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Nephrol Dial Transplant (2001) 16: 448-451
© 2001 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

The evolving pattern of calciphylaxis: therapeutic considerations

Francisco Llach

Nephrology Division, Newark Beth Israel Medical Center, Newark, NJ 07112, USA

Keywords: hyperparathyroidism; calcium load; hyper-phosphataemia; phosphorous; uraemia

Introduction

The syndrome of calciphylaxis has evolved over the last three decades. In 1962, Selye first described a syndrome in the experimental animal [1] and postulated that two steps are required to produce ectopic systemic calcification. First, a systemic sensitization induced by agents such as parathyroid hormone (PTH), vitamin D or a diet high in calcium (Ca) and phosphorus (P). Secondly after a time interval (the ‘critical period’) exposure to appropriate challenging agents by subcutaneous injection which results in macroscopically visible deposits of calcium salts (hydroxapatite) systemically and at the site of injection within 2 to 3 days. The challenging agents include local trauma, iron salt, egg albumin, polymycin and glucocorticoids. Selye named the syndrome calciphylaxis. A few years later a syndrome characterized by peripheral ischaemic tissular necrosis, vascular calcifications and cutaneous ulcerations was reported in uraemic patients, and because of its resemblance to Selye's animal model, it was . . . [Full Text of this Article]

Therapeutic considerations

Notes

References


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