Paricalcitol reduces proteinuria but does not modify peritoneal protein loss in patients on peritoneal dialysis
- PMID: 23364628
- DOI: 10.3265/Nefrologia.pre2012.Oct.11635
Paricalcitol reduces proteinuria but does not modify peritoneal protein loss in patients on peritoneal dialysis
Abstract
Introduction: Paricalcitol, a selective activator of Vitamin D receptors, is successfully used as a treatment of hyperparathyroidism secondary to chronic kidney disease (CKD). In addition, it has been proposed for reducing proteinuria in patients with CKD. Nonetheless, little is known about its effect on peritoneal protein loss in patients on peritoneal dialysis (PD).
Objectives: To analyse the efficiency of oral paricalcitol in secondary hyperparathyroidism control in PD patients and to verify its effect on urinary and peritoneal effluent protein loss.
Material and method: Prospective study with a 12-month follow-up on a cohort of PD patients. Invention consisted of the introduction of paricalcitol for the treatment of secondary hyperparathyroidism. Paricalcitol was dosed according to parathyroid hormone (PTH): 1mg/day for patients with PTH < 500 pg/ml, and 2mg/day for those with higher PTH levels. Epidemiological, clinical and analytical data were analysed.
Results: 38 patients (56 ± 19 years, 55% women, 16% diabetics, technique time (14 ± 10 months) were included in the study. Thirty-three of them received 1mg/day of paricalcitol; the rest received 2mg/day. The use of paricalcitol was associated with a PTH decrease of 30.7 ± 6.8% (P<.001) after 12 months of treatment with no changes in calcium (8.82 ± 0.96 vs. 9.02 ± 0.91; P = .153) and phosphate levels (4.78 ± 0.63 vs. 4.93 ± 0.77; P = .693). Patients did not modify treatment concurrent with phosphate binders over the study period, nor did they change the cinacalcet dosage. However, fewer patients needed it by the end of the study. The PTH baseline levels were independent indicators of its decrease (b = 0.689, P = .018), and the rest of the analysed parameters were not affected. Over the study period there was a proteinuria decrease (0.79 ± 0.41 vs. 0.64 ± 0.36 g/day, P = .034) with no changes in renal function (7.2 ± 1.1 vs. 6.3 ± 0.9 ml/min, P =.104). Similarly, no differences were found in in the percentages of patients taking renin-angiotensin system inhibitors (71 vs. 68 %, P = .472) or the doses needed. There was no significant change in peritoneal protein loss (5.8 ± 1.9 vs. 6.0 ± 2.2g/24h, P = .731) nor in serum albumin levels (3.7 ± 1.1 vs. 3.7 ± 1.2g/dl, P = .697).
Conclusions: The use of oral paricalcitol reduces PTH levels safely and substantially in patients on PD. Their use is associated with a proteinuria decrease and is not linked to a decrease of glomerular filtration rate or changes in the medication that could modify it. We have found no modification in the amount of peritoneal protein loss.
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