British Journal of Radiology 75 (2002),74-77 © 2002 The British Institute of Radiology
Metastatic pulmonary calcification in renal failure: a new HRCT pattern
R K Lingam, BSc (Hon), MRCP, FRCR
1
J Teh, BSc, MRCP, FRCR
2
A Sharma, MRCP, FRCR
1 and
E Friedman, MRCP, FRCR
1
1Department of Diagnostic Radiology, Royal London Hospital, London E1 1BB and 2Department of Diagnostic Radiology, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3 7LD, UK
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Abstract
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A 56-year-old male with chronic renal failure presented with a 6 month history of progressive dyspnoea. High resolution CT of the chest showed multiple, peripheral, centrilobular nodules in the upper and mid zones, consistent with metastatic pulmonary calcification. Some of these pulmonary nodules showed ring calcification, a pattern that to our knowledge has not been described before. Calcification was also seen in the segmental pulmonary arteries, bronchi, trachea and subcutaneous vessels of the chest wall.
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Introduction
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Metastatic pulmonary calcification (MPC) is a well known complication of end-stage renal failure (ESRF) and its treatment. It is usually asymptomatic or has a benign course [1], but in some cases can cause fulminant respiratory failure and early death [2]. High resolution CT (HRCT), with its excellent sensitivity in the detection of small amounts of calcification, is being increasingly used to diagnose MPC. Several CT patterns have been documented to date [2, 3]. We present a case of MPC in a patient with ESRF whose HRCT images demonstrated multiple, peripheral, centrilobular nodules in the upper and mid zones with ring calcification, a pattern that, to our knowledge, has not been previously described.
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Case report
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A 56-year-old male with ESRF, treated with renal transplantation, was referred for HRCT for evaluation of an abnormal chest radiograph. He had persisting dsypnoea for 6 months. Lung function tests demonstrated normal lung volumes but a markedly reduced transfer factor and transfer coefficient (40% and 57% of predicted values, respectively). The patient first presented with ESRF, as a result of chronic glomerulonephritis in 1970. He was on maintenance haemodialysis until 1984 when chronic ambulatory peritoneal dialysis was commenced. In 1987 he received his third cadaveric renal transplant and had a stable baseline creatinine (Cr) level of 180 µmol l-1 (60120 µmol l-1). There was evidence of ischaemic heart disease with normal left ventricular and valvular function on echocardiography. Renal function deteriorated over the last year, with an average Cr level of 320 µmol l-1 following several insults including contrast nephropathy, pyelonephritis and diuretic toxicity. At one stage an elevated parathormone level at 76 pg ml-1 (1065 pg ml-1) was recorded. Serum calcium level remained stable at 2.4 mmol l-1 (2.22.6 mmol l-1) and phosphate at 1.7 mmol l-1 (0.81.4 mmol l-1). Renal biopsy showed evidence of chronic glomerulopathy.
Chest radiography (Figure 1a
) demonstrated multiple, ill defined, peripheral, symmetrically distributed nodules in the upper and mid zones. The lung bases were spared and opacities were not dense enough to suggest calcification. Multiple calcified blood vessels were seen in the subcutaneous tissues of the chest wall (Figure 1b
). A chest radiograph obtained 5 months earlier had a similar appearance, whereas a chest radiograph obtained 8 months previously showed only chest wall vascular calcification.

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Figure 1. (a) Posteroanterior chest radiograph showing multiple, ill defined, peripheral opacities both in the upper and mid zones. (b) Magnified view of the left supraclavicular fossa showing vascular calcification in the subcutaneous tissues.
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HRCT of the chest (Figure 2
), using 1 mm collimation at 10 mm intervals (Siemens Somatom Plus 4 scanner; Siemens, Erlangen, Germany), showed multiple centrilobular nodules situated peripherally approximately 1 cm from the pleural edge. There was a symmetrical distribution involving the apices and the mid zones. Many of the nodules were confluent. Several nodules demonstrated calcification (180 HU) that was either diffuse or ring-like, with a central lucency. No consolidation or ground-glass opacity was seen. A thin rim of calcification surrounded the trachea, main bronchi, segmental pulmonary arteries and the vessels of the chest wall. There was no evidence of pulmonary fibrosis.

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Figure 2. (a,b) Magnified images of the mediastinum (level 35, window 550) and lung (level -500, window 1500) showing ring calcification of the pulmonary nodules (straight arrows) and calcification of the segmental pulmonary arteries (curved arrows).
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Discussion
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Multifocal pulmonary parenchymal calcification is associated with infection, especially histoplasmosis and varicella zoster pneumonia, MPC, silicosis, diffuse parenchymal amyloidosis, alveolar microlithiasis, haemosiderosis secondary to mitral stenosis and fat embolism associated with adult respiratory distress syndrome. It also occurs in treated metastases and in metastatic malignancies such as osteogenic sarcoma, chondrosarcoma, mucin-producing adenocarcinomas and thyroid malignancies [4]. In the clinical context of chronic renal failure, the most likely cause for pulmonary parenchymal calcification is MPC. The patient had no clinical history of dust exposure, cardiac problems or malignancy. Mantoux test was negative. Although both diffuse pulmonary amyloidosis and alveolar microlithiasis can cause progressive dyspnoea and pulmonary calcification on HRCT, their HRCT patterns are somewhat different. The calcified nodules in diffuse parenchymal amyloidosis are located predominantly in the subpleural areas of the mid and lower zones and are associated with hilar lymphadenopathy, interlobular septal thickening, consolidation and ground-glass opacities [5]. The calcified pulmonary nodules in alveolar microlithiasis are smaller (about 1 mm in diameter), typically occur in the lower zones and the paracardiac regions and may be associated with apical bullae and subpleural cysts [5]. Although a possible limitation of this case is the lack of pathological proof to support the diagnosis of MPC, this is not required owing to the characteristic appearance of calcium combined with the clinical history and the serial chest radiographs.
MPC occurs in disease states with concurrent derangement of calcium and phosphorus metabolism. It is most commonly seen in chronic renal failure [1, 3] but has been described in primary and secondary hyperparathyroidism, D hypervitaminosis, milk-alkali syndrome, diffuse myelomatosis and extensive bone malignancy. Abnormal pulmonary and cardiac calcifications have been reported at autopsy in 4080% of patients with ESRF [2, 6]. MPC is characterized by diffuse calcium deposition in the lung. Pathologically, it is an interstitial process with calcium deposited in the alveolar septa and bronchial walls and, to a lesser extent, in bronchioles and pulmonary arterioles [6]. Calcium deposition can lead to interstitial fibrosis in severe cases and can result in respiratory insufficiency [2, 6].
Conventional chest radiography is of little help in diagnosing MPC. First, it is insensitive in depicting small amounts of calcification, probably owing to the small size of calcium deposits and the high tube potential (kV) techniques used [7]. Second, changes on chest radiography are not specific. MPC has been described as confluent or patchy airspace opacities simulating pulmonary oedema or pneumonia that do not improve despite treatment of these conditions [1, 2]. Although the density in most of the reported cases is not sufficiently high to suggest calcification, the opacities in some cases are massively calcified or become progressively more dense when left untreated. MPC can also appear as a diffuse interstitial process or as discrete or confluent calcified nodules [2, 7].
CT, especially HRCT, is much more sensitive than chest radiography in detecting small amounts of calcification and is increasingly used in the diagnosis of MPC, thereby obviating the need for open lung biopsy [1]. Three patterns of pulmonary calcification have been described in the literature. The first pattern is multiple diffuse calcified nodules that are either distributed throughout the whole lung [2] or show a predilection for the apices [2, 3] or the bases [2]. The second pattern is diffuse or patchy areas of ground-glass opacity or consolidation [2]. Finally, MPC may appear as a confluent high attenuation parenchymal consolidation in a predominantly lobar distribution, mimicking lobar pneumonia [3]. Several authors have also described calcification in the bronchial walls, myocardium and within the vessels of the chest wall [1, 2, 8]. The combination of pulmonary and vascular calcification is said to be characteristic of MPC [2]. We describe a HRCT pattern with peripheral, symmetrical, centrilobular nodules in the upper and mid zones. One recent case report [8] described subpleural nodules in the lower lobe, but the HRCT images showed ground-glass opacification and consolidation. We also noted ring calcification of these nodules, which, to our knowledge, has not been previously described. Although histology was not obtained in this case, calcium deposition in the bronchioles, alveolar septa and pulmonary arterioles is well established in histopathological studies of MPC in cases of renal failure. We postulate that the ring calcification demonstrated on HRCT represents changes in these areas.
This case also shows calcification in the segmental pulmonary arteries, trachea and bronchi. Pulmonary arterial calcification is rare and has, so far, only been described in a few patients with prolonged pulmonary hypertension and in the Eisenmenger syndrome [9]. Pulmonary arteriolar calcification seen on CT in MPC has been described [8]. Tracheobronchial calcification is described quite commonly in the elderly and also in cases of MPC, tracheopathia osteochondroplastica and, more rarely, in children [2, 10].
With the advent of CT and HRCT, it is becoming increasingly easy to make an ante-mortem diagnosis of MPC, thereby obviating the need for open lung biopsy. It is therefore important for the radiologist to recognize the HRCT patterns of this relatively common disease process afflicting patients with chronic renal failure.
Received for publication June 28, 2001.
Accepted for publication July 24, 2001.
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References
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Kuhlman JE, Ren H, Hutchins GM, Fishman EK. Fulminant pulmonary calcification complicating renal transplantation: CT demonstration. Radiology 1989;173:45960.[Abstract/Free Full Text]
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