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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+Negl+Trop+Dis
2017 ; 11
(5
): e0005615
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Lp25 membrane protein from pathogenic Leptospira spp is associated with
rhabdomyolysis and oliguric acute kidney injury in a guinea pig model of
leptospirosis
#MMPMID28505191
Abreu PAE
; Seguro AC
; Canale D
; Silva AMGD
; Matos LDRB
; Gotti TB
; Monaris D
; Jesus DA
; Vasconcellos SA
; de Brito T
; B Magaldi AJ
PLoS Negl Trop Dis
2017[May]; 11
(5
): e0005615
PMID28505191
show ga
Acute kidney injury (AKI) from leptospirosis is frequently nonoliguric with hypo-
or normokalemia. Higher serum potassium levels are observed in non-survivor
patients and may have been caused by more severe AKI, metabolic disarrangement,
or rhabdomyolysis. An association between the creatine phosphokinase (CPK) level
and maximum serum creatinine level has been observed in these patients, which
suggests that rhabdomyolysis contributes to severe AKI and hyperkalemia. LipL32
and Lp25 are conserved proteins in pathogenic strains of Leptospira spp., but
these proteins have no known function. This study evaluated the effect of these
proteins on renal function in guinea pigs. Lp25 is an outer membrane protein that
appears responsible for the development of oliguric AKI associated with
hyperkalemia induced by rhabdomyolysis (e.g., elevated CPK, uric acid and serum
phosphate). This study is the first characterization of a leptospiral outer
membrane protein that is associated with severe manifestations of leptospirosis.
Therapeutic methods to attenuate this protein and inhibit rhabdomyolysis-induced
AKI could protect animals and patients from severe forms of this disease and
decrease mortality.