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we present the case of a patient who was HCV positive and who developed two different glomerular processes&#44; one in his native kidneys and one in his renal transplant&#44; both related to the aforementioned virus&#46;<span class="elsevierStyleSup">2&#44;7-13</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION OF THE CLINICAL CASE</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">A 56 year-old male with a personal history of alcoholic hepatitis&#44; who in 1995 was admitted for a nephrotic syndrome&#44; microhaematuria and renal failure &#40;creatinine 1&#46;5mg&#47;dl&#41; study&#46; The physical examination revealed the presence of oedemas&#44; hepatomegaly and purpuric lesions on his lower limbs&#46; The study &#40;Table 1&#41; showed a positive serology for the HCV&#44; with the remaining serologies being negative&#46; It also revealed positive cryoglobulin&#46; A renal biopsy was performed&#44; revealing a renal parenchyma with seven glomeruli with diffuse involvement&#44; increased cellularity and a mesangial matrix with a lobular appearance&#44; basement membranes with images of double contour&#44; irregular thickening of the capillary walls and interstitial fibrosis&#46; Direct immunofluorescence revealed C3 granular parietal glomerular deposits and the electron microscopy showed subendothelial deposits&#44; swollen endothelial cells and mesangial expansion &#40;Figure 1&#41;&#46; The patient was diagnosed with MPGN associated with HCV with positive cryoglobulins&#46;</p><p class="elsevierStylePara">The patient was referred to the Digestive System Clinic to assess HCV treatment on a whole&#46; A liver biopsy was performed&#44; which revealed cirrhosis of the liver &#40;P-3&#44; L-2&#44; F-3&#41;&#46; Given these results&#44; we started treatment with interferon alpha&#44; initially without achieving a sustained viral response&#44; and subsequently with its pegylated form for 48 weeks achieving a negative viral load&#46; Four months after completion of treatment&#44; he had an episode of acute pericarditis with presence of HCV in the pericardial fluid coinciding with a further increase in viral load&#46; The patient had had poor clinical tolerance to both previous treatments and it was decided not to initiate further treatment&#46; Another complication that he presented was inflammatory arthritis of his major joints&#46;</p><p class="elsevierStylePara">From a renal perspective&#44; antiproteinuric therapy was introduced with renin-angiotensin-aldosterone system blockade&#44; despite which the patient developed progressive renal failure and finally began haemodialysis in 2007&#46; In November 2009&#44; he received his first kidney transplant from a donor who had died from spontaneous cerebral haemorrhage&#46; The donor had HLA typing&#58; DR1&#44; DRX&#44; B14&#44; B35&#44; A11&#44; A30&#44; and a history of alcoholism&#44; with creatinine in the moment of removal of 1mg&#47;dl and negative proteinuria&#46; Immunosuppression was performed with corticosteroids&#44; mycophenolic acid and tacrolimus&#46; Renal progression was excellent and there was immediate renal function&#46; Thirteen months after transplantation&#44; the patient developed non-nephrotic proteinuria and microhaematuria with red blood cell casts&#44; while maintaining normal renal function&#46; An autoimmunity study was performed &#40;Table 1&#41;&#59; donor-specific antibodies&#44; cytomegalovirus antigenaemia and serum CRP &#40;polymerase enzyme chain reaction&#41; levels for the BK virus were negative&#44; and the renal Doppler ultrasound was normal&#46; Given the suspected recurrence of the underlying disease&#44; we opted for a renal biopsy&#46; The optical microscopy showed a renal parenchyma with ten glomeruli with marked mesangial expansion&#44; mild fibrosis and tubular atrophy&#46; Immunofluorescence revealed granular mesangial IgA and C3 deposits&#44; and electron microscopy showed mesangial expansion of cells and matrix with abundant homogeneous electron deposits&#46; The C4d immunohistochemistry techniques were negative &#40;Figure 2&#41;&#46; The patient was diagnosed with <span class="elsevierStyleItalic">de novo</span> IgA mesangial GN in the graft&#44; and the dose of corticosteroids and mycophenolic acid were increased without clinical biochemical improvement&#46; After the start of antiproteinuric treatment with blockade of the renin-angiotensin-aldosterone system by angiotensin receptor antagonist &#40;ARA II&#41; and the subsequent association of spironolactone&#44; a negative proteinuria result was achieved&#44; although with a small deterioration renal function that is currently stabilised &#40;Figure 3&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">De novo</span> GN in the renal graft are defined as a glomerular disease that appears after a renal transplantation&#44; which is different from the primary nephropathy and they are the third most common cause for loss of graft at 10 years after transplantation&#46; Their prevalence in the publications is highly variable due to&#58; the different criteria and protocol for carrying out renal biopsies&#44; the fact that in some cases there is only optic microscopy without immunofluorescence or electron microscope&#44; not being able to carry out the differential diagnosis safely with other forms of the disease&#44; the total count of <span class="elsevierStyleItalic">de novo</span> GN and recurrences of the original disease and the presence of a renal disease of unknown origin&#46; The most common forms are membranous nephropathy&#44; focal segmental glomerulosclerosis&#44; MPGN&#44; thrombotic microangiopathy secondary to drug intake and nephritis due to basement membrane antibodies&#44; associated with Alport&#8217;s syndrome&#46;<span class="elsevierStyleSup">1&#44;2</span> The presence of <span class="elsevierStyleItalic">de novo</span> IgA GN is uncommon&#46;<span class="elsevierStyleSup">14-19</span> With regard to the clinical course&#44; <span class="elsevierStyleItalic">de novo</span> GN appear late&#44; normally from one year after the transplantation&#44; in contrast to recurrences&#44; which usually appear in the first weeks after transplantation&#46;<span class="elsevierStyleSup">1</span> Graft survival&#44; both in recurrences and in <span class="elsevierStyleItalic">de novo</span> GN is clearly lower than in patients who do not develop any glomerular process&#46;<span class="elsevierStyleSup">20</span></p><p class="elsevierStylePara">We report the case of a patient with nephrotic syndrome&#44; in whose study we note a positive serology for the HCV and positive cryoglobulins&#46; The renal biopsy shows an MPGN associated with a chronic infection due to the HCV&#46; This entity may appear in a primary form &#40;idiopathic&#41; or as secondary to the deposit or in situ formation of immune complexes in the glomerulus&#44; caused by diseases with chronic activation of the immune system &#40;such as infections due to the hepatitis B and C viruses&#41;&#44; autoimmune diseases&#44; and the inability to remove immune complexes and some tumours&#46;<span class="elsevierStyleSup">21</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">After receiving his first renal transplant&#44; the patient displayed proteinuria and microhaematuria with red blood cell casts&#44; and a recurrence of his baseline disease was initially suspected&#44; which occurs in 20-30&#37; of cases&#44;<span class="elsevierStyleSup">1&#44;2</span> but the histopathological study revealed the presence of a <span class="elsevierStyleItalic">de novo</span> IgA GN&#46; The aetiology of the second GN is uncertain&#46; Initially&#44; it could be related to the presence of chronic liver disease in the recipient&#46;<span class="elsevierStyleSup">13</span> Secondly&#44; the possibility is considered that the donor has a non-diagnosed IgA GN without proteinuria at the time of transplantation&#46; The donor had a history of alcoholism and was a carrier of HLA-B35&#44; which are factors associated with this glomerulopathy&#44;<span class="elsevierStyleSup">13&#44;22</span> although&#44; we do not know if they had previously presented abnormalities in renal function or urinary sediment&#46; No renal biopsy was carried out on the graft before the transplantation and the contralateral kidney was not transplanted because it carried a renal cyst&#46; This possibility seems more remote to us&#44; given that what is described in literature suggests that IgA deposits in the transplanted kidney disappear soon after transplantation&#46;<span class="elsevierStyleSup">23</span></p><p class="elsevierStylePara">The HCV is a small RNA virus &#40;30-38nm&#41; with a lipid envelope and it belongs to the <span class="elsevierStyleItalic">Flaviviridae </span>family&#46; This virus may result in the appearance of some renal diseases&#46; Furthermore&#44; renal disease patients have a higher risk of becoming infected by the HCV because they have greater direct or indirect contact with blood from other patients &#40;transfusions&#44; haemodialysis&#44; transplantations&#41;&#46; In haemodialysis centres in the United States&#44; a prevalence of 8-10&#37; of patients infected by HCV and an incidence of 1-3&#37; new cases per year has been described&#46; It has been related to different renal diseases&#44; however&#44; the most common are type I MPGN&#44; which is associated with type II mixed cryoglobulinaemia and to a lesser extent&#44; non-cryoglobulinaemic MPGN and membranous GN&#46; Small series and isolated cases have also been described that associate infection due to HCV with other processes&#44; both glomerular &#40;focal and segmental glomerulosclerosis&#44; immunotactoid and fibrillary glomerulopathy&#44; acute post-infectious GN and IgA GN<span class="elsevierStyleSup">7-12</span>&#41; and non-glomerular &#40;tubulointerstitial nephritis and thrombotic microangiopathy&#41;&#46;<span class="elsevierStyleSup">3&#44;11</span></p><p class="elsevierStylePara">This history may suggest that both glomerular processes in our patient are associated with infection due to HCV&#46; In the first GN&#44; MPGN&#44; the association with the virus is well documented and supported by many epidemiological studies&#44; clinical cases&#44; trials and experimental work&#46;<span class="elsevierStyleSup">3&#44;24</span> The relationship between the HCV and the second glomerular process&#44; <span class="elsevierStyleItalic">de novo</span> IgA GN&#44; is less common&#46; At the start of the 1990s&#44; the link between the HCV and this GN was not known&#44; although the link between the latter and chronic alcoholic liver disease was known&#46;<span class="elsevierStyleSup">25&#44;26</span> However&#44; over the years&#44; isolated cases<span class="elsevierStyleSup">7-10</span> and series of cases<span class="elsevierStyleSup">11</span> of IgA GN in native kidneys have been described&#46; There are also cases of patients in whom&#44; after completing the antiviral treatment with interferon and ribavirin and achieving a sustained viral response&#44; the liver profile and the urinary sediment normalised&#46;<span class="elsevierStyleSup">7&#44;27</span> The prevalence of IgA GN in HCV patients varies between 0&#37; and 6&#37; according to the series&#44; although in other geographical regions such as Saudi Arabia or Japan&#44; there are greater frequencies&#46;<span class="elsevierStyleSup">10&#44;11&#44;28</span> Sansonno et al&#46; have confirmed the presence of viral RNA in the glomeruli and viral core particles both in glomeruli and tubules of IgA patients&#44; although in a lower percentage than in other glomerulopathies such as MPGN and membranous GN&#46; These data suggest that the HCV has a role in the pathogenesis of IgA GN in these patients&#46;<span class="elsevierStyleSup">29</span></p><p class="elsevierStylePara">Various renal diseases have been described in patients who have the HCV after receiving a renal transplant &#40;MPGN&#44; membranous GN&#44; minimal change disease&#44; thrombotic microangiopathy&#44; acute rejection&#44; chronic rejection&#41;&#46; With regard to <span class="elsevierStyleItalic">de novo</span> GN&#44; the HCV was associated with membranous GN and MPGN&#46;<span class="elsevierStyleSup">3-5</span> Its potential aetiological role in <span class="elsevierStyleItalic">de novo</span> IgA GN is unknown&#46; We displayed the cases described in literature of IgA GN&#44; along with their progression in Table 2&#46; There is a notable case described by Francisco et al&#46; of a black chronic kidney disease patient attributed to nephroangiosclerosis secondary to non-biopsied high blood pressure&#44; without haematuria&#46; The patient acquired the infection due to the HCV after receiving various transfusions when he was on renal replacement therapy&#44; in the form of haemodialysis&#44; developing chronic liver disease&#46; He eventually received a renal graft from a deceased donor&#46; A renal biopsy was carried out two weeks after the transplant&#44; and it displayed an acute rejection without lesions or deposits suggestive of IgA GN&#46; After three years&#44; he developed non-nephrotic range proteinuria&#44; and a renal biopsy was carried out with IgA GN being diagnosed&#46;<span class="elsevierStyleSup">15</span> In the other cases of <span class="elsevierStyleItalic">de novo</span> IgA GN described&#44; we do not have recipients&#8217; HCV serology data&#46; In our case&#44; the diagnosis of <span class="elsevierStyleItalic">de novo</span> IgA coincides with an increase in the HCV viral load&#44; which indicates active RNA replication&#46; This&#44; along with the effect of immunosuppression and the virus itself could modulate the response of lymphocytes and the production of antibodies&#44; thus generating an imbalance between antigens and antibodies which&#44; along with the susceptibility of the renal graft&#44; would influence the long-term genesis of <span class="elsevierStyleItalic">de novo</span> GN&#46;<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">Lastly&#44; we wish to highlight the favourable progression made by our patient&#44; similar to that presented in other cases of <span class="elsevierStyleItalic">de novo</span> IgA GN without crescents in the renal biopsy&#44; a marker of poor prognosis in renal graft relapses&#46;<span class="elsevierStyleSup">14-19</span> Our patient did not display crescents but was HCV positive&#44; which is described as a risk factor for the development of proteinuria&#44; chronic rejection&#44; glomerular lesions&#44; infections and decrease of the survival&#44; both of the graft and the receiver&#46;<span class="elsevierStyleSup">5&#44;6</span><span class="elsevierStyleItalic">De novo</span> IgA GN appeared while the patient was being treated with the triple immunosuppressant therapy &#40;corticosteroids&#44; mycophenolic acid and tacrolimus&#41;&#46; However&#44; the control of proteinuria was not achieved despite the increase in the dose of steroids and mycophenolic acid&#46; Lastly&#44; blockade of the renin-angiotensin-aldosterone system was carried out by ARA II and spironolactone&#44; with a decrease in proteinuria but a slight deterioration in renal function&#44; which is currently stable&#46; The patient is being treated with mycophenolic acid as part of his immunosuppressant therapy&#44; although the use of mycophenolic acid in the treatment of IgA nephropathy is still controversial&#46;<span class="elsevierStyleSup">30</span></p><p class="elsevierStylePara">In summary&#44; in this pathogenesis&#44; the HCV is related to different renal diseases&#44; amongst them MPGN and IgA GN&#46; In our case&#44; we believe that infection due to the HCV could have contributed to the pathogenesis of both glomerular processes&#44; although&#44; we cannot rule out that <span class="elsevierStyleItalic">de novo</span> IgA GN could be secondary to chronic liver disease&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12067&#95;16025&#95;48635&#95;en&#95;f1120672&#46;jpg" class="elsevierStyleCrossRefs"><img src="12067_16025_48635_en_f1120672.jpg" alt="Native kidney biopsy"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Native kidney biopsy</p><p class="elsevierStylePara"><a href="grande&#47;12067&#95;16025&#95;48636&#95;en&#95;f2120672&#46;jpg" class="elsevierStyleCrossRefs"><img src="12067_16025_48636_en_f2120672.jpg" alt="Biopsy of the renal transplant"></img></a></p><p class="elsevierStylePara">Figure 2&#46; Biopsy of the renal transplant</p><p class="elsevierStylePara"><a href="grande&#47;12067&#95;16025&#95;48637&#95;en&#95;f3120672&#46;jpg" class="elsevierStyleCrossRefs"><img src="12067_16025_48637_en_f3120672.jpg" alt="Progression of renal function and proteinuria"></img></a></p><p class="elsevierStylePara">Figure 3&#46; Progression of renal function and proteinuria</p><p class="elsevierStylePara"><a href="grande&#47;12067&#95;16025&#95;48638&#95;en&#95;t112067&#46;jpg" class="elsevierStyleCrossRefs"><img src="12067_16025_48638_en_t112067.jpg" alt="Analytic progression and complementary tests"></img></a></p><p class="elsevierStylePara">Table 1&#46; Analytic progression and complementary tests</p><p class="elsevierStylePara"><a href="grande&#47;12067&#95;16025&#95;48639&#95;en&#95;t212067&#46;jpg" class="elsevierStyleCrossRefs"><img src="12067_16025_48639_en_t212067.jpg" alt="Review of the cases of de novo IgA glomerulonephritis in patients with renal transplants "></img></a></p><p class="elsevierStylePara">Table 2&#46; Review of the cases of de novo IgA glomerulonephritis in patients with renal transplants </p>"
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        "resumen" => "<p class="elsevierStylePara">La glomerulonefritis &#40;GN&#41; membranoproliferativa puede asociarse patog&#233;nicamente con la infecci&#243;n por el virus de la hepatitis C &#40;VHC&#41;&#44; como numerosos casos cl&#237;nicos han mostrado&#46; La posible relaci&#243;n entre VHC y GN IgA&#44; por el contrario&#44; ha sido sugerida solamente en casos aislados&#46; La nefropat&#237;a IgA recurre hasta en un 50&#160;&#37; de los casos tras el trasplante renal&#44; pero es poco frecuente que aparezca como una GN <span class="elsevierStyleItalic">de novo</span>&#46; Presentamos el caso de un paciente con infecci&#243;n cr&#243;nica por VHC y hepatopat&#237;a&#44; que desarrolla dos patolog&#237;as glomerulares diferentes a lo largo de su evoluci&#243;n&#58; GN membranoproliferativa en sus ri&#241;ones nativos&#44; proceso que caus&#243; una insuficiencia renal terminal&#44; y GN IgA <span class="elsevierStyleItalic">de novo</span> en el ri&#241;&#243;n trasplantado&#46; Se discute la posible relaci&#243;n patog&#233;nica de ambos procesos glomerulares con la infecci&#243;n por VHC&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara"><span class="elsevierStyleItalic">Membranoproliferative glomerulonephritis &#40;GN&#41; may be pathogenically associated with infection due to the hepatitis C virus &#40;HCV&#41; as many clinical cases have shown&#46; The potential relationship between the HCV and IgA GN&#44; by contrast&#44; has been suggested only in isolated cases&#46; IgA nephropathy recurs in up to 50&#37; of cases after renal transplantation&#44; but it is uncommon for it to appear as a de novo GN&#46; We report the case of a patient with chronic infection due to the HCV and liver disease&#44; who developed two different glomerular diseases during its progression&#58; membranoproliferative GN in his native kidneys&#44; a process that caused terminal renal failure and de novo IgA GN in the transplanted kidney&#46; The potential pathogenic relationship of both glomerular processes with infection due to the HCV is discussed&#46;</span></p>"
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