Journal Information
Vol. 28. Num. 5.October 2008
Pages 475-573
Vol. 28. Num. 5.October 2008
Pages 475-573
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Metastatic pulmonary calcinosis
Calcinosis pulmonar metástasica
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Raquel Montoiro Alluéa, Alfonso Perez Trullenb, Silvia Moreno Loshuertosc
a Servicio de Medicina Intensiva, Hospital Cl??nico Universitario Lozano Blesa, Zaragoza, Zaragoza, Espa??a,
b Servicio de Neumolog??a, Hospital Cl??nico Universitario Lozano Blesa, Zaragoza, Zaragoza, Espa??a,
c Servicio de Nefrolog??a, Hospital Santa B??rbara, Soria, Soria, Espa??a,
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La calcinosis pulmonar metastásica (CPM) es un proceso infrecuente, de etiología desconocida, asociada a una amplia variedad de procesos tanto benignos como malignos. Cuya implicación fisiopatológica es el depósito de calcio en la membrana basal epitelial y vascular del alveolo, paredes bronquiales y capa media de las arterias pulmonares. Dando lugar a una repuesta intersticial linfoproliferativa y fibrosis pulmonar. La importancia de diagnosticar de forma precoz esta complicación radica en que las calcificaciones pulmonares, en este tipo de alteración en concreto, pueden ser potencialmente reversibles con un tratamiento adecuado y precoz.
To the editor: Metastatic pulmonary calcinosis (MPC) is an uncommon process of unknown etiology associated to a wide variety of both benign and malignant conditions. Pathophysiologically, MPC consists of calcium deposition in the epithelial and vascular basement membrane of alveoli, bronchial walls, and media layer of pulmonary arteries, resulting in a lymphoproliferative interstitial response and pulmonary fibrosis. The significance of early diagnosis of this complication lies in the fact that pulmonary calcifications, in this particular condition, may be potentially reversible with adequate, early treatment.
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To the editor: Metastatic pulmonary calcinosis (MPC) is an uncommon process of unknown etiology associated to a wide variety of both benign and malignant conditions. Pathophysiologically, MPC consists of calcium deposition in the epithelial and vascular basement membrane of alveoli, bronchial walls, and media layer of pulmonary arteries, resulting in a lymphoproliferative interstitial response and pulmonary fibrosis. The significance of early diagnosis of this complication lies in the fact that pulmonary calcifications, in this particular condition, may be potentially reversible with adequate, early treatment.



We report the case of a 37-year-old male, a former smoker with no known drug allergies and a history of kidney

transplant for chronic renal failure (CRF) secondary to membranoproliferative glomerulonephritis, systemic arterial hypertension, and acute myocardial infarction. Routine chest Xrays of the patient showed an alveolarinterstitial pattern in both upper lobes, predominately on the left side, with no respiratory symptoms, and was therefore admitted to hospital for diagnostic work-up. Blood and chemistry laboratory test results included: hemoglobin 6.9 g/dL, hematocrit 20.9%, WBCs 9.500/mm3 with normal differential count, platelet count 195,000/mm3, ESR 135 mm, iron metabolism and coagulation study within normal limits, except for fibrinogen increase to 766 mg/dL. Basal glucose 86 mg/dL, creatinine 8.6 mg/dL, urea 119 mg/dL, sodium 138 mEq/L, potassium 4.3 mEq/L, chloride 100 mEq/L, calcium 9.23 mg/dL, phosphorus 7.83 mg/dL, parathormone 2,475 pg/mL, normal TSH, C-reactive protein 1.65 mg/dL, beta-2-microglobulin 20.80 mcg/mL, lipid profile, proteinogram, and liver function within normal ranges. Diagnostic tests included a high-resolution CT scan (fig. 1) that showed highdensity bilateral involvement of middle and upper pulmonary fields consistent with calcifications. Radiographic bone series revealed advanced vascular calcifications. Functional respiratory test results included: forced vital capacity (FVC), 4.22 L (81.2 % of

predicted); forced expiratory volume in the first second (FEV1), 3.60 L (88.4 % of predicted); FEV1/FVC, 85.1 %; RV, 2.04 L (109.4 % of predicted); TLC, 6.23 (91.2 % of predicted). CO diffusion was moderately decreased in absolute values, partially corrected with AV measured, suggesting loss of alveolar units for exchange. Bronchoscopy visualized a bronchial tree with whitish images of a hard consistency, linear and parallel to each other and diffusely distributed in both lungs, consistent with metastatic calcifications. BAL and transbronchial pulmonary biopsy were performed and confirmed diagnosis.



In 1855, Virchow first described metastatic pulmonary calcinosis. This is usually associated to changes in calcium and phosphorus metabolism and to systemic and local pH. The most common cause of metastatic calcifications is chronic renal failure, and other less common causes include primary and secondary hyperparathyroidism, kidney transplant, osteopetrosis, hypervitaminosis D, and malignant diseases such as multiple myeloma, leukemia,

parathyroid carcinoma, and others. A high prevalence (up to 60%-80% in certain series) is found in patients with chronic renal failure undergoing hemodialysis. Chest X-rays are poorly sensitive for diagnosis of this condition, while the greater sensitivity of high-resolution CT allows for detecting small calcifications. Clinical course is usually silent, and most patients remain asymptomatic, as occurred in the onereported here. If calcium deposits are extensive, a decreased diffusion, a restrictive functional pattern, and hypoxemia may be seen. Pulmonary fibrosis may occur in most severe cases, leading to respiratory insufficiency and even death.
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