- Email: [email protected]
Nomenclature of the Oxford classification of IgA nephropathy: do we need to be careful?
letter to the editor
significant difference between gp120–cell membrane Gb3 binding and HIV target cell infection. In addition, the known receptors/co-receptors for gp120 on T cells can be expressed within the non-DRM fraction and then recruited to detergent resistant membranes after gp120–viral target cell binding,6 and so initial binding within the non-detergent resistant membrane fraction does not exclude a later role for cholesterol in HIV internalization. 1. Mikulak J, Singhal PC. HIV-1 entry into human podocytes is mediated through lipid rafts. Kidney Int 2009; 77: 72–73. 2. Khan F, Proulx F, Lingwood CA. Detergent-resistant globotriosy ceramide may define verotoxin/glomeruli restricted hemolytic uremic syndrome pathology. Kidney Int 2009; 75: 1209–1216. 3. Percherancier Y, Lagane B, Planchenault T et al. HIV-1 entry into T-cells is not dependent on CD4 and CCR5 localization to sphingolipid-enriched, detergent-resistant, raft membrane domains. J Biol Chem 2003; 278: 3153–3161. 4. Popik W, Alce TM. CD4 receptor localized to non-raft membrane microdomains supports HIV-1 entry. Identification of a novel raft localization marker in CD4. J Biol Chem 2004; 279: 704–712. 5. Lund N, Ramkumar S, Olsson ML et al. The human Pk histo-blood group antigene provides protection against HIVinfection. Blood 2009; 113: 4980–4991. 6. Popik W, Alce TM, Au WC. Human immunodeficiency virus type 1 uses lipid raft-colocalized CD4 and chemokine receptors for productive entry into CD4(+) T cells. J Virol 2002; 76: 4709–4722.
Clifford A. Lingwood1 1
Molecular Structure & Function Program, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada Correspondence: Clifford A. Lingwood, Molecular Structure & Function Program, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada. E-mail: [email protected]
Organization3 and is much more sensible. As such, its nomenclature could preferably be changed to ‘consensus schema’ or ‘formulation’ to truly reflect the unique endeavor and the methodology adopted in this effort, or else it could be changed to ‘working classification’ for the following reasons. (2) I also assume this is not an end point classification of IgA nephropathy (IgAN). There is certainly room for evolution, as the authors also agree in discussion, as more realistic validation studies are being carried out on a wide spectrum of cases in routine clinical practice in different parts of the world. Moreover, the contribution of immunofluorescence and electron microscopic studies has not been evaluated in this schema. It will be worth exploring this aspect of the study of IgAN to see if they add any value to mere light microscopic scoring of the renal biopsies adopted in this classification. The future will definitely see more molecular genetic studies further refining the crude prognostic criteria that we have at hand now and true prognostic classes of IgAN may emerge. Retention of the word ‘classification’ in the option of nomenclature of ‘working classification’ will prevent us from repenting in future for not using it, should this picture emerge in future. This approach has been successfully adopted by the Banff working classification of renal allograft pathology.4 1.
2.
Nomenclature of the Oxford classification of IgA nephropathy: do we need to be careful? Kidney International (2010) 77, 74; doi:10.1038/ki.2009.370
To the Editor: I have read with great interest the article published recently in your esteemed journal entitled ‘The Oxford classification of IgA nephropathy: rationale, clinicopathologic correlations, and classification’.1 This is a unique and huge effort by the members of the International IgA Nephropathy Working Group in trying to standardize the reporting of pathological criteria of importance in the prognostication of this most common form of primary glomerulopathy worldwide.2 I have a few points to make regarding the nomenclature of this scheme. I understand that these are conceptual and related to nomenclature, rather than substantial and related to contents of the study, and that they merit some consideration by the worthy authors of this scheme. The points are as follows: (1) I believe this effort is not the so-called ‘splitters’ approach to classification of diseases, inasmuch as no artificial classes are defined and the cases are lumped into these. The approach adopted in this classification is more akin to the Revised European-American Classification of Lymphoid Neoplasms (REAL) by the World Health 74
3.
4.
Cattran DC, Coppo R, Cook T et al. The Oxford classification of IgA nephropathy: rationale, clinicopathologic correlations, and classification. Kidney Int 2009; 76: 534–545. Julian BA, Waldo FB, Rifai A et al. IgA nephropathy, the most common glomerulonephritis worldwide. A neglected disease in the United States? Am J Med 1988; 84: 129–132. Harris NL, Jaffe ES, Diebold J et al. The World Health Organization classification of neoplasms of the hematopoietic and lymphoid tissues: report of the Clinical Advisory Committee meeting – Airlie House, Virginia, November, 1997. Hematol J 2000; 1: 53–66. Racusen LC, Solez K, Colvin RB et al. The Banff 97 working classification of renal allograft pathology. Kidney Int 1999; 55: 713–723.
Muhammed Mubarak1 1 Histopathology Department, Sindh Institute of Urology and Transplantation, Karachi, Pakistan Correspondence: Muhammed Mubarak, Department of Histopathology, SIUT, Civil Hospital, Karachi-74200, Pakistan. E-mail: [email protected]
Response to ‘Nomenclature of the Oxford classification of IgA nephropathy: do we need to be careful?’ Kidney International (2010) 77, 74–75; doi:10.1038/ki.2009.371
We thank Dr Muhammed Mubarak1 for his comments regarding our new classification of immunoglobulin A nephropathy.2 We agree that optional words could have been used and were explored. This is why, in part, there are additional descriptors in the title to help explain what we Kidney International (2010) 77, 72–75
significant difference between gp120–cell membrane Gb3 binding and HIV target cell infection. In addition, the known receptors/co-receptors for gp120 on T cells can be expressed within the non-DRM fraction and then recruited to detergent resistant membranes after gp120–viral target cell binding,6 and so initial binding within the non-detergent resistant membrane fraction does not exclude a later role for cholesterol in HIV internalization. 1. Mikulak J, Singhal PC. HIV-1 entry into human podocytes is mediated through lipid rafts. Kidney Int 2009; 77: 72–73. 2. Khan F, Proulx F, Lingwood CA. Detergent-resistant globotriosy ceramide may define verotoxin/glomeruli restricted hemolytic uremic syndrome pathology. Kidney Int 2009; 75: 1209–1216. 3. Percherancier Y, Lagane B, Planchenault T et al. HIV-1 entry into T-cells is not dependent on CD4 and CCR5 localization to sphingolipid-enriched, detergent-resistant, raft membrane domains. J Biol Chem 2003; 278: 3153–3161. 4. Popik W, Alce TM. CD4 receptor localized to non-raft membrane microdomains supports HIV-1 entry. Identification of a novel raft localization marker in CD4. J Biol Chem 2004; 279: 704–712. 5. Lund N, Ramkumar S, Olsson ML et al. The human Pk histo-blood group antigene provides protection against HIVinfection. Blood 2009; 113: 4980–4991. 6. Popik W, Alce TM, Au WC. Human immunodeficiency virus type 1 uses lipid raft-colocalized CD4 and chemokine receptors for productive entry into CD4(+) T cells. J Virol 2002; 76: 4709–4722.
Clifford A. Lingwood1 1
Molecular Structure & Function Program, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada Correspondence: Clifford A. Lingwood, Molecular Structure & Function Program, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada. E-mail: [email protected]
Organization3 and is much more sensible. As such, its nomenclature could preferably be changed to ‘consensus schema’ or ‘formulation’ to truly reflect the unique endeavor and the methodology adopted in this effort, or else it could be changed to ‘working classification’ for the following reasons. (2) I also assume this is not an end point classification of IgA nephropathy (IgAN). There is certainly room for evolution, as the authors also agree in discussion, as more realistic validation studies are being carried out on a wide spectrum of cases in routine clinical practice in different parts of the world. Moreover, the contribution of immunofluorescence and electron microscopic studies has not been evaluated in this schema. It will be worth exploring this aspect of the study of IgAN to see if they add any value to mere light microscopic scoring of the renal biopsies adopted in this classification. The future will definitely see more molecular genetic studies further refining the crude prognostic criteria that we have at hand now and true prognostic classes of IgAN may emerge. Retention of the word ‘classification’ in the option of nomenclature of ‘working classification’ will prevent us from repenting in future for not using it, should this picture emerge in future. This approach has been successfully adopted by the Banff working classification of renal allograft pathology.4 1.
2.
Nomenclature of the Oxford classification of IgA nephropathy: do we need to be careful? Kidney International (2010) 77, 74; doi:10.1038/ki.2009.370
To the Editor: I have read with great interest the article published recently in your esteemed journal entitled ‘The Oxford classification of IgA nephropathy: rationale, clinicopathologic correlations, and classification’.1 This is a unique and huge effort by the members of the International IgA Nephropathy Working Group in trying to standardize the reporting of pathological criteria of importance in the prognostication of this most common form of primary glomerulopathy worldwide.2 I have a few points to make regarding the nomenclature of this scheme. I understand that these are conceptual and related to nomenclature, rather than substantial and related to contents of the study, and that they merit some consideration by the worthy authors of this scheme. The points are as follows: (1) I believe this effort is not the so-called ‘splitters’ approach to classification of diseases, inasmuch as no artificial classes are defined and the cases are lumped into these. The approach adopted in this classification is more akin to the Revised European-American Classification of Lymphoid Neoplasms (REAL) by the World Health 74
3.
4.
Cattran DC, Coppo R, Cook T et al. The Oxford classification of IgA nephropathy: rationale, clinicopathologic correlations, and classification. Kidney Int 2009; 76: 534–545. Julian BA, Waldo FB, Rifai A et al. IgA nephropathy, the most common glomerulonephritis worldwide. A neglected disease in the United States? Am J Med 1988; 84: 129–132. Harris NL, Jaffe ES, Diebold J et al. The World Health Organization classification of neoplasms of the hematopoietic and lymphoid tissues: report of the Clinical Advisory Committee meeting – Airlie House, Virginia, November, 1997. Hematol J 2000; 1: 53–66. Racusen LC, Solez K, Colvin RB et al. The Banff 97 working classification of renal allograft pathology. Kidney Int 1999; 55: 713–723.
Muhammed Mubarak1 1 Histopathology Department, Sindh Institute of Urology and Transplantation, Karachi, Pakistan Correspondence: Muhammed Mubarak, Department of Histopathology, SIUT, Civil Hospital, Karachi-74200, Pakistan. E-mail: [email protected]
Response to ‘Nomenclature of the Oxford classification of IgA nephropathy: do we need to be careful?’ Kidney International (2010) 77, 74–75; doi:10.1038/ki.2009.371
We thank Dr Muhammed Mubarak1 for his comments regarding our new classification of immunoglobulin A nephropathy.2 We agree that optional words could have been used and were explored. This is why, in part, there are additional descriptors in the title to help explain what we Kidney International (2010) 77, 72–75