To examine the relationship between the length of the predialysis period and the pathogenesis of diabetic end-stage renal failure, we retrospectively studied 58 hemodialyzed patients (36 males, 22 females; 62.8±10.6 (SD) years). They were subgrouped into group A (n=34) or B (n=29), respectively, depending on whether hemodialysis was started less or more than 2 years after their serum creatinine concentration had reached 2mg/dL.
Group A patients were ten years younger than those of group B, and showed significantly higher urinary protein excretion, lower plasma albumin concentration, and larger renal size. The incidence of cerebral infarction was higher in group B. Multiple regression analysis demonstrated that the length of predialysis period was well correlated with both patients' age and renal size. These findings suggest that the major pathogenesis of renal failure is microangiopathic glomerulosclerosis in group A, and macroangiopathic nephrosclerosis in group B. The length of the predialysis period in each case must reflect the different involvements of these two mechanisums. Especially, in older hemodialyzed diabetic patients, the number of which has been increasing in recent years, nephrosclerosis may play a larger role in diabetic nephropathy.

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The effects of differential albumin leakage from the dialyzer on glycoalbumin (GA) levels were investigated. Forty-six chronic hemodialysis patients used either dialyzer PS [Polysulfone, removal rate (β₂-MG)=0.7, albumin leakage=2.85(g/session)] or dialyzer MRC [Modified reproductive cellulose, removal rate (β₂-MG)=0.3, albumin leakage=1.7(g/session)]. Patients were classified by glucose tolerance and allotted dialyzer into 4 groups: nonDM-PS (n=13), nonDM-MRC (n=12), DM-PS (n=11), DM-MRC (n=10). GA levels were measured at 4 points: before use of the dialyzer, 2 months, 6 months, and 12 months after the use of the dialyzer.
Changes in GA levels exhibited significant differences depending on whether dialyzer PS or MRC was used. In the nonDM-PS and DM-PS groups, GA values decreased significantly 2 months after beginning to use dialyzer PS, then returned to control levels after 6 months. In the nonDM-MRC and DM-MRC groups, there was no significant change in GA levels throughout the year.
These results indicate that increased albumin leakage from the dialyzer may cause acute reduction of GA levels. However, GA levels appear to be modified by other effects over the long term.

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Cardiovascular disease is a leading cause of morbidity and mortality in patients with end-stage renal disease (ESRD). We previously reported that DSE is useful to detect coronary artery disease. The present study investigated the utility of DSE in predicting cardiac events after testing. Forty patients with ESRD who underwent DSE were classified into three groups; DSE demonstrated ischemia in 10 (group A), a normal study in 14 (group M) and side effects in 16 (group S). These forty patients were then followed for cardiac events after DSE and 38 patients of these 40 could be successfully followed. The mean follow-up duration was 24±10 months and the average age was 65±10 years. The cardiac event rate was higher in group A (75%) and group S (69%) than in group M (14%) (p<0.04). A positive DSE provides useful prognostic information for cardiac events in patients with chronic renal failure.

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We experienced 2 patients who developed heparin-induced thrombocytopenia (HIT) a few years after the initiation of hemodialysis therapy. Both patients demonstrated anti-PF 4/heparin complex antibody (HIT antibody) prior to symptomatic onset. Case 1, a 68-year-old woman. She had been treated chronic kidney disease by dialysis using heparin as an anticoagulant since 2001. We initially detected HIT antibody in her blood in April 2002. In August 2002, she developed HIT with blood coagulation in the circuit using heparin. Thereafter, we changed anticoagulant to nafamostat mesilate. HIT antibody remains positive in this patient. Case 2, a 71-year-old man. He had been treated chronic kidney disease on dialysis using heparin as anticoagulant since 1996. He had shown episodes of vascular access clotting between 2000 and 2004. HIT antibody was detected in his blood in April 2002. After the last episode of vascular clotting on 2004, he developed HIT with blood coagulation in the circuit using heparin. Thereafter, we changed argatroban as an anticoagulant. HIT antibody remains positive in this patient. We measured HIT antibodies for 129 dialysis patients in our clinic in 2002. As a result, 5 (3.9%) patients was found to have HIT antibody. We must carefully monitor the cases with HIT antibody, even if the patients do not initially show any signs of HIT. It is likely that HIT may develop during afuture dialysis session.

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We report a 64-year-old male on chronic hemodialysis for 12 years, who was complicated by spontaneous renal rupture and diverticulitis. The patient had a history of recurrent diverticulitis since 2002. In February 2003, the patient developed tarry stool, progression of anemia and abdominal pain. Additionally, a tender mass measuring 5cm×7cm was palpable in the left abdomen. He was referred to our hospital for further examination. On enhanced computed tomography (CT) of the abdomen, a large hematoma was demonstrated in the region of the left kidney. Renal arteriogram confirmed the presence of hemorrhage from the left renal artery and angioembolization was performed. Colon fibers showed numerous diverticula and coagulations. The source of melena was not evident, but diverticulitis was highly suspected. When hemodialysis patients develop abdominal pain, renal rupture should be considered as part of the differential diagnosis as well as gastroenterological lesion.

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