title: Hyperphosphaturia after kidney transplantation in syngeneic rats: effects on nephrocalcinosis and bone metabolism?
abstract: BACKGROUND
  Studies on kidney transplantation have thus far mainly dealt with surgical techniques, immunology, and transplant tolerance. Disturbed mineral metabolism after renal denervation has not received much attention. Basic physiological research in short-term experiments has shown that experimental renal denervation in rats leads to parathormone (PTH)-independent hyperphosphaturia (HPU). HPU and other metabolic complications also have been described after clinical kidney transplantation. Furthermore, there is an unexpected increase in the risk of bone fracture. However, these studies have examined an organism pre-damaged with regard to the parathyroid and immunosuppression. Experimental investigations in syngeneic rats were performed to see whether HPU also occurs after transplantation and thus after denervation and which target organs are involved.
  
  
  METHODS
  Thirty-six male Lewis rats subjected to laparotomy (n = 12), unilateral nephrectomy (n = 12), or unilateral transplantation and bilateral nephrectomy (n = 12) were observed for 18 weeks.
  
  
  RESULTS
  Animals that underwent transplantation had a significant loss of phosphate in the urine not associated with decreased calcium, phosphate, or magnesium in bone. Stability test showed no deterioration, despite a slight increase in the bone parameters of alkaline phosphatase, cyclic AMP, and hydroxyproline with unchanged calciotropic hormones. Nephrocalcinosis was not observed. Parallel to HPU, there was a compensatory reduction in fecal phosphate excretion.
  
  
  CONCLUSIONS
  The loss of phosphate after clinical kidney transplantation in the predamaged parathyroid hormone control system as well as immunosuppression and a surprising increase in the incidence of bone fractures may be explained by the denervation-related loss of phosphate. The lack of intestinal counter-regulation could be an important pathomechanism.
authors.affiliation: Department of Urology, Klinikum Benjamin Franklin, Freie Universität, Berlin, Germany. straub@medizin.fu-berlin.de
authors.forename: B
authors.initials: B
authors.lastname: Straub
authors.forename: M
authors.initials: M
authors.lastname: Müller
authors.forename: R
authors.initials: R
authors.lastname: Heicappell
authors.forename: M
authors.initials: M
authors.lastname: Schrader
authors.forename: C
authors.initials: C
authors.lastname: Goessl
authors.forename: K
authors.initials: K
authors.lastname: Miller
mesh_terms: D000241:Adenosine; D000493:Allopurinol; D000818:Animals; D001842:Bone and Bones / Q000378:metabolism*; D002114:Calcinosis / Q000209:etiology*; D004195:Disease Models, Animal; D005978:Glutathione; D007328:Insulin; D007674:Kidney Diseases / Q000209:etiology*; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000502:physiology; D008297:Male; D009392:Nephrectomy; D009926:Organ Preservation; D019188:Organ Preservation Solutions; D010710:Phosphates / Q000652:urine*; D011887:Raffinose; D051381:Rats; D011917:Rats, Inbred Lew; D020858:Tissue and Organ Harvesting; D014185:Transplantation, Isogeneic; D016482:Urinalysis
chemical_list: D007328:Insulin; D019188:Organ Preservation Solutions; D010710:Phosphates; C055206:University of Wisconsin-lactobionate solution; D000493:Allopurinol; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose