Focal Segmental Glomerulosclerosis: Difference between revisions

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* FSGS is broadly categorized into primary (idiopathic) and secondary forms, and such distinction carries both prognostic and therapeutic implications<ref name=":0">Sangameswaran KD, Baradhi KM. [https://www.ncbi.nlm.nih.gov/books/NBK532272/ Focal Segmental Glomerulosclerosis].2019 Available from:https://www.ncbi.nlm.nih.gov/books/NBK532272/ (last accessed 21.10.2020)</ref>
* FSGS is broadly categorized into primary (idiopathic) and secondary forms, and such distinction carries both prognostic and therapeutic implications<ref name=":0">Sangameswaran KD, Baradhi KM. [https://www.ncbi.nlm.nih.gov/books/NBK532272/ Focal Segmental Glomerulosclerosis].2019 Available from:https://www.ncbi.nlm.nih.gov/books/NBK532272/ (last accessed 21.10.2020)</ref>
== Epidemiology  ==
== Epidemiology  ==
 
* The exact incidence and prevalence data of FSGS is difficult to ascertain due to significant racial and geographical differences in incidence. The estimated incidence of FSGS is about 7 per 1 million with a prevalence of 4%.  
The exact incidence and prevalence data of FSGS is difficult to ascertain due to significant racial and geographical differences in incidence.  
 
The estimated incidence of FSGS is about 7 per 1 million with a prevalence of 4%.  
* In the United States, approximately 50% of nephrotic syndrome is attributed to FSGS.  
* In the United States, approximately 50% of nephrotic syndrome is attributed to FSGS.  
* The prevalence of FSGS has gradually increased over the years, and it is the most common primary glomerular process contributing to [[Chronic Kidney Disease|end-stage renal disease]] in the United States.  
* The prevalence of FSGS has gradually increased over the years, and it is the most common primary glomerular process contributing to [[Chronic Kidney Disease|end-stage renal disease]] in the United States.  
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== Characteristics/Clinical Presentation  ==
== Characteristics/Clinical Presentation  ==
 
* Children with focal segmental glomerular sclerosis (FSGS) typically present with the full-blown nephrotic syndrome ([[Peripheral Edema|edema]], massive proteinuria, hypoalbuminemia, hypercholesterolemia).  
It is possible for there to be no signs or symptoms when in the early stages of FSGS. Typically the first sign that a patient commonly recognizes is edema, especially in the legs, and sudden weight gain.<ref name="University">University of North Carolina Kidney Center. Focal Segmental Glomerulosclerosis (FSGS). Available at: http://www.unckidneycenter.org/kidneyhealthlibrary/fsgs.html. Accessed March 16, 2011.</ref>
* Adults can have nephrotic or sub-nephrotic proteinuria, [[Blood Pressure|hypertension]], microscopic hematuria, or present with renal insufficiency.  
 
* Patients with primary FSGS often have profound hypoalbuminemia and edema, but these are rare in secondary forms<ref name=":0" />.
Signs and Symptoms: <ref name="University" /><ref name="Rao">Rao TS, Soman AS. eMedicine from WebMD. Focal Segmental Glomerulosclerosis. February 17, 2009. Available at: http://emedicine.medscape.com/article/245915-overview. Accessed March 16, 2011.</ref><ref name="McMillan">McMillan JI. The Merck Manuals Online Medical Library. Nephrotic Syndrome (Focal Segmental Glomerulosclerosis). January 2010. Available at: http://www.merckmanuals.com/professional/sec17/ch235/ch235c.html#sec17-ch235-ch235c-879. Accessed March 16, 2011.</ref><ref name="Patel">Patel P. Medline Plus. Focal Segmental Glomerulosclerosis. May 20, 2009. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000478.htm. Accessed March 16, 2011.</ref><br>&nbsp;&nbsp;&nbsp;&nbsp; • Massive proteinuria and foamy urine appearance<br>&nbsp;&nbsp;&nbsp;&nbsp; • Edema, swelling and associated weight gain<br>&nbsp;&nbsp;&nbsp;&nbsp; • Hypertension<br>&nbsp;&nbsp;&nbsp;&nbsp; • Renal dysfunction with increased creatinine levels<br>&nbsp;&nbsp;&nbsp;&nbsp; • Hypoalbuminemia<br>&nbsp;&nbsp;&nbsp;&nbsp; • Hyperlipidemia<br>&nbsp;&nbsp;&nbsp;&nbsp; • Microscopic hematuria is occasionally present<br>&nbsp;&nbsp;&nbsp;&nbsp; • Fatigue<br>&nbsp;&nbsp;&nbsp;&nbsp; • Poor appetite<br>&nbsp;&nbsp;&nbsp;&nbsp; • Headache<br>&nbsp;&nbsp;&nbsp;&nbsp; • Itchy skin<br>&nbsp;&nbsp;&nbsp;&nbsp; • Shortness of air<br>&nbsp;&nbsp;&nbsp;&nbsp; • Nausea
 
== Associated Co-morbidities  ==
 
See etiology/causes for a full list of co-morbidities associated with primary and secondary FSGS.<br>
 
== Medications  ==
 
The goals of pharmacotherapy are to preserve renal function, reduce morbidity, and to prevent complications.<ref name="Rao" /> Patients with FSGS should be treated with angiotensin inhibition, an ACE inhibitor or an angiotensin II receptor blocker in order to help decrease protein loss and blood pressure.<ref name="McMillan" /> Patients with nephrotic syndrome should be treated with a statin. The primary disorder should be treated in patients with secondary FSGS. A trial of immunosuppressive therapy, corticosteroids and sometimes cytotoxic drugs, is indicated in idiopathic FSGS if proteinuria reaches the nephrotic range or if renal dysfunction is present.<ref name="McMillan" />  


== Diagnostic Tests/Lab Tests/Lab Values  ==
== Diagnostic Tests/Lab Tests/Lab Values  ==


A Urinalysis is commonly used to evaluate Blood Urea Nitrogen (BUN), serum creatinine, and 24-hour urinary protein excretion.<ref name="McMillan" /> A Urinalysis usually reveals large amounts of protein, along with hyaline and broad waxy casts, whereas RBC casts are generally absent.<ref name="Rao" /> A Kidney biopsy however, is the most definitive way to establish the diagnosis of FSGS. The biopsy typically shows focal and segmental hyalinization of the glomeruli, often with immunostaining showing IgM and complement (C3) deposits in a nodular and coarse granular pattern.<ref name="McMillan" /> In HIV-associated FSGS, an ultrasound generally reveals large echogenic kidneys.<ref name="Rao" />  
A Urinalysis is commonly used to evaluate Blood Urea Nitrogen (BUN), serum creatinine, and 24-hour urinary protein excretion.<ref name="McMillan">McMillan JI. The Merck Manuals Online Medical Library. Nephrotic Syndrome (Focal Segmental Glomerulosclerosis). January 2010. Available at: http://www.merckmanuals.com/professional/sec17/ch235/ch235c.html#sec17-ch235-ch235c-879. Accessed March 16, 2011.</ref> A Urinalysis usually reveals large amounts of protein, along with hyaline and broad waxy casts, whereas RBC casts are generally absent.<ref name="Rao">Rao TS, Soman AS. eMedicine from WebMD. Focal Segmental Glomerulosclerosis. February 17, 2009. Available at: http://emedicine.medscape.com/article/245915-overview. Accessed March 16, 2011.</ref> A Kidney biopsy however, is the most definitive way to establish the diagnosis of FSGS. The biopsy typically shows focal and segmental hyalinization of the glomeruli, often with immunostaining showing IgM and complement (C3) deposits in a nodular and coarse granular pattern.<ref name="McMillan" /> In HIV-associated FSGS, an ultrasound generally reveals large echogenic kidneys.<ref name="Rao" />  


== Etiology/Causes  ==
== Etiology/Causes  ==
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* Viral causes include [[HIV/AIDS|HIV]], parvo B19, CMV, [[Cytomegalovirus (CMV) Infection|EBV]], [[Hepatitis A, B, C|hepatitis]] C, and Simian virus.
* Viral causes include [[HIV/AIDS|HIV]], parvo B19, CMV, [[Cytomegalovirus (CMV) Infection|EBV]], [[Hepatitis A, B, C|hepatitis]] C, and Simian virus.
Drugs
Drugs
* Drugs associated with FSGS include heroin, interferon, lithium, pamidronate, mTOR inhibitors, anabolic steroid
* Drugs associated with FSGS include heroin, interferon, lithium, pamidronate, mTOR inhibitors, anabolic steroid<ref name=":0" />


== Systemic Involvement<ref name="Rao" />  ==
== Systemic Involvement<ref name="Rao" />  ==
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“Severe hypertension with a diastolic blood pressure of 120 mmHg or more is not uncommon, especially in African American patients with renal insufficiency. Rarely, patients experience severe renal failure with signs and symptoms of advanced uremia (nausea, vomiting, bleeding, seizures) or altered mental status.”  
“Severe hypertension with a diastolic blood pressure of 120 mmHg or more is not uncommon, especially in African American patients with renal insufficiency. Rarely, patients experience severe renal failure with signs and symptoms of advanced uremia (nausea, vomiting, bleeding, seizures) or altered mental status.”  


== Medical Management (current best evidence) ==
== Medical Management  ==
 
* Glucocorticoids (daily or every other day) are the first line of treatment in children and adults with focal segmental glomerular sclerosis (FSGS). Patients who are resistant or intolerant to steroids are treated with immunosuppressive therapy with calcineurin inhibitors (CNI), mycophenolate mofetil, or rituximab.  
Some of the medical management for FSGS can already be found in the medication section above. However, treatment for FSGS can be divided into nonspecific or specific treatment.  
* In patients with subnephrotic proteinuria, adaptive FSGS, a trial of RAS inhibition, and sodium restriction can be tried.  
 
* In other secondary forms of FSGS, removing the offending agent or treating the underlying disorder is recommended.  
'''Nonspecific Treatment'''<ref name="Rao" /><br>“Treatment goals include maintenance of adequate nutrition, minimization or elimination of proteinuria, and prevention of complications resulting from edema. Controlling hypertension is one of the most important aspects of overall management. Lowering lipid levels is necessary to reduce cardiovascular risk and to possibly delay the progression of renal disease. It is recommended to reduce salt intake to 2g of sodium and to also alter the use of diuretics accordingly. A high level of protein intake may further aggravate proteinuria, adversely affecting renal function. Current recommendations advise intake of 1-1.3g of high biologic protein per kilogram of body weight and a reduction of fat intake.”
* Optimization of blood pressure, treatment of edema with diuretics, statin therapy for hypercholesterolemia and anticoagulation in select patients at risk for thrombosis/embolization are indicated.
 
* Children respond within a few weeks, but adults may take months to respond. <ref name=":0" />
'''Specific Treament'''<ref name="Rao" /><br>“Idiopathic FSGS is difficult to treat because of its highly variable clinical course. The specific treatment approach is still experimental, and no consensus has evolved because of a lack of prospective controlled trials. However, current evidence is mostly derived from retrospective analyses and favors the use of prolonged corticosteroid therapy, 6 months or longer, to induce remission in patients with idiopathic FSGS.”
 
== Physical Therapy Management (current best evidence)  ==
 
Due to varying results in case studies and case reports it is however recommended to also monitor patients for bone marrow suppression, and encourage them to drink adequate fluids to prevent hemorrhagic cystitis.<ref name="Rao" /> Despite attempts, some patients continue to deteriorate and progress to ESRD.<ref name="Rao" /> As a Physical Therapist we should have the appropriate tools and resources to inform the patient and their families about treatment choices for ESRD and how to control hypertension and hyperlipidemia. Regular exercise or sports and an appropriate diet should be encouraged in order to help decrease or maintain blood pressure and cholesterol levels. Appropriately informing our patients could also help them in choosing among maintenance hemodialysis, continuous ambulatory peritoneal dialysis, or cadaver or living donor transplantation, when appropriate.<ref name="Rao" />  


Although there are no published studies on exercise or physical therapy management and its effect on FSGS, as physical therapists we must be able to screen for this disease based on patient and family history, etiology/cause, and signs and symptoms. We should ask questions regarding the possible presence of kidney pain that may produce referral patterns, any history of kidney problems, do you have a family history of kidney disease, are you urinating blood or notice any changes in urine, drug use, etc. All of these questions evolve around the characteristics of FSGS and the primary and secondary causes of FSGS. As mentioned in the systemic involvement section, on physical examination patient’s typically present normal except for edema, we should also ask follow up question regarding the edema. If suspicious of a kidney problem, or specifically FSGS, refer to a Medical Doctor for further evaluation. {{#ev:youtube|mvvsSDQS4G4}}<ref>Alonzo Mourning. Overcomes Disease and Inspires Others. Available from: http://www.youtube.com/watch?v=mvvsSDQS4G4 [Last Accessed 04/05/11]</ref>  
== Physical Therapy Management  ==
* Regular [[Therapeutic Exercise|exercise]] or sports and an appropriate diet should be encouraged in order to help decrease or maintain blood pressure and cholesterol levels.
* [[Renal Rehabilitation]] if available is recommended
* Appropriately informing our patients could also help them in choosing among maintenance hemodialysis, continuous ambulatory peritoneal dialysis, or cadaver or living donor transplantation, when appropriate.<ref name="Rao" />
{{#ev:youtube|mvvsSDQS4G4}}<ref>Alonzo Mourning. Overcomes Disease and Inspires Others. Available from: http://www.youtube.com/watch?v=mvvsSDQS4G4 [Last Accessed 04/05/11]</ref>  


== Dietary Management (current best evidence) ==
== Dietary Management  ==


Low sodium or sodium free diets, as well as Vitamin D supplementation are usually recommended to patients with FSGS.<ref name="Patel" /> This is important to help lower high lipid values that can place a patient at risk for cardiovascular complications and could help delay the progression toward End Stage Renal Disease.&nbsp;<br>
Low sodium or sodium free diets, as well as Vitamin D supplementation are usually recommended to patients with FSGS.<ref name="Patel">Patel P. Medline Plus. Focal Segmental Glomerulosclerosis. May 20, 2009. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000478.htm. Accessed March 16, 2011.</ref> This is important to help lower high lipid values that can place a patient at risk for cardiovascular complications and could help delay the progression toward End Stage Renal Disease.&nbsp;  


== Differential Diagnosis  ==
== Differential Diagnosis  ==
Line 88: Line 75:
*A 67-year-old woman with chronic proteinuria<ref name="Osunkoya">Osunkoya A, Agte S, Laszik Z. A 67-year-old woman with chronic proteinuria. Focal segmental and global glomerulosclerosis with light microscopic and ultrastructural features consistent with Fabry disease. Archives of Pathology &amp; Laboratory Medicine. 2006 June; 130(6):e93-e95.</ref> [view article in ''[http://web.ebscohost.com.libproxy.bellarmine.edu/ehost/pdfviewer/pdfviewer?sid=02c64f0a-d93c-4b61-bc8a-96ea3f5a66f1%40sessionmgr15&vid=2&hid=12 Archives of Pathology &amp; Laboratory Medicine]]''  
*A 67-year-old woman with chronic proteinuria<ref name="Osunkoya">Osunkoya A, Agte S, Laszik Z. A 67-year-old woman with chronic proteinuria. Focal segmental and global glomerulosclerosis with light microscopic and ultrastructural features consistent with Fabry disease. Archives of Pathology &amp; Laboratory Medicine. 2006 June; 130(6):e93-e95.</ref> [view article in ''[http://web.ebscohost.com.libproxy.bellarmine.edu/ehost/pdfviewer/pdfviewer?sid=02c64f0a-d93c-4b61-bc8a-96ea3f5a66f1%40sessionmgr15&vid=2&hid=12 Archives of Pathology &amp; Laboratory Medicine]]''  
*Successful treatment of recurrent focal segmental glomerulosclerosis after kidney transplantation by plasmapheresis and rituximab<ref name="Hristea">Hristea D, et al. Successful treatment of recurrent focal segmental glomerulosclerosis after kidney transplantation by plasmapheresis and rituximab. Transplant International. 2007 January; 20(1):102-105.</ref> [[http://www.ncbi.nlm.nih.gov/pubmed/17181660 view article abstract on Pubmed]]
*Successful treatment of recurrent focal segmental glomerulosclerosis after kidney transplantation by plasmapheresis and rituximab<ref name="Hristea">Hristea D, et al. Successful treatment of recurrent focal segmental glomerulosclerosis after kidney transplantation by plasmapheresis and rituximab. Transplant International. 2007 January; 20(1):102-105.</ref> [[http://www.ncbi.nlm.nih.gov/pubmed/17181660 view article abstract on Pubmed]]
== Resources    ==
The Nephcure Foundation: http://www.nephcure.org/<br>National Kidney Foundation: http://www.kidney.org/
== References  ==
== References  ==


Revision as of 08:05, 21 October 2020

Original Editors - Jessie O'Donley from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Lead Editors -

Definition/Description[edit | edit source]

Focal Segmental Glomerulosclerosis (FSGS) is a kidney disease that involves the formation of scar tissue in the glomeruli.

  • Frequently encountered cause of nephrotic syndrome, accounting for 40% of cases in adults and 20% in children.
  • Histologically, it is characterized by segmental scarring, involving a part of the glomerulus, and affects some but not all glomeruli sampled.
  • Recent research has shed light on the pathogenesis of FSGS which is podocyte injury and damage, leading to protein loss and subsequent development of focal sclerosing lesions.
  • FSGS is broadly categorized into primary (idiopathic) and secondary forms, and such distinction carries both prognostic and therapeutic implications[1]

Epidemiology[edit | edit source]

  • The exact incidence and prevalence data of FSGS is difficult to ascertain due to significant racial and geographical differences in incidence. The estimated incidence of FSGS is about 7 per 1 million with a prevalence of 4%.
  • In the United States, approximately 50% of nephrotic syndrome is attributed to FSGS.
  • The prevalence of FSGS has gradually increased over the years, and it is the most common primary glomerular process contributing to end-stage renal disease in the United States.
  • The increasing incidence is likely due to improved recognition and detection of the entity, with a better understanding of the pathophysiology of podocyte injury and development of therapy targeting mediators of such injury[1].

Characteristics/Clinical Presentation[edit | edit source]

  • Children with focal segmental glomerular sclerosis (FSGS) typically present with the full-blown nephrotic syndrome (edema, massive proteinuria, hypoalbuminemia, hypercholesterolemia).
  • Adults can have nephrotic or sub-nephrotic proteinuria, hypertension, microscopic hematuria, or present with renal insufficiency.
  • Patients with primary FSGS often have profound hypoalbuminemia and edema, but these are rare in secondary forms[1].

Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]

A Urinalysis is commonly used to evaluate Blood Urea Nitrogen (BUN), serum creatinine, and 24-hour urinary protein excretion.[2] A Urinalysis usually reveals large amounts of protein, along with hyaline and broad waxy casts, whereas RBC casts are generally absent.[3] A Kidney biopsy however, is the most definitive way to establish the diagnosis of FSGS. The biopsy typically shows focal and segmental hyalinization of the glomeruli, often with immunostaining showing IgM and complement (C3) deposits in a nodular and coarse granular pattern.[2] In HIV-associated FSGS, an ultrasound generally reveals large echogenic kidneys.[3]

Etiology/Causes[edit | edit source]

Recent research has shed light on the pathogenesis and etiology of focal segmental glomerular sclerosis (FSGS), which is podocyte injury. Several genetic and acquired causes of podocyte injury have been identified.

Genetic

  • Several genes encoding slit diaphragm proteins, cell membrane proteins, cytoskeleton proteins, nuclear proteins, mitochondrial proteins, and lysosomal proteins have been identified to be abnormal/mutated leading to loss of integrity of glomerular filtration barrier resulting in FSGS.

Circulating Permeability Factor

  • Primary FSGS has long been thought to be due to the presence of circulating permeability factors/cytokines which causes foot process effacement and proteinuria. These include cardiotrophin-like cytokine factor 1, apoA1b, anti-CD40 Ab and suPAR.[5][6][7]

Viruses

  • Viral causes include HIV, parvo B19, CMV, EBV, hepatitis C, and Simian virus.

Drugs

  • Drugs associated with FSGS include heroin, interferon, lithium, pamidronate, mTOR inhibitors, anabolic steroid[1]

Systemic Involvement[3][edit | edit source]

“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 End Stage Renal Disease (ESRD) is 6-8 years, although wide variations in the time course occur. One of the key factors that determine renal survival is the persistence and degree of proteinuria. In patients with unresponsive massive proteinuria of greater than 10 g/d, most will develop ESRD within 5 years.” 

“Pleural effusion and ascites may be present; pericardial effusions are rare. Gross edema may predispose patients to ulcerations and infections in dependent areas, such as the lower extremity. Abdominal pain, a common finding in children, may be a sign of peritonitis. Rarely, xanthomas may be evident in association with severe hyperlipidemia. In many patients, physical examination findings are normal except for generalized or dependent edema.”

“Severe hypertension with a diastolic blood pressure of 120 mmHg or more is not uncommon, especially in African American patients with renal insufficiency. Rarely, patients experience severe renal failure with signs and symptoms of advanced uremia (nausea, vomiting, bleeding, seizures) or altered mental status.”

Medical Management[edit | edit source]

  • Glucocorticoids (daily or every other day) are the first line of treatment in children and adults with focal segmental glomerular sclerosis (FSGS). Patients who are resistant or intolerant to steroids are treated with immunosuppressive therapy with calcineurin inhibitors (CNI), mycophenolate mofetil, or rituximab.
  • In patients with subnephrotic proteinuria, adaptive FSGS, a trial of RAS inhibition, and sodium restriction can be tried.
  • In other secondary forms of FSGS, removing the offending agent or treating the underlying disorder is recommended.
  • Optimization of blood pressure, treatment of edema with diuretics, statin therapy for hypercholesterolemia and anticoagulation in select patients at risk for thrombosis/embolization are indicated.
  • Children respond within a few weeks, but adults may take months to respond. [1]

Physical Therapy Management[edit | edit source]

  • Regular exercise or sports and an appropriate diet should be encouraged in order to help decrease or maintain blood pressure and cholesterol levels.
  • Renal Rehabilitation if available is recommended
  • Appropriately informing our patients could also help them in choosing among maintenance hemodialysis, continuous ambulatory peritoneal dialysis, or cadaver or living donor transplantation, when appropriate.[3]

[4]

Dietary Management[edit | edit source]

Low sodium or sodium free diets, as well as Vitamin D supplementation are usually recommended to patients with FSGS.[5] This is important to help lower high lipid values that can place a patient at risk for cardiovascular complications and could help delay the progression toward End Stage Renal Disease. 

Differential Diagnosis[edit | edit source]

Potential differential diagnoses:[3]
     • minimal-change disease
     • mesangial proliferative glomerulonephritis
     • membranoproliferative glomerulonephritis
     • membranous glomerulonephritis

Case Reports/ Case Studies[edit | edit source]

References[edit | edit source]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Sangameswaran KD, Baradhi KM. Focal Segmental Glomerulosclerosis.2019 Available from:https://www.ncbi.nlm.nih.gov/books/NBK532272/ (last accessed 21.10.2020)
  2. ↑ 2.0 2.1 McMillan JI. The Merck Manuals Online Medical Library. Nephrotic Syndrome (Focal Segmental Glomerulosclerosis). January 2010. Available at: http://www.merckmanuals.com/professional/sec17/ch235/ch235c.html#sec17-ch235-ch235c-879. Accessed March 16, 2011.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Rao TS, Soman AS. eMedicine from WebMD. Focal Segmental Glomerulosclerosis. February 17, 2009. Available at: http://emedicine.medscape.com/article/245915-overview. Accessed March 16, 2011.
  4. ↑ Alonzo Mourning. Overcomes Disease and Inspires Others. Available from: http://www.youtube.com/watch?v=mvvsSDQS4G4 [Last Accessed 04/05/11]
  5. ↑ Patel P. Medline Plus. Focal Segmental Glomerulosclerosis. May 20, 2009. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000478.htm. Accessed March 16, 2011.
  6. ↑ Glick A. Focal segmental glomerulosclerosis: a case study with review of pathophysiology. Nephrology Nursing Journal. 2007 March; 34(2):176-183.
  7. ↑ Lim A, Lydia A, Rim H, Dowling J, Kerr P. Focal segmental glomerulosclerosis and Guillain-Barre syndrome associated with Campylobacter enteritis. Internal Medicine Journal. 2007 October; 37(10):724-728.
  8. ↑ Lowik M, Groenen P, LP, et al. Focal segmental glomerulosclerosis in a patient homozygous for a CD2AP mutation. Kidney International. 2007 November; 72(10):1198-1203.
  9. ↑ Osunkoya A, Agte S, Laszik Z. A 67-year-old woman with chronic proteinuria. Focal segmental and global glomerulosclerosis with light microscopic and ultrastructural features consistent with Fabry disease. Archives of Pathology & Laboratory Medicine. 2006 June; 130(6):e93-e95.
  10. ↑ Hristea D, et al. Successful treatment of recurrent focal segmental glomerulosclerosis after kidney transplantation by plasmapheresis and rituximab. Transplant International. 2007 January; 20(1):102-105.


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