Acute tumoral calcinosis due to severe hyperphosphatemia in a maintenance hemodialysis patient

Abstract

We report the case of a maintenance hemodialysis patient with severe hyperphosphatemia (26.6 mg/dL) who developed acute tumoral calcinosis. The patient started receiving maintenance hemodialysis after being diagnosed with type 2 diabetes mellitus. The patient's phosphate levels suddenly increased. He had not taken the prescribed phosphate binders for the past 5 years. He noticed swelling of the palmar aspects of his right thumb, which was diagnosed as tumoral calcinosis. His serum phosphate level reached 26.6 mg/dL. He started taking medication to lower his serum phosphate levels. The patient had a long history of eating convenience foods. As food additives in convenience foods could be a major source of phosphate, the patient corrected this habit by replacing convenience foods with special foods for dialysis patients. His symptoms improved along with the decrease in his serum phosphate levels. The main reason for the abrupt decrease in phosphate levels could be the correction of his dietary habits. Therefore, phosphate levels in processed foods should be carefully considered in dialysis patients.

Surgical treatment of uremic tumoral calcinosis: a case report and concise review of the literature

“…The exact mechanism of UTC is still unknown,so no approved effective therapy currently exists.Surgery may not be the rst option due to the presence of multiple co-morbidities and higher risk of recurrence,the underlying disorder is primarily treated [30][31] .A low-phosphate diet is an essential rst step,primary treatment modalities consists of phosphate binders [32][33] and antacids, if this is ineffective,increasing urinary phosphate excretion by the administration of acetazolamide might be bene cial [34] ,this has been shown to reduce size of TC lesions to various degrees. Sevelamer may result in a decrease in serum phosphate level,but the response in the described cases in the literature was inconsistent,the bene ts are limited and it could not prevent the progression of the lesion [35] .Medical therapy is also used for TC patients,using low-calcium dialysate solutions, high-ux hemodialysis and increased length and frequency of hemodialysis treatments [36] .Fatehi et al [37] reported a case that keeping on hemodialysis improved the symptoms and reduced the mass of the lesion.Surgical resection should be considered when calcinosis causes severe pain, neurologic dysfunction or joint function limitations [38] .In addition,parathyroidectomy and renal transplantation have been performed,the role of parathyroidectomy is still controversial [39] ,it usually achieves remarkable resolution in dialysis patients with severe hyperparathyroidism and elevated serum alkaline phosphatase(ALP) [40] ,but in the absence of secondary hyperparathyroidism with a markedly elevated PTH, parathyroidectomy should be avoided as it may not improve calcium and phosphorus control or favorably affect the underlying process [41] .Successful renal transplantation can provides complete resolution of UTC by inducing a negative calcium balance [42][43][44][45] .…”

A New Disease Concept in the Age of Processed Foods—Phosphorus-Burden Disease; including CKD–MBD Concrete Analysis and the Way to Solution

“…As a result, hypocalcemia occurs and parathyroid hormone (PTH) is stimulated, causing hyperparathyroidism. Finally, it was found that PTH causes excessive mobilization of P and calcium from bone, resulting in vascular calcification and ectopic mass calcification [ 6 ]. On the other hand, in patients with renal dysfunction, the dysregulation of the αKlotho-FGF-receptor prevents the signaling of the P diuretic factor FGF23, resulting in hyperphosphatemia and vascular calcification.…”

Juxta-articular tumoral calcinosis associated with the temporomandibular joint: a case report and concise review

“…In such patients, medical treatment may have a role. Treatment modalities such as calcium-depleted electrolytic bath [13], phosphate binders [14, 16], calcitonin, bisphosphonate [16] and diet restriction of phosphate were used to restore phosphate and calcium metabolism. This has been shown to reduce size of TC lesions to various degrees.…”