Idiopathic nephrotic syndrome (NS) in children is most commonly due to minimal change nephrotic syndrome and can be successfully treated with steroid therapy. However 10-15% of children with nephrotic syndrome are diagnosed with FSGS, which is resistant to steroid therapy and many other immunosuppressive drugs, and is associated with poor outcome. Approximately 50% of patients with FSGS progress to ESRD within 5-10 years and in about 30% of children, FSGS can recur after transplantation.(1) African-American children are at significantly higher risk for FSGS.(2) Recent studies indicate that primary FSGS is a heterogeneous disorder caused by genetic mutations in nearly a third of cases and as yet undefined immunological defects in the remaining cases.(3) Immune mediated FSGS has been associated with a circulating permeability factor, which is thought to increase glomerular permeability to albumin, leading to proteinuria and contributes to sclerotic lesions in FSGS. Presence of the FSPF is defined as permeability activity >0.5. (4) Current therapies for FSGS include plasmapheresis and many immunosuppressive agents that include cyclosporine, tacrolimus, mycophenolate mofetil, rituximab, and drugs that decrease proteinuria such as angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) with inconsistent outcome. Additionally, these drugs have long-term consequences of immunosuppression and some drugs such as cyclosporine and tacrolimus affect renal function adversely when used for prolonged periods of time. (5) There is an urgent need for investigating benign therapies such as galactose. If proven to be useful, it may present a safe alternative or an adjunct to currently available therapies.