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The Symptoms Of Kidney Insufficenecy With Abnormal Phosphorus Metabolism

2018-08-13 10:05

Phosphorus can inhibit PTH’s bone calcium release, interfere with intestinal reabsorption and redeposit calcium salt in bone. Phosphorus can also inhibit the hydroxylation of vitamin d in kidney tissue.

Clinically, a series of manifestations caused by phosphorus metabolism disorder are mainly caused by hyperphosphatemia and secondary hyperparathyroidism. High phosphorus can itself induce metastatic calcification and tissue damage, while cutaneous and subcutaneous tissue metastatic calcification are manifested as itching, while corneal calcification causes banded keratoma.The combined subcapsular calcification showed acute irritation symptoms and ” diseased eyes”. Renal calcification can cause renal damage and become one of the mechanisms of renal disease progression. Other rare metastatic calcifications are soft tissue necrosis, tumor calcium deposition disease, etc. When the calcium-phosphorus deposition exceeds 60 – 70, the risk of metastatic calcification obviously increases. However, even in CRF, the blood calcium level can be better adjusted. Therefore, it is mainly determined by the phosphorus level. It is generally believed that the blood phosphorus level exceeds 4 mmol / l ( 12 mg / dl ), which indicates that the phosphorus load in the body increases. When the blood phosphorus level exceeds 4 to 5 mmol / l ( 12 to 15 mg / dl ), the risk of metastatic calcification increases significantly.

Secondary hyperparathyroidism mainly causes osteodystrophy, with clinical manifestations of proximal myopathy, soft tissue calcification and bone disease. Bone disease mainly includes the following series of manifestations:

It is characterized by incomplete mineralization of bone and formation of various kinds of bone. Its mechanism is low calcium, high phosphorus, decreased activity of 1,25 – ( oh ) 2vd 3 and increased PTH. Other diseases, such as acidosis, uremic toxin, and aluminum poisoning and malnutrition are also related.

Mainly caused by PTH, osteoclast activity increases and bone salt dissolves, showing spongiform disease and cancellous bone trabecula formation.

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