Parathyroidectomy after kidney transplantation Ferreira GF et al. guidelines are currently lacking, and thus, laboratory data, clinical symptoms and imaging data should all be con- sidered. A previous report suggested a possible deleterious effect of total parathyroidectomy with immediate auto- transplantation on long-term kidney graft survival.8 Although the present study demonstrated an acute dete- rioration of renal function in the acute period after parathyroidectomy, renal function was similar to baseline and the control group at the final follow up. This suggests that the deterioration only persists short term. Group that contained patients undergoing some urological surgeries with a greater interference in renal function, the difference observed in the first week remained unchanged. The present paper clearly shows that acute changes in renal function are not the same after parathyroidectomy and other comparable operations not involving the parathyroid glands, leading one to consider anesthetic or post-trauma effects on these variables.10 Indeed, one study demonstrated that renal function after total parathyroidectomy without immediate autotransplantation did not differ even from that of patients undergoing subtotal parathyroidectomy.11 This study emphasizes that persistent HPT is an important surgical disease in kidney transplant patients, as parathyr- oidectomy accounted for approximately 31% (28 of 90) of all operative diseases of these patients. Cinacalcet may play an effective role in the clinical management of such patients12, but the drug is not yet available for patients in Brazil. The results presented here demonstrate that parathyroi- dectomy, which is an important therapeutic modality for kidney transplant patients, appears to be safe for kidney function irrespective of the technique employed. Notwith- standing, determining the mechanism involved in the acute deterioration of renal function that occurs shortly after parathyroidectomy may permit better patient selection and determination of the most appropriate type of parathyr- oidectomy in kidney-transplanted patients.13 Acute renal changes after parathyroidectomy are also seen in some patients undergoing parathyroidectomy for primary HPT. In the past, these alterations were clinically evidenced by the presence of oliguria, but it is now possible to observe a significant elevation in creatinine shortly after the surgery.14 Clinically evident renal failure may occur even in more recent cases.15,16 Much has been said in the literature about the hemody- namic effects of PTH on the kidney,17-19 but precise mechanisms for long-term alterations in renal function have not been proposed. Moreover, contradictory information has been presented.4 In 1983, Pang et al. suggested that different segments of the PTH molecule might have specific activities.20 It seems reasonable to speculate that the variable patterns of creatinine change after parathyroidectomy may result from the activity of another parathyroid substance or of a PTH fragment. PTH-related protein (PTHrP) is an autocrine/paracrine peptide expressed in renal tubules and vasculature that may play an important role in regulating overall renal function. It was first identified as a tumor-derived protein responsible for humoral hypercalcemia of malignancy.21 PTHrP is homologous to PTH in the N-terminal region, suggesting a possible basis for the similarity of this peptide’s actions to those of PTH when secreted into the systemic circulation by malignant tumors. Experimental analysis has shown that PTHrP can act as an endogenous vasorelaxant, modulating renal responses to vasoactive stimuli.16 This effect suggests 434 CLINICS 2011;66(3):431-435 the possibility that calcineurin inhibitors, which act as powerful glomerular vasoconstrictors, might worsen creati- nine levels.22 In any case, both the acute and chronic effects of high levels of PTH on kidney function deserve further study, as apparently contradictory results have been described.23,24 REFERENCES 1. Messa P, Sindici C, Cannella G, Miotti V, Risaliti A, Gropuzzo M, et al. Persistent secondary hyperparathyroidism after renal transplantation. 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