Post-renal transplant hypophosphatemia, a common disorder during the first two weeks after transplantation, has an incidence rate of 50-80%. Transplanted kidney plays a major role in this type of hypophosphatemia. The alterations in proximal tubular brush border membrane trafficking of type IIa sodium/phosphate cotransporters mediated by drugs and phosphotonins account for this reduction of serum phosphate level and the role of parathyroid hormone (PTH) as a mediator of this type of hypophosphatemia has been called into question. In the present study, we investigated the role PTH as a mediator of post-renal transplant hypophosphatemia in our patients. In this prospective study, serum phosphate (P), calcium (Ca), creatinine (Cr), alkaline phosphatase and intact parathyroid hormone (iPTH) levels of 393 patients (male/female ratio=257/136) were evaluated during two weeks after successful renal transplantation within three years. Hypophosphatemia developed in 76% of patients with mean serum phosphate and intact PTH levels of 2.00±0.26 mg/dl and 108±14 ng/ml respectively. In nonhypophosphatemic group (24% of patients) mean serum P and iPTH concentrations were 3.93±1.17 mg/dl and 150±51 ng/ml. There was no significant difference in intact parathyroid hormone, calcium and alkaline phosphatase values between hypophosphatemic and nonhypophosphatemic group of patients (P>0.05), but the difference in serum creatinine levels between these two groups was statistically meaningful (P value=0.001). Parathyroid hormone appears not to be involved in the development of post-renal transplant hypophosphatemia, but the occurrence of this type of hypophosphatemia is related to the function of transplanted kidney.