Oral paricalcitol as antiproteinuric agent in chronic kidney disease.

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 30-90 mL/min/1.73 m² and proteinuria >400 mg/d with a stable dose of ACE inhibitor or ARB for at least 3 months were recruited. Patients received oral paricalcitol 1 µg/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 2806 mg/d and fell to 2199 mg/d at month 6 (p<.0001) and 1931.5 mg/d at month 12 (P<.0001). Patients with >3000 mg/d baseline proteinuria (n=12) saw smaller relative reductions in proteinuria (5956.9±2492.6 mg/d to 4220.4±2613 mg/d at 12 months) than patients with <3000 mg/d baseline proteinuria (1371±627.5 mg/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 1-3 g/d.

Oral paricalcitol as antiproteinuric agent in chronic kidney disease

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/1.73m2 and proteinuria >400mg/d with a stable dose of ACE inhibitor or ARB for at least 3 months were recruited. Patients received oral paricalcitol 1µg/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±627.5 mg/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 (AU)

Introducción: La vitamina D posee un efecto regulatorio del eje renina-angiotensina-aldosterona, jugando, por lo tanto, un papel importante en cuanto a proteinuria se refiere. Presentamos nuestra experiencia en el uso de paricalcitol como antiproteinúrico. Métodos: Incluimos 36 pacientes con un eGFR of 30-90 ml/min/1,73 m2 y proteinuria > 400 mg/d con dosis estables de inhibidores del SRAA durante 3 meses. Se le admistró durante 12 meses 1 µg/día de paricalcitol. Como objetivo primario estudiamos el descenso de proteinuria; como secundarios cambios en Cr, eFG, calcio, fósforo, iPTH, 25(OH)vitD, PCR y tension arterial. Resultados: La proteinuria media fue 2806 mg/d cayendo hasta 2199 mg/d en el mes 6 (p < 0,0001) y 1931,5 mg/d a los 12 meses (p < 0,0001). Aquellos con una proteinuria basal > 3000 mg/d (n=12) sufrieron una menor disminución (5956,9 ± 2492,6 mg/d a 4220,4 ± 2613 mg/d en mes 12) respecto a aquellos con una proteinuria < 3000 mg/d (1371 ± 627,5 mg/d a 821,3 ± 491,5 mg/d en mes 12). No se objetivaron cambios en tension arterial, eGFR y PCR. Los cambios en calcio, fósforo, iPTH y vitamina D 25(OH) fueron estadísticamente significativos. Conclusión: Nuestro estudio demuestra una reducción importante de proteinuria con dosis bajas de paricalcitol en pacientes con IRC, que es de particular importancia en aquellos con porteinuria basal entre 1-3 g/d (AU)

[FGF-23: just a phosphate metabolism regulator or something else?]. / FGF-23: ¿solo regulador del metabolismo del fósforo o algo más?

Endocrine communication between the bone, kidney, and the intestine is involved in maintaining appropriate serum phosphate concentrations, which is critical for the maintenance of skeletal integrity and is central to signal transduction and cell metabolism. In addition, hyperphosphatemia is statistically associated with vascular calcification, increased morbidity and mortality; because of this, phosphate regulation has become an important field of research. In this sense, fibroblast growth factor 23 (FGF-23) has been identified as a new hormone involved in phosphate regulation through feedback mechanisms involving parathyroid hormone and vitamin D. Given what the kidney is the primary site for regulation of phosphate levels and the principal target for FGF-23, its discovery has changed the understanding of disordered mineral metabolism in chronic kidney disease, especially now, since there is clinical evidence in favor of FGF-23 playing a central role for the pathogenesis of sHPT.

FGF-23: ¿solo regulador del metabolismo del fósforo o algo más? / FGF-23: just a phosphate metabolism regulator or something else?

En el organismo, la regulación de los niveles adecuados de fósforo se debe a la coordinación entre el esqueleto, el riñón y el intestino. El fósforo es un elemento crítico para el mantenimiento de la integridad del esqueleto, así como para la comunicación de numerosos procesos celulares. Además, la hiperfosfatemia ha sido estadísticamente asociada con calcificación vascular e incremento de la morbimortalidad, por lo que el control del fósforo se ha convertido en un importante campo de investigación. En este sentido, el factor de crecimiento fibroblástico 23 (FGF-23) ha aparecido como la nueva hormona implicada en la regulación del fósforo. Dado que el riñón es el principal órgano de regulación de los niveles de fósforo y el principal órgano diana de FGF-23, este factor ha suscitado un gran interés en el campo de la nefrología, especialmente al ser reconocido como el factor central del desarrollo del hiperparatiroidismo secundario (AU)

Endocrine communication between the bone, kidney, and the intestine is involved in maintaining appropriate serum phosphate concentrations, which is critical for the maintenance of skeletal integrity and is central to signal transduction and cell metabolism. In addition, hyperphosphatemia is statistically associated with vascular calcification, increased morbidity and mortality; because of this, phosphate regulation has become an important field of research. In this sense, fibroblast growth factor 23 (FGF-23) has been identified as a new hormone involved in phosphate regulation through feedback mechanisms involving parathyroid hormone and vitamin D. Given what the kidney is the primary site for regulation of phosphate levels and the principal target for FGF-23, its discovery has changed the understanding of disordered mineral metabolism in chronic kidney disease, especially now, since there is clinical evidence in favor of FGF-23 playing a central role for the pathogenesis of sHPT (AU)