Idiopathic nephrotic syndrome (INS) in childhood is usually responsive to oral steroid therapy. However, 10% of cases remain steroid resistant. While approximately 50% of these children respond to intensified immunosuppressive treatment, the remaining ‘multidrug-resistant’ children show persistent proteinuria and ultimately progress to renal failure. A circulating glomerular permeability factor (PF) may be involved in many of these cases (Savin et al 1996) . This notion is supported by the frequent recurrence of FSGS after renal transplantation (Hoyer et al 2001), its removal by plasmapheresis (Artero et at.1994) and transplacental transfer of PF from a mother with FSGS to her newborn causingcongenital nephrotic syndrome (Kemper at el 2001).

Galactose is a monosaccharide, similar to fructose and glucose. It has been identified as one of 8 essential sugars needed in the diet for proper cell development and functioning of the human body. Galactose occurs in two different structurally related forms; L(-) Galactose and D(+) Galactose. D(+) Galactose is prevalent throughout the animal and plant kingdoms, and is produced within the human body in a range of 2- to 10-grams per day. As a micronutrient, galactose is not toxic, except in patients withthe rare metabolic condition of galactosemia.
D-Galactose is an integral component of glycoproteins, glycolipids and proteoglycans, integral components of the plasma membranes that surround all animal cells. They form a protective barrier around cells; yet they also mediate their contact to the surrounding milieu, the extracellular matrix and neighboring cells.
In the glomerulus, galactose interacts with the podocyte glycocalyx and is thought to bind to the PF forming a galactose-PF complex which gets cleared by macrophages, hence preventing it from interacting with the glycocalyx (Savin et al 2008).

Based on this action, oral galactose administrationmay be helpful in reducing proteinuria in patients with multidrug resistant nephrotic syndrome (De Smet et al. 2009, Kopač et al.2011, Mishra et al, 2014).De Smet et al (2009) reported a 48-year-old male with a nephrotic syndrome secondary to FSGS resistant to corticosteroids, immunosuppression and plasmaphaeresis. The patient was given oral galactose as a last resort treatment at 10 gm BID for 6 months, which was followed by remission of his nephrotic syndrome that correlated with a reduction of focal segmental permeability factor (FSPF) activity. This case is the first report of a long-standing remission of an FSPF-associated nephrotic syndrome on oral galactose therapy.
Kopac et al. (2011) described the case of a three-year-old boy with nephrotic syndrome secondary to FSGS resistant to corticosteroids, cyclophosphamide and tacrolimus. The patient was given oral galactose as a last resort treatment at a dose of 0.2 g/kg twice a day for one month, within which proteinuria decreased by 50%.
Mishra et al (2014) reported reduction in proteinuria by 55% and rise in serum albumin levels after a 90-day course of glactose along with immunosuppressive drugs in three patients of steroid resistant nephrotic syndrome with FSGS histology. However, benefit was duration dependent.
By contrast, Sgambat et al (2014) did not observe anyantiproteinuric effect in a series of 7 cases. The negative findings in this study may have been influencedby the fact that the patients had long standing disease with extensive interstitial fibrosis.

A first controlled trial of galactose in multidrug resistant NS showed promising results but failed to reach enrollment targets (Trachtman et al. BMC Nephrology 2015). Hence, the conflicting anecdotal information regarding a proteinuria-lowering effect of galactose is awaiting resolution by well-designed controlled clinical trials. Therefore, the present trial has been planned to find out the effect of oral galactose in reduction of protenuria from baseline after 3 months of therapy in children with multidrug resistant nephrotic syndrome.