Focal segmental glomerulosclerosis natural history, complications and prognosis: Difference between revisions

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==Prognosis==
==Prognosis==
More than half the patients with focal or segmental glomerulosclerosis develop [[chronic kidney failure]] within 10 years.
The most important poor prognostic factors in focal segmental glomerulosclerosis (FSGS) are(0):
*Massive or nephrotic-range proteinuria
*Level of serum creatinine > 1.3 mg/dL
*Collapsing variant on morphological appearance
*Presence of tubulointerstitial fibrosis
*Absence of remission or partial remission
*Black race
 
According to a 10-year study in 1999, Approximately 50% of patients with heavy proteinuria in the nephrotic-range progress to end-stage renal disease (ESRD) within 3-8 years.(Korbet 1999) In converse, patients with non-nephrotic range proteinuria often have a better prognosis, with a 10-year survival reaching > 80%.<ref name="pmid10382985">{{cite journal| author=Korbet SM| title=Clinical picture and outcome of primary focal segmental glomerulosclerosis. | journal=Nephrol Dial Transplant | year= 1999 | volume= 14 Suppl 3 | issue=  | pages= 68-73 | pmid=10382985 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10382985  }} </ref> While spontaneous remission is highly uncommon in FSGS, occurring in less than 6% of patients, the degree of proteinuria may predict the probability of spontaneous remission.<ref name="pmid10382985">{{cite journal| author=Korbet SM| title=Clinical picture and outcome of primary focal segmental glomerulosclerosis. | journal=Nephrol Dial Transplant | year= 1999 | volume= 14 Suppl 3 | issue=  | pages= 68-73 | pmid=10382985 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10382985  }} </ref>
 
 
 
Serum creatinine > 1.3 mg/dL and interstitial fibrosis > 20% on pathological analysis have been associated with worse renal outcomes.<ref name="pmid10382985">{{cite journal| author=Korbet SM| title=Clinical picture and outcome of primary focal segmental glomerulosclerosis. | journal=Nephrol Dial Transplant | year= 1999 | volume= 14 Suppl 3 | issue=  | pages= 68-73 | pmid=10382985 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10382985  }} </ref> The extent of proteinuria, serum creatinine, and extent of fibrosis on pathological observation have been positively correlated.<ref name="pmid10382985">{{cite journal| author=Korbet SM| title=Clinical picture and outcome of primary focal segmental glomerulosclerosis. | journal=Nephrol Dial Transplant | year= 1999 | volume= 14 Suppl 3 | issue=  | pages= 68-73 | pmid=10382985 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10382985  }} </ref>
 
 
While collapsing variant, commonly seen in HIV-induced FSGS, is associated with poorer outcomes, tip variant correlates with better outcomes.<ref name="pmid16518352">{{cite journal| author=Thomas DB, Franceschini N, Hogan SL, Ten Holder S, Jennette CE, Falk RJ et al.| title=Clinical and pathologic characteristics of focal segmental glomerulosclerosis pathologic variants. | journal=Kidney Int | year= 2006 | volume= 69 | issue= 5 | pages= 920-6 | pmid=16518352 | doi=10.1038/sj.ki.5000160 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16518352  }} </ref> According to Korbet and colleagues, the remission of proteinuria is negatively associated with progression to ESRD in FSGS.<ref name="pmid10382985">{{cite journal| author=Korbet SM| title=Clinical picture and outcome of primary focal segmental glomerulosclerosis. | journal=Nephrol Dial Transplant | year= 1999 | volume= 14 Suppl 3 | issue=  | pages= 68-73 | pmid=10382985 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10382985  }} </ref>


==References==
==References==

Revision as of 22:02, 3 December 2013

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief:’’’ Cafer Zorkun, M.D., Ph.D. [2]

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Overview

Natural History

Complications

Prognosis

The most important poor prognostic factors in focal segmental glomerulosclerosis (FSGS) are(0):

  • Massive or nephrotic-range proteinuria
  • Level of serum creatinine > 1.3 mg/dL
  • Collapsing variant on morphological appearance
  • Presence of tubulointerstitial fibrosis
  • Absence of remission or partial remission
  • Black race

According to a 10-year study in 1999, Approximately 50% of patients with heavy proteinuria in the nephrotic-range progress to end-stage renal disease (ESRD) within 3-8 years.(Korbet 1999) In converse, patients with non-nephrotic range proteinuria often have a better prognosis, with a 10-year survival reaching > 80%.[1] While spontaneous remission is highly uncommon in FSGS, occurring in less than 6% of patients, the degree of proteinuria may predict the probability of spontaneous remission.[1]


Serum creatinine > 1.3 mg/dL and interstitial fibrosis > 20% on pathological analysis have been associated with worse renal outcomes.[1] The extent of proteinuria, serum creatinine, and extent of fibrosis on pathological observation have been positively correlated.[1]


While collapsing variant, commonly seen in HIV-induced FSGS, is associated with poorer outcomes, tip variant correlates with better outcomes.[2] According to Korbet and colleagues, the remission of proteinuria is negatively associated with progression to ESRD in FSGS.[1]

References

  1. 1.0 1.1 1.2 1.3 1.4 Korbet SM (1999). "Clinical picture and outcome of primary focal segmental glomerulosclerosis". Nephrol Dial Transplant. 14 Suppl 3: 68–73. PMID 10382985.
  2. Thomas DB, Franceschini N, Hogan SL, Ten Holder S, Jennette CE, Falk RJ; et al. (2006). "Clinical and pathologic characteristics of focal segmental glomerulosclerosis pathologic variants". Kidney Int. 69 (5): 920–6. doi:10.1038/sj.ki.5000160. PMID 16518352.

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