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Most cases of adult type IgA nephropathy (IgAN) have an insidious onset and asymptomatic course. However, some patients reveal recurrent macroscopic haematuria following episodes of respiratory or urinary tract infections. In order to clarify the correlation between clinical features and histological alterations or prognosis, 42 cases of early stage IgAN and 40 cases with acute exacerbation episodes were investigated and compared with a control group. Early stage cases were defined as having had a renal biopsy within 1 year after the first detection of urinary abnormalities, and had normal urinary findings within the 12 months before the first detection of urinary abnormalities. Acute exacerbation cases were defined as macroscopic haematuria or worsening of urinary abnormalities after acute infectious episodes and undergoing a renal biopsy within 120 days after the onset of these episodes. The early stage cases had better renal function and lower systolic and diastolic blood pressure than that of control group. They also showed milder changes in mesangial cell proliferation, mesangial matrix increase, totally sclerotic glomeruli, and tubulointerstitial changes. However, it is important to note that glomerular and interstitial sclerotic changes were observed even in early stage cases. Endothelial detachment was noticed more frequently in the early stage cases. Acute exacerbation cases revealed lesions of endocapillary proliferation, mesangiolysis and endothelial detachment more frequently, although these changes were segmental in each glomerulus. There was no statistical difference in disease prognosis between cases with and without acute exacerbation. These data indicated that there are characteristic histological changes in early stage cases and acute exacerbation cases of IgAN.

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A 24-year-old woman was admitted to Toyosaka Hospital with proteinuria, hematuria, lymphopenia, hypocomplementemia, positive anti-nuclear antibody (ANA), and elevation of anti-streptolysin O (ASO). Renal biopsy specimen revealed diffuse mesangial and endocapillary glomerulonephritis with crescent formation and duplication of the capillary loop on light microscopic examination. Mild to moderate proliferation of mesangial matrix and cells were observed. On immunofluorescence (IF) examination, deposition of IgG, IgA, IgM, C1q, C3, and C4 to the mesangium and capillary wall were observed. By electron microscopy (EM), mesangial, subendothelial, and subepithelial deposits were recognized. However, microtubular structure in glomerular endothelial cells, fingerprint structures, and circumferential mesangial interposition were not observed by EM. The patient was referred to our hospital, but there was no change in her proteinuria 3 weeks after admission. The elevation of ASO, hypocomplementemia, and endocapillary proliferation suggested acute glomerulonephritis, while lymphocytopenia, positive ANA, the persistent hypocomplementemia, and various deposits detected by IF and EM suggested lupus nephritis; however, she did not fulfill the classification criteria of systemic lupus erythematosus. We started prednisolone (40 mg/day) with the diagnosis of chronic glomerulonephritis revealing diffuse mesangial and endocapillary proliferative glomerulonephritis, but it was not effective for the proteinuria. Quinapril (10 mg/day) and losartan (25 to 50 mg/day) were administered and the proteinuria decreased. It is possible that this use of an angiotensin converting-enzyme inhibitor and an angiotensin II receptor antagonist was effective in reducing the proteinuria in this patient.