Hyperphosphatemia-induced hyperparathyroidism in 5/6 nephrectomized rats: development of a new animal model.
(41/179)
BACKGROUND: We require a stable model to understand the molecular mechanism by which isolated hyperphosphatemia induces hyperparathyroidism secondary to chronic renal failure. The present study established a rat model of hyperphosphatemia-induced secondary hyperparathyroidism in chronic renal failure. METHODS: Twenty-nine rats with 5/6 nephrectomy (Nx) were divided into three groups and were fed for 10 weeks on a high phosphate diet (1.2% phosphate) starting from three different post-Nx time points. Parathyroid hormone mRNA in parathyroid gland was measured by real-time PCR and parathyroid cell hyperplasia was tested by proliferating cell nuclear antigen (PCNA) assay. RESULTS: The 10 rats fed a high phosphate diet starting from the fourth week post-Nx had isolated hyperphosphatemia and excess synthesis/secretion of parathyroid hormone, and hyperplasia of the parathyroid glands were induced (r = 0.86 - 0.97, P < 0.001), but the levels of serum calcium and 1, 25 (OH)2D3 did not change. CONCLUSION: A rat model of hyperphosphatemia-induced secondary hyperparathyroidism in chronic renal failure was established by 5/6 Nx and 10 weeks-high phosphate diet starting from the fourth week post-Nx. (+info)
Hyperostosis and hyperphosphataemia syndrome: a diagnostic dilemma.
(42/179)
The syndrome of hyperostosis and hyperphosphataemia (HHS) is very rare. It can mimic bone infections and tumours. A nine-year-old girl presented with pain in her left lower leg. Radiographs showed patchy sclerosis in the tibial diaphysis. Investigations were normal except for hyperphosphataemia. Open biopsy showed chronic inflammation. Bacterial cultures were negative. Four months later, she had pain in the other leg. On evaluation for hyperphosphataemia, there was increased renal reabsorption of phosphates. She responded to analgesics. In patients between six and 16 years of age, HHS must be considered when there is painful diaphyseal swelling of long bones associated with isolated hyperphosphataemia. The painful episodes can recur. Surgical decompression can be considered if conservative treatment methods are ineffective. (+info)
Adequate phosphate binding with lanthanum carbonate attenuates arterial calcification in chronic renal failure rats.
(43/179)
Iron-magnesium hydroxycarbonate (fermagate): a novel non-calcium-containing phosphate binder for the treatment of hyperphosphatemia in chronic hemodialysis patients.
(45/179)
Newly discovered mutations in the GALNT3 gene causing autosomal recessive hyperostosis-hyperphosphatemia syndrome.
(47/179)
BACKGROUND AND PURPOSE: Periosteal new bone formation and cortical hyperostosis often suggest an initial diagnosis of bone malignancy or osteomyelitis. In the present study, we investigated the cause of persistent bone hyperostosis in the offspring of two consanguineous parents. METHODS: Clinical assessment, imaging, and direct sequencing were used to elucidate the etiology of the condition seen in the patient. RESULTS: Radiological examination revealed periosteal reaction, diaphysitis, and cortical hyperostosis, suggesting osteomyelitis or a bone neoplasm. The clinical and radiological features were also reminiscent of hyperostosis with hyperphosphatemia (HHS), a rare autosomal recessive disease manifesting with recurrent, transient, and painful swelling of the long bones. The identification of two novel heterozygous pathogenic mutations in the GALNT3 gene confirmed a diagnosis of HHS. INTERPRETATION: Molecular analysis represents an invaluable tool in the differential diagnosis of persistent cortical hyperostosis. (+info)
Vascular calcification and secondary hyperparathyroidism of severe chronic kidney disease and its relation to serum phosphate and calcium levels.
(48/179)