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Diagnosis: IgA Nephropathy
With parietal (capillary) IgA deposition and concomitant (non-dominant) IgG and IgM glomerular deposition

It is now accepted that the diagnosis of IgA nephropathy depends on the demonstration of glomerular IgA-dominant or codominant, involving the mesangium with or without staining of peripheral capillary loops (Haas M. J Nephrol. 2005;18:676-80 [PubMed link]; Jennette JC. Am J Kidney Dis 1988;12:348-52 [PubMed link]) Close to 50% of cases of IgA nephropathy contain mesangial deposits of IgG and approximately 50% contain mesangial deposits of IgM. C3 is detected in glomeruli in more than 90% of cases and C1q in around of 10% (Haas M. J Nephrol. 2005;18:676-80 [PubMed link]).

In this case the presecence of IgM, IgG, C3, and C1q (C1q only traces) to raise the possibility of other immune-complex mediated glomerulonephritis (GN), however there are not clinical or laboratory test suggesting it. Moreover, IgA staining was more intense that other immunoglobulins, a feature very unusual in immune-complex mediated GN, like lupus nephritis. Even so, rare cases have been reported in which a patient who developed systemic lupus erythematosus had a renal biopsy showing a mesangial proliferative or membranous lesion with predominant IgA deposits months to several years prior to developing clinical and serologic manifestations of SLE. C3 and C1q staining was weak and does not suggest C3 nephropathy or C1q nephropathy.

It is frequent to find IgA deposits on the glomerular capillary walls in IgA nephropathy, until 38% of the cases according to several authors. Electron microscopic findings reveale that location of the dense deposits is subepithelial (near to 50%), intramembranous (near to 65%), and subendothelial (near to 24%) (Yoshimura M, et al. Am J Kidney Dis. 1987;9:404-9 [PubMed link]).

Some authors report that crescent formation is more frequently found in patients with capillary deposits than those with only mesangial deposits, especially higher in those with subepithelial deposits. Also, capillary deposits are associated to heavier proteinuria. It is frequent that in patients with acute exacerbations, manifested by an abrupt increase in urinary protein and development of macroscopic hematuria, capillary IgA deposits be detected. It is suggested that capillary IgA deposition is closely related to clinical and histologic activities of IgA nephropathy and is considered to be an important factor responsible for the progression of the disease (Yoshimura M, et al. Am J Kidney Dis. 1987;9:404-9 [PubMed link]).

It is reported in a study that high levels of proteinuria might be due to alterations of the size barrier and/or anionic sites of GBM in IgA nephropathy (Tomino Y et al. J Clin Lab Anal. 1989;3:101-7 [PubMed link])

See the chapter IgA Nephropathy and Schönlein-Henoch purpura of our Tutorial.

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Bibliography

• Haas M. Histology and immunohistology of IgA nephropathy. J Nephrol. 2005;18(6):676-80. [PubMed link]
• Tomino Y, Yagame M, Eguchi K, Miyazaki M, Nomoto Y, Sakai H, Shirato I, Ito K. Detection of anionic sites and immunoglobulin A deposits in the glomerular capillary walls from patients with IgA nephropathy. J Clin Lab Anal. 1989;3(2):101-7. [PubMed link]
• Jennette JC. The immunohistology of IgA nephropathy. Am J Kidney Dis. 1988;12(5):348-52. [PubMed link]
• Yoshimura M, Kida H, Abe T, Takeda S, Katagiri M, Hattori N. Significance of IgA deposits on the glomerular capillary walls in IgA nephropathy. Am J Kidney Dis. 1987;9(5):404-9. [PubMed link]

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