@entity14104 after kidney transplantation in syngeneic @entity35 : effects on XXXX and bone metabolism?

@entity14104 @entity174 @entity11604 @entity1391 @entity1919 @entity720 @entity460 @entity35 @entity4727 @entity1760
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 @entity35 leads to parathormone ( @entity4727 )-independent @entity14104 ( @entity14104 ). @entity14104 and other metabolic complications also have been described after clinical kidney transplantation. Furthermore, there is an unexpected increase in the risk of @entity174 . However, these studies have examined an organism pre-damaged with regard to the parathyroid and immunosuppression. Experimental investigations in syngeneic @entity35 were performed to see whether @entity14104 also occurs after transplantation and thus after denervation and which target organs are involved. METHODS: Thirty-six male Lewis @entity35 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 @entity1391 in the urine not associated with decreased @entity460 , @entity1391 , or @entity1760 in bone. Stability test showed no deterioration, despite a slight increase in the bone parameters of alkaline phosphatase, @entity1919 , and @entity720 with unchanged calciotropic hormones. @entity11604 was not observed. Parallel to @entity14104 , there was a compensatory reduction in fecal @entity1391 excretion. CONCLUSIONS: The loss of @entity1391 after clinical kidney transplantation in the predamaged parathyroid hormone control system as well as immunosuppression and a surprising increase in the incidence of @entity174 may be explained by the denervation-related loss of @entity1391 . The lack of intestinal counter-regulation could be an important pathomechanism.
