Calcium-Carbonate-Induced Calciphylaxis

Campistol, Josep M.; Almirall, Jaume; Martin, E; Torrás, A; Revert, L

doi:10.1159/000185393

Cited by 27 publications

(12 citation statements)

References 5 publications

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“…8 Furthermore, high doses of calcium carbonate have been associated with CUA, which reversed following its discontinuation. 9 On the other hand, protracted hyperphosphatemia remains an important predisposing factor. This is especially seen in adynamic bone lesion and patients who have had parathyroidectomies.…”

Section: Discussionmentioning

confidence: 99%

Calcific uremic arteriopathy in a patient with long-standing uremia and severe hyperparathyroidism

et al. 2006

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Calcific uremic arteriopathy (CUA) is a rare complication of uremia. Its pathogenesis is not known, and there is no well-defined treatment for it. In this report we describe CUA in a patient with end-stage renal failure who had undergone hemodialysis (HD) for 12 years. The patient developed end-stage renal failure 12 years prior to this report because of chronic glomerulonephritis, and was managed by HD. He had a renal transplant soon after initiation of HD, but this graft failed within a month because of acute rejection, and HD was resumed. He became hepatitis C positive 2 years later, and tests showed the development of impaired liver function. A year prior to this report, the patient developed tubercular ascites and responded well to antituberculous drugs. Six months prior to this report he noticed the development of multiple ulcerations in his toes and digits with ischemic pain. These lesions slowly increased in number and size. The patient was managed by strictly controlling phosphorus and by anticoagulation, followed by parathyroidectomy. This led to complete healing of most ischemic lesions and improvement of others. We attribute the CUA in this patient to prolonged hyperphosphatemia and hyperparathyroidism. Control of hyperphosphatemia, parathyroidectomy, local care, and anticoagulation are important therapeutic measures for this rare but life-threatening complication of chronic uremia.

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Section: Discussionmentioning

confidence: 99%

Calcific uremic arteriopathy in a patient with long-standing uremia and severe hyperparathyroidism

et al. 2006

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“…Most of the risk factors described point overwhelmingly to an altered calcium and phosphate milieu (Table 1), although CUA may occur in patients with serum calcium, phosphate and PTH concentrations in target ranges. Major risk factors for CUA include white race, younger age, elevated serum calcium or phosphate concentration, calcium3phosphate product and PTH concentrations (5), lower serum albumin, elevated serum alkaline phosphatase, and protein C and/or S deficiency (16)(17)(18)(19)(20)(21). Local trauma, obesity (body mass index.30), liver disease, and use of systemic corticosteroids and warfarin have also been found to be independent risk factors (4,5,(16)(17)(18).…”

Section: Risk Factorsmentioning

confidence: 99%

“…Warfarin likely promotes the development of CUA by reducing functional protein C levels and blocking vitamin K-dependent carboxylation of the matrix GLA protein, which is a local inhibitor of vascular calcification (22,23). Use of calcium supplements has been associated with increased risk of calciphylaxis in some (19,24), but not, all studies (7,17). Recent studies have suggested that parenteral iron may also be associated with development of CUA (25,26).…”

Section: Risk Factorsmentioning

confidence: 99%

Painful Skin Ulcers in a Hemodialysis Patient

Sprague

2014

Clinical Journal of the American Society of Nephrology

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SummaryCalciphylaxis, also referred to as calcific uremic arteriolopathy, is a relatively rare but well described syndrome that occurs most commonly in patients with late stage CKD. It is characterized by very painful placques or subcutaneous nodules and violaceous, mottled skin lesions that may progress to nonhealing ulcers, tissue necrosis, and gangrene with a 1-year mortality rate >50%. The pathogenesis of calciphylaxis is poorly understood. Risk factors include female sex, obesity, hyperphosphatemia, hypercalcemia, hyperparathyroidism, longer dialysis vintage, hypercoagulable states, and use of calcium-containing phosphate binders and warfarin. Treatment strategies for calciphylaxis are limited by inadequate understanding of its pathophysiology. Therapy is generally focused on correcting disturbances of calcium, phosphorus, and parathyroid hormone metabolism. Additional therapy focuses on decreasing inflammation and on dissolution of tissue calcium deposits with sodium thiosulfate and/or bisphosphonates. Successful treatment generally results in improvement of pain and healing of the lesions within 2-4 weeks, but the disorder generally takes many months to completely resolve.Clin J Am Soc Nephrol 9: 166-173, 2014. doi: 10.2215/CJN.00320113Case Description Abhijit Naik, MD (Renal Fellow). A 54-year-old white man was referred from an outside dialysis clinic for evaluation of necrotic skin lesions. He had a 10-year history of diabetes and hypertension, with ESRD secondary to diabetes. His history was also significant for coronary artery disease, with two prior myocardial infarctions and atrial fibrillation. He had been undergoing thrice-weekly hemodialysis for 2 years with a Kt/V between 1.3-1.4. Three months before presentation he noticed several small firm and very painful nodules on both anterior thighs. He stated that after several weeks the lesions became much larger, black, and spread to the lateral thighs and buttocks. He was treated with mupirocin ointment and a vascular evaluation revealed normal blood flow in his legs. Aside from these painful lesions, he stated that he generally felt "ok." Dialysis had been proceeding without problems. He denied chest pain, dyspnea, abdominal pain, or any gastrointestinal complaints. Review of systems was otherwise unremarkable. He never smoked and drank alcohol very infrequently. Medications included aspirin, amiodarone, simvastatin, famotidine, glipizide, clopidogrel, sevelamer carbonate, hydrocodone, and gabapentin. He had no known allergies.On examination his vital signs were as follows: temperature, 98.8°F; heart rate, 80 beats per minute; BP, 94/60 mmHg, with no orthostatic changes; and respiratory rate, 20 breaths per minute. His BP was generally low, with systolic BP averaging between 90 and 100 mmHg. He was an ill appearing male in mild distress from extremity pain. His lungs were clear and a cardiovascular examination revealed a regular rate and rhythm with a 2/6 holosystolic murmur. His abdomen had normal bowel sounds and was mildly distended with some asc...

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“…The serum phosphorus concentration may be lower by using non-calcium-containing phosphate binders (e.g., sevelamer) and intensifying hemodialysis as to increase removal of phosphorus. Calcium supplements and vitamin D should be avoided, as they are known risk factors for the development of calciphylaxis [52][53][54]. In addition, the use of dialysates containing low calcium concentrations has also been recommended [55].…”

Section: Management Of Calciphylaxismentioning

confidence: 99%

Proceedings: Pathogenesis and Treatment of Renal Osteodystrophy

2003

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Renal osteodystrophy is the term used to describe the many different patterns of the skeletal abnormalities that occur in patients with chronic kidney disease. The main two conditions are osteitis fibrosa, characterized by high bone turnover, increased osteoclastic and osteoblastic activity, and high levels of circulating parathyroid hormone (PTH) and adynamic bone disease characterized by low bone turnover and low levels of circulating PTH. Retention of phosphorus, decreased levels of calcitriol in blood, decreased levels of serum ionized calcium, reduced numbers of vitamin D receptors and calcium sensors in the parathyroid gland, and skeletal resistance to the calcemic action of PTH play a major role in the development of renal osteodystrophy. This review will describe the current approach for the treatment of renal osteodystrophy.

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Calcium-Carbonate-Induced Calciphylaxis

Cited by 27 publications

References 5 publications

Calcific uremic arteriopathy in a patient with long-standing uremia and severe hyperparathyroidism

Calcific uremic arteriopathy in a patient with long-standing uremia and severe hyperparathyroidism

Painful Skin Ulcers in a Hemodialysis Patient

Proceedings: Pathogenesis and Treatment of Renal Osteodystrophy

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