Metabolic syndrome and chronic kidney disease in Okinawa, Japan.

We assessed the prevalence of chronic kidney disease (CKD) in a hospital-based screening program in Okinawa, Japan. The significance of metabolic syndrome as a determinant of CKD was examined using multivariate logistic regression analysis. A total of 6980 participants, aged 30-79 years, participated in a screening program in Tomishiro Chuo Hospital. Metabolic syndrome was defined according to the criteria of the Adult Treatment Panel III (ATP III). Data were also analyzed according to the modified criteria of the National Cholesterol Education Program (NCEP) that defines abdominal obesity as a waist circumference of > oe =85 cm in men and > or =90 cm in women. CKD was defined as dipstick proteinuria (> or =1+) or a reduced glomerular filtration rate (GFR). GFR was estimated using the abbreviated Modification of Diet in Renal Disease (MDRD) formula. The prevalence of metabolic syndrome and CKD was 12.8 and 13.7%, respectively. Metabolic syndrome was a significant determinant of CKD (adjusted odds ratio (OR) 1.537 and 95% confidence interval (CI) 1.277-1.850, P<0.0001). The adjusted OR (95% CI) was 1.770 (1.215-2.579, P=0.0029) for those with four metabolic syndrome risk factors compared to those with no metabolic syndrome risk factors. Metabolic syndrome was a significant determinant for younger participants (<60 years; OR 1.686, 95% CI 1.348-2.107, P<0.0001), but not for older participants (> or =60 years; OR 1.254, 95% CI 0.906-1.735, NS). The relationship between the number of metabolic syndrome risk factors and the prevalence of CKD was linear using the modified criteria. The results suggest that metabolic syndrome is a significant determinant of CKD in men under 60 years of age, in Okinawa, Japan.

[A case of Goodpasture's syndrome with massive pulmonary hemorrhage ameliorated by cyclophosphamide pulse therapy].

A 22-year-old woman was admitted to our hospital for evaluation of fever, renal dysfunction, and a 3-month-history of macrohematuria. Laboratory evaluation revealed proteinuria (1.8 g/day), hypoproteinemia, microcytic microchromic anemia, renal failure (blood urea nitrogen 30.3 mg/dl, serum creatinine 4.0 mg/dl), and positive serum antiglomerular basement membrane (anti-GBM) antibody. Renal biopsy revealed cellular crescents in all 8 glomeruli and partial rupture of the GBM. The interstitium showed severe inflammatory cell infiltration. Immunofluorescent examination revealed linear deposits of IgG and C3 along the GBM. Pulmonary biopsy revealed linear deposits of IgG along the alveolar basement membrane in the immunofluorescent examination. A diagnosis of Goodpasture's syndrome was made because all of the diagnostic criteria were fulfilled. After admission, the patient's renal function deteriorated rapidly. Hemodialysis was started, and the patient was treated with methylprednisolone pulse therapy and oral prednisolone with double filtration plasma pheresis (DFPP). However, her renal function did not improve. On the 30th hospital day, she showed hemoptysis, and a chest X-ray and CT revealed massive bilateral pulmonary hemorrhage. Despite treatment with pulsed methylprednisolone, oral prednisolone (80 mg/day), and DFPP, the pulmonary hemorrhage improved only transiently, worsening again 5 days later. Cyclophosphamide pulse therapy was administered. After this treatment, the patient's pulmonary manifestations and pulmonary hemorrhage improved. At the present time she is on maintenance dialysis therapy without pulmonary manifestations. These findings suggest that cyclophosphamide pulse therapy is effective against Goodpasture's syndrome with massive pulmonary hemorrhage showing resistance to other conventional therapy.

Successful treatment of a non-haemophilic patient with inhibitor to factor VIII by double-filtration plasmapheresis.

Factor VIII (FVIII) inhibitors appear in 3-20% of haemophilia A patients after injection of FVIII concentrates. However, autoantibodies to FVIII are also reported in non-haemophiliacs. In these patients FVIII inhibitor disappears spontaneously or diminishes in response to immunosuppressive therapy. However, a few patients show resistance to immunosuppressive therapy. We describe a non-haemophilic elderly patient with acquired FVIII inhibitor who failed to respond to prednisolone. He was treated with double-filtration plasmapheresis (DFPP) which resulted in a very rapid reduction in inhibitor levels and resolution of symptoms.

A possible mechanism for increased cerebrovascular permeability in diabetic rats: effects of insulin and 2-deoxy-glucose.

1. Cerebrovascular permeability estimated as Evans blue extravasation significantly increased during insulin-induced hypoglycemia in both non-diabetic and diabetic rat groups. 2. Cerebrovascular permeability also increased significantly during 2-deoxy-glucose-induced intracellular glycopenia in both groups. 3. When a blood glucose level was fixed, cerebrovascular permeability showed no more significant change despite the hyperinsulinemic state in both groups. 4. Results suggest that hypoglycemia and/or intracellular glycopenia seems to be the major factor for increases in cerebrovascular permeability.