The clinical implications of thin basement membrane nephropathy (TBMN) in renal transplantation must be considered from the perspectives of both the allograft recipient and the donor. Most individuals with TBMN have a benign course, but some develop end-stage renal failure (ESRF) and undergo transplantation. ESRF in patients with TBMN often results from the presence of additional glomerular or interstitial lesions and some of these, such as immunoglobulin (Ig)A disease, may recur in the renal allograft and affect outcome. In addition, individuals with TBMN always must be distinguished from those with glomerular membrane thinning due to Alport syndrome. This is not only to enable appropriate genetic counseling but also to anticipate the possible complication of posttransplant anti-glomerular basement membrane disease. From the perspective of the live renal donor, donation from individuals with TBMN (or carriers of X-linked Alport syndrome with thinned membranes) remains controversial because the risks remain unknown. Any effects of the thinned membranes themselves on allograft function are unclear. Further advances in our understanding of the clinical, pathologic, and molecular features of TBMN should result in improved assessment of potential live donors and help stratify those at risk for renal impairment.