Oral paricalcitol as antiproteinuric agent in chronic kidney disease
- Autores: Alberto de Lorenzo, Laura Salanova Villanueva, Andrew S. Bomback, María Moya, Francisco Coronel, Carmen Bernis Carro, José Antonio Sánchez Tomero, Vicente Álvarez
- Localización: Nefrología: publicación oficial de la Sociedad Española de Nefrología, ISSN 0211-6995, Vol. 33, Nº. 5, 2013, págs. 709-715
- Idioma: inglés
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Resumen
Background:
Vitamin D has an important regulatory effect on the renin-angiotensin-aldosterone system, playing a central role in the regulation of proteinuria. We therefore studied the antiproteinuric effect of paricalcitol.
Methods:
36 patients with an estimated GFR of 30-90mL/ min/1.73m 2 and proteinuria >400mg/d with a stable dose of ACE inhibitor or ARB for at least 3 months were recruited. Patients received oral paricalcitol 1?g/day for 12 months. Primary endpoint was decrease in proteinuria from baseline. Secondary endpoints were changes in creatinine, eGFR, serum levels of calcium, phosphorus, iPTH, 25(OH)vitD, C-Reactive Protein and blood presure.
Results:
Mean proteinuria was 2806mg/d and fell to 2199mg/d at month 6 (p<.0001) and 1931.5mg/d at month 12 ( P <.0001). Patients with >3000mg/d baseline proteinuria (n=12) saw smaller relative reductions in proteinuria (5956.9±2492.6mg/d to 4220.4±2613mg/d at 12 months) than patients with <3000mg/d baseline proteinuria (1371±627.5mg/d to 821.3±491.5mg/d at 12 months). There were no changes in BP, eGFR and CRP. We observed significant changes in serum levels of calcium, phosphorus, iPTH, 25(OH) vitamin D.
Conclusion:
Our study shows an important reduction in proteinuria with a low dose of oral paricalcitol in CKD, that is particularly robust with baseline proteinuria between 1-3g/d
