and other inflamed organs through the alternative pathway because its specific inhibition results in higher serum levels. It is interesting that complement activation through immune complexes is not significant in this setting because anti-DNA levels, and presumably anti-DNA immune complexes, did not change.
3.5. Proteinuria and pyuria are reduced in CRIg-Fc treated mice
Renal damage is a frequent and serious complication in SLE patients and is manifested clinically, among others, with proteinuria, hematuria and pyuria. Proteinuria and pyuria were measured and analyzed following a 16 hour collection of urine from CRIg-Fc and control treated mice. Both protein and leukocyte levels increased significantly in the control mice by 14 weeks of age (proteinuria: 14 weeks p = 0.006; 15 weeks p = 0.018; 16 weeks p = 0.001) (pyuria: 14 weeks p = 0.005; 15 weeks p = 0.048; 16 weeks p = 0.001) as compared to the CRIg treated mice (Figs. 2E/F). This suggests there is decreased kidney inflammation in MRL/lpr mice following CRIg-Fc treatment.
3.6. Renal pathology is diminished in CRIg-Fc treated mice
To further assess kidney damage, we evaluated renal histopathology of 16-week old mice. PAS staining of kidney sections demonstrated greater glomerular inflammation in the control mice as compared to the CRIg-Fc treated animals (Fig. 3A). Blinded analysis of these kidney sections demonstrated a significant reduction in glomerular pathology in CRIg-Fc treated mice (p b 0.0001)