CALCIPHYLAXIS: A SEVERE COMPLICATION OF RENAL DISEASE

An 82-year-old man with end-renal disease, who had been receiving he modialysis for five years, presented with a three-month history of erythematous patches on his legs. Clinical examination showed multiple painful cutaneous ulcerations coated with dark eschar, surrounded by indurated, violaceous plaques (figure 1). An important laboratory finding was a markedly elevanted phosphate concentration (1.95 {normal 0.87-1.45} mmol/L), associated with normal concentrations of calcium and parathyroid hormone. Histopathologic evaluation showed intramural deposition of calcium in several subcutaneous arterioles (appendix 1, avalaible at www.cmaj.ca/lookup/suppl/doi:10.1503/emaj.110046/-/DC 1). Radiologic

examination showed calcification of the large arteries of the leg (appendix 2, available at www.cmaj.ca/lookup/suppl/doi:10.1503/emaj.110046/-/DC 1).caciphylaxis was diagnosed. surgical debridement was performed, and the patient was given culture directed intravenous antibiotic therapy, resulting in an improvement in the skin lesions. However, his general condition worsened, and he eventually died of septicemia. Calciphylaxis, also known as calcific uremic arteriolopathy, is a microvasculer occlusion syndrome with mural calcification of arterioles leading to severe ischemia of the tissue. It occurs in up to 4% of patients undergoing long-term dialysis, but sporadic instances in patients with normal renal function have also been reported. In addition to kidney failure, other risk factors include obesity, female sex, with race, liver disease, use of systemic corticosteroids, decreased albumin levels and elevated calcium-phosphorus

product.parathyroid hormone is often found to be abnormal. Mortality associated one-year rate of survival of 45%. The pathogenesis of calciphylaxis may be linked to an imbalance of homeostasis in the bones. Excisional biopsy should be done to confirm the diagnosis. The main differential diagnoses incluse pyoderma gangrenosum, coagulopathies and arteriosclerotic ulcers. although there are no guidelines on therapy, treatment usually consists of surgical debridement of necroticlesions of the underlying metabolic disturbances. Prosessing result have been reported after treatment with cinacalcet and sodium thiosulfate.

CALCIPHYLAXIS: KOMPLIKASI PARAH PENYAKIT GINJAL.

Seorang pria 82-tahun dengan akhir penyakit ginjal, yang telah menerima dia modialysis selama lima tahun, disajikan dengan sejarah tiga bulan memperbaiki eritematosa pada kakinya. Pemeriksaan klinis menunjukkan ulserasi kulit yang menyakitkan beberapa dilapisi dengan eschar gelap, dikelilingi oleh indurated, plak lembayung. Temuan laboratorium penting adalah konsentrasi fosfat nyata elevanted (1,95} {yang normal 0,871,45 mmol / L), dikaitkan dengan konsentrasi normal kalsium dan hormon paratiroid. Evaluasi histopatologi menunjukkan deposisi intramural kalsium dalam arteriol beberapa subkutan (lampiran 1, avalaible di www.cmaj.ca/lookup/suppl/doi:10.1503/emaj.110046//DC 1). Pemeriksaan radiologis menunjukkan kalsifikasi arteri besar dari kaki (lampiran 2, tersedia di www.cmaj.ca/lookup/suppl/doi:10.1503/emaj.110046/-/DC 1). Caciphylaxis didiagnosis. debridemen dilakukan, dan pasien diberi terapi diarahkan budaya antibiotik intravena, mengakibatkan perbaikan dalam lesi kulit. Namun, kondisi umum memburuk, dan ia akhirnya meninggal karena septikemia. Calciphylaxis, juga dikenal sebagai arteriolopathy uremik kalsifikasi, adalah oklusi microvasculer sindrom dengan kalsifikasi mural arteriol menyebabkan iskemia jaringan parah. Ini terjadi pada sampai dengan 4% dari pasien yang menjalani dialisis jangka panjang, namun kasus sporadis pada pasien dengan fungsi ginjal normal juga telah dilaporkan. Selain gagal ginjal, faktor risiko lain termasuk obesitas, jenis kelamin perempuan, dengan ras, penyakit hati, penggunaan kortikosteroid sistemik, penurunan kadar albumin dan peningkatan kalsium-fosfor hormon product.parathyroid sering ditemukan normal. Kematian terkait satu tahun tingkat kelangsungan hidup 45%. Patogenesis calciphylaxis mungkin berhubungan dengan ketidakseimbangan

homeostasis dalam tulang. Eksisi biopsi harus dilakukan untuk mengkonfirmasi diagnosis. Diagnosis diferensial utama pioderma gangrenosum incluse, koagulopati dan bisul arteriosclerotic. meskipun tidak ada pedoman pada terapi, pengobatan biasanya terdiri dari debridement bedah necroticlesions dari gangguan metabolik yang mendasari. proses hasilnya telah dilaporkan setelah pengobatan dengan cinacalcet dan natrium tiosulfat.