Proteinuria After Kidney Transplantation

Proteinuria is a relatively frequent complication in both adults and children after kidney transplantation (40%–80%). It is usually mild and predominantly of tubular origin and is caused mainly by rejection, mTOR inhibitors, or hypertension; however, proteinuria could also be in the nephrotic range and of glomerular origin if caused by the recurrence of idiopathic FSGS or rejection. Proteinuria is a risk factor impacting graft and patient survival in adults and graft survival in children. Proteinuria should be assessed by protein/creatinine ratio regularly in pediatric kidney transplant recipients. In children with idiopathic FSGS, proteinuria should be assessed daily during the first 2–3 weeks post-transplant to enable prompt diagnosis of recurrence. The etiology of proteinuria should be identified (recurrence, rejection, mTOR-inhibitors, hypertension, etc.). If no apparent cause is found, a graft biopsy should be considered. Antiproteinuric therapy is primarily focused on treating the causes of the proteinuria, and this is usually done using Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBs). The long-term follow-up goal should be normalization of proteinuria with a protein/creatinine ratio < 20 mg/mmol (200 mg/g). Because of the role elevated blood pressure may play in exacerbating proteinuria, antihypertensive medications should be used in those who are resistant to initial antiproteinuric therapy to achieve lower BP.