Renal Endothelin in FK506-Induced Nephrotoxicity in Spontaneously Hypertensive Rats
Why the study?
Does TAK-044 improve renal dysfunction in spontaneously hypertensive rats with FK506-induced nephrotoxicity?
Population
Spontaneously hypertensive rats with FK506-induced nephrotoxicity
Comparison
TAK-044 (ET/ET antagonist) 3 mg/day, s.c… vs FK506 alone (implied)
Design
Preclinical
Follow-up
14 days
Authors
Discussion
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Member takes
Implication
Does not restore GFR despite partial vasoconstriction relief in rats; leaves open dominant mechanisms of FK506 nephrotoxicity beyond endothelin.
Structured PICO
Does TAK-044 improve renal dysfunction in spontaneously hypertensive rats with FK506-induced nephrotoxicity?
P
Population
Spontaneously hypertensive rats with FK506-induced nephrotoxicity
I
Intervention
TAK-044 (ET(A)/ET(B) antagonist) 3 mg/day, s.c. continuous administration
C
Comparator
FK506 alone (implied)
O
Outcome
Renal dysfunction (glomerular filtration rate and renal vasoconstriction)surrogate
Although endothelin-1 gene expression is involved in FK506-induced renal vasoconstriction, endothelin does not play a major role in the overall FK506-induced renal dysfunction.
Cite This Study
Uchida et al. (1998) studied this question.