Endotoxin removal column containing polymyxin B immobilized fiber is useful for the treatment of the patient with Vibrio vulnificus septicemia.

A case of primary septicemia due to Vibrio vulnificus infection is reported. The patient was successfully treated with appropriate antibiotic therapy, drainage, and debridement of the necrotic tissues and direct hemoperfusion (DHP) using polymyxin B immobilized fiber (PMX-F). The effectiveness of DHP using PMX-F, which removes endotoxin in the circulating blood for the treatment of septic shock and multiple organ dysfunction occurring due to this fulminant infectious disease, is discussed.

Changes in prevalence of anti-HCV antibodies associated with preventive measures among hemodialysis patients and dialysis staff.

The latest prevalence of hepatitis C virus (HCV) infection was evaluated in 548 Japanese patients undergoing hemodialysis, and 216 members of the hospital dialysis staff. An assay of anti-HCV antibodies was performed using both first- and second-generation immunoenzymatic tests, and anti-HCV specificity was confirmed with a second-generation recombinant immunoblot assay. Of 548 hemodialysis patients, 90 (16.4%) were positive with first-generation, and 166 (30.3%) with second-generation tests. These rates were significantly higher than those for either hospital staff members (0.5% and 2.3%; p < 0.01) or healthy blood donors (0.98% and 1.30%; p < 0.001). Patients with a history of blood transfusion tended to have a higher positivity rate for anti-HCV than did the non-transfused group (35.4% vs. 25.7% with second generation tests; p < 0.05). Positivity for anti-HCV was related to the duration of hemodialysis. Only a few patients seroconverted during the 2-year, 5-month period between the previous and present studies. Although hemodialysis patients remain a high-risk group for HCV infection, the prevalence of anti-HCV antibodies has decreased recently thanks to the use of erythropoietin for renal anemia, the universal screening of blood donors for anti-HCV antibodies, and improvements in infection control measures for this virus.

[A case of secondary amyloidosis complicated with ulcerative colitis].

A 54 year-old woman who had had 4 years history of ulcerative colitis (UC) was admitted to our hospital because of recently developed proteinuria and leg edema. On admission, laboratory findings disclosed massive proteinuria, hypoalbuminemia, acceleration of ESR and elevated of CRP. Her abdominal symptom was remitted. Renal biopsy showed amyloid deposition in glomeruli and arteriole. Amyloid deposition was also found on rectal biopsy. She had no evidence of familial amyloidosis and multiple myeloma. In this case, amyloid deposition might be developed after UC. Secondary amyloidosis due to UC was extremely rare, only 3 cases including ours were reported in Japan.

Significance of guanidino compounds in non-dialyzed patients with chronic renal failure.

Various guanidino compounds were determined in 48 non-dialyzed patients with chronic renal failure. The patients were divided into two groups, as follows: group A, chronic glomerulonephritis and polycystic kidney; and group B, diabetes nephropathy, lupus nephritis and renal amyloidosis. Six kinds of guanidino compounds in the serum were measured by high performance liquid chromatography. Although guanidinosuccinic acid (GSA), methylguanidine (MG) and taurocyamine (G-TAU) were inversely related to deterioration of renal function, arginine and guanidinoacetic acid were not correlated with the serum creatinine and urea nitrogen (SUN) levels. GSA was increased exponentially with decrease in renal function as compared to SUN. The ratio of methylguanidine to creatinine (MG/CRN) was significantly higher in the patients of group B than those of group A (P less than 0.05) in the range of creatinine 2.0-8.0 mg/dl. MG/CRN showed a negative correlation with the progression rate of renal dysfunction (P less than 0.01). It is suggested that GSA might be a more sensitive marker for renal dysfunction than SUN at the end stage of chronic renal failure, and MG/CRN might represent another indicator reflecting the activity of the causal renal disease and progression rate of renal failure. Furthermore, G-TAU could be a potent substance indicating the disease state. From these results, it is concluded that determinations of guanidino compounds in the serum might be useful for recognizing of the state of chronic renal failure.

IgA nephritis associated with plasminogen abnormalities.

Two patients with IgA nephritis associated with hereditary plasminogen abnormalities are described. One patient had dysplasminogenemia and the other had plasminogen deficiency. In both patients, renal biopsy specimens showed significant arteriosclerotic changes in addition to mesangial proliferation. Increased fibrinopeptide A concentration in their plasma suggested increased thrombin generation. In one patient, no systemic arteriosclerosis coexisted, judging from normal optic fundi and the absence of neurological and cardiac abnormalities. In IgA nephritis, renal vascular hyalinosis is often observed, probably resulting from vascular injury. Thus, it was suggested that the decreased fibrinolysis and renal vascular injury of these patients synergistically induced more fibrin thrombi and accelerated arteriosclerosis of the kidney. These cases imply the important role of fibrinolytic disorders in the progression of IgA nephritis.

A case of acute interstitial nephritis induced by flurbiprofen.

Recently, acute interstitial nephritis (AIN) presenting nephrotic syndrome and renal failure induced by nonsteroidal anti-inflammatory drug (NSAID) has been recognized with increasing frequency. We described here a 43-year-old woman who developed this type of nephropathy after taking NSAID for rheumatoid arthritis. Flurbiprofen (Froben) was assumed to be a causal drug based on a clinical course and a positive result of lymphocyte transformation test. Withdrawal of flurbiprofen therapy led no sufficient improvement, and high-dose steroid therapy done 15 months after the onset resulted in only a minor improvement. So far as we know, this was the second case of AIN associated with flurbiprofen and the youngest in NSAID-induced AIN with irreversible chronic renal insufficiency.