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Results for “Calciphylaxis”

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At least 559 records · Page 31Linked to original sources
PubMed2005

Cutaneous necrosis by calcific uremic arteriolopathy.

BACKGROUND: Calcific uremic arteriolopathy is a rare and serious disorder characterized by systemic medial calcification of the arteries and tissue ischemia. Most often it is found in patients with chronic renal failure on dialysis and in renal transplant recipients with secondary hyperparathyroidism. METHODS: We report six patients with end-stage renal disease [five on hemodialysis (one with a nonfunctioning renal graft) and one on peritoneal dialysis] who developed painful livedo reticularis and skin necrosis of the limbs. All had secondary hyperparathyroidism and elevated calcium-phosphorus product. Our patients presented with the following clinical features: white race (six patients), hypoalbuminemia (three patients), diabetes (one patient), and obesity (four patients). RESULTS: Subtotal parathyroidectomy was performed in three cases. Despite this procedure, two patients died; one patient survived and his lesions healed. One patient was treated with aggressive wound care and hemodialysis (with low dialysate calcium concentration and Renagel phosphorus binders) and one patient received only local wound care, both with improvement of their lesions. In one case, no therapy was performed because the patient died immediately after diagnosis. CONCLUSIONS: The three patients who survived (Cases 4, 5 and 6) had distal lesions, normal serum albumin, and an early diagnosis. There was a relationship between the outcome of the patients and these factors, rather than the type of treatment received.

Adult↗
PubMed1968

Calcergy inhibited by calciphylactic challengers.

The subcutaneous calcification effected in the rat at sites directly treated with calcergens, such as lead acetate, CeCl(3), CaCl(2), and KMnO(4), is inhibited by simultaneous local application of various calciphylactic challengers, but not by many other compounds.

Aluminum↗
PubMed1991

Fulminant calcinosis in two patients after kidney transplantation.

The first patient had total parathyroidectomy (PTX) with autografting 2 years before. She developed disabling soft-tissue calcifications following kidney transplantation. After reduction of the autograft--a complete removal was not possible--the subcutaneous calcifications regressed. In the second patient, fulminant necrotizing vascular calcinosis developed after successful renal transplantation. Total PTX without autotransplantation was carried out, and progression of the vascular disease was ceased. In both patients, the parathyroid hormone was elevated but not the calcium-phosphate product. We suggest that fulminant calcinosis in patients with kidney transplants requires PTX.

Adult↗
PubMed1993

Mathematical formulation to help identify the patient at risk of ischemic tissue necrosis--a potentially lethal complication of chronic renal failure.

Ischemic tissue necrosis (ITN) has been described as a complication of hyperparathyroidism (HPT) in patients with end-stage renal disease (ESRD) and is associated with a mortality rate of up to 80%. Early recognition of ITN is important but difficult. Optimal treatment is controversial. Based on an analysis of the English literature and a recent clinical experience, a mathematical expression to aid in the identification of high-risk patients (2 x [CaPO(4) - 5] x alkaline phosphatase x PTH ratio) was developed. The values for this expression were calculated in 3 recently reported cases and our case (n = 4). The values were compared with those of a group of 54 hyperparathyroid chronic hemodialysis patients (controls); the mean values were significantly different (p < 0.001). The expression, consisting of 4 easily measured laboratory values, appears to differentiate patients with this complication of ITN from patients with only severe HPT. Ten new additional cases were evaluated using the equation; the sensitivity of the equation was 80% and the specificity 92%, positive predictive value was 66% and the negative predictive value 96%. Long-term validation of this equation is required but it appears to be discriminatory and, thus, promising, given the potentially lethal consequences of ITN.

Adult↗
PubMed2006

Heart of stone.

Explore the source record for details and available documents.

Adult↗
PubMed2006

Successful management of critical limb ischemia with intravenous sodium thiosulfate in a chronic hemodialysis patient.

Vascular calcification is common among hemodialysis (HD) patients and contributes to the development of peripheral arterial disease. A 57-year-old Japanese man who had been on HD for 30 years was referred to us for severe pain with multiple ulcers on his toes and fingers. He was an ex-smoker and had no diabetes mellitus. On admission, he had ulcers on his big toes bilaterally and right 2nd - 4th fingers. Peripheral pulses were strong and his ankle-brachial pressure index was above 1.3. Laboratory data were as follows: calcium 9.9 mg/dl, albumin 3.3 g/dl, phosphate 3.0 mg/dl, Ca x P product 30, and parathyroid hormone 98 pg/ml. He had a parathyroidectomy in 1998 and 1999. X-rays of his hands and legs showed diffuse subcutaneous arteriolar calcification. Angiography revealed no local stenotic lesions. Despite intensive therapies including hyperbaric oxygen therapy, painful gangrene developed on his right big toe and the pain was so intense that he could not go to sleep in a supine position. We infused intravenous sodium thiosulfate (20 g) 3 times weekly, based on previous reports. Within 4 - 5 days, he experienced rapid and dramatic symptom relief. The score of the visual analogue pain scale improved from 10/10 - 2/10. The signs of ischemia, measured by transcutaneous partial oxygen pressure and thermography, improved significantly. During the infusion of sodium thiosulfate, the patient complained of nausea, vomiting and hyperosmia. These adverse symptoms were resolved after discontinuation of the infusion. Pain relief was sustained and he could walk after 2 weeks of infusion. Our case supports the use of sodium thiosulfate as a novel therapeutic choice for critical limb ischemia with severe vascular calcification in chronic HD patients.

Calcinosis↗