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A 50-year-old man diagnosed as having AGA(Churg-Strauss syndrome) was administered steroid. After treatment with mizoribine, hyperuricemia and acute renal failure occurred as side effects of this drug. Accordingly we started dialysis treatment, terminated mizoribine treatment, and administered allopurinol dosage. Hemodialysis was necessary every day for 11 days and his renal function recovered after one month. In 67Ga scintigraphy, accumulation of 67Ga was seen in the kidney.

Background: Lipid abnormalities are frequently found in end-stage renal disease (ESRD), and abnormal lipid metabolism may contribute to the progression of renal disease. Previous investigators have reported that apolipoprotein E (apoE) has an important role in lipoprotein metabolism and that the process of lipoprotein catabolism varies according to the apoE phenotype. In addition, the relative frequency of the apoE alleles is different among the races. In this study, we investigated the allele frequency of apoE phenotypes and evaluated the impact of apoE polymorphism on lipid profile in Japanese patients with renal disease., Methods: ApoE phenotypes were determined using isoelectric focusing and Western blotting in 592 Japanese patients with renal disease [86 out of 107 patients with glomerulonephritis had proteinuria of not less than 0.25 g per 24 hr and 485 with ESRD; 448 were on hemodialysis (HD), and 37 were on continuous ambulatory peritoneal dialysis (CAPD)]. The allele frequency and apoE phenotype distribution were estimated by the gene-counting method. Serum lipid parameters related to lipid metabolism were measured after at least a 12-hour fast., Results: The allele frequency of the three major apoE phenotypes (apoE2, apoE3, and apoE4) in 107 glomerulonephritis patients (epsilon 2; 0.037, epsilon 3; 0.860, epsilon 4; 0.103) was almost identical to that in the normal control population (epsilon 2; 0.036, epsilon 3; 0.848, epsilon 4; 0.115). However, 86 glomerulonephritis patients with proteinuria had higher allele frequency of apoE2 (epsilon 2; 0.052, P < 0.01) and apoE4 (epsilon 4; 0.140, P < 0.001) and lower allele frequency of apoE3 (epsilon 3; 0.808, P < 0.001) than the controls. Furthermore, ESRD patients had higher allele frequency of apoE2 (epsilon 2; 0.058, P < 0.01) and lower allele frequency of apoE4 (epsilon 4; 0.091, P < 0.05) than the controls. Higher prevalence of nephrotic syndrome was found in proteinuric glomerulonephritis patients with apoE2. The impact of apoE polymorphism on serum lipid profile in patients with glomerulonephritis, HD, and CAPD was different from that generally expected., Conclusions: The higher frequency of apoE2 in ESRD patients suggests that apoE2 is a possible genetic predisposition to ESRD in a Japanese population. The impact of apoE2 and apoE4 on lipid profile in patients with renal disease was unique and different from that in the normal population.

Vancomycin therapy is frequently used for peritonitis in patients on peritoneal dialysis, but the emergence of resistance has been reported. We evaluated the efficacy of a single intraperitoneal dose of vancomycin for peritonitis in peritoneal dialysis patients. We assessed 24 episodes of peritonitis in 16 patients, and compared clinical parameters between responders and nonresponders. Vancomycin was effective for 12 patients (18 out of 24 episodes, 75.0%). Nonresponders had a significantly higher initial C-reactive protein level and dialysis fluid leukocyte count, and the mean serum albumin over three months before onset was significantly lower than in responders. Patients with a serum albumin level 3.0 g/dl or more were significantly more likely to respond than those with a level less than 3.0 g/dl. In conclusion, it seems reasonable for peritonitis patients with a mild inflammatory response and a serum albumin 3.0 g/dl or more to receive intraperitoneal vancomycin on an outpatient basis.

Recently, involvement of remnant-like particle cholesterol (RLP-C) in atherosclerosis was reported, but this parameter has not been adequately investigated in hemodialysis (HD) patients. The present study investigated the relationship between the RLP-C level and total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), lipid peroxides (malone dialdehyde, MDA), apolipoprotein (Apo) A-I, and ApoB. In addition, the fractions of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), LDL, and HDL in serum lipoproteins were determined by disk polyacrylamide gel electrophoresis. The relationship between the RLP-C level and three atherogenic indices was also studied. The RLP-C level in HD patients (8.2 +/- 6.7 mg/dl) was significantly higher than that in normal controls (2.7 +/- 1.3 mg/dl). The RLP-C level showed a significant positive correlation with the levels of TC, TG, LDL-C, MDA, ApoB, VLDL(%), and IDL(%), as well as a negative correlation with HDL(%). However, there was no correlation with age or the duration of HD. RLP-C also showed significant positive correlations with the (TC -HDL-C)/HDL-C ratio and the (VLDL + LDL)/HDL ratio, as well as a negative correlation with the ApoA-I/ApoB ratio. These results suggest that RLP-C may be a potential indicator of atherogenic risk in HD patients.

To clarify the role of apolipoprotein E (apo E) in the formation of amyloid deposits, we examined specimens from 11 patients with renal amyloidosis who underwent renal biopsy by an immunohistochemical method using a monoclonal antibody (murine IgG1). Apo E was distributed in the amyloid deposits of all patients in a pattern similar to that obtained with Congo red staining. Strong positive staining for apo E was found on the amyloid deposits in the glomeruli. These results suggest that apo E is a common constituent of amyloid fibrils and that it may be a useful marker for immunohistochemical studies of systemic amyloidosis including renal amyloidosis.

In order to define the role of cytokines in mesangial cell pathophysiology, we measured the mitogenic activity of recombinant human platelet-derived growth factor AA (rhPDGF-AA), rh interleukin-1 alpha (rhIL-1 alpha) and rh tumor necrosis factor-alpha (rhTNF-alpha) in cultured human mesangial cells, and investigated the effect of the calcium channel blocker nicardipine hydrochloride on their cell mitogenic activity. DNA synthesis in mesangial cells, stimulated by rhPDGF-AA, rhIL-1 alpha or rhTNF-alpha, was measured using [3H]TdR up take and similar investigations, with nicardipine hydrochloride added to the above, were conducted. The results showed DNA synthesis in cultured human mesangial cells were stimulated by rhPDGF-AA, rhIL-1 alpha and rhTNF-alpha, and this effect was reduced by the addition of nicardipine hydrochloride. Since rhPDGF-AA, rhIL-1 alpha and rhTNF-alpha are released by the inflammatory cells which infiltrate glomeruli, these cytokines may be involved in the mechanisms of mesangial cell proliferation observed in immune-mediated mesangial proliferative glomerulonephritis. Nicardipine hydrochloride reduced DNA synthesis in cultured human mesangial cells in response to these cytokines, suggesting possible application in medical therapy for immune-mediated mesangial proliferative glomerulonephritis.

We report an 18-year old woman who had glomerulocystic kidney disease (GCKD) without a family history of renal disease or hypertension and no known congenital abnormalities. Her renal function was normal. Renal biopsy showed cystic dilatation of the Bowman's spaces and atrophy of the glomerular tufts. Electron microscopy revealed specific changes in the basement membranes of noncystic glomeruli, suggesting a congenital origin for her renal pathology. This relatively rare case contrasts with the usual presentation of GCKD in neonates or children.