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Presenter: Ida, Fernandes, Sao Baeolo, Brazil
Authors: Caldas H., Fernandes I., Braile D., Goloni-Bertollo E., Kawasaki-Oyama R., Baptista M., Abbud-Filho M.
MESENCHYMAL STEM CELLS AND CELLULAR TRANSPLANTATION
H. Caldas1, I.M. Fernandes1, D.M. Braile1, E. Goloni-bertollo1, R.S. Kawasaki-oyama1, M.A.S. Baptista1, M. Abbud-filho2
1Medicine, Medical School - FAMERP, Sao Jose do Rio Preto/BRAZIL, 2Medicina, FAMERP/Funfarme, sao Jose do Rio preto/BRAZIL
Body: Introduction: Different routes for the administration of bone marrow derived cells (BMDC) have been proposed to treat the progression of chronic kidney disease (CKD). In this study, we investigatedwhether: 1) bovine pericardium-(BP) scaffold for cell therapy would retard progression of CKD; 2) cell therapy impacts differently distinct degrees of mass reduction (5/6 or 2/3 CKD models). Methods:Treatment consisted of BP seeded with either mesenchymal stem cells (BPMSC) or mononuclear cells (BPMO). Renal function and 24-hours proteinuria (PT24h) were measured at 0, 45, and 90 days aftersurgery. Histological evaluation was performed in all groups. Results: After 90 days animals the group CKD2/3 treated with BPMSC had sCr in levels similar to Sham (S) (BPMSC= 7.6% vs S= 5.2%; P=NS)and lower than the untreated groups (BPMSC= 7.6% vs CKD2/3= 48.2% vs BP= 39%; P=0.043). Following treatment with BPMSC CLcr was higher than in untreated animals (S=1.05 ± 0.20 vs CKD2/3= 0.40± 0.12 vs BP= 0.34 ± 0.09 vs BPMSC= 0.65 ± 0.22 vs BPMO= 0.50 ± 0.07ml/min; P< 0.0001) while PT24h was similar to S group (S= 5.4 ± 1.14 vs BPMSC= 4.92 ±2.4mg/24h [P=NS] vs CKD2/3= 27 ± 16.7 vs BP= 20.2 ± 4.7 vs BPMO= 10 ± 2.8mg/24h; P=0.0005). Progression of CKD2/3 measured by 1/Cr slopes was reduced by BPMSC (S= 0.884 ±0.91 vs BPMSC= 0.78 ± 0.81 [P=NS] vs CKD2/3= -0.24 ± 0.03 vs BP= -0.20 ± 0.09; P=0.0343). BPMO did not significantly affect sCr, Clcr, or PT24h of CKD2/3 animals. In the CKD5/6model both treatments were effective to prevent increases in sCr (CKD5/6= 128% vs BP= 168% vs BPMSC= 78.6% vs BPMO= 72.4%; P<0.0001). PT24h decreased significantly in treated groups after 45 days(S= 2.8 ± 1.64 vs CKD5/6= 123.8 ± 112 vs BP= 51.6 ± 32 vs BPMSC= 20.8 ± 26.4 vs BPMO= 9.6 ± 6.6 mg/24h; P=0.0117). This effect seemed to persist at 90 day in spiteof not reach statistical significance; (S= 5.4 ± 1.14 vs CKD5/6= 151 ± 109 vs BP= 116 ± 48,7 vs BPMSC= 46,5 ± 37.7 vs BPMO= 66.1 ± 61.38mg/24h; P=0.012) anddecreases in Clcr was observed in untreated groups (S= 1.1 ± 0.2 vs CKD5/6= 0.25 ± 0.17 vs BP= 0.22 ± 0.09 vs BPMSC= 0.46 ± 0.10 vs BPMO= 0.53 ± 0.15ml/min;P<0.0001). Progression of disease in the CKD5/6 model was partially retarded also by both treatments (CKD5/6= -0.493 ± 0.04 vs BP= -0.53 ± 0.10 vs BPMSC= -0.35 ± 0.12 vs BPMO=-0.32 ± 0.13; P=0.016), although in a less intense way than that observed in the CKD2/3 model. Histological evaluation showed significantly less renal damage in the remnant kidney of treatedrats in both models using both types of BMDC. Conclusions: Our results demonstrate that 1) BP combined to BMDC did retard the progression of experimental CKD; 2) cellular therapy seems to be moreeffective when given in less severe stages of CKD; 3) BP seeded with BMDC can be an alternative route to cellular therapy.
Disclosure: All authors have declared no conflicts of interest.
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