2010 - TTS International Congress


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Mesenchymal Stem Cells and Cellular Transplantation

93.5 - Biomaterial seeded with bone marrow derived cells did retard progression and impact differently distinct stages of chronic kidney disease

Presenter: Ida, Fernandes, Sao Baeolo, Brazil
Authors: Caldas H., Fernandes I., Braile D., Goloni-Bertollo E., Kawasaki-Oyama R., Baptista M., Abbud-Filho M.

BIOMATERIAL SEEDED WITH BONE MARROW DERIVED CELLS DID RETARD PROGRESSION AND IMPACT DIFFERENTLY DISTINCT STAGES OF CHRONIC KIDNEY DISEASE

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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