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2016 ; 27
(11
): 3271-3277
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Loss of Kynurenine 3-Mono-oxygenase Causes Proteinuria
#MMPMID27020856
Korstanje R
; Deutsch K
; Bolanos-Palmieri P
; Hanke N
; Schroder P
; Staggs L
; Bräsen JH
; Roberts IS
; Sheehan S
; Savage H
; Haller H
; Schiffer M
J Am Soc Nephrol
2016[Nov]; 27
(11
): 3271-3277
PMID27020856
show ga
Changes in metabolite levels of the kynurenine pathway have been observed in
patients with CKD, suggesting involvement of this pathway in disease
pathogenesis. Our recent genetic analysis in the mouse identified the kynurenine
3-mono-oxygenase (KMO) gene (Kmo) as a candidate gene associated with
albuminuria. This study investigated this association in more detail. We compared
KMO abundance in the glomeruli of mice and humans under normal and diabetic
conditions, observing a decrease in glomerular KMO expression with diabetes.
Knockdown of kmo expression in zebrafish and genetic deletion of Kmo in mice each
led to a proteinuria phenotype. We observed pronounced podocyte foot process
effacement on long stretches of the filtration barrier in the zebrafish knockdown
model and mild podocyte foot process effacement in the mouse model, whereas all
other structures within the kidney remained unremarkable. These data establish
the candidacy of KMO as a causal factor for changes in the kidney leading to
proteinuria and indicate a functional role for KMO and metabolites of the
tryptophan pathway in podocytes.
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