Discussion

DR. STEVEN N. EMANCIPATOR (Pathologist, University Hos-pitals of Cleveland, and Associate Professor of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio): Given the different pathologic and clinical features of these two patients, it is perhaps surprising that they share the same diagnosis: IgA nephropathy (IgAN). Diverse as these two examples are, they do not represent the clinical extremes of IgAN, namely, the acute nephritic syndrome with acute renal failure, and the nephrotic syndrome. Nor are diffuse, proliferative, necrotizing nephritis or minimal change by light microscopy—the pathologic poles of IgAN—illustrated by these two patients. In addition, whereas the second patient is likely to develop end-stage renal disease, the first patient is likely to maintain good renal function, at least for the next 20 years. Nevertheless, both patients are typical examples of IgAN, a syndrome defined by the predominant deposition of IgA within the glomerulus.

The first phase of investigation of IgAN consisted of a descriptive collation of clinical and/or pathologic features; several excellent recent reviews, including a prior Nephrology Forum, distill these original series, and reach similar conclusions about the disorder's attributes [1—7]. Nearly all patients with IgAN (95%) have hematuria sometime during the course of the disease. Its severity ranges from episodic macrohematuria (54% of patients), which often is superimposed on persistent