AUTHOR’S REPLY

Year : 2016  |  Volume : 4  |  Issue : 2  |  Page : 140-141

Non-lupus glomerulonephritis in a patient with systemic lupus erythematosus. Saudi J Med Med Sci 2015;3:241-4.

Emad Abdallah¹, Bassam Al-Helal², Reem Asad², Faisal Shehab³, Abdulrahman Al-Rashidi^4
1 Department of Nephrology, Theodor Bilharz Research Institute, Cairo, Egypt
² Department of Internal Medicine, Nephrology Unit, Al-Adan Hospital, Kuwait
³ Department of Internal Medicine, Al-Adan Hospital, Kuwait
⁴ Department of Internal Medicine, Rheumatology Unit, Al-Adan Hospital, Kuwait

Correspondence Address:
Emad Abdallah
Department of Nephrology, Theodor Bilharz Research Institute, Cairo
Egypt

DOI: 10.4103/1658-631X.178371

PMID: 30787718

1. Several novel susceptibility genes for SLE and IgAN have been identified in recent genome-wide association studies. Since both LN and IgAN are autoimmune renal diseases, they might share common disease mechanisms that overlap with genetic tendency. This is recently supported by the demonstration of shared genetics between IgAN and SLE. ^[1],[2]
   In our case, pathologiclly, this nonlupus form of glomerulonephritis should be considered as IgAN in patients with SLE rather than LN because the prominent IgA deposits in the mesangium dominated the histological picture, and significant proliferation was absent ^[3] and our case may support that both LN and IgAN are autoimmune renal diseases, they might share common disease mechanisms that overlap with genetic tendency. However, Vuong, et al. ^[4] did not support an overlap in genetic susceptibility between patients with IgAN or SLE and reveal no specific importance of SLE associated SNPs for the presence of lupus nephritis (LN). In addition, geographic differences in genetic susceptibility to SLE and IgAN ^[5] must be taken into consideration. Hence, we need further and more studies to support these genetic associations between IgAN and LN in different geographical regions.
   In addition, according to the recommendations of Churg et al., ^[6] class IV LN is defined by diffuse distribution of subendothelial deposits regardless of the pattern of proliferation and the presence of large subendothelial depositions of immunoglobulins without activation of the complement system and proliferation is exceptional and although C1q, C3, C4, and IgG depositions are more common in typical LN, IgA deposition can also be seen. ^[7] Thus, our case with predominant mesangial IgA deposits may be proposed to be a special subtype of LN.
2. Human immunodeficiency virus (HIV) infection associated with a variety of glomerulonephritides, including IgAN, membranoproliferative glomerulonephritis (GN), membranous nephropathy, lupus-like GN, immunotactoid glomerulopathy, and fibrillary GN. ^[8] However, despite low prevalence of HIV in Kuwait (0.1%), ^[9] HIV infection was considered by us ^[3] and HIV infection was negative in our patient.

References

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2.	Zhou XJ, Cheng FJ, Zhu L, Lv JC, Qi YY, Hou P, et al. Association of systemic lupus erythematosus susceptibility genes with IgA nephropathy in a Chinese cohort. Clin J Am Soc Nephrol 2014;9:788-97.
3.	Abdallah E, Al-Helal B, Asad R, Shehab F, Al-Rashidi A. Non-lupus glomerulonephritis in a patient with systemic lupus erythematosus. Saudi J Med Med Sci 2015;3:241-4.
4.	Vuong MT, Gunnarsson I, Lundberg S, Svenungsson E, Wramner L, Fernström A, et al. Genetic risk factors in lupus nephritis and IgA nephropathy - No support of an overlap. PLoS One 2010;5:e10559.
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9.	List of Countries by HIV/AIDS Adult Prevalence Rate. Available from: http://www.en.wikipedia.org/wiki/List_of_countries_by_HIV/AIDS_adult_prevalence_rate. [Last accessed on 2015 Sep 11].