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During an observation period of 1-2 years in 2 different districts in Japan, 104 patients were found to have upper respiratory infections caused by group A streptococci. Fourty-nine of these patients were followed prospectively to determine if renal involvement would occur. Twelve patients developed transient serum complement (CH50) depression and urinary abnormality, and 2 of these developed mild hypertension. The latent period was from 1-8 weeks after the streptococcal infection. Renal biopsies of the 12 patients with "asymptomatic" of "subclinical" acute poststreptococcal glomerulonephritis (APSGN) were examined by light, immunofluorescent and electron microscopy. Glomerular lesions ranged from mild proliferative changes to the classical pathology seen in APSGN. The 12 patients were followed for 10 years. Two of them developed persistent or intermittent hematuria, and renal biopsies obtained 4 years after the initial infection revealed mesangial proliferative glomerulonephritis without IgA deposits. The remaining patients showed no abnormal findings after the acute episode. These findings suggested that glomerular involvement after group A streptococcal infection is frequent and mesangial proliferative glomerulonephritis, which was found to develop in some, may rank with IgA nephropathy as a major cause of unexplained microscopic hematuria.

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We studied the significance of a streptococcal protein (preabsorbing Ag) (PA-Ag) in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN). This protein was isolated from nephritogenic streptococci. Purification of PA-Ag was achieved by chromatography, followed by Sephadex IEF. A single protein band at pH 4.7 was identified as PA-Ag. The m.w. was 43,000. Rabbit antisera against PA-Ag and sera of patients with APSGN showed identical precipitation lines by immunodiffusion. Antibodies to PA-Ag were found to be present in 30 of 31 patients with APSGN, in 1 of 36 patients with uncomplicated group A streptococcal upper respiratory tract infections, and in 1 of 36 normal adults. By using immunoelectrophoresis, it was found that PA-Ag activates the alternate pathway of C. Other water-soluble streptococcal fractions, used as controls, did not activate the C system. The demonstration that PA-Ag is present in the glomeruli in the early phase of APSGN and its ability to activate C3 and factor B suggest that PA-Ag may be involved in the pathogenesis of APSGN, via in situ C activation.

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Hypercalcemia is an uncommon complication of childhood renal tumors. It is exclusively seen in infants 6 months of age or younger with malignant rhabdoid tumor of the kidney (MRTK) or congenital mesoblastic nephroma (CMN). Secretion of parathormone or prostaglandin E2 by the tumor cells is responsible for the hypercalcemia in most of these patients. Bone metastasis has been notably absent in these patients, and the hypercalcemia completely resolves with the removal of the tumor. Hypercalcemia in itself probably does not have any prognostic significance; however, it may serve as a tumor marker in some patients. Early recognition and effective management of this complication may prevent the acute life-threatening as well as the longstanding complications of this serious metabolic disorder.

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To investigate the role of circulating immune complexes (CIC) in the pathogenesis of acute poststreptococcal glomerulonephritis (AGN), sera were obtained serially from 13 patients with biopsy-proven AGN, 16 patients with group A streptococcal infection, and 20 age- and sex-matched controls. Samples were analysed for Clq-binding activity (Clq-BA), levels of IgG, IgA, IgM, C3 and C4, and antibody titres to streptococcal enzymes. Significant elevation of Clq-BA was observed in 11 patients (84.5%) with AGN and 7 patients (44%) with streptococcal infection alone. The data suggest that CIC do not necessarily cause glomerular damage, but rather represent a systemic inflammatory response in patients with group A streptococcal infection.

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The presence and localization of antigenic sites in glomeruli of 14 patients with acute poststreptococcal glomerulonephritis (AGN) were studied by immunofluorescein and immunoferritin technics. Labeled IgG fractions from the same patients were used for the identification of antigenic sites. The staining capacity of these IgG fractions depended on the time when sera were obtained. Staining was minimal during the first week, and increased up to the fourth or fifth week. Glomeruli, however, stained only when renal tissue was obtained during the early phase of the disease. Precise localization of antigenic sites was determined with ferritin-conjugated patients' IgG. Segmental deposition of ferritin was observed in the mesangial matrix and on the endothelial side of the glomerular basement membrane. Subepithelial electron-dense deposits contained no or very few ferritin particles. In contrast, ferritin-conjugated antihuman IgG was distributed diffusely in the mesangial matrix, on the endothelial side of the basement membrane and in subepithelial deposits. These findings suggest that, during the early stage of acute poststreptococcal glomerulonephritis, free antigen is present in the glomeruli of patients with this disease.

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Fluorescein-labeled immunoglobulin G fractions from serums of patients with acute glomerulonephritis and from many normal serums stained the glomerular basement membrane and mesangium of renal tissue from patients with early acute glomerulonephritis; these serums did not stain the corresponding tissues from patients with any other kidney disease. Previous absorption of the serum fraction with frozen and thawed nephritogenic beta hemolytic streptococci abolished all staining. Other bacteria studied did not abolish the staining. Only the plasma membrane of the streptococcus absorbed the immunoglobulin G fraction; such absorption eliminated staining. Fluorescein-labeled antiserums against streptococcal plasma membrane had staining properties similar to patients' serums.

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