Correspondence

Case 12-1995: Acute Postinfectious Glomerulonephritis

N Engl J Med 1995; 333:524-525August 24, 1995

Article

To the Editor:

In his discussion of Case 12-1995 (April 20 issue)1 on acute renal failure of glomerular origin, Black mentions the possibility of IgA nephropathy as a cause of glomerular hematuria. He cites our study 2 of patients with acute renal failure associated with episodes of macroscopic hematuria, but he misinterprets our conclusions. We found that decreased renal function in IgA nephropathy correlated closely with the presence of red-cell casts in the tubular lumen, accompanied by signs of tubular necrosis, and not with the presence of glomerular crescents, as Black states. At the time of the disappearance of macroscopic hematuria, every patient in our study spontaneously recovered normal renal function, without immunosuppressive treatment. Similar findings have been reported by others.3,4 The mechanisms of the tubular damage that accompanies some episodes of glomerular hematuria have not been elucidated. Massive crescent formation has also been described in IgA nephropathy; this seems to be a very uncommon complication with a poor prognosis.

Manuel Praga, M.D.
Hospital 12 de Octubre, 28041 Madrid, Spain

4 References

1
Case Records of the Massachusetts General Hospital (Case 12-1995). N Engl J Med 1995;332:1083-1089
Full Text | Web of Science | Medline

2
Praga M, Gutierrez Millet V, Navas JJ, et al. Acute worsening of renal function during episodes of macroscopic hematuria in IgA nephropathy. Kidney Int 1985;28:69-74
CrossRef | Web of Science | Medline

3
Kincaid-Smith P, Ryan GB, Dowling JP, Nicholls K. Acute renal failure in mesangial IgA nephropathy. Contrib Nephrol 1984;40:182-186
Medline

4
Delclaux C, Jacquot C, Callard P, Kleinknecht D. Acute reversible renal failure with macroscopic haematuria in IgA nephropathy. Nephrol Dial Transplant 1993;8:195-199
Web of Science | Medline

Author/Editor Response

Dr. Black replies:

To the Editor: Praga suggests that I misinterpreted data in his paper when I stated that “acute renal failure, which is usually reversible, can occur and may be associated with glomerular crescent formation” in patients with IgA nephropathy. However, among six patients with acute renal failure from whom biopsy specimens were obtained in the study of patients with IgA nephropathy by Praga et al., four had glomerular crescent formation. The authors concluded that the crescent formation was not the cause of the acute renal failure. This issue was not the premise of my discussion; I simply wished to indicate that IgA nephropathy can cause acute renal failure and that the renal insufficiency may be associated with glomerular crescents. The importance of crescentic glomerulonephritis in the pathogenesis of acute renal failure in IgA nephropathy has been described elsewhere.1-3

Robert M. Black, M.D.
St. Vincent Hospital, Worcester, MA 01604

3 References