We report the case of a 48-year-old woman with chronic renal failure secondary to tubulointerstitial nephritis.
The patient had received replacement therapy with long-term HD and had undergone two kidney transplants with transplantectomies: the first was due to acute humoral rejection and the second due to acute humoral and vascular rejection.
He resumed hemodialysis treatment in March 2005.
Serum levels of intact parathyroid hormone (iPTH) were intermittently high.
Previously, the patient had been treated with calcitriol for short periods of time, since the administration caused hypercalcemia and hyperfatemia.
In January 2006, she had severe SHPT (with higher levels of iPTH than those presented in previous months).
Ultrasound revealed a hyperechogenic nodular image in the medial zone of the left thyroid lobe, compatible with parathyroid gland hypertrophy.
A radiological series showed signs of hyperparathyroidism in the bones of both hands and wrists and VC in the radial and interdigital arteries.
Mammography showed multiple linear VC in both breasts.
1.
The patient was treated only with calcium carbonate.
Subsequently, they were added to calcitriol and sevelamer (800 mg with main meals), a chelating agent (P), and the dose of oral phosphate carbonate was reduced.
Figure 5 shows serum Ca, P and iPTH levels.
Hyperphosphoremia was controlled after two months of treatment, and the level of Ca-P product was adequate, but iPTH levels increased to 734 pg/ml, so treatment was changed.
Oral calcitriol was replaced by 30 mg of oral cinacalcet once a day and intravenous alphacalcidol (2 μg) immediately after hemodialysis.
The doses of calcium carbonate and sevelamer did not change.
1.
Two months later, the calcimetic dose was reduced due to hypocalcemia levels (7.6 mg/dl).
Treatment with intravenous vitamin D and calcium carbonate was maintained, and the dialysate calcium was changed from 2.5 to 3 mEq/l.
During the following six months, the levels of all parameters were within the range recommended by the KDOQI guidelines.
Excessive suppression of iPTH (138 pg/ml) and potential hypercalcaemia (9.4 mg/dl) were observed in November 2006, therefore treatment with carbonate and alphacalcium was discontinued.
In January 2007 treatment with sevelamer (800 mg with main meals) and a minimum weekly calcimetic dose (30 mg on Mondays) was continued, resulting in good control of mineral metabolism, with cinacalcet resulting in good control.
During this period, it was observed that in the radiological series the interdigital artery calcifications had a more structured appearance and that the bone had a more structured appearance.
Mammography also showed regression of QoL.
Initial linear calcifications were sustained by irregular grades.
