Figure 1.
The method of measuring peritoneal calcification (PC).
PC located in the abdominal wall and bowel wall was circled as the region of interest. The software ImageJ quantified the calcification areas of more than 150 Hounsfield units (table in the figure). The Tenckhoff catheter and vascular calcification were excluded from measurement.
Table 1.
Comparisons of the clinical characteristics of peritoneal dialysis (PD) patients without (group 1) and with (group 2) peritoneal calcification (PC).
Table 2.
Comparisons of the PD associated characteristics of the 2 groups without (group 1) and with (group 2) peritoneal calcification (PC).
Table 3.
Independent determinants for presenting PC or not using multiple logistic regression analysis with adjustment for PD vintage.
Table 4.
Correlations between the severity of peritoneal calcification and clinical or PD associated characteristics in patients with PC (n = 50).
Table 5.
Independent determinants of the severity of PC, in patients with detectable PC on CT scan, using multiple linear regression analysis.
Table 6.
Comparison of various outcomes and morbidity targets between the 2 groups.
Figure 2.
Kaplan-Meier survival analysis was used to compare outcomes between patients without (group 1; n = 133) and with (group 2; n = 50) peritoneal calcification.
There was no significant difference between the 2 groups in event free survival of mortality (A), technique failure (B), hospitalization (C), and peritonitis (D).
Figure 3.
Proposed pathogenesis of peritoneal calcification.
Unphysiologic dialysate and peritonitis episodes stimulate mesothelial cells which secret calcification inhibitors (matrix Gla protein, MGP) and other cytokines. Some other calcification inhibitor (fetuin A) and cytokines are also across the capillary wall from the circulation. These cytokines might transform the mesenchymal cells into osteocyte-like cells to induce following calcification. In addition, blood provide calcium and vitamin D to facilitate calcification.