Tissue Calcification In Patients Research Articles

Treatment of a soft tissue calcification in a patient receiving peritoneal dialysis

Chronic Kidney Disease patients suffer from Mineral and Bone Disorder (CKD-MBD) leading to increased vascular and soft-tissue calcification. The prevalence of soft tissue calcification in dialysis patients is not well described, and most cases describe such calcifications in hemodialysis patients. We describe a case of a massive soft tissue calcification in the right gluteal region in a peritoneal dialysis patient. The patient had severe pain and were disabled. The treatment was converted to an intensive hemodialysis regimen with a minimal calcium load and high dose of cinacalcet. During the treatment, the calcification diminished rapidly from a diameter of 26.6 to 2.9 cm, and the patient symptoms were relieved, leaving the patient with no pain or restriction in mobilization.

Differences in associated factors between aortic and mitral valve calcification in hemodialysis

Increased prevalence of aortic and mitral valve calcification has been reported in patients on hemodialysis, but it remains unknown whether aortic and mitral valve calcification arise from similar pathogenesis. We detected heart valve calcification using two-dimensional echocardiography, and we related valve calcification to various clinical parameters in patients treated with hemodialysis three times a week for more than 1 year. In 112 patients (77 men and 35 women, age 67+/-10 years, duration on hemodialysis 95+/-67 months), aortic and mitral valve calcification were observed in 84 (75.0%) and 58 (51.7%) patients, respectively. Aortic valve calcification was associated with increased age, higher serum calcium, lower serum albumin, lower total cholesterol and higher high-sensitivity C-reactive protein. Multivariate analysis showed that increased age and higher serum calcium were independently associated with aortic valve calcification. Conversely, mitral valve calcification was associated with increased age, higher high-sensitivity C-reactive protein and higher serum beta(2)-microglobulin, but not with higher serum calcium. In multivariate analysis, increased age and higher serum beta(2)-microglobulin were independently associated with mitral valve calcification. Serum beta(2)-microglobulin was associated with longer duration on hemodialysis, malnutrition inflammation (lower serum albumin and higher high-sensitivity C-reactive protein) and dyslipidemia. Considering the results in previous studies showing that the distribution of beta(2)-microglobulin amyloid deposition was consistent with that of tissue calcification in patients on hemodialysis, beta(2)-microglobulin may have pathogenic roles in valve calcification.

Calcinose pseudotumorale de localisation inhabituelle chez un patient hémodialysé

Tumour-like calcinosis is a rare cause of tissue calcification in patients on maintenance haemodialysis for chronic renal failure. Its estimated incidence is between 0.5 and 7% of haemodialysis patients. A 29-year-old male patient was referred to our department with a large cervical mass lesion increasing in size for two months. The patient had been on maintenance haemodialysis for one year for chronic renal failure during which time he reported multiple episodes of cervical trauma. Cervical MRI demonstrated a 11 x 9 cm calcified tumoral mass extending to the cervical muscles and the lower cervical spine (C6, C7, T1), accompanied by C6 osteolysis. Laboratory studies revealed secondary hyperparathyroidism with elevated calcium-phosphorus product. The patient underwent parathyroidectomy and several weeks later, there was a dramatic regression of the tumoral calcinosis. Renal transplantation was performed secondarily with no recurrence of the tumoral calcification after six years of follow-up. Tumour-like calcinosis of the lower cervical spine with osteolysis of the cervical vertebrae is very rare. The principal contributing factors are hyperparathyroidism, elevation of calcium-phosphorus product and local trauma. Optimal treatment of these calcifications remains controversial. While surgical resection of the mass is commonly recommended, in our case report, despite the initial aggressiveness of the lesion, surgery was not performed and treatment of hyperparathyroidism alone was sufficient to ensure dramatic improvement with complete resolution of the calcinosis within few weeks.

Renal osteodystrophy: present and future

Evidence is accumulating to indicate that certain abnormalities in mineral metabolism and/or their clinical management can lead to the development of vascular and soft tissue calcifications in patients with end-stage renal disease. Although the long-term consequences of vascular calcification in chronic renal failure have yet to be fully defined, the disorder may contribute to the high mortality rate from cardiovascular causes in patients undergoing long-term dialysis. The relationship between vascular calcification and cardiovascular disease in those with end-stage renal disease needs to be thoroughly evaluated, and substantial changes in the clinical management of patients undergoing dialysis may be appropriate. Phosphate retention and hyperphosphatemia have long been recognized as contributors to vascular and soft tissue calcification in chronic renal failure. Several recent reports indicate, however, that the use of large oral doses of calcium as phosphate-binding agents particularly in patients with persistently elevated serum phosphorus levels, may increase the risk of vascular calcification. Concurrent therapy with supra-physiological doses of calcitriol and other vitamin D sterols to manage secondary hyperparathyroidism leads to episodes of hyperphosphatemia and hypercalcemia, which can further aggravate soft tissue and vascular calcification. The phosphate-binding ion exchange resin sevelamer is now available for clinical use in the United States. It does not contain either calcium or aluminum, and other calcium- and aluminum-free phosphate-binding agents are being developed. These compounds make it possible to manage phosphate retention in patients with chronic renal failure without the risks associated with the sustained ingestion of large daily doses of calcium or aluminum. Several new vitamin D analogs are now available to treat secondary hyperparathyroidism due to chronic renal failure. These compounds may be less likely than calcitriol to enhance intestinal calcium and phosphorus absorption and to promote calcium and phosphorus release from bone. The therapeutic use of new vitamin D sterols as alternatives to calcitriol may permit clinicians to effectively manage secondary hyperparathyroidism while reducing the risks of soft tissue calcification in patients who require vitamin D therapy.

Soft Tissue Calcification in Renal Failure

Disorders of phosphorus, calcium, and vitamin D are common in patients with renal failure. Medical management, including dietary phosphorus restriction, administration of phosphate binding agents, and calcium and vitamin D sterol supplementation, must be instituted to control serum concentrations of these substances because of the loss of normal homeostatic mechanisms. If these measures are not employed, soft tissue calcification and hyperparathyroidism may result. We report the case of a 22-year-old woman with endstage renal disease treated with continuous ambulatory peritoneal dialysis who developed secondary hyperparathyroidism and tumorous calcinosis as a result of noncompliance with dietary phosphorus restriction and phosphate-binding agent therapy. The etiology and treatment of soft tissue calcification in patients with renal disease are discussed. Compliance with dietary restrictions and phosphate binding agents is frequently problematic in this population. Pharmacists should play an active role in educating patients with renal disease on the consequences of noncompliance with dietary and drug therapy.