FP358PARICALCITOL THERAPY IMPROVES LEFT VENTRICULAR HYPERTROPHY IN RENAL TRANSPLANT PATIENTS WITH SECONDARY HYPERPARATHYROIDISM

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INTRODUCTION AND AIMS: Left ventricular hypertrophy (LVH) is common in renal transplant recipients (RTRs), and represents an independent predictor of cardiovascular events and death. Several factors are believed to be responsible for the development and maintenance of LVH, including high PTH levels. Oral paricalcitol has been shown to be effective and safe in the treatment of secondary hyperparathyroidism (SHPT) in RTRs, and attenuating myocardial hypertrophy in experimental models. In humans, the impact of paricalcitol therapy on cardiac hypertrophy is less clear. The aim of our study was to evaluate the impact of paricalcitol therapy on LVH in a group of RTRs with SHPT. METHODS: On this purpose we selected 24 RTRs (group A) with LVH and SHPT and compared them to 25 RTRs (group B) not treated with vitamin D analogs and with progressive increase in PTH levels. SHPT was defined as PTH levels 1.5 times higher than the high normal limits, while LVH was defined as a LV mass index (LVMi) > 95 g/m2 in female, and > 115 g/m2 in male. Other inclusion criteria in the group A were: renal transplant vintage ≥ 12 months; increased PTH levels for at least 6 months before the study; serum calcium < 10.2 mg/dl; serum phosphate < 4.5 mg/dl; renal function, assessed by eGFR, steadily > 15 ml/min/1.73 m2. Treatment with paricalcitol was started at mean dose of 1 µg/day, and reduced to 1 µg on the other day when sCa levels were > 10.5 mg/dl, or FECa > 0.020%, and/or sPO4 > 4.5 mg/dl. Paricalcitol administration was temporarily stopped when sCa levels were > 11 mg/dl. On average every 6 weeks were evaluated: sCr, eGFR, sCa, sPO4, total alkaline phosphatase (t-ALP), FECa, FEPO4, proteinuria, cyclosporine, and tacrolimus serum levels. Serum PTH levels were assessed every three months. RESULTS: After 18 months of treatment in the group A there was a significant reduction of PTH levels from 202 ± 157 to 105 ± 42 pg/ml (P<0.01), of t-ALP from 101 ± 40 to 76 ± 17 mU/ml (P<0.01), of diastolic blood pressure from 80 ± 6 to 75 ± 7 mmHg (P<0.05), and of LVMi from 136 ± 21 to 113 ± 29 g/m2 (P<0.01), - 17 ± 15% from baseline, the presence of LVH was reduced from 100% at baseline to 54% at F-U. Serum calcium levels showed a modest increase just only during the first 12 months of treatment. During the study were recorded only two episodes of hypercalcemia that required a temporary interruption of paricalcitol treatment, and two episodes of isolated hypercalciuria that required reduction of paricalcitol dose to 1 µg every other day. Throughout the study renal function was stable in all patients. There were no changes in the dosage of antihypertensive therapy and number of patients treated. The modest proteinuria present at baseline showed no modifications. In the group B there was an increase of PTH levels from 131 ± 77 to 160 ± 82 pg/ml (P=NS), while there was a significant increase in proteinuria from 140 ± 86 to 501 ± 896 mg/g Cr (P<0.01), and of LVMi from 114 ± 27 to 125 ± 16 g/m2 (P<0.01), + 8 ± 16% from baseline, the presence of LVH went from 52% at baseline to 80% at F-U. There were no significant changes of the other parameters evaluated. CONCLUSIONS: Our results suggest that SHPT plays an important role in the development and maintenance of LVH and that its correction with paricalcitol has a favorable impact on the progression of LVH.

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