A 56-year-old man, with a personal history of alcoholic hepatitis, who in 1995 was admitted to the hospital to be studied for nephrotic syndrome, microhaematuria and renal insufficiency (creatinine 1.5 mg/dl). Physical examination revealed oedema, hepatomegaly and purpuric lesions on the lower limbs. The study showed positive serology for HCV, the rest of the serologies negative and positive cryoglobulins. A renal biopsy showed renal parenchyma with seven glomeruli with diffuse involvement, increased cellularity and lobular mesangial matrix, basement membranes with double-contour images, irregular thickening of the capillary walls and interstitial fibrosis. Direct immunofluorescence showed glomerular parietal granular C3 deposits and electron microscopy showed subendothelial deposits, swollen endothelia and mesangial enlargement. The patient was diagnosed with HCV-associated MPGN with positive cryoglobulins.

The patient was referred to the gastrointestinal clinic for joint evaluation of HCV treatment. A liver biopsy was performed which revealed liver cirrhosis (P-3, L-2, F-3). With these results, treatment with interferon alpha was started, initially without achieving a sustained viral response, and subsequently in its pegylated form for 48 weeks, achieving a negative viral load. Four months after the end of treatment, he presented an episode of acute pericarditis with HCV in the pericardial fluid coinciding with a new increase in viral load. The patient had had poor clinical tolerance to both previous treatments and it was decided not to start new therapies. Other complications included inflammatory arthritis of large joints.
From the renal point of view, antiproteinuric treatment with renin-angiotensin-aldosterone system blockade was started, despite which the patient developed progressive renal failure and finally started haemodialysis in 2007. In November 2009, he received his first deceased donor kidney transplant due to a spontaneous cerebral haemorrhage. The donor had HLA typing: DR1, DRX, B14, B35, A11, A30 and a history of enolism, with creatinine at the time of extraction of 1 mg/dl and negative proteinuria. Immunosuppression with corticosteroids, mycophenolic acid and tacrolimus was performed. Renal evolution was excellent and renal function was immediate. Thirteen months after transplantation, the patient developed non-nephrotic proteinuria and microhaematuria with haematic casts, but maintained normal renal function. An autoimmunity study, donor-specific antibodies, as well as antigenemia for cytomegalovirus and serum PCR (polymerase enzyme chain reaction) for BK virus were negative, and renal Doppler ultrasound was normal. Given the suspicion of recurrence of the underlying disease, it was decided to perform a renal biopsy. Light microscopy showed renal parenchyma with ten glomeruli with marked mesangial enlargement, mild fibrosis and tubular atrophy. Immunofluorescence showed granular mesangial deposits of IgA and C3, and electron microscopy showed mesangial enlargement of cells and matrix with abundant homogeneous electrodense deposits. Immunohistochemistry for C4d was negative. A diagnosis of de novo IgA mesangial GN in the graft was made, and the dose of corticosteroids and mycophenolic acid was increased without clinical-biochemical improvement. After starting antiproteinuric treatment, with blockade of the renin-angiotensin-aldosterone system by means of an angiotensin II receptor antagonist (ARA II) and the subsequent association of spironolactone, proteinuria became negative, although with a slight deterioration of renal function, currently stabilised.