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Focal Segmental Glomerulosclerosis Treatment & Management

  • Author: Sreepada TK Rao, MD, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jun 06, 2016
 

Medical Care

Treatment of focal segmental glomerulosclerosis (FSGS) can be divided into nonspecific and specific treatment.

In patients with primary or secondary FSGS (non-nephrotic or nephrotic) and proteinuria, the initial approach consists of optimal blood pressure (BP) control and the use of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). For patients who remain non-nephrotic or become non-nephrotic after 6 months of therapy, this remains the primary therapeutic approach.[32]

In patients with secondary FSGS and nephrotic-range proteinuria, the mainstay of therapy remains BP control and ACEIs and ARBs, along with disease-specific treatment if available (eg, antiretroviral therapy in HIV-associated nephropathy). Patients who are persistently nephrotic after a course of conservative therapy or who present with complications from nephrotic syndrome require more aggressive treatment with prednisone or immunosuppressive agents.[32]

Nonspecific treatment

Nonspecific treatment goals in patients with nephrotic syndrome include maintenance of adequate nutrition, minimization or elimination of proteinuria, and prevention of complications resulting from edema. Control of hypertension is one of the most important aspects of overall management. Lowering of lipid levels is necessary to reduce cardiovascular risk and to possibly delay the progression of renal disease.

The mainstay of treatment is reduction in daily salt intake to 2 g of sodium (6 g of salt) and the use of diuretics in varying doses and combinations. A high level of protein intake may further aggravate proteinuria, adversely affecting renal function. Current recommendations call for an intake of 1-1.3 g of high biologic value protein per kilogram of body weight and a reduction of fat intake.

In most patients, loop diuretics (eg, furosemide) are needed to promote diuresis. Patients with massive edema with impaired oral absorption may require intravenous administration. In patients with refractory conditions, addition of other diuretics (eg, metolazone) and potassium-sparing agents (eg, spironolactone, triamterene) facilitates diuresis and prevents hypokalemia.

Rarely, some patients (especially children) with intractable edema may need intravenous albumin and mannitol in a hospital setting to initiate diuresis. Protracted use of intravenous albumin should be discouraged; the regimen is expensive and ineffective, because most of the infused albumin is lost in the urine.

ACEIs and ARBs are nonspecific agents that reduce proteinuria because of their antihypertensive and intrarenal hemodynamic effects of reducing glomerular capillary pressure and resistance. ACEIs and ARBs are effective in reducing protein loss even in normotensive patients. These agents do not eliminate proteinuria completely or reverse the primary glomerular disease process.

Since most patients with idiopathic FSGS develop hypertension, which further contributes to renal functional deterioration, meticulous attention must be paid to maintain BP in the reference range. All classes of antihypertensive agents, which effectively lower BP, have a beneficial effect in reducing proteinuria. In many patients, combination antihypertensive therapy may be needed to maintain normal blood pressure.

Another nonspecific therapy is the use of lipid-lowering agents to control hyperlipidemia. The statin class of drugs is better tolerated than some of the older agents.

Specific treatment

Idiopathic FSGS is a difficult disease to treat because of its highly variable clinical course. The specific treatment approach is still empirical, and no consensus has evolved because of a lack of prospective controlled trials. Spontaneous remissions are very rare, probably occurring in less than 5% of patients. In those with non-nephritic proteinuria, many physicians use only the nonspecific measures outlined above, and the general consensus is that aggressive approaches should be used in persistently nephritic patients. Ultimately, prognosis in nephritic FSGS patients is determined by their response to prednisone and other immunosuppressive agents.

Steroid therapy

Current evidence, mostly derived from retrospective analyses, favors prolonged corticosteroid therapy (6 mo or longer) to induce remission in patients with idiopathic FSGS.

Since long-term steroid therapy may lead to serious toxicity, patient counseling and close monitoring for adverse effects are essential before embarking on such a protracted regimen. The current approach calls for initiating therapy with prednisone in a dose of 1 mg/kg (60-80 mg/d) for 2-6 months or longer, depending on patient response as assessed by presence or absence of edema; 24-hour urine protein excretion; creatinine clearance; and serum creatinine, albumin, and lipid levels.

Studies indicate that 30-60% of patients may undergo complete or partial remission to such a regimen, and relapses are frequent when steroids are discontinued. Complete remission is protein excretion of less than 200-300 mg/d, and partial response is excretion of 200-3500 mg/d, or a greater than 50% reduction in baseline proteinuria. In children, results from several studies show a remission of proteinuria in 11% of patients, persistence of nephrotic syndrome (NS) with preservation of renal function in 31%, decline in the glomerular filtration rate in 23%, and development of end-stage renal disease (ESRD) in 21%. In adults, 10-year renal survival in nephrotic patients ranges from 25-55%, compared with 85-90% in patients with mild proteinuria.

In general, patients with tip lesions on histology are more responsive to corticosteroids, with excellent renal preservation compared with those with other forms of FSGS. Blacks and patients with collapsing FSGS are generally refractory to treatment and progress to renal failure. In responding patients, the goal is to titrate prednisone to the lowest dose to stop or reduce proteinuria and to prevent relapses. Use of steroids on alternate days can also reduce toxicity. Some have used a combination of prednisone and a cytotoxic agent such as cyclophosphamide as initial therapy to reduce the dose and duration of corticosteroids.

The optimal treatment duration is uncertain. Some authorities recommend the use of steroids indefinitely.

Other agents

In patients who are refractory to 2-3 months of prednisone therapy, the recommendation is to reduce the steroid dose and to add cyclophosphamide (2.5 mg/kg [150-200 mg/d]). Monitor patients for bone marrow suppression, and encourage them to drink adequate fluids to prevent hemorrhagic cystitis. Prolonged use of cyclophosphamide may lead to gonadal toxicity. Therefore, persisting with cyclophosphamide beyond 3 months in patients who do not respond is unwise.

Guidelines from Kidney Disease/Improving Global Outcomes (KDIGO) suggest considering calcineurin inhibitors (cyclosporine or tacrolimus) as first-line therapy for patients with relative contraindications or intolerance to high-dose corticosteroids (eg, uncontrolled diabetes, psychiatric conditions, severe osteoporosis).[33]

Randomized controlled trials and uncontrolled studies indicate that cyclosporine (CsA) in a dose of 5-10 mg/kg/d may be beneficial in patients unresponsive to prednisone and cyclophosphamide. Few limited studies have employed tacrolimus. Since both of these calcineurin inhibitors can cause nephrotoxicity, the recommendation is to avoid them in patients with renal insufficiency.

Because of favorable results in other glomerular diseases, mycophenolate mofetil (MMF) has also been evaluated in FSGS. Although the experience is limited, the suggested dose is 750-1000 mg twice daily in patients who are refractory to corticosteroids and in whom calcineurin inhibitors may not be appropriate.

To assess whether treatment with MMF and oral pulses of dexamethasone (DEXA) was more effective than treatment with CsA alone for steroid-resistant FSGS, a National Institutes of Health–sponsored multicenter randomized controlled trial, the largest study to date, was conducted in 138 patients aged 2-40 years. At the end of the 52-week treatment period, the incidence of complete and partial remissions was 33% in the MMF and DEXA group compared with 46% in the CsA group, which was not significantly different. A critical analysis of this study highlights the limitations of current practices in the treatment of the individual patient with FSGS.[31]

Isolated reports have suggested that in patients who are refractory to steroids and cyclophosphamide, treatment with other immunosuppressive agents, such as tacrolimus (Prograf) and sirolimus (Rapamune), may be beneficial in inducing remissions. In a prospective study of 44 patients with steroid-resistant nephrotic syndrome due to FSGS, 48 weeks of treatment with oral tacrolimus given in combination with prednisolone resulted in complete remission in 17 patients (38.6%) and partial remission in 6 patients (13.6%). Resistance to tacrolimus was observed in 21 patients (47.7%). Mean time to remission was 15.2 ± 6 weeks.[34]

Among the patients who achieved complete remission, relapse occurred in five (21.7%) after the tacrolimus dose was tapered and in 7 (30.4%) after tacrolimus was stopped. Reversible and irreversible nephrotoxicity occurred in 7 (15.9%) and 4 patients (9%), respectively. Tacrolimus-related diarrhea was observed in 10 patients (22.7%), infections in 19 patients (43.1%), and impaired fasting glucose and diabetes mellitus in 10 patients (22.7%).[34]

Rituximab has proved effective for maintenance of remission in frequently relapsing FSGS and for treatment of remission, including in kidney transplant recipients.[35, 36] Kronbichler and colleagues, in a systematic review of 14 studies involving 86 adult patients with either steroid-dependent or frequently relapsing minimal change disease or FSGS, found that rituximab treatment significantly reduced the number of relapses per year from a mean of 1.3 before treatment to none after treatment. Rituximab treatment decreased proteinuria from 2.43 g/day to 0 g/day (P < 0.001), increased serum albumin from 2.9 to 4.0 g/dL, and decreased the need for immunosuppression.[37]

Despite all attempts, some patients continue to deteriorate and progress to ESRD. Counsel patients and their families early regarding treatment choices for ESRD. A well-informed patient can choose among maintenance hemodialysis, continuous ambulatory peritoneal dialysis, or cadaver or living donor transplantation. FSGS may recur in the transplanted kidney, but most nephrologists do not consider this a contraindication for renal transplantation.[38]

In October 2013, the FDA approved the Liposorber LA-15 System to treat children with primary FSGS either before kidney transplantation, or after kidney transplantation in which there is recurrence of FSGS.[39] This product is an extracorporeal blood processing system that removes certain lipoproteins from the blood; it was previously approved to lower low density lipoprotein cholesterol (LDL-C) in selected patients with familial hypercholesterolemia.[39]

Approval was based on two studies in children with FSGS. One study showed normal or near normal renal function in most children who had had a high risk for progression to ESRD but who achieved remission of FSGS following treatment with the system.[39] The second study reported that posttransplant children who were treated with the Liposorber LA-15 System had less excretion of protein in their urine relative to children not treated with the system.[39]

Small studies have found benefit with use of galactose, abatacept, and adalimumab.[40, 41]

Subcutaneously injected adrenocorticotropic hormone (ACTH) gel may have some efficacy for treatment of FSGS, especially in treatment-resistant or relapsing cases. In a study of 24 patients with nephrotic syndrome from idiopathic FSGS, Hogan et al reported that treatment with ACTH gel resulted in full remission in two patients and partial remission in five patients. However, two responders relapsed during follow-up and 21 patients experienced adverse events, including one episode of new-onset diabetes, which resolved after stopping ACTH, and two episodes of acute kidney injury.[42]

Secondary FSGS

Management of secondary FSGS is directed toward the etiology or associated disorder. For example, in HIV-associated FSGS, highly active antiretroviral therapy (HAART) is associated with remission of proteinuria and preservation of renal function.[16] Current guidelines call for initiation of HAART therapy in patients with HIV who have nephropathy irrespective of CD4 count and viral load. In selected patients with HIV and FSGS, corticosteroid therapy is associated with a significant improvement and, in some patients, discontinuation of dialysis therapy. In heroin-associated FSGS, discontinuation of the drug may result in remission of proteinuria and improvement in renal function.

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Diet

Daily salt intake should be reduced to 2 g of sodium (6 g of salt). Potassium supplementation may be needed in patients treated with diuretics who develop hypokalemia.

High protein intake may further aggravate proteinuria, adversely affecting renal function. Current recommendations call for an intake of 1-1.3 g of high biologic value protein per kilogram of body weight and a reduction of fat intake.

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Contributor Information and Disclosures
Author

Sreepada TK Rao, MD, FACP Professor, Department of Medicine, State University of New York Downstate Medical Center

Sreepada TK Rao, MD, FACP is a member of the following medical societies: American Society of Hypertension, International Society of Nephrology, American Society of Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Chike Magnus Nzerue, MD, FACP Professor of Medicine, Associate Dean for Clinical Affairs, Meharry Medical College

Chike Magnus Nzerue, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Acknowledgements

Anjana S Soman, MD Staff Physician, Department of Pathology, Quest Diagnostics

Anjana S Soman, MD is a member of the following medical societies: American Society for Clinical Pathology and College of American Pathologists

Disclosure: Nothing to disclose.

References
  1. Del Rio M, Kaskel F. Evaluation and management of steroid-unresponsive nephrotic syndrome. Curr Opin Pediatr. 2008 Apr. 20(2):151-6. [Medline].

  2. Thomas DB. Focal segmental glomerulosclerosis: a morphologic diagnosis in evolution. Arch Pathol Lab Med. 2009 Feb. 133(2):217-23. [Medline].

  3. 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].

  4. Rao TKS. Renal complications in HIV disease. Med Clin North Am. 1996 Nov. 80(6):1437-51. [Medline].

  5. 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].

  6. 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].

  7. 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].

  8. D'Agati VD. The spectrum of focal segmental glomerulosclerosis: new insights. Curr Opin Nephrol Hypertens. 2008 May. 17(3):271-81. [Medline].

  9. 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].

  10. 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.

  11. 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].

  12. Cunningham EE, Zielezny MA, Venuto RC. Heroin-associated nephropathy. A nationwide problem. JAMA. 1983 Dec 2. 250(21):2935-6. [Medline].

  13. Friedman EA, Tao TK. Disappearance of uremia due to heroin-associated nephropathy. Am J Kidney Dis. 1995 May. 25(5):689-93. [Medline].

  14. Rao TKS, Nicastri AD, Friedman EA. Natural history of heroin-associated nephropathy. N Engl J Med. 1974 Jan 3. 290(1):19-23. [Medline].

  15. 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].

  16. D''Agati V, Appel GB. HIV infection and the kidney. J Am Soc Nephrol. 1997 Jan. 8(1):138-52. [Medline].

  17. Kimmel PL, Bosch JP, Vassalotti JA. Treatment of human immunodeficiency virus (HIV)-associated nephropathy. Semin Nephrol. 1998 Jul. 18(4):446-58. [Medline].

  18. 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].

  19. 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].

  20. 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].

  21. 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].

  22. Shankland SJ, Pollak MR. A suPAR circulating factor causes kidney disease. Nat Med. 2011 Aug 4. 17(8):926-7. [Medline].

  23. 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].

  24. 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].

  25. 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].

  26. 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].

  27. Genovese G, Friedman DJ, Ross MD, et al. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science. 2010 Aug 13. 329(5993):841-5. [Medline]. [Full Text].

  28. 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].

  29. 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].

  30. 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].

  31. 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].

  32. Korbet SM. Treatment of primary FSGS in adults. J Am Soc Nephrol. 2012 Nov. 23(11):1769-76. [Medline].

  33. [Guideline] Kidney Disease/Improving Global Ooutcomes. KDIGO Clinical Practice Guideline for Glomerulonephritis (GN). Kidney Int. June 2012. 2 suppl 2:[Full Text].

  34. 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].

  35. 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].

  36. 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].

  37. 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].

  38. Kang HG, Ha IS, Cheong HI. Recurrence and Treatment after Renal Transplantation in Children with FSGS. Biomed Res Int. 2016. 2016:6832971. [Medline]. [Full Text].

  39. 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.

  40. Han KH, Kim SH. Recent Advances in Treatments of Primary Focal Segmental Glomerulosclerosis in Children. Biomed Res Int. 2016. 2016:3053706. [Medline].

  41. 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].

  42. 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].

  43. 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].

  44. 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].

  45. 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].

  46. Korbet SM. Angiotensin antagonists and steroids in the treatment of focal segmental glomerulosclerosis. Semin Nephrol. 2003 Mar. 23(2):219-28. [Medline].

  47. Korbet SM. Treatment of primary focal segmental glomerulosclerosis. Kidney Int. 2002 Dec. 62(6):2301-10. [Medline].

  48. 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].

  49. 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].

  50. Rudnicki M. FSGS Recurrence in Adults after Renal Transplantation. Biomed Res Int. 2016. 2016:3295618. [Medline].

 
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