Introduction: Hyperphosphatemia is an important symptom of chronic kidney disease-mineral bone disorder (CKD-MBD). Various oral phosphate binders have been used, but have not been very effective, especially for severe secondary hyperparathyroidism (SHPT) in patients undergoing maintenance dialysis. Maintenance dialysis patients with severe SHPT can develop hypophosphatemia for several months after parathyroidectomy without elevated alkaline phosphatase. Based on these clinical phenomena, we hypothesized that high levels of parathyroid hormone (PTH) might inhibit intestinal phosphorus absorption which mediated by sodium-dependent phosphorus transporters.
Methods: Forty BALB/c mice were divided into four groups. Mice in group 1 were given an intravenous injection of normal saline as the control group. Mice in groups 2, 3, and 4 were given PTH(1- 34) in doses of 40 μg/100 g, 200 μg/100 g, and 400 μg/100 g body weight intravenously, respectively. All mice were euthanized 8 hours after the injection. The mRNA and protein expression of sodium-dependent phosphorus transporter NPT-2b and Pit-1 on the membrane of the intestinal epithelial cells was detected by real-time polymerase chain reaction (PCR) and western blot analysis, respectively.
Results: In group 4, intestinal epithelial NPT-2b and Pit-1 protein expression was significantly decreased, whereas in groups 2 and 3, no significant changes were found.
Conclusion: A high PTH level decreases the protein expression of NPT-2b and Pit-1 in the intestinal mucosa.