|Association of histologic variants in FSGS clinical trial with presenting features and outcomes.|
|PMID: 23220425 Owner: NLM Status: MEDLINE|
|BACKGROUND AND OBJECTIVES: FSGS histologic variants have correlated with outcomes in retrospective studies. The FSGS Clinical Trial provided a unique opportunity to study the clinical impact of histologic variants in a well defined prospective cohort with steroid-resistant primary FSGS.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Renal biopsies of 138 FSGS Clinical Trial participants aged 2-38 years enrolled from 2004 to 2008 were analyzed using the Columbia classification by core pathologists. This study assessed the distribution of histologic variants and examined their clinical and biopsy characteristics and relationships to patient outcomes.
RESULTS: The distribution of histologic variants was 68% (n=94) FSGS not otherwise specified, 12% (n=16) collapsing, 10% (n=14) tip, 7% (n=10) perihilar, and 3% (n=4) cellular. Individuals with not otherwise specified FSGS were more likely to have subnephrotic proteinuria (P=0.01); 33% of teenagers and adults had tip or collapsing variants compared with 10% of children, and subjects with these variants had greater proteinuria and hypoalbuminemia than not otherwise specified patients. Tip variant had the strongest association with white race (86%) and the lowest pathologic injury scores, baseline creatinine, and rate of progression. Collapsing variant had the strongest association with black race (63%, P=0.03) and the highest pathologic injury scores (P=0.003), baseline serum creatinine (P=0.003), and rate of progression. At 3 years, 47% of collapsing, 20% of not otherwise specified, and 7% of tip variant patients reached ESRD (P=0.005).
CONCLUSIONS: This is the first prospective study with protocol-defined immunomodulating therapies confirming poor renal survival in collapsing variant and showing better renal survival in tip variant among steroid-resistant patients.
|Vivette D D'Agati; Joan M Alster; J Charles Jennette; David B Thomas; James Pullman; Daniel A Savino; Arthur H Cohen; Debbie S Gipson; Jennifer J Gassman; Milena K Radeva; Marva M Moxey-Mims; Aaron L Friedman; Frederick J Kaskel; Howard Trachtman; Charles E Alpers; Agnes B Fogo; Tom H Greene; Cynthia C Nast|
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|Type: Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural Date: 2012-12-06|
|Title: Clinical journal of the American Society of Nephrology : CJASN Volume: 8 ISSN: 1555-905X ISO Abbreviation: Clin J Am Soc Nephrol Publication Date: 2013 Mar|
|Created Date: 2013-03-08 Completed Date: 2013-08-26 Revised Date: 2014-01-10|
Medline Journal Info:
|Nlm Unique ID: 101271570 Medline TA: Clin J Am Soc Nephrol Country: United States|
|Languages: eng Pagination: 399-406 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
Adrenal Cortex Hormones / therapeutic use
Biological Markers / blood
Creatinine / blood
European Continental Ancestry Group
Glomerulosclerosis, Focal Segmental / drug therapy, ethnology, pathology*
Hypoalbuminemia / ethnology, pathology
Immunosuppressive Agents / therapeutic use
Kidney / drug effects, pathology*
Kidney Failure, Chronic / ethnology, pathology
Predictive Value of Tests
Proportional Hazards Models
Proteinuria / ethnology, pathology
Severity of Illness Index
United States / epidemiology
|DK063455/DK/NIDDK NIH HHS; DK063490/DK/NIDDK NIH HHS; DK063549/DK/NIDDK NIH HHS; DK80095/DK/NIDDK NIH HHS; UL1 TR000124/TR/NCATS NIH HHS; UO1-DK063385/DK/NIDDK NIH HHS|
|0/Adrenal Cortex Hormones; 0/Biological Markers; 0/Immunosuppressive Agents; AYI8EX34EU/Creatinine|
Nat Rev Nephrol. 2013 Feb;9(2):65
Clin J Am Soc Nephrol. 2013 Mar;8(3):344-6 [PMID: 23430205 ]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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