Calcinosis cutis and renal failure

Kolton, B.

doi:10.1001/archderm.110.2.256

Cited by 19 publications

(19 citation statements)

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“…Calcification of the skin (known as calcinosis cutis), characterized by the deposition of hydroxyapatite crystal in the derma, is a rare soft tissue calcification [4,5]. Contrary to common tumoral calcinosis, characterized by subcutaneous and juxta-articular location with a large size and a tendency to progressive enlargement, calcinosis cutis exhibits a predilection around the greater joints, axillae, medial thighs, flexural areas and iliac crests, and presents as nodules or plaques which may become fluctuant, break down and extrude chalky contents, as in our case [6]. Calcinosis cutis has been historically divided into 3 types including: (i) the more common dystrophic form in patients with damaged skin resulting from inflammation (e.g., scleroderma) and normal serum levels of calcium and phosphate; (ii) the less common metastatic form resulting from abnormal levels of calcium or phosphate, and (iii) the very rare idiopathic form [6].…”

Section: Discussionmentioning

confidence: 75%

Diffuse Calcinosis and Intradermal Tophi in a Uremic Patient: Effect of Low-Calcium Hemodialysis and Mechanism of Hypercalcemia

Hsu

Lee²,

Wang³

et al. 2004

Blood Purif

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Soft tissue calcification is a frequent complication in end-stage renal disease (ESRD) patients with a high serum calcium-phosphate product, but systemic involvement of both the visceral organs and skin is rarely seen. We report on a newly diagnosed ESRD patient with gouty nephropathy who had initial presentations of extensive intradermal tophi, diffuse calcinosis, and hypercalcemia. He received maintenance hemodialysis (HD) with low-calcium dialysate (1.25 mEq/l) for 11 months. Although the above complications diminished, serum calcium remained elevated. Thereafter, unexpected cervical lymphadenitis from a Mycobacterium tuberculosis (TB) infection with high extra-renal production of calcitriol was found. Serum calcium levels normalized only after anti-TB treatment for 2 months. We thought that this patient might have had occult TB infection before the start of HD, which resulted in calcitriol production and hypercalcemia. In addition, concomitant hyperphosphatemia in chronic renal failure contributed to severe diffuse calcinosis. After the initiation of HD therapy, both the elevated serum calcitriol levels and accelerated resolution and mobilization of diffuse calcinosis from low-calcium HD contributed to persistent hypercalcemia.

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Section: Discussionmentioning

confidence: 75%

Diffuse Calcinosis and Intradermal Tophi in a Uremic Patient: Effect of Low-Calcium Hemodialysis and Mechanism of Hypercalcemia

Hsu

Lee²,

Wang³

et al. 2004

Blood Purif

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“…Classic metastatic calcinosis [2] due to chronic renal failure occurs with secondary hyperparathyroidism when the C axP product is much higher than 70. The calcium deposits occur most frequently in the abdominal mucosa, the lungs, the kidney or the heart and much more rarely in the skin.…”

Section: Metastatic Calcinosismentioning

confidence: 99%

Chronic Renal Failure and Skin Calcifications

Poesen

Heidbüchel²,

Morren³

1995

Dermatology

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“…Trois tableaux cliniques avec dépôts calciques sans nécrose Dépôts intradermiques [22][23][24][25], Des papules, nodules ou plaques apparaissent brusquement, souvent après grattage, essentiellement au voisinage des grosses articulations et des plis. Décoloration brunâtre [23]. blanchâtre [25], érythémateuse [23].…”

Section: Tableaux Cliniquesunclassified

“…Décoloration brunâtre [23]. blanchâtre [25], érythémateuse [23]. elles tendent à s'ombiliquer et à exprimer un matériel crayeux [22], Dépôts hypodermiques (7.24.26].…”

Section: Tableaux Cliniquesunclassified

“…11.12], Il apparaît logique dès lors de rapprocher les différents tableaux clini ques et de les intégrer dans une entité unique avec une étiopathogénie semblable et une approche thérapeutique identique. La raison pour laquelle les calcinoses n'entraînent pas de phénomène de nécrose dans certains cas [22][23][24][25][26][27][28] reste obscure.…”

Section: Mécanisme Des Nécrosesunclassified

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Calciphylaxie?

Bourlond¹,

Eggers²,

Willocx³

et al. 1989

Dermatology

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A patient with end-stage renal failure on chronic hemodialysis, with secondary hyperparathyroidism and hyperphosphatemia, developed widespread and painful necrotic lesions involving the skin and the subcutaneous fat of the left leg and the lower portion of the abdomen. On X-ray examination the areas showed severe soft tissue as well as vascular calcification. The literature is reviewed and the pathogenetic factors are analyzed: high product of calcium and phosphate; hyperparathyroidism, calciphylaxis. Subtotal parathyroidectomy is considered the best treatment, because it may result in rapid cure of the cutaneous ulcers.

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Calcinosis cutis and renal failure

Cited by 19 publications

References 0 publications

Diffuse Calcinosis and Intradermal Tophi in a Uremic Patient: Effect of Low-Calcium Hemodialysis and Mechanism of Hypercalcemia

Diffuse Calcinosis and Intradermal Tophi in a Uremic Patient: Effect of Low-Calcium Hemodialysis and Mechanism of Hypercalcemia

Chronic Renal Failure and Skin Calcifications

Calciphylaxie?

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