A 23-year-old male with end-stage renal disease (ESRD) on haemodialysis for 3.5 years after a failed renal transplant, presented to our medical centre in October of 2012 for evaluation of a dilated aortic root. His history is notable for Caroli disease, autosomal recessive polycystic kidney disease, bilateral nephrectomy followed by renal transplantation at age 6, aortic regurgitation. A CT scan of the chest was obtained to further characterize the thoracic aorta. Diffuse high attenuation centrilobular nodules were identified throughout both lungs, greatest in the upper lobes compatible with metastatic calcifications (Fig. 1). The patient did not have any pre existing pulmonary disease. His parathyroid hormone (PTH) was 133 pmol/L the year before and he underwent a parathyroidectomy in May 2012. Alkaline phosphatase levels ranged from 50 to 67 U/L. He reported several hospitalizations after the parathyroidectomy for hypocalcaemia and tetany. On further inquiry, patient reported taking 30 tabs of calcium carbonate 1000 mg a day as both a calcium supplement and as a phosphate binder. He had been on a 1.75 mmol/L calcium bath on haemodialysis sessions. The patient underwent a CT scan of the chest a year before at our institution, which did not reveal the calcifications (Fig. 2). He had serum calcium values from 1.5 to 2 mmol/L, ionized calcium 0.85 mmol/L, phosphate 1.125 to 1.5 mmol/L, PTH 1.8 pmol/L, vitamin D (1,25OH) 32.88 pmol/L, vitamin D (25OH) 65.8 nmol/L. Metastatic calcifications in ESRD patients can demonstrate both visceral and non-visceral involvement. Visceral calcification may occur in the lungs, stomach, kidney heart and muscles. Non-visceral calcification mainly affects the small to medium arteries of the dermis and subcutaneous tissues. While, the exogenous calcium load in our patient coincides chronologically with the development of pulmonary calcification, it does not imply causation. We also acknowledge that although a CT scan a year before the parathyroidectomy did not reveal any calcifications, the calcifications may have been developing prior to the parathyroidectomy. There are reports of metastatic calcification in dialysis patients with no apparent metabolic abnormalities. Evidence suggests that administration of excessive calcium might be an important contributor to calcification in chronic kidney disease. 1 Calcium when provided during dialysis or by calcium-based binders in chronic kidney disease (CKD) enters the body rather rapidly. The bone exchangeable calcium pool (ECP) is able to buffer an acute calcium load in healthy subjects. The minute-to-minute calcium regulation depends on this mechanism without any obvious contribution of other factors like parathyroid hormone. Reduction in the bone ECP plasticity in some patients with CKD leads to short lasting increases in calcium as observed during haemodialysis and during ingestion of calcium containing phosphate binders. This could contribute to and partially explain the propensity of these subjects to develop extraosseous calcifications...
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