Warfarin-Induced Pulmonary Metastatic Calcification and Calciphylaxis in a Patient With End-stage Renal Disease

Cadavid, Juan Camilo Pérez; Divietro, Matthew; Torres, Elio; Fumo, Peter; Eiger, Glenn

doi:10.1378/chest.10-1322

Cited by 22 publications

(14 citation statements)

References 14 publications

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“…Warfarin has been associated with vascular calcification in patients receiving dialysis, and an initial concern for dabigatran causing calciphylaxis in our patient was raised; however, to our knowledge, no data have shown an association between dabigatran and calciphylaxis . Our patient had previously been taking warfarin before transitioning to dabigatran, and this was hypothesized to have contributed to her development of calciphylaxis as well as her additional risk factors including female sex, obesity, and renal failure …”

Section: Discussionmentioning

confidence: 80%

Management of Dabigatran‐Associated Bleeding with Two Doses of Idarucizumab Plus Hemodialysis

et al. 2016

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Vitamin K antagonists have been a mainstay of treatment for patients requiring anticoagulation for atrial fibrillation, but direct oral anticoagulants, such as dabigatran, have become increasingly prescribed. Compared with warfarin, dabigatran has a significantly lower risk of life-threatening bleeding; however, bleeding events can still occur, supporting the need for effective reversal strategies. Idarucizumab was recently approved by the U.S. Food and Drug Administration to reverse the anticoagulant effects of dabigatran when life-threatening bleeding occurs or an urgent need for an invasive medical procedure exists. Before idarucizumab's approval, reversal strategies included hemodialysis, coagulation factor replacement, and, in the setting of acute ingestion, activated charcoal. We describe the case of a 58-year-old, obese woman with a history of atrial fibrillation who developed acute kidney injury while taking dabigatran 150 mg twice/day, resulting in coagulopathy. Despite receiving idarucizumab 5 g and hemodialysis, there was a rebound increase in prothrombin time (PT) and activated partial thromboplastin time (aPTT) values, prompting administration of an additional 5-g dose of idarucizumab and continued hemodialysis, with subsequent PT and aPTT values remaining within their appropriate ranges. To our knowledge, this is the first case report to describe the successful use of repeat dosing of idarucizumab with hemodialysis to reverse the anticoagulant effects of dabigatran. Although two doses of idarucizumab were given to our patient, this dosing regimen is not the current standard of practice. Administration of idarucizumab and the use of additional reversal strategies should involve an assessment of each individual patient's severity of bleeding and subsequent risk of thrombosis. Due to the recent availability of idarucizumab and varying success with alternative reversal strategies, additional knowledge is needed for the optimal reversal of anticoagulation from dabigatran.

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Section: Discussionmentioning

confidence: 80%

Management of Dabigatran‐Associated Bleeding with Two Doses of Idarucizumab Plus Hemodialysis

et al. 2016

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“…Multiple case reports have noted an association with calciphylaxis after warfarin initiation even in the absence of ESRD 10 11. One case highlighted onset of calciphylaxis and metastatic pulmonary calcification temporally related to warfarin use 12. The underlying mechanism for development of these lesions remains theoretical with several known associations clinically and biochemically.…”

Section: Discussionmentioning

confidence: 99%

Curious case of calciphylaxis leading to acute mitral regurgitation

et al. 2014

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Calciphylaxis is uncommon and typically seen in patients with end-stage renal disease. It has been defined as a vasculopathic disorder characterised by cutaneous ischaemia and necrosis due to calcification, intimal fibroplasia and thrombosis of pannicular arterioles. We present the case of a 74-year-old woman with chronic kidney disease stage III who developed calciphylaxis leading to mitral valve calcification, chordae tendineae rupture and acute mitral regurgitation. Although an alternative explanation can typically be found for non-uraemic calciphylaxis, her evaluation did not reveal any usual non-uraemic causes including elevated calcium–phosphorus product, hyperparathyroidism, or evidence of connective tissue disease. Her wounds improved with sodium thiosulfate, pamidronate, penicillin and hyperbaric oxygen therapies but she ultimately decompensated with the onset of acute mitral regurgitation attributed to rupture of a previously calcified chordae tendineae. This case highlights an unusual case of calciphylaxis without clear precipitant as well as a novel manifestation of the disease.

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“…Although the exact pathophysiology is not known, risk factors identified from case series suggest causative mechanisms. A role for increased calcium, phosphate, and/or PTH levels is indicated by numerous case reports on calciphylaxis in the context of primary hyperparathyroidism and severe hyperphosphatemia , but many cases are described without any calcium phosphate derangement and with normal PTH. Other risk factors are female gender, obesity, diabetes mellitus .…”

Section: Calciphylaxismentioning

confidence: 99%

Extraosseous Calcification in End‐stage Renal Disease: From Visceral Organs to Vasculature

Molenaar

Reekum

Rookmaaker

et al. 2014

Seminars in Dialysis

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In earlier days, periarticular accumulations of calcium phosphate causing tumor-like depositions were considered the result of passive precipitation and referred to as metastatic calcifications. From sophisticated computer tomographic studies and growing insight, we have learned that calcifications in the cardiovascular system are far more threatening and in fact one of the most important sequela of end-stage renal disease. The histologic characteristic of uremia-related calcification is arteriosclerosis of the media. In addition, there is atherosclerosis of the intima, due to the high prevalence of classic cardiovascular risk factors in renal disease. The two vascular features can frequently exist at different sites in the vasculature. Novel diagnostic techniques are helping to elucidate the pathogenetic mechanisms of active conversion of vascular smooth muscle cells to osteochondritic cells. Through this process, extensive calcification of the central and peripheral vasculature ensues, influenced by different promotors and inhibitors. Calciphylaxis is a special form of extraosseous calcification leading to skin necrosis. The factors that trigger the development of calciphylaxis are not completely understood, but this syndrome shares part of the pathophysiologic basis of extraosseous calcification in general. However, the therapeutic approach must be prompt and aggressive, because of the poor prognosis. Frequently, a fatal outcome cannot be avoided in calciphylaxis.

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Warfarin-Induced Pulmonary Metastatic Calcification and Calciphylaxis in a Patient With End-stage Renal Disease

Cited by 22 publications

References 14 publications

Management of Dabigatran‐Associated Bleeding with Two Doses of Idarucizumab Plus Hemodialysis

Management of Dabigatran‐Associated Bleeding with Two Doses of Idarucizumab Plus Hemodialysis

Curious case of calciphylaxis leading to acute mitral regurgitation

Extraosseous Calcification in End‐stage Renal Disease: From Visceral Organs to Vasculature

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