Focal Segmental Glomerulosclerosis
- Author: Sreepada TK Rao, MD, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
Focal segmental glomerulosclerosis (FSGS) is one of the most common causes of primary glomerular diseases in adults. The condition causes asymptomatic proteinuria or nephrotic syndrome with or without renal insufficiency. Generally, FSGS is a progressive form of kidney disease, accounting for 2.3% of patients with end-stage renal disease (ESRD).
Signs and symptoms
The most common clinical presenting feature of FSGS (>70% of patients) is nephrotic syndrome, characterized by generalized edema, massive proteinuria, hypoalbuminemia, and hyperlipidemia. However, the natural history of FSGS is variable and can range from edema that is difficult to manage, to proteinuria that is refractory to corticosteroids and other immunosuppressive agents, to worsening hypertension and a progressive loss of renal function.
In the collapsing form of FSGS, the disease is marked by severe hypertension, more massive proteinuria, a very poor response to corticosteroids, and a much faster rate of progression to ESRD. In human immunodeficiency virus (HIV)–associated FSGS, the renal functional deterioration is rapid, leading to ESRD within a few weeks to 1 year.
See Clinical Presentation for more detail.
Although clinical features are suggestive, a diagnosis of FSGS is established only by histopathology findings. In massively obese patients, FSGS is a diagnosis of exclusion.
Examination of patients with FSGS may include the following findings:
Abdominal pain: Common in children; may be sign of peritonitis
Ulcerations and infections in dependent regions
Severe hypertension (diastolic blood pressure of ≥120 mm Hg): Commonly seen in black patients, especially those with renal insufficiency 
Urinalysis: Large amounts of protein; hyaline and broad waxy casts
Serum creatinine concentration or creatinine clearance: Usually within reference range
Albumin levels: Generally low
Lipid studies: Hyperlipidemia
In patients with idiopathic FSGS, investigational findings for an underlying etiology—such as systemic lupus erythematosus (serum complement C4/C3 levels, antinuclear antibody/anti-DNA titers), hepatitis B or C infection, or vasculitis (antineutrophil cytoplasmic antibody titers, serum protein electrophoresis)—are generally negative.
In patients with suspected secondary FSGS, obtain HIV antibody, CD4, and viral load studies; serology for hepatitis B and C; and parvovirus testing.
Ultrasonographic findings of the kidneys include the following in FSGS:
Early stages: Normal or large kidneys with increased echogenicity, suggesting diffuse intrinsic medical renal disease
Advanced renal failure: Small and shrunken kidneys, indicating severe glomerular scarring and interstitial fibrosis
HIV-associated disease: Generally, large echogenic kidneys
Kidney biopsy is the most definitive way to confirm the diagnosis. Findings are as follows:
Segmental solidification of the glomerular tuft: Characteristic lesion
Segmental obliteration of glomerular capillaries by accumulation of acellular matrix and hyaline deposits, along with adhesion to the Bowman capsule
Fusion of diffuse foot process, predominantly in the sclerotic segments; morphologic subsets may occur
HIV-associated FSGS: Collapsing glomerular lesions with microcystic dilatation of renal tubules and tubuloreticular inclusions in endothelial and mesangial cells [4, 5]
See Workup for more detail.
Nonspecific, general management
Control hypertension, including pharmacotherapy (eg, diuretics, antihypertensives)
Reduce lipid levels
Reduce daily salt and protein intake
Nephrotic syndrome: Maintain adequate nutrition, minimize/eliminate proteinuria, prevent complications from edema
Idiopathic FSGS is difficult to treat due to its highly variable clinical course. The specific treatment approach is still empirical; no consensus has evolved due to a lack of prospective controlled trials.
The general consensus is for an aggressive approach in persistently nephritic patients to induce remission (eg, use of corticosteroids and immunosuppressive agents). Precautions in managing patients with idiopathic FSGS include the following:
Patient counseling and close monitoring for adverse effects of long-term steroid therapy
Monitoring for bone marrow suppression; encourage adequate fluid intake to prevent hemorrhagic cystitis
Avoiding prolonged use of cyclophosphamide, particularly in nonresponsive cases
Early patient and family counseling about treatment choices for ESRD
Avoiding cyclosporine in patients with renal insufficiency who have refractory FSGS
Management of secondary FSGS is directed toward the etiology or associated disorder, such as the following:
HIV-associated FSGS: Highly active antiretroviral therapy (HAART); corticosteroids and/or discontinuation of dialysis in selected patients
Heroin-associated FSGS: Discontinuation of the drug
Some patients with FSGS continue to deteriorate and progress to ESRD. Treatment options include the following:
Continuous ambulatory peritoneal dialysis
Cadaver or living donor renal transplantation
The following medications are used in the management of FSGS:
Immunosuppressants (eg, prednisone, cyclophosphamide)
Loop diuretics (eg, furosemide)
Potassium-sparing diuretics (eg, spironolactone, triamterene)
Other diuretics (eg, metolazone)
Volume expanders (eg, albumin)
Osmotic agents (eg, mannitol)
Angiotensin-converting enzyme inhibitors
Angiotensin receptor blockers
Focal segmental glomerulosclerosis (FSGS), first described in 1957, is currently recognized as one of the most common causes of primary glomerular diseases in adults, and the incidence of FSGS has been increasing in recent years.[6, 7] FSGS causes asymptomatic proteinuria or nephrotic syndrome (NS) with or without renal insufficiency. In adults undergoing renal biopsy for evaluation of proteinuria, FSGS accounts for 35% of all cases and up to 80% of cases in African-American patients. Generally, FSGS is a progressive form of kidney disease, accounting for 2.3% of patients with end-stage renal disease (ESRD).
Although clinical features are suggestive, a diagnosis of FSGS is confirmed only by histopathology findings. The disease represents several patterns of glomerular injury, and biopsy findings provide no insights into the pathogenesis. FSGS arises through idiopathic (primary) or secondary causes.
Therapy for FSGS includes nonspecific measures (eg, nutrition) and symptomatic treatment. Current evidence, mostly derived from retrospective analyses, favors prolonged corticosteroid therapy to induce remission in patients with idiopathic FSGS.
Etiologic agents or mechanisms that initiate glomerular injury which lead to glomerulosclerosis are largely unknown, except in certain animal models of viral-induced renal disease. The primary pathophysiologic process in FSGS is an injury inherent within or directed to podocytes. Foot process effacement, proliferation of mesangial, endothelial, and epithelial cells in the early stages, followed by shrinkage/collapse of glomerular capillaries all lead to scarring (glomerulosclerosis).[8, 9]
Proposed mechanisms include viral- or toxin-mediated damage or intrarenal hemodynamic changes such as glomerular hyperperfusion and high intraglomerular capillary pressure. FSGS initially begins in the deeper juxtamedullary glomeruli and subsequently extends to the superficial nephrons. The characteristic lesion is a segmental solidification of the glomerular tuft, usually in the perihilar region and sometimes in the peripheral areas, including the tubular pole.
The extent of lesions varies in different portions of the kidney, ranging from normal unaffected glomerulus to segmental sclerosis and, eventually, global glomerulosclerosis as the disease progresses. Diffuse foot process fusion occurs, predominantly in the sclerotic segments, although partial effacement may be observed in normal-appearing lobules.
Many morphologic subsets, such as a cellular variant (endocapillary and extracapillary hypercellularity), a collapsing variant (FSGS with mesangial hypercellularity), and FSGS with tip lesions, have been described.[2, 9] Whether these diverse lesions reflect different pathogenesis or account for the differences in the prognoses in patients with FSGS is unclear. To better comprehend some aspects of pathogenesis, FSGS can be classified as primary (idiopathic) or secondary.
Primary (idiopathic) FSGS
Primary (idiopathic) FSGS includes the following:
FSGS with hyalinosis
Progression from minimal-change disease
Progression from immunoglobulin M (IgM) nephropathy
Progression from mesangial proliferative glomerulonephritis
Superimposed on other primary glomerulonephritis conditions (eg, membranous glomerulonephritis, immunoglobulin A [IgA] nephropathy)
Variants of primary FSGS include the following:
Cellular variant (endocapillary and extracapillary hypercellularity)
FSGS with mesangial hypercellularity
FSGS with glomerular tip lesions
Drugs associated with FSGS include the following :
Intravenous heroin [11, 12, 13, 14]
Viruses associated with FSGS include the following:
Hemodynamic factors in patients with reduced renal mass include the following:
Hemodynamic causes in patients without reduced renal mass include the following:
Massive obesity 
Sickle cell nephropathy
Congenital cyanotic heart disease
Lymphomas and other malignancies have been associated with FSGS. Genetic cases may be familial or sporadic. Scarring may lead to FSGS subsequent to postinfectious glomerulonephritis. Miscellaneous other conditions associated with FSGS include the following:
In other words, factors as diverse as infections, inflammations, toxins, and intrarenal hemodynamic alterations can initiate injury to cells and lead to glomerulosclerosis.
A pathogenic classification of FSGS has also been proposed, as follows:
Primary alteration of epithelial cells - Includes FSGS from idiopathic, viral-associated, drug-induced, and genetic disorders
Secondary to reduction in nephron mass or hemodynamic adaptation - Includes FSGS seen in patients who are obese and those with a single kidney, renal dysplasia/agenesis, reflux nephropathy, sickle cell disease, hereditary nephropathies, and other primary glomerular diseases
This classification also does not contribute much to the understanding of the pathogenesis of FSGS.
Another classification, often referred to as Columbia classification, recognizes five histologic variants of primary FSGS, as follows:
FSGS not otherwise specified
Collapsing forms of FSGS
These histologic variants may predict response to immunomodulating agents but do not provide insights into the pathogenesis of FSGS.
Protein mutations and circulating factors
The discovery that mutations in several proteins that play critical roles in podocyte structure, function, or both not only cause FSGS but can predict disease phenotype such as steroid responsiveness has advanced the understanding of the pathophysiology of FSGS.[20, 21, 22] For example, people with causal mutations in TRPC6 or NPHS2 do not respond well to immunosuppressive therapy; however, when they receive kidney transplants, the disease does not usually recur.
Consistent with these findings, Mele et al found that mutations in MYO1E, which encodes a nonmuscle class I myosin, are correlated with childhood-onset, glucocorticoid-resistant FSGS. The observation that in some cases FSGS can occur de novo in renal transplants and may occur immediately after transplantation has led to speculation that circulating factors in plasma may engender podocytopathy.
The nature of these circulating factors linked to the development of FSGS is being constantly clarified as findings continue to come to light. Proposed candidate molecules include hemopexin, vascular endothelial growth factor, and cardiotrophinlike cytokine-1. One candidate that has been studied the most is the soluble form of urokinase receptor (suPAR).
Wei et al have shown that elevated levels of soluble form of urokinase receptor (suPAR) was present in the plasma of two-thirds of patients with FSGS. Furthermore, high levels of suPAR were predictive of FSGS recurrence, and lowering suPAR levels by plasmapheresis led to disease remission.
In some cases of idiopathic FSGS, other yet-to-be identified circulating factors may be involved. Recently, the same group has analyzed circulating suPAR levels in 2 cohorts of patients with biopsy proven FSGS. This included 70 patients from a North America–based FSGS clinical trial and 94 patients from Europebased, steroid-resistant nephrotic syndrome, compared with age- and sex-matched control subjects. They found strong associations between change in circulating suPAR levels with different therapeutic regimens and with remission of proteinuria.
Not all patients with FSGS have elevated suPAR levels, a fact consistent with the suggestion that FSGS is not a disease but a pattern of renal injury that may follow many forms of primary podocyte insults.
The search for other permeability factors, genetic variations in different races, mutations of many proteins involved in podocyte function (eg, as podocin and others) is the focus of ongoing research efforts. Genetic variation in circulating apolipoprotein Apol1 predisposes to FSGS in African Americans, although the putative mechanisms are unknown. Mutations of podocyte proteins are more often associated with familial forms of FSGS.
Typically, idiopathic FSGS is observed in persons aged 18-45 years, although no age group is exempt from the disease. In children with NS, FSGS is found in 7-10% of renal biopsies; incidence is much greater in those who are resistant to steroid and cyclophosphamide therapy. In adults, the lesion is more common in men and is observed in 20-30% of patients with NS. Incidence of FSGS is 3-7 times higher in young black men as compared with whites.
The reported annual incidence rates for FSGS is 5 cases per million population in whites, compared with 24 cases per million population in African Americans. This increased incidence is partly explained by variants of 2 important podocyte function proteins; nonmuscle myosin heavy chain-9 and apolipoprotein Apol1 is found in about 60% of African American patients compared with 5% in whites.[28, 29]
The annual incidence of secondary FSGS in patients who are addicted to intravenous heroin is 30 times higher (611 cases per million population). In selected urban centers in the United States, heroin-associated FSGS accounted for 11.4% of end-stage renal disease (ESRD) patients in the 1970s and 1980s, although the disease gradually disappeared in the 1990s. Most patients with HIV-associated FSGS are young black men (mean age, 33 y; male-to-female ratio, 10:1),[11, 12, 3] 50% are intravenous drug abusers, and the remaining are either gay or bisexual men, heterosexual contacts of infected persons, or children with HIV infection. HIV-associated FSGS is distinctly rare in whites. In the United States and elsewhere, more than 95% of patients are black.
The incidence of HIV-associated FSGS in children has practically disappeared because of serologic screening of all transfused products, screening of pregnant mothers, and effective use of antiretroviral drugs during pregnancy and childbirth.
The annual incidence of ESRD attributed to idiopathic FSGS increased 11 fold (from 0.2% to 2.3%) between 1980 and 2000. In black and white patients in the United States, idiopathic FSGS is now the commonest cause of ESRD resulting from primary glomerular disease.
FSGS lesions are observed in about 10% of renal biopsies performed for the evaluation of proteinuria.
The natural history of FSGS varies a great deal. A typical course runs from edema that is difficult to manage, to proteinuria refractory to corticosteroids and other immunosuppressive agents, to worsening hypertension and progressive loss of renal function. In patients who do not respond to therapy, the average time from the onset of gross proteinuria to ESRD is 6-8 years, although wide variations in the time course occur. One of the key factors that determines renal survival is the persistence and degree of proteinuria. Achievement of a remission, whether spontaneous or induced by immunosuppressive therapy, is associated with a good renal outcome.
In patients who are unresponsive to therapy and who continue to have massive proteinuria of greater than 10 g/d, most develop ESRD within 5 years. The prognosis is much worse in black patients compared with white patients. In the collapsing form of FSGS, the disease is marked by severe hypertension, more massive proteinuria, a very poor response to corticosteroids, and a much faster rate of progression to ESRD.
The prevalence rate is much higher in blacks than in whites. In one large epidemiologic study, the annual incidence of FSGS in patients aged 18-45 years was 20 cases per million population in blacks, a rate seven times higher than that of individuals who are not black. On the other hand, the annual incidence of secondary FSGS in patients addicted to intravenous heroin is 30 times higher (611 cases per million population). As previously noted, most subjects with HIV-associated FSGS are young black men.
The reported annual incidence rates for FSGS is 5 cases per million population in whites, compared with 24 cases per million population in African Americans. In recent years, the incidence of heroin-associated FSGS has drastically decreased.
Sex- and age-related variance
In adults, the lesion is three to four times more common in men than women.
Typically, idiopathic FSGS is observed in persons aged 18-45 years, although no age group is exempt from the disease. In children with NS, FSGS is found in 7-10% of renal biopsy specimens; incidence is much greater in those who are resistant to steroid and cyclophosphamide therapy.
Del Rio M, Kaskel F. Evaluation and management of steroid-unresponsive nephrotic syndrome. Curr Opin Pediatr. 2008 Apr. 20(2):151-6. [Medline].
Thomas DB. Focal segmental glomerulosclerosis: a morphologic diagnosis in evolution. Arch Pathol Lab Med. 2009 Feb. 133(2):217-23. [Medline].
Freedman BI, Hicks PJ, Bostrom MA, et al. Polymorphisms in the non-muscle myosin heavy chain 9 gene (MYH9) are strongly associated with end-stage renal disease historically attributed to hypertension in African Americans. Kidney Int. 2009 Jan 28. [Medline].
Rao TKS. Renal complications in HIV disease. Med Clin North Am. 1996 Nov. 80(6):1437-51. [Medline].
Winston JA, Burns GC, Klotman PE. The human immunodeficiency virus (HIV) epidemic and HIV-associated nephropathy. Semin Nephrol. 1998 Jul. 18(4):373-7. [Medline].
Haas M, Spargo BH, Coventry S. Increasing incidence of focal-segmental glomerulosclerosis among adult nephropathies: a 20-year renal biopsy study. Am J Kidney Dis. 1995 Nov. 26(5):740-50. [Medline].
Kitiyakara C, Eggers P, Kopp JB. Twenty-one-year trend in ESRD due to focal segmental glomerulosclerosis in the United States. Am J Kidney Dis. 2004 Nov. 44(5):815-25. [Medline].
D'Agati VD. The spectrum of focal segmental glomerulosclerosis: new insights. Curr Opin Nephrol Hypertens. 2008 May. 17(3):271-81. [Medline].
Barisoni L, Schnaper HW, Kopp JB. Advances in the biology and genetics of the podocytopathies: implications for diagnosis and therapy. Arch Pathol Lab Med. 2009 Feb. 133(2):201-16. [Medline].
Rao TKS, Nicastri AD, Friedman EA. The nephropathies of drug addiction and acquired immunodeficiency syndrome. Renal Pathology. New York, NY: JB Lippincott; 1989. 340-56.
Cunningham EE, Brentjens JR, Zielezny MA, et al. Heroin nephropathy. A clinicopathologic and epidemiologic study. Am J Med. 1980 Jan. 68(1):47-53. [Medline].
Cunningham EE, Zielezny MA, Venuto RC. Heroin-associated nephropathy. A nationwide problem. JAMA. 1983 Dec 2. 250(21):2935-6. [Medline].
Friedman EA, Tao TK. Disappearance of uremia due to heroin-associated nephropathy. Am J Kidney Dis. 1995 May. 25(5):689-93. [Medline].
Rao TKS, Nicastri AD, Friedman EA. Natural history of heroin-associated nephropathy. N Engl J Med. 1974 Jan 3. 290(1):19-23. [Medline].
Bruggeman LA, Dikman S, Meng C, et al. Nephropathy in human immunodeficiency virus-1 transgenic mice is due to renal transgene expression. J Clin Invest. 1997 Jul 1. 100(1):84-92. [Medline].
D''Agati V, Appel GB. HIV infection and the kidney. J Am Soc Nephrol. 1997 Jan. 8(1):138-52. [Medline].
Kimmel PL, Bosch JP, Vassalotti JA. Treatment of human immunodeficiency virus (HIV)-associated nephropathy. Semin Nephrol. 1998 Jul. 18(4):446-58. [Medline].
Verani RR. Obesity-associated focal segmental glomerulosclerosis: pathological features of the lesion and relationship with cardiomegaly and hyperlipidemia. Am J Kidney Dis. 1992 Dec. 20(6):629-34. [Medline].
D'Agati VD, Alster JM, Jennette JC, Thomas DB, Pullman J, Savino DA. Association of histologic variants in FSGS clinical trial with presenting features and outcomes. Clin J Am Soc Nephrol. 2013 Mar. 8(3):399-406. [Medline].
Tryggvason K, Patrakka J, Wartiovaara J. Hereditary proteinuria syndromes and mechanisms of proteinuria. N Engl J Med. 2006 Mar 30. 354(13):1387-401. [Medline].
Winn MP, Conlon PJ, Lynn KL, et al. A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis. Science. 2005 Jun 17. 308(5729):1801-4. [Medline].
Shankland SJ, Pollak MR. A suPAR circulating factor causes kidney disease. Nat Med. 2011 Aug 4. 17(8):926-7. [Medline].
Mele C, Iatropoulos P, Donadelli R, et al. MYO1E mutations and childhood familial focal segmental glomerulosclerosis. N Engl J Med. 2011 Jul 28. 365(4):295-306. [Medline].
McCarthy ET, Sharma M, Savin VJ. Circulating permeability factors in idiopathic nephrotic syndrome and focal segmental glomerulosclerosis. Clin J Am Soc Nephrol. 2010 Nov. 5(11):2115-21. [Medline].
Wei C, El Hindi S, Li J, Fornoni A, et al. Circulating urokinase receptor as a cause of focal segmental glomerulosclerosis. Nat Med. 2011 Jul 31. 17(8):952-60. [Medline].
Wei C, Trachtman H, Li J, Dong C, Friedman AL, Gassman JJ. Circulating suPAR in two cohorts of primary FSGS. J Am Soc Nephrol. 2012 Dec. 23(12):2051-9. [Medline].
Kopp JB, Smith MW, Nelson GW, Johnson RC, Freedman BI, Bowden DW. MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis. Nat Genet. 2008 Oct. 40(10):1175-84. [Medline].
Kopp JB, Nelson GW, Sampath K, Johnson RC, Genovese G, An P. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy. J Am Soc Nephrol. 2011 Nov. 22(11):2129-37. [Medline].
Deegens JK, Wetzels JF. Immunosuppressive treatment of focal segmental glomerulosclerosis: lessons from a randomized controlled trial. Kidney Int. 2011 Oct. 80(8):798-801. [Medline].
Gipson DS, Trachtman H, Kaskel FJ, et al. Clinical trial of focal segmental glomerulosclerosis in children and young adults. Kidney Int. 2011 Oct. 80(8):868-78. [Medline].
Korbet SM. Treatment of primary FSGS in adults. J Am Soc Nephrol. 2012 Nov. 23(11):1769-76. [Medline].
[Guideline] Kidney Disease/Improving Global Ooutcomes. KDIGO Clinical Practice Guideline for Glomerulonephritis (GN). Kidney Int. June 2012. 2 suppl 2:[Full Text].
Ramachandran R, Kumar V, Rathi M, Nada R, Jha V, Gupta KL, et al. Tacrolimus therapy in adult-onset steroid-resistant nephrotic syndrome due to a focal segmental glomerulosclerosis single-center experience. Nephrol Dial Transplant. 2014 Oct. 29(10):1918-24. [Medline].
Garrouste C, Canaud G, Büchler M, Rivalan J, Colosio C, Martinez F, et al. Rituximab for Recurrence of Primary Focal Segmental Glomerulosclerosis After Kidney Transplantation: Clinical Outcomes. Transplantation. 2016 Apr 13. 17 (2):79-82. [Medline].
Ruggenenti P, Ruggiero B, Cravedi P, Vivarelli M, Massella L, et al. Rituximab in steroid-dependent or frequently relapsing idiopathic nephrotic syndrome. J Am Soc Nephrol. 2014 Apr. 25 (4):850-63. [Medline]. [Full Text].
Kronbichler A, Kerschbaum J, Fernandez-Fresnedo G, Hoxha E, Kurschat CE, Busch M, et al. Rituximab treatment for relapsing minimal change disease and focal segmental glomerulosclerosis: a systematic review. Am J Nephrol. 2014. 39(4):322-30. [Medline].
FDA approves new pediatric use for Liposorber Apheresis System [news release]. October 10, 2013. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm370931.htm. Accessed: October 15, 2013.
Han KH, Kim SH. Recent Advances in Treatments of Primary Focal Segmental Glomerulosclerosis in Children. Biomed Res Int. 2016. 2016:3053706. [Medline].
Beer A, Mayer G, Kronbichler A. Treatment Strategies of Adult Primary Focal Segmental Glomerulosclerosis: A Systematic Review Focusing on the Last Two Decades. Biomed Res Int. 2016. 2016:4192578. [Medline].
Hogan J, Bomback AS, Mehta K, Canetta PA, Rao MK, Appel GB, et al. Treatment of idiopathic FSGS with adrenocorticotropic hormone gel. Clin J Am Soc Nephrol. 2013 Dec. 8 (12):2072-81. [Medline]. [Full Text].
Chun MJ, Korbet SM, Schwartz MM, et al. Focal segmental glomerulosclerosis in nephrotic adults: presentation, prognosis, and response to therapy of the histologic variants. J Am Soc Nephrol. 2004 Aug. 15(8):2169-77. [Medline].
Crook ED, Habeeb D, Gowdy O, et al. Effects of steroids in focal segmental glomerulosclerosis in a predominantly African-American population. Am J Med Sci. 2005 Jul. 330(1):19-24. [Medline].
Kitiyakara C, Eggers P, Kopp JB. Twenty-one-year trend in ESRD due to focal segmental glomerulosclerosis in the United States. Am J Kidney Dis. 2004 Nov. 44(5):815-25. [Medline].
Korbet SM. Angiotensin antagonists and steroids in the treatment of focal segmental glomerulosclerosis. Semin Nephrol. 2003 Mar. 23(2):219-28. [Medline].
Korbet SM. Treatment of primary focal segmental glomerulosclerosis. Kidney Int. 2002 Dec. 62(6):2301-10. [Medline].
Stirling CM, Mathieson P, Boulton-Jones JM, et al. Treatment and outcome of adult patients with primary focal segmental glomerulosclerosis in five UK renal units. QJM. 2005 Jun. 98(6):443-9. [Medline].
Troyanov S, Wall CA, Miller JA, et al. Focal and segmental glomerulosclerosis: definition and relevance of a partial remission. J Am Soc Nephrol. 2005 Apr. 16(4):1061-8. [Medline].
Rudnicki M. FSGS Recurrence in Adults after Renal Transplantation. Biomed Res Int. 2016. 2016:3295618. [Medline].