Focal segmental glomerulosclerosis (FSGS) is a group of glomerular diseases with focal segmental distribution of glomerulosclerosis as the basic pathological change. The etiology includes three major categories: primary, secondary and genetic, and the pathological subtypes are collapsed, tip, cellular, hilar and non-specific. Focal staged glomerulosclerosis (FSGS) can occur at any age and accounts for 7% to 20% of patients with childhood nephrotic syndrome and a significantly higher proportion in adult nephrotic syndrome. FSGS is more prevalent in African-Latin American patients than in Caucasians and accounts for approximately 80% of all causes of nephrotic syndrome. In patients with focal segmental glomerulosclerosis (FSGS), 100% have varying degrees of proteinuria, more than 60% have nephrotic syndrome, about 50% have varying degrees of hematuria, and 1/3 have hypertension and renal insufficiency at presentation, often with manifestations of impaired tubular function. In persistent nephrotic syndrome, if left untreated, more than 50% of patients will enter end-stage renal disease within 5 to 10 years. Spontaneous remission of proteinuria is uncommon in FSGS patients (<6%) and therefore the importance of achieving remission with pharmacological therapy needs to be emphasized. The specific approach to treating patients with FSGS nephrotic syndrome is controversial, with only few randomized controlled trials. Because of the low rate of complete remission in patients treated with glucocorticoids alone, long-term high-dose use is often accompanied by significant glucocorticoid side effects. Therefore, the preferred treatment options are high-dose glucocorticoids [prednisone 1 mg/kg?d)] combined with cyclophosphamide or low-dose glucocorticoids [prednisone <0.5 mg/(kg?d)] combined with cyclosporine. Tacrolimus [0.05-0.1 mg/kg-d) at trough blood concentrations of 5-10 ng/ml] may be effective in patients who are not responding to cyclosporine therapy. For glucocorticoid-dependent patients with recurrent relapses, cyclophosphamide, cyclosporine, azathioprine, and morte-macrolimus (1-2g/d for 3-6 months) may be beneficial for prolonging the maintenance of remission. Overall, the adult meta-analysis showed complete remission rates of 30% to 60% and partial remission rates of 30% after treatment. The remaining 40% to 50% were ineffective. Prolonging the duration of hormone therapy (up to 6 months) results in higher remission rates, but complications associated with hormone therapy also increase, and many patients, especially those who are elderly, obese, and have other comorbidities, are unable to tolerate long or repeated courses of hormone therapy. Complete remission of urinary protein after hormone therapy remains the best indicator of prognosis, and partial remission of urinary protein also plays an important role in predicting patients' long-term prognosis. Cytotoxic drugs are also effective in treating hormone-sensitive FSGS patients, with complete remission rates of up to 51% and partial remission rates of up to 23%. the indications for cytotoxic drugs in FSGS patients are similar to those for hormone-sensitive MCD patients. However, remission rates in patients with hormone-resistant FSGS treated with cytotoxic agents are low. The most optimistic retrospective studies to date report complete and partial remission rates of only 17% and 7% in adult patients, and 52% and 17% in pediatric patients, respectively. A recent meta-analysis of randomized controlled trials on FSGS nephrotic syndrome in children showed no significant difference in complete remission rates with oral cyclophosphamide combined with prednisone compared with prednisone alone (in one trial, n=53; RR 1.01, 95%, confidence interval 0.75 to 1.47). It is generally accepted that cytotoxic drug treatment of hormone-resistant FSGS does not increase the remission rate, but has the potential to prolong the duration of maintenance of remission. Rituximab or plasma exchange may be used for patients who fail to respond to the above treatments. However, these drugs are expensive and can also be associated with some serious complications, limiting their clinical use. Recently, some foreign studies have suggested that there is a circulating permeability factor in the blood of FSGS patients, and it has been found that galactose can reduce the activity of the circulating permeability factor, thus helping FSGS patients to reduce urinary protein. Some clinical observations have found that oral administration of galactose to patients who have failed the above treatment can have satisfactory clinical efficacy in reducing urinary protein. Since galactose is a commonly used food additive, it has an unparalleled safety profile compared to hormones and cytotoxic drugs or treatments such as rituximab or plasma exchange; it is also inexpensive and non-toxic, and if its efficacy in reducing urinary protein can be clinically proven, its medical future is quite promising.