Focal segmental glomerulosclerosis (FSGS) is a histopathologic finding of scarring (sclerosis) of glomeruli and damage to renal podocytes.[2][3] This process damages the filtration function of the kidney, resulting in protein presence in the urine due to protein loss.[3] FSGS is a leading cause of excess protein loss—nephrotic syndrome—in children and adults in the US.[4] Signs and symptoms include proteinuria and edema.[2][5]Kidney failure is a common long-term complication of the disease.[5][6] FSGS can be classified as primary, secondary, or genetic, depending on whether a particular toxic or pathologic stressor or genetic predisposition can be identified as the cause.[7][8][9] Diagnosis is established by renal biopsy,[2][10] and treatment consists of glucocorticoids and other immune-modulatory drugs.[11] Response to therapy is variable, with a significant portion of patients progressing to end-stage kidney failure.[5] An American epidemiological study 20 years ago demonstrated that FSGS is estimated to occur in 7 persons per million, with cisgender male African-Americans at higher risk.[12][13][7]
^Kitiyakara C, Eggers P, Kopp JB (November 2004). "Twenty-one-year trend in ESRD due to focal segmental glomerulosclerosis in the United States". Am J Kidney Dis. 44 (5): 815–25. doi:10.1016/S0272-6386(04)01081-9. PMID15492947.
^ abcRydel JJ, Korbet SM, Borok RZ, Schwartz MM (April 1995). "Focal segmental glomerular sclerosis in adults: presentation, course, and response to treatment". Am J Kidney Dis. 25 (4): 534–42. doi:10.1016/0272-6386(95)90120-5. PMID7702047.
^Korbet SM, Schwartz MM, Lewis EJ (June 1994). "Primary focal segmental glomerulosclerosis: clinical course and response to therapy". Am J Kidney Dis. 23 (6): 773–83. doi:10.1016/s0272-6386(12)80128-4. PMID8203357.
^Kitiyakara C, Kopp JB, Eggers P (March 2003). "Trends in the epidemiology of focal segmental glomerulosclerosis". Semin Nephrol. 23 (2): 172–82. doi:10.1053/snep.2003.50025. PMID12704577.