Tumoral calcinosis due to severe hyperphosphatemia and secondary hyperparathyroidism without vascular calcification in a hemodialysis patient.

We report a case of a 32-year-old man who was undergoing chronic hemodialysis and had hyperphosphatemia and secondary hyperparathyroidism (SHPT) with multiple tumoral calcinosis (TC) lesions refractory to drug therapy. Total parathyroidectomy and autotransplantation were performed, and he recovered from TC within 3 months. Several soft-tissue calcifications were present, but neither computed tomography (CT) before diagnosis nor CT performed 12 months after surgery detected evidence of vascular calcification (VC), despite persistence of hyperphosphatemia. This patient had a high calcium (Ca) × phosphate (P) product and calciprotein particles, and high serum Ca and P levels are important risk factors for both TC and VC. P plays a crucial role in regulation of VC, but the absence of VC in our case suggests a specific circumstance in which VC does not progress even under a high phosphatemic state, and that P alone may be insufficient for VC progression. TC in our patient was probably due to severe SHPT and continuous high serum P and Ca × P product levels, but the absence of VC suggests that the pathophysiologic process leading to VC requires further investigation, particularly in chronic kidney disease.