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Dear Editor, I read with great interest the article by Altay et al. [1]. The authors made an association between hepatic hydatid disease and different glomerulonephritides including IgA nephropathy and MPGN. The article is important because hydatid disease is endemic in many parts of the world. However, a number of limitations, none of which was mentioned in the study, deserve attention. First, and in my opinion the most important one, is that the authors did not use a control group matched for age, gender and other major aetiologic factors for renal disease. Thus, we cannot be sure whether haematuria and proteinuria in the study population are products of simple chance or because of hepatic hydatid disease. These results do not show an increased frequency of glomerulonephritides in patients with hydatid cyst disease. Second, it seems paradoxical that none of the patients who had renal cysts (5% of the study population) had evidence of renal injury. How do the authors explain this finding? If it is said that the mechanism of injury is immune-mediated, the same immune mechanisms should also be the same for the patients with renal cysts. Third, did the authors exclude patients with hypertension? We know that hypertension, with diabetes mellitus, is one of the major causes of renal disease. And again, there is no mention about the status of angiotensin-converting enzyme inhibitor and/or angiotensin receptor blocker use. Thus, a number of aetiologic factors such as hypertension, analgesic use, etc., which may be responsible for impaired kidney function, have not been appropriately controlled. IgA nephropathy is fairly common among renal biopsies. The frequency of IgA nephropathy reaches up to 35% of all renal biopsies [2]. Fourth, two of the biopsy-proven IgA nephropathy patients improved after treatment for the underlying hydatid cyst disease. Two other cases progressed despite therapy. We also know that spontaneous remission rates are fairly high in IgA nephritis and membranous nephropathy even in the absence of immunosuppressive therapy [3,4]. Thus, the lack of a consistent response to hydatid disease treatment in half of the patients in the absence of a control group and the lack of data about antihypertensive treatment modalities make it hard to draw definitive causal relations between hydatid disease and glomerulonephritis. And finally, one should be cautious in using the term ‘hydatid nephropathy’, until an unequivocal causal relationship was proved. Conflict of interest statement. None declared. References 1 Altay M, Unverdi S, Altay FA, et al. Renal injury due to hepatic hydatid disease, Nephrol Dial Transplant , 2010, vol. 25 (pg. 2611- 2615) Google Scholar CrossRef Search ADS PubMed 2 Schena FP. Survey of the Italian Registry of Renal Biopsies: frequency of the renal diseases for 7 consecutive years. The Italian Group of Renal Immunopathology, Nephrol Dial Transplant , 1997, vol. 12 (pg. 418- 426) Google Scholar CrossRef Search ADS PubMed 3 Polanco N, Gutiérrez E, Covarsí A, et al. Grupo de Estudio de las Enfermedades Glomerulares de la Sociedad Española de Nefrología. Spontaneous remission of nephrotic syndrome in idiopathic membranous nephropathy, J Am Soc Nephrol , 2010, vol. 21 (pg. 697- 704) Google Scholar CrossRef Search ADS PubMed 4 Glassock RJ. IgA nephropathy: challenges and opportunities, Cleve Clin J Med , 2008, vol. 75 (pg. 569- 576) Google Scholar CrossRef Search ADS PubMed © The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org Oxford University Press
Nephrology Dialysis Transplantation – Oxford University Press
Published: Sep 21, 2010
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