Description:
<jats:title>Abstract</jats:title>
<jats:sec>
<jats:title>Background and Aims</jats:title>
<jats:p>The progression of IgA nephropathy (IgAN) has been associated with Mannose -Binding Lectin levels (both excess or deficiency). The MBL deficiency, is associated with the rs5030737, the rs1800450 and the rs1800451, who represent the “O” allele. Since lectin pathway deregulation may impact on IgA progression on native kidney we hypothesized that the presence of the “O” allele and therefore MBL deficiency, could influence also the graft survival in recipients with a biopsy-proven diagnosis of IgAN on native kidneys. Therefore we investigated the role of MBL “O” allele in kidney transplant recipients with IgAN.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Method</jats:title>
<jats:p>We enrolled 32 kidney transplant recipients with biopsy-proven IgAN on the native kidney. The region in MBL encompassing the SNPs rs5030737, rs1800450 and rs1800451were amplified using PCR and analyzed by Sanger sequencing.Clinical data at baseline and during the follow-up were collected from patients’ records. An eGFR &lt;60mL/min/1.73m2 (MDRD equation) was considered as main outcome at univariate and multivariate analyses.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Results</jats:title>
<jats:p>The 38% of patients carry the“O” allele and 62% of patients the “A” allele which is associated with the wild genotype. No difference between the two groups as for demographic features, donor and transplant-related variables has been found. Interestingly we found that patients with the “O” allele had a worse graft outcome (P = 0.01) during a mean follow-up of 151 months (Figure 1). The “O” allele was an independent predictor for the graft survival in a Cox survival analysis model adjusted for donor's and recipient's age, acute rejection, and disease recurrence (HR 0.046; 95% I.C. 0.005-0.423; P = 0.01). Moreover we found a link between the genetic background and the MBL serum level (Figure 2).</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Conclusion</jats:title>
<jats:p>Our study suggest a potential role of the MBL deficiency in the long term graft dysfunction in kidney transplant recipient with IgAN.</jats:p>
</jats:sec>