Minimal-change nephropathy and chronic hepatitis C infection: coincidental or associated?

great majority of our patients presented the same 419delG mutation that also produce a truncate protein, and may be comparable with the above defect. Lack of heart defects in the majority of our patients lessens the likelihood of the podocin protein defect being associated with cardiac defects. We suggest re-evaluation of the association, because it cannot be excluded that in the Frishberg study group, one hitherto uncharacterized gene causing the heart defect has been co-inherited with NPHS2 [6]. A new genetic approach in the Arab cohort could also lead to the definitive comprehension of the reason for the heart defect associated with nephrotic syndrome in this particular cohort, and form the basis for a characterization of new genes involved in familial heart defects.