Does Secondary Hyperparathyroidism Play a Primary Role in Causing Peritoneal Calcification in Patients on CAPD?

P calcification is occasionally observed in patients on long-term continuous ambulatory peritoneal dialysis (CAPD). Extraosseous calcium deposits are often seen in patients with secondary hyperparathyroidism (HPT) undergoing long-term hemodialysis (HD). Thus, secondary HPT may be considered a candidate for the major cause of peritoneal calcification. In past decades, a large number of patients with secondary HPT have been treated with HD, but peritoneal calcification in these patients is rarely reported. If secondary HPT plays a major role in peritoneal calcification, why is calcium deposit not found exclusively in the peritoneum but is found in the vascular bed or subcutaneous tissue in these HD patients? We have observed peritoneal calcification in 3 of 23 patients (17 males, 6 females; mean age 50 ± 6 years; mean period on CAPD 8.1 ± 1.4 years) on CAPD for longer than 7 years. We analyzed these patients by comparing them with 30 ageand sexmatched HD patients with secondary HPT (23 males, 7 females; mean age 51 ± 5 years; mean period on HD 16.6 ± 4.1 years). The prevalence of peritoneal calcification detected by computed tomography was significantly higher (χ2 = 4.1, p < 0.05) in CAPD patients (13%; 3 of 23 patients) than in HD patients (0%; 0 of 30), despite a shorter history of dialysis. In contrast, the incidence of extraperitoneal ectopic calcification revealed by radiographs and echocardiographs was significantly lower (χ2 = 4.2, p < 0.05) in CAPD patients (0%; 0 of 23) than in HD patients (17%; 5 of 30). Serum intact parathyroid hormone level was lower (p < 0.05) in CAPD patients (138 ± 104 pg/mL) than in HD patients (225 ± 88 pg/mL). However, no differences in serum calcium (9.4 ± 0.7 vs 9.6 ± 1.0 mg/dL) or phosphate levels (5.8 ± 0.9 vs 5.7 ± 0.7 mg/dL) were observed between CAPD and HD patients. Neither significant parathyroid overactivity nor abnormal calcium and phosphate metabolism is always associated with peritoneal calcification in CAPD patients (1,2). The only common factor of peritoneal calcification reported so far is long-term CAPD (over 7 years) (1–3). Extraosseous calcification in sites other than the peritoneum, which is a relatively common observation in long-term HD patients with secondary HPT, is hardly recognized in CAPD patients. Of course, there is a possibility that extraperitoneal calcification may increase if patients continue to receive CAPD therapy for long periods. On the other hand, peritoneal calcification is rarely reported in HD patients (4). These findings clearly indicate that HPT is not the sole cause of peritoneal calcification in longstanding CAPD therapy. Other mediators, such as exposure to hypertonic dialysate (2), repeated peritonitis, acetate buffer, and ferrous substance, probably also promote peritoneal calcification under the condition in which the peritoneum is incessantly exposed to nonphysiological hypertonic glucose solution. In HD patients, the absence of these factors may explain the low prevalence of calcium deposits in the peritoneum. Peritoneal calcification can be considered part of the spectrum of sclerosing peritonitis (5), which shows hyalinization, fibrosis, and inflammatory cell infiltration in the peritoneum. This pathological picture is associated with atherosclerosis with calcium plaques often seen in patients with diabetes (5). Thus, we speculate that, in CAPD patients, similar pathogenic processes may occur in the peritoneum after long-term exposure to high concentrations of glucose equivalent to nearly 4000 mg/dL serum glucose concentration.