Title: The Effects of Renal Osteodystrophy Treatment on Bone Histology
Abstract: Patients with chronic renal disease are at risk for not just rickets and osteomalacia, but also renal osteodystrophy, a complex bone disease. Renal osteodystrophy is a wide term that encompasses all biochemical abnormalities as well as skeletal symptoms in chronic kidney disease patients. The effects of calcium, phosphorous, and vitamin D deficiency on bone turnover, mineralization, and extraskeletal calcifications, as well as their effects on bone turnover, mineralization, and extraskeletal calcifications, are all key components of this disorder. Renal osteodystrophy has traditionally been defined as the outcome of hyperparathyroidism caused by hyperphosphatemia and hypocalcemia, both of which are caused by decreased phosphate excretion by the injured kidney. The inability of the damaged kidneys to convert vitamin D3 into its active form, calcitriol, results in low levels of activated vitamin D3. Phosphate binders, vitamin D compounds, and calcimimetics are the most common treatments for renal osteodystrophy. .Because of their effects on bone turnover, mineralization, and volume, aluminum-containing phosphate binders have been demonstrated to be toxic to bone. Renal osteodystrophy (ROD) begins with a decrease of kidney function (about a 50% reduction in glomerular infiltration rates). ROD affects nearly all patients with severe chronic kidney disease (CKD), and a link has been established between histologic alterations in bone turnover and vascular calcifications .Patients with chronic renal disease are at risk for not just rickets and osteomalacia, but also renal osteodystrophy, a complex bone disease. Renal osteodystrophy is a wide term that encompasses all biochemical abnormalities as well as skeletal symptoms in chronic kidney disease patients. The effects of calcium, phosphorous, and vitamin D deficiency on bone turnover, mineralization, and extraskeletal calcifications, as well as their effects on bone turnover, mineralization, and extraskeletal calcifications, are all key components of this disorder. Renal osteodystrophy has traditionally been defined as the outcome of hyperparathyroidism caused by hyperphosphatemia and hypocalcemia, both of which are caused by decreased phosphate excretion by the injured kidney. The inability of the damaged kidneys to convert vitamin D3 into its active form, calcitriol, results in low levels of activated vitamin D3. Phosphate binders, vitamin D compounds, and calcimimetics are the most common treatments for renal osteodystrophy. .Because of their effects on bone turnover, mineralization, and volume, aluminum-containing phosphate binders have been demonstrated to be toxic to bone. Renal osteodystrophy (ROD) begins with a decrease of kidney function (about a 50% reduction in glomerular infiltration rates). ROD affects nearly all patients with severe chronic kidney disease (CKD), and a link has been established between histologic alterations in bone turnover and vascular calcifications .
Publication Year: 2021
Publication Date: 2021-01-01
Language: en
Type: article
Access and Citation
AI Researcher Chatbot
Get quick answers to your questions about the article from our AI researcher chatbot