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Calciphylaxis, also known as calcific uremic arteriolopathy (CUA) or “Grey Scale”, is a rare syndrome characterized by painful skin lesions.The pathogenesis of calciphylaxis is unclear but believed to involve calcification of the small blood vessels located within the fatty tissue and deeper layers of the skin, blood clots, and eventual death of skin cells due to lack of blood flow. [1]
Calcinosis cutis is an uncommon condition marked by calcium buildup in the skin and subcutaneous tissues. Calcinosis cutis can range in intensity from little nodules in one area of the body to huge, crippling lesions affecting a vast portion of the body. [1]
The term nephrocalcinosis is used to describe the deposition of both calcium oxalate and calcium phosphate. [1] It may cause acute kidney injury. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification in radiology. [2] It is caused by multiple different conditions and is determined by progressive kidney dysfunction.
Calcinosis is the formation of calcium deposits in any soft tissue. [1] It is a rare condition that has many different causes. These range from infection and injury to systemic diseases like kidney failure .
Phosphate nephropathy or nephrocalcinosis [1] is an adverse renal condition that arises with a formation of phosphate crystals within the kidney's tubules. This renal insufficiency is associated with the use of oral sodium phosphate (OSP) such as C.B. Fleet's Phospho soda and Salix's Visocol, for bowel cleansing prior to a colonoscopy.
Hypercalciuria is the condition of elevated calcium in the urine. Chronic hypercalciuria may lead to impairment of renal function, nephrocalcinosis, and chronic kidney disease. Patients with hypercalciuria have kidneys that excrete higher levels of calcium than normal, for which there are many possible causes. Calcium may come from one of two ...
The kidney fails to respond adequately to PTH, which normally promotes phosphaturia and calcium reabsorption, or to FGF-23, which also enhances phosphate excretion. [2] In addition, there is evidence at the tissue level of a downregulation of vitamin D receptor and of resistance to the actions of PTH.
However, both the acute and chronic form of this illness involve renal impairment which is a key contributor to the hypercalcemia seen in people with MAS. Cope and Burnett believe that the kidney damage caused by ingesting high amounts of calcium and alkali occurs first which subsequently makes removal of calcium from the body difficult. [3] [16]
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