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F Ginevri

Publications and source records attributed to F Ginevri.

78 records · Page 5Linked to original sources
PubMedDate not supplied

Cytotoxic molecule mRNA expression in chronically rejected human kidney allografts.

The pathogenesis of immunological and nonimmunological components that cause chronic kidney allograft nephropathy (CAN), is not yet completely understood. To explore the possible contribution of alloreactive cytotoxic T cells, we analyzed the transcription of cytotoxic molecules such as granzyme B and perforin using semiquantitative RT-PCR on surgically removed grafts obtained from two groups: group 1 (n = 10) were cases of CAN; group 2 (n = 3) had no CAN. Among group 1 kidneys, granzyme-B was expressed in 7 of 10, whereas perforin was detectable in 9 of 10 cases; their detection was not related to the presence of superimposed signs of acute graft lesions. Cytotoxic molecules were never found in group 2 kidneys. These results show that explanted chronically rejected grafts display cytotoxic molecule transcripts in addition to Th2 type cytokines, such as IL-10, IL-3, and IL-6, suggesting that both cellular and humoral alloreactive mechanisms may play important roles in CAN pathogenesis.

Antigens, CD↗
PubMedDate not supplied

[Polyomavirus BK-associated nephropathy after kidney transplantation].

Polyomavirus BK (BKV) infection has been lately recognized as a major cause of renal allograft dysfunction. BKV-related interstitial nephropathy (PVAN) may affect 1-10% of renal allograft recipients, occurring more frequently in the first 6 months after transplantation. Progression to irreversible allograft failure has been observed in up to 45% of all cases; thanks to increased PVAN awareness and improved diagnostic techniques, the rate of graft loss has lowered, more consistently in centres with active screening and intervention programs. PVAN pathogenesis is characterized by multiple synergizing factors, among which immunodepression plays a key role. PVAN diagnosis requires the evaluation of a renal biopsy showing polyomavirus cytopathic changes and confirming BKV through an ancillary technique such as immunohistochemistry. Given the focal nature of the disease, early diagnosis may be difficult to obtain. Thus, quantification of BKV-DNA in plasma has been suggested as surrogate marker for PVAN. To date, given the lack of controlled trials, there is no consensus on a 'standard' management of PVAN. However, evidence based on reported observations suggests that a step-wise reduction of immunosuppression, preceded by pulsed steroids in case of coexistent acute rejection, may improve outcomes. Additional options may be represented by drugs with antiviral activity, such as cidofovir, leflunomide or quinolones. Application of a preventive treatment based on viremia monitoring has been recently proposed.

Adrenal Cortex Hormones↗
PubMedDate not supplied

[Clinical aspects of the nephropathy in Schoenlein-Henoch syndrome].

Fourty-four children with Henoch-Schoenlein nephritis were studied at the onset of the nephropathy and during a follow-up from 6 to 110 months. The extra-renal manifestations were purpura (100%), abdominal pain (63.5)% or melena (27%), arthlagias (61.5%), neurological symptoms with convulsions (4.5%) and retinal involvement (4.5%). The clinical presentation of the nephropathy consisted in haematuria and proteinuria (41%), isolated haematuria (30%), acute renal failure (ARF) (23%), nephrotic syndrome (4%) or isolated proteinuria (2%). Hypertension was present in 17 patients. Renal biopsy was performed in 18 patients and the glomerular changes were graded according to the classification of ISKDC; the renal histopathology ranged from minimal lesions to severe crescentic glomerulonephritis and was found to correlate with clinical state. Twenty-four patients, who showed severe clinical presentation and/or diffuse mesangial proliferation with high proportion of crescents, received a corticosteroid therapy. Most of our patients followed a relatively benign course: all but one of patients with ARF have normal renal function at the end of follow-up and no patients with less severe renal presentation got a bad outcome. Only 2 patients showed relapse of nephropathy and purpura at the 6th and 8th year of follow-up, respectively. After 24 months of follow-up the clinical outcome of a group of 19 patients receiving corticosteroid therapy was not very different from that of 11 untreated patients.

Acute Kidney Injury↗