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2015 ; 11
(2
): 76-87
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Causes and pathogenesis of focal segmental glomerulosclerosis
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Fogo AB
Nat Rev Nephrol
2015[Feb]; 11
(2
): 76-87
PMID25447132
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Focal segmental glomerulosclerosis (FSGS) describes both a common lesion in
progressive kidney disease, and a disease characterized by marked proteinuria and
podocyte injury. The initial injuries vary widely. Monogenetic forms of FSGS are
largely due to alterations in structural genes of the podocyte, many of which
result in early onset of disease. Genetic risk alleles in apolipoprotein L1 are
especially prevalent in African Americans, and are linked not only to adult-onset
FSGS but also to progression of some other kidney diseases. The recurrence of
FSGS in some transplant recipients whose end-stage renal disease was caused by
FSGS points to circulating factors in disease pathogenesis, which remain
incompletely understood. In addition, infection, drug use, and secondary
maladaptive responses after loss of nephrons from any cause may also cause FSGS.
Varying phenotypes of the sclerosis are also manifest, with varying prognosis.
The so-called tip lesion has the best prognosis, whereas the collapsing type of
FSGS has the worst prognosis. New insights into glomerular cell injury response
and repair may pave the way for possible therapeutic strategies.
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