We present the case of a 48-year-old woman with chronic renal failure secondary to tubulointerstitial nephropathy. The patient had received long-term HD replacement therapy and had undergone two renal transplants with transplantectomies: the first was due to acute humoral rejection and the second due to acute humoral and vascular rejection. She resumed haemodialysis treatment in March 2005.
Serum intact parathyroid hormone (iPTH) values were intermittently high. Previously, the patient had been treated with calcitriol for short periods of time, as the administration caused hypercalcaemia and hyperphosphataemia.
In January 2006, she developed severe SHPTH (with higher iPTH levels than in previous months). Parathyroid ultrasound revealed a hyperechogenic pseudonodular image in the posteromedial area of the left thyroid lobe, which was compatible with hypertrophy of the parathyroid gland. A radiological series showed signs of hyperparathyroidism in the bones of both hands and wrists and CV in the radial and interdigital arteries. Mammography showed multiple linear VC in both breasts.

The patient was treated with calcium carbonate alone. Subsequently, oral calcitriol and sevelamer (800 mg with main meals), a phosphate (P)-chelating agent, were added to the regimen and the dose of calcium carbonate was reduced. Figure 5 shows serum Ca, P and iPTH levels. Hyperphosphataemia was brought under control after two months of treatment, and the Ca-P product level was adequate, but iPTH levels increased to 734 pg/ml, so treatment was changed. Oral calcitriol was replaced by oral cinacalcet 30 mg once daily and intravenous alfacalcidol (2 µg) immediately after haemodialysis. The doses of calcium carbonate and sevelamer were not changed.

Two months later, the calcimimetic dose was reduced due to hypocalcaemia levels (7.6 mg/dl). Treatment with intravenous vitamin D and calcium carbonate was maintained, and the calcium in the dialysate was changed from 2.5 to 3 mEq/l.
Over the next six months, the levels of all parameters remained within the range recommended by the KDOQI guidelines. In November 2006, excessive suppression of iPTH (138 pg/ml) and potential hypercalcaemia (9.4 mg/dl) were observed and treatment with calcium carbonate and alfacalcidol was discontinued. In January 2007, treatment was continued with sevelamer (800 mg with main meals) and a minimal weekly dose of calcimimetic (30 mg cinacalcet on Mondays and Fridays), resulting in good control of mineral metabolism.
During this period, it could be observed that in the radiological series the calcifications of the interdigital artery had disappeared and the bone had a more structured appearance. Mammography also showed regression of the VCs. The initial linear calcifications were replaced by irregular calcifications.