A 56-year-old man with a history of alcoholic hepatitis was admitted in 1995 for the study of nephrotic syndrome, microhematuria and renal failure (creatinine 1.5 mg/dl).
Physical examination revealed edema, hepatomegaly and purpuric lesions in the lower limbs.
The study showed positive serology for HCV, other negative serology and positive cryoglobulins.
A renal biopsy showed a renal parenchyma with seven glomeruli with diffuse involvement, increased cellularity and mesangial matrix of lobular aspect, irregular interstitial double contour with interstitial images.
Immunofluorescence showed parietal glomerular deposits of C3 in the parietal bones, and direct granular electronic deposits showed subendothelial deposits, swelling endothelium and mesangial expansion.
The patient was diagnosed with HCV-associated GNP with positive cryoglobulins.
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The patient was referred to the Gastroenterology Unit to assess HCV treatment jointly.
A liver biopsy showed liver cirrhosis (P-3, L-2, F-3).
With these results, treatment with alpha interferon was established, initially without achieving viral response and later in its pegylated form for 48 weeks achieving viral load negativization.
Four months after the end of treatment, the patient developed an episode of acute pericarditis complaining of HCV in the pericardial fluid and new viral load increase.
The patient had had poor clinical tolerance to both previous treatments and it was decided not to initiate new therapies.
Other complications included inflammatory arthritis of the large intestine.
From the renal point of view, antiprotein blockade was established with renina-angiotensin-aldosterone system, despite which the patient developed progressive renal failure and finally started hemodialysis in 2007.
In November 2009 he received his first kidney transplant from deceased donor due to spontaneous cerebral hemorrhage.
The donor had HLA typing: DR1, DRX, B14, B35, A11, A30 and a history of alcoholism, with creatinine at the time of extraction of 1 mg/dl and negative proteinuria.
Immunosuppression was performed with corticosteroids, mycophenolic acid and tacrolimus.
The renal evolution was excellent and presented immediate renal function.
Thirteen months after transplantation, the patient developed non-nephrotic proteinuria and microhematuria with voiding gels but maintained normal renal function.
A study of autoimmunity, specific donor antibodies, as well as antigenemia for cytomegalovirus and PCR (polymerase chain reaction) serum for BK virus was performed, which were negative, and the renal echo-fixation was normal.
Due to the suspicion of recurrence of the underlying disease, a renal biopsy was performed.
A renal parenchyma was observed with ten glomeruli with marked mesangial enlargement, mild fibrosis and tubular necrosis.
Immunofluorescence showed granular mesangial deposits IgA and C3, and electron microscopy showed mesangial expansion and matrix with abundant homogeneous depositions.
Immunohistochemical techniques for C4d were negative.
De novo mesangial IgA GN was diagnosed in the graft, increasing the dose of corticoids and mycophenolic acid without clinical-biochemical improvement.
After the start of antiproteins treatment, with blockade of renina-angiotensin system was negative, using a receiver of beta-aldosterone (ARA) and the association was later confirmed with renal tubular deterioration, proteinuria decreased.
