Abstract
IgA nephropathy is now accepted as a clinicopathologic entity characterized by diffuse glomerular mesangial deposition of IgA as the predominant immunoglobulin [1, 2]. As pointed out by Berger in his first description, clinical presentation and symptoms as well as glomerular aspects by light microscopy vary from patient to patient. Some present with recurrent macroscopic hematuria while in the others the disease is discovered by “chance” finding of proteinuria. Although the mode of presentation of IgA nephropathy may be influenced by renal biopsy policy, obvious differences are observed between pediatric and adult reports, on the one hand, and among different countries, on the other. For instance, in France, gross hematuria is the presenting symptom in 40% of adults and 80% of children [3, 4] while, in Japan, gross hematuria is the initial symptom in only 14% of adults and children [5]. In the majority of patients, the evolution is chronic during several years with persistent urinary abnormalities. Episodes of macroscopic hematuria are more frequent during the first years of the course and then tend to disappear [3, 4, 6, 7]. Long-standing clinical remission may occur in a few patients, especially in children [7]. However, 15–25% of all patients develop progressive renal failure [6, 8]. A few of them follow a direct, rapid course to terminal renal failure and are thus referred to as having “malignant” IgA nephropathy [9]. Hypertension develops during the course in a significant number of cases [6, 8, 10, 11] preceding or not the appearance of renal insufficiency.
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© 1987 Martinus Nijihoff Publishing, Boston
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Droz, D. (1987). IgA Nephropathy: Clinicopathologic Correlations. In: Clarkson, A.R. (eds) IgA Nephropathy. Topics in Renal Medicine, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2039-5_7
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DOI: https://doi.org/10.1007/978-1-4613-2039-5_7
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