subjects and 5 uninephrectomized renal transplant donors. On the basis of the parathyroid function tests, we divided the patients into three groups. In Group 1 (5 patients) serum calcium, NcAMP and PTH were all normal; these patients had resolved hyperparathyroidism. In Group 2 (6 patients) serum calcium, NcAMP and PTH. were all raised; these patients had persistent hypercalcemic hyperparathyroidism. In Group 3 (14 patients) serum calcium was normal but either NcAMP or iPTH or both were raised; these patients had persistent normocalcemic hyperparathyroidism. These three groups did not differ significantly in duration of graft survival, creatinine clearance, type or dose of immunosuppressive therapy, or serum levels of vitamin D metabolites.

Keywords

Serum Calcium Renal Transplant Patient Renal Allograft Recipient Phosphate Reabsorption Single Kidney 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    H.N. Ward, R.C. Pabico, B.A. McKenna and R.B. Freeman, The The renal handling of phosphate by renal transplant patients: correlation with serum parathyroid hormone, cyclic 3′,5′ — adenosine monophosphate urinary excretion, and allograft function, Adv. Exp. Med. Biol. 81:173 (1977).PubMedGoogle Scholar
  2. 2.
    N.D. Vaziri, R.E. Nellans, R.M. Brueggemann, C.H. Barton and D.C. Martin. Renal tubular dysfunction in transplanted kidneys. Southern Med. J. 72:530 (1979).PubMedCrossRefGoogle Scholar
  3. 3.
    M. Garabedian, C. Silve, D. Levy, A. Bourdeau, A. Ulmann, M. Broyer and S. Balsan, Chronic hypophosphatemia in kidney transplanted children and young adults, Adv. Med. Biol 128:249, (1980).Google Scholar
  4. 4.
    R.C. Pabico, B.A. McKenna and R.B. Freeman, Renal function before and after unilateral nephrectomy in renal donors, Kidney Int. 8:166 (1975).CrossRefGoogle Scholar
  5. 5.
    S.G. Massry, J.W. Coburn, D.B.N. Lee, J. Jowsey, C.R. Kleeman, Skeletal resistance to parathyroid hormone in renal failure. Ann. Intern. Med. 78:357 (1973).PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • M. Kleerekoper
    • 1
  • R. S. Bernstein
    • 1
  • C. Cruz
    • 1
  • N. W. Levin
    • 1
  • A. M. Parfitt
    • 1
  1. 1.Department of MedicineHenry Ford HospitalDetroitUSA

Personalised recommendations