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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2012  |  Volume : 23  |  Issue : 2  |  Page : 369-370
Author's Reply

MC Specialty Hospital, P. O. Box 7832 Dubai, United Arab Emirates

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Date of Web Publication28-Feb-2012

How to cite this article:
Jabur WL. Author's Reply. Saudi J Kidney Dis Transpl 2012;23:369-70

How to cite this URL:
Jabur WL. Author's Reply. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2021 Feb 28];23:369-70. Available from: https://www.sjkdt.org/text.asp?2012/23/2/369/93183
I have read with interest the queries high­lighted by Dr. Muhammed Mubarak about the article I have published in your journal.

As you know, IgAN is the most common glo-merular disease worldwide. However, there has been no consensus about the classification to correlate the clinical and the pathological presentations of the disease. I endeavored to highlight in this article the controversial cre-scentic lesion that has been cited in two his­toric classifications (although not the latest), and to address the importance of the necrotic lesion we frequently encounter in the context of proliferative glomerulonephritis in general, and the crescentic prototype in particular. I opted to include Henoch Schonlein Purpura (HSP) in the discussion for being synonymous to IgAN in its intrarenal pathology.

I have few points to highlight in the context of answering the queries raised in the men­tioned letter.

Although the association between IgAN and minimal change disease (MCD) is widely re­cognized as mentioned, the co-existence of HSP and MCD is not described to the best of my knowledge.

The aim of the article was to highlight the diverse clinical correlation of IgAN and its systemic vasculitis corollary of HSP and also to address, in particular, the controversial lesion of extra-capillary proliferation and capillary necrosis encountered in the context of the variable light microscopic presentations of IgAN. It was aimed to shed light on the clas­sifications and the criteria cited to identify crescentic glomerulonephritis in general, and the Lee-Haas classification in particular.

The intensity of IgA deposition is of no sig­nificance, neither for the diagnosis nor for assessing the prognosis, and it is well known that any deposition of IgA immunoglobulin (more than trace) in the absence of C1q is indicative of IgAN.

In the Lee-Hass classification, the severity of glomerular disease in IgAN was featured by the extent of glomerular sclerosis and glome-rular crescents, without an obvious discrimi­nation between cellular and fibrous crescents, which explicitly points to chronic lesions. They linked the crescentic lesions to glome-rular sclerosis on the one hand and, more im­portantly, to tubular atrophy and interstitial inflammation on the other hand. However, they were arguably considering the aforementioned lesions with the acute lesions of mesangial proliferative glomerulonephritis in focal seg-mental, diffuse or global patterns of compa­rable grades of severity, which I think is quite confusing regarding the guidelines for therapy and management thereof. Therefore, I pro­posed the consideration of vascular necrosis as the definite acute glomerular lesion, particu­larly when accompanied by the presence of cellular crescents, as the hallmark of an active disease process that clearly warrants an ag­gressive treatment that might lead to reversal of the lesions. Moreover, I suggested two dis­tinctive patterns of involvement outlining IgAN in general; first is the vascular pattern charac­terized predominantly by capillary necrosis and extra-capillary cellular crescents, which is less frequently encountered than the more common mesangial pattern including sclerosis and the proliferative lesions, with a third mixed pattern, giving the fact that the me-sangium and the sub-endothelial space (as highlighted) are potentially a continuum. Also, I tried to categorize the necrotic crescentic glomerulonephrtitis encountered in the context of IgAN and uniquely representing a pre­dominant vascular involvement, which is clearly distinctive from the classical crescentic glomerulopnephritis. I believe that it is critical for the diagnosis and treatment stratification to know the percentage or spread of the crescen-tic lesion whenever there is predominantly cellular crescents and an association with ca­pillary necrosis. It was clearly highlighted in the mentioned classifications and categorized according to its prevalence on light micros­copic examination, which I think was an arbi­trary classification confused with other feat­ures indicative of a chronic and acute disease in the same basket.

Capillary deposition of immunoglobulins is common in HSP, as I have shown by the EM picture cited in the article, but it is widely recognized as a poor prognostic feature in IgAN, not in HSP as shown in the concerned patient.

All the deliberations I was discussing in the mentioned article were undoubtedly concerning IgAN, and it is absolutely not applicable to HSP by any means to asses its severity or prognosis.

I assumed retrospectively that the nephrotic syndrome was inflicted by a concurrent MCD due to the swift improvement and reversal of the nephrosis. Consequently, further biopsy was neither contemplated nor indicated to evaluate the histopathological improvement that would have been induced by prednisolone therapy.

I agree that the latest Oxford classification of IgA nephropathy might have addressed this issue in a more thorough and dedicated approach.

Correspondence Address:
Wael Latif Jabur
MC Specialty Hospital, P. O. Box 7832 Dubai
United Arab Emirates
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