Key result
DDAH overexpression decreased plasma ADMA levels and inhibited the deterioration of renal dysfunction, peritubular capillary loss, and tubulointerstitial fibrosis in a rat model of CKD.
Why the study?
Does DDAH overexpression prevent progression of renal dysfunction in a rat model of chronic kidney disease?
Population
Rat remnant kidney model (five-sixths subtotal nephrectomy)
Comparison
Recombinant adenovirus vector encoding DDAH-I… vs Control vector expressing bacterial…
Design
Preclinical
Authors
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Hypothesis-generating in rat CKD; does not support clinical use of DDAH modulation.
Does DDAH overexpression prevent progression of renal dysfunction in a rat model of chronic kidney disease?
DDAH overexpression lowers ADMA levels and prevents the progression of renal dysfunction and fibrosis in a rat model of chronic kidney disease.
Matsumoto et al. (2007) studied Chronic Kidney Disease (rat model). Recombinant adenovirus vector encoding DDAH-I (Adv-DDAH) vs. Control vector (Adv-LZ) or hydralazine (Hyz) was evaluated on Renal dysfunction, peritubular capillary loss, and tubulointerstitial fibrosis. DDAH overexpression decreased plasma ADMA levels and inhibited the deterioration of renal dysfunction, peritubular capillary loss, and tubulointerstitial fibrosis in a rat model of CKD.
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