Hiroharu Kubota

IgA Nephropathy and Henoch-Schönlein Purpura Nephritis with Anterior Uveitis

Two patients with IgA nephropathy and a patient with Henoch-Schönlein purpura nephritis each associated with anterior uveitis are described. As anterior uveitis accompanying IgA nephropathy improved, renal manifestations were relieved. The patient with Henoch-Schönlein purpura nephritis suffered from not only anterior uveitis but also keratitis. It is suggested that immune mechanisms which induce IgA nephropathy may play a role in the development of anterior uveitis and keratitis.

Glomerular Deposition of Hageman Factor in IgA Nephropathy

Glomerular localization of Hageman factor and fibrin-related antigen (FRA) was examined in 31 cases of IgA nephropathy by immunofluorescent techniques. Hageman factor was observed in 21 cases (68%) and FRA in 24 cases (77%). It is suggested that blood coagulation occurs and fibrin is formed in the glomerulus of IgA nephropathy.

Elevated serum secretory IgA in patients with IgA nephropathy.

Serum secretory IgA was measured to elucidate the significance of secretory IgA in patients with IgA nephropathy. The levels of serum secretory IgA and IgA were, respectively, 6.8 +/- 3.5 micrograms/ml and 231.0 +/- 69.2 mg/dl in the controls and 11.8 +/- 3.2 micrograms/ml and 385.3 +/- 78.7 mg/dl in the patients. The levels of serum secretory IgA and IgA in the patients were significantly higher than those in controls (p less than 0.01). Elevated serum secretory IgA may reflect the excessive state of the IgA-secreting system in IgA nephropathy patients.

Mechanism of Urinary Erythrocyte Deformity in Patients with Glomerular Disease

Hiroharu Kubota, MD, Second Department of Internal Medicine, Hirosaki University, School of Medicine, 5 Zaifucho, Hirosaki 036 (Japan) Dear Sir, Birch and Fairley [1,2] and Birch et al. [3] described glomerular bleeding giving rise to a wide range of morphological alterations in red cells such as dysmorphic red cells. In these alterations, we suspect that the doughnut type of deformity is the most characteristic (fig. 1). The mechanism of urinary erythrocyte deformity in patients with glomerular disease is considered to be the result of continuous changes in osmotic pressure and urinary pH in tubuli [2, 3]. However, in our experiments no doughnut-type erythrocytes were seen under osmotic pressure changes and there were no differences in urinary pH between the dysmorphic group (48 cases) and isomor-phic group (35 cases). In glomerular hematuria, another important factor was the passage of erythrocytes through the glomerular capillary wall composed of endothelium, basement membrane and foot process of epithelium [4, 5]. In view of the important finding that erythrocytes were distorted by passage through the ruptured glomerular capillary wall, we carried out further experiments as follows. 1 ml venous blood in 100 ml saline was incubated at 38 ¤C for 30 min. About 50 mm Hg pressure was applied to the suspended erythrocytes filtered by 3 kinds of membrane filters (pore size: 5 and 3 μm, fibrin-coated 5-μm narrowing in size). The filtrates were examined by phasecontrast microscopy and scanning electron microscopy. In this experiment, doughnut-type erythrocytes were seen in the fibrin-coated 5-μm membrane filter group and

Intraglomerular Lipid Deposition in Experimental Focal Glomerular Sclerosis in the Rat

Hiroshi Ohsawa, Second Department of Internal Medicine, Hirosaki University School of Medicine, 5 Zaifucho, Hirosaki Aomori 036 (Japan) Dear Sir, It is well known that focal glomerular sclerosis is observed in rats by administration of puromycin amino-nucleoside (AN). Although the pathogenesis of glomerular sclerosis in this model is still unknown, some hypotheses have been reported, such as mesangial overloading [1]. A recent report [2] suggests that chronic renal disease may be mediated by abnormalities of lipid metabolism. We studied the intraglomerular lipid deposition in this model and analyzed the intraglomerular lipid. AN (1.5 mg/l00 g of body weight) was injected daily, first for a week, and then again 6 weeks later. AN-treated rats and control rats were sacrificed monthly from the 3rd to the 6th month. Kidney tissues were observed by light microscopy and electron microscopy. To examine the intraglomerular lipid deposition, sections stained with Sudan III were observed and lipid extracted from isolated glomeruli was analyzed by thin layer chromatogra-phy. Isolated glomeruli were obtained by the sieving method. At the sacrifice, blood was sampled to measure total protein, creatinine and lipid according to the standard method. Urinary protein was measured by sulfosali-cylic acid method. After 3 months, 87% of the glomeruli revealed glomerular sclerosis in AN-treated rats. Electron microscopy showed that the main pathologic change in sclerosis was an increasing of mesangial matrix. Lipid deposition was seen in 95% of the sclerotic glomeruli, especially in the sclerotic lesions. Morphological changes were not observed in control rats. Serum levels of total protein and creatinine were normal in each group. Significant pro-teinuria and hyperlipemia were observed in AN-treated rats, but not in control rats. Thin layer chromatography revealed that the intraglomerular lipid consisted of cholesterol ester and triglyceride (fig. 1). Grond et al. [1,3] suggested that mesangial accumulation of macromolecular substance leads to glomerular sclerosis [1, 3]. The lipid deposition has some relation to the development of focal