Table 2.
Parameter | Endostatin | PEDF | KLF-2 |
CG0:CG1 | No patients | No patients | No patients |
CG0:CG2 | 0.4724 | 0.9253 | 0.8644 |
CG0:CG3 | 0.2708 | 0.2405 | 0.5530 |
CT0:CT1 | 0.5116 | 0.0099 | 0.8414 |
CT0:CT2 | 0.0154 | 0.7330 | 0.8486 |
CT0:CT3 | 0.5214 | 0.1317 | 0.4685 |
CV0:CV1 | 0.8230 | 0.3523 | 0.7985 |
CV0:CV2 | 0.4617 | 0.0556 | 0.2313 |
CV0:CV3 | 0.3913 | 0.9644 | 0.8748 |
CI0:CI1 | 0.7157 | 0.0409 | 0.7638 |
CI0:CI2 | 0.0439 | 0.9279 | 0.8167 |
CI0:CI3 | 0.6165 | 0.1559 | 0.4942 |
Regression analyses did not reveal any correlation between endostatin, PEDF or KLF-2 with the degree of renal dysfunction (as judged by serum creatinine concentration) or clinical parameters (data not shown). There was, however, significant correlation between endostatin, PEDF and KLF-2 levels in the urine. Analysis of correlation between endostatin, PEDF and KLF-2 levels and histological parameters of glomerular, tubulointerstitial and vascular disease in CAD-1–3 revealed a tight correlation between endostatin or PEDF with the severity of tubular and interstitial injury, but none showed correlation with the degree of glomerular involvement.