To investigate morphological changes in the peritoneal membrane of CAPD patients during exposure to dialysate, peritoneal membrane specimens were collected by biopsy from the patients without evidence of peritonitis and clinicopathological study was performed using these specimens. Of those listed with the Peritoneal Biopsy Registry, 65 patients who had no history of peritonitis were used as the subjects. The morphology of the peritoneal membrane immediately after the introduction of CAPD was used for comparison. Biopsy of the peritoneal membrane was performed in each patient at the time of catheter withdrawal.
CAPD was discontinued due to decreased ultrafiltration in 18 patients and for reasons other than insufficient ultrafiltration in 47 patients (catheter exit-site and tunnel infection in 13, catheter position shift in 6, abdominal surgery in 3, psychiatric reason in 10, death in 6, renal transplantation in 2 and others in 7).
To compare the duration of CAPD and peritoneal morphology, the subjects were divided by the duration of CAPD, that is, 36 patients whose CAPD duration was less than 5 years were assigned to Group 1 and 29 patients whose duration was 5 years or longer to Group 2. Then the clinical and histopathological findings were compared between these two groups. The peritoneal tissue samples were examined morphologically by light, transmission, and scanning electron microscopy.
The localization of advanced glycation end products (AGEs), collagen (I, II, III, IV, VI), gelatin, fibronectin, laminin, matrix metalloproteinase (MMP-1, MMP-2, MMP-9), and tissue inhibitors of metalloproteinases (TIMP-1, TIMP-2) in the peritoneum were observed by immunohistochemical techniques. Excluding the 14 patients who demonstrated peritoneal morphology similar to that observed immediately after the introduction of CAPD, peritoneal thickening was observed in specimens from remaining 57 patients. These specimens were further classified into fibrotic peritoneal thickening (peritoneal fibrosis) and sclerotic peritoneal thickening (peritoneal sclerosis). The peritoneal morphology demonstrated time course changes after long-term exposure to dialysate. Peritoneal thickening observed in patients whose duration of CAPD was less than 5 years was classified as peritoneal fibrosis caused by the growth of collagen III originally present in the submesothelial connective tissue and mesothelial cells present on the surface of peritoneal membrane. As the fluid removal function was not decreased, there was no problem in continuing CAPD. However, peritoneal sclerosis occurred after 5 years of CAPD.
Collagen fibers in the submesothelial connective tissue became degenerated and gelatinized, and mesothelium was absent from the surface, demonstrating a pathology clearly different from that of peritoneal fibrosis. Clinically, a decrease in fluid removal was observed, which is a change that might cause intestinal obstruction. It was considered that these two changes were caused by the exposure of the peritoneal membrane to the high concentration of glucose in the dialysate. In such case, the growth factor is stimulated by AGEs, causing proliferation of fibroblasts and collagen in the submesothelial connective tissue, leading to peritoneal fibrosis.
Furthermore, the aggravation of peritoneal fibrosis to peritoneal sclerosis is conceivably due to the gelatinization of collagen by AGEs that are accumulated in the proliferating collagen fiber. In this regard, it is necessary to differentiate peritoneal fibrosis from peritoneal sclerosis when the peritoneal morphology of CAPD patients is evaluated in the future.

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To elucidate the clinical features, diagnosis and treatment efficacy, we examined 8 patients with tuberculosis receiving maintenance hemodialysis in our hospital and affiliated institutions. This study involved three males and five females aged 28 to 72 (59.6±4.9) years. Pulmonary tuberculosis was detected in two patients and extrapulmonary tuberculosis in six (peritonitis, neck lymphadenitis, pericarditis, spondylitis, intestinal tuberculosis). Four of six patients with extrapulmonary tuberculosis had old pulmonary lesions. The duration from initiation of hemodialysis to onset of tuberculosis was significantly shorter in the diabetic group (n=4) than in the non-diabetic group (6.5±4.0 vs 108±67.1 months; p<0.05). Mycobacterium tuberculosis could be demonstrated in only one patient by culture and polymerase chain reaction (PCR) examination. The other patients had been diagnosed as having tuberculosis based on treatment response and diagnostic imaging or biopsy findings. All patients were successfully treated with anti-tuberculosis drugs; two patients with pulmonary tuberculosis received three drugs (isoniazid, INH; rifampicin, RFP; streptomycin, SM), six with extrapulmonary tuberculosis received INH and RFP. These findings suggest that the incidence of extrapulmonary tuberculosis in hemodialysis patients is high and the onset of tuberculosis in diabetic patients is frequently simultaneous with starting dialysis therapy. Therapeutic diagnosis may be needed in dialysis patients suspected of tuberculosis infection, because it is difficult to detect Mycobacterium tuberculosis by culture or PCR.

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We encountered a family demonstrating two cases (mother and her daughter) of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) with end-stage renal failure. A3243G point mutation of the mitochondrial DNA (mtDNA) was detected in each case. To treat uremia, continuous ambulatory peritoneal dialysis (CAPD) was considered preferable to hemodialysis (HD), because of impaired cardiac function in both cases. They successfully received CAPD more than 23 months (mother) and 40 months (daughter). There were no complications due to lactic acidosis during the CAPD period in either case. In conclusion, CAPD could be an appropriate way to manage MELAS patients with chronic renal failure complicated by cardiomyopathy.

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A 60-year-old male, undergoing regular hemodialysis therapy since 1994 presented with dyspnea and pyrexia just after the hemodialysis session. The patient had been well until 2 days before, when sore throat and general fatigue developed. Repeated chest radiographs demonstrated rapidly progressive pulmonary infiltration, and blood gas analysis disclosed severe hypoxia. The patient was intubated, and clinically diagnosed as having acute lung injury based on the criteria proposed by an American-European Consensus Conference. After the administration of high-dose corticosteroid (methyl-prednisolone, 500mg×3days) and imipenem, both pulmonary infiltration on chest radiograph and hypoxia improved immediately. The patient was extubated 2 days after the intubation, and followed a stable clinical course.

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Consciousness disturbances in untreated end stage renal failure are referred to as uremic encephalopathy, which is now rare in Japan as dialysis therapy is readily available. We describe two chronic renal failure (CRF) patients who developed consciousness disturbances attributable to hypermagnesemia.
Case 1. A 77-year-old man with CRF due to diabetic nephropathy was transferred to our hospital because of appetite loss and drowsiness. Serum creatinine and blood urea nitrogen (BUN) levels were 4.31 and 64mg/dL, respectively. The serum magnesium (Mg) level was found to be as high as 7.3mg/dL. The calcium level was 5.8mg/dL. He had cutaneous flushing and respiratory insufficiency caused by respiratory depression in addition to pneumonia. The serum Mg level decreased after hemodialysis with improvement of consciousness disturbances. However, the serum Mg level rose again on the next day, and an additional hemodialysis session was needed.
Case 2. A 78-year-old woman with rheumatoid arthritis developed urinary tract infection which induced acute deterioration of CRF. She demonstrated general fatigue and disorientation. The serum Mg, creatinine and BUN levels were 7.1, 6.56 and 96mg/dL, respectively. Her consciousness level was normalized as the Mg levels decreased after three successive days of hemodialysis.
Both of these patients demonstrated rather mild azotemia and developed consciousness disturbances during the use of magnesium oxide. Of our 78 patients starting hemodialysis in the past two years, only these two patients demonstrated toxic serum Mg levels. We suggest that the use of Mg can cause symptomatic hypermagnesemia in patients with acute deterioration of CRF, and that hypocalcemia may worsen the manifestations of hypermagnesemia.
Conclusions: As Mg toxicity is a serious and potentially fatal condition, early and accurate diagnosis must be made especially in CRF patients with consciousness disturbances. Hemodialysis is effective for the treatment, but postdialysis rebound of the serum Mg level must be carefully observed.

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We report a case of ethylene glycol poisoning in a 64-year-old man, who was admitted because of severe clouding of consciousness. The results of laboratory tests on admission showed marked metabolic acidosis and hyperkalemia. We diagnosed ethylene glycol poisoning because of typical crystals in urine sediment. The patient was immediately given ethanol and started on continuous hemodiafiltration, followed by intermittent hemodialysis. We could save the life of this patient without persistent physical disturbance.

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