Kidney international
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Kidney international · Aug 2004
Clinical TrialThe urine-blood PCO gradient as a diagnostic index of H(+)-ATPase defect distal renal tubular acidosis.
Urine pH during acidemia and urine PCO2 upon alkalization both may be useful to indicate H+ secretion from collecting ducts. The urine anion gap has been used to detect urinary NH4+ for differential diagnosis of hyperchloremic metabolic acidosis. We have previously demonstrated that the lack of normal H(+)-ATPase may underlie secretory defect distal renal tubular acidosis (dRTA). In this study we evaluated the diagnostic value of the urine-blood (U-B) PCO2 in H(+)-ATPase defect dRTA, and compared it with that of urine pH and urine anion gap during acidemia. ⋯ The U-B PCO2 during NaHCO3 loading is an excellent diagnostic index of H(+)-ATPase defect dRTA.
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Kidney international · Aug 2004
EPO and alpha-MSH prevent ischemia/reperfusion-induced down-regulation of AQPs and sodium transporters in rat kidney.
Ischemia-induced acute renal failure (ARF) is known to be associated with significant impairment of urinary concentrating ability and down-regulation of renal aquaporins (AQPs) and sodium transporters in rats. We tested whether treatment with erythropoietin (EPO) or alpha-melanocyte-stimulating hormone (alpha-MSH) in combination with EPO reduces the renal ischemia/reperfusion (I/R) injury and prevents the down-regulation of renal AQPs and major sodium transporters. ⋯ EPO and/or alpha-MSH treatment significantly prevent I/R-induced injuries such as urinary-concentrating defects and down-regulation of renal AQPs and sodium transporters.
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Kidney international · Aug 2004
ReviewEndothelial injury and dysfunction: role in the extension phase of acute renal failure.
The pathophysiology of ischemic acute renal failure (ARF) involves a complex interplay between renal hemodynamics, tubular and endothelial cell injury, and inflammatory processes. A growing body of evidence supports the contribution of altered renal vascular function, especially at the microvascular level, in initiating and subsequently extending the initial tubular injury. The extension phase of ischemic ARF involves continued reduction in renal perfusion, ongoing hypoxia, and inflammatory processes that occur during reperfusion and contribute to continued tubular cell injury. ⋯ Vascular congestion, edema formation, diminished blood flow, and infiltration of inflammatory cells have been documented in the corticomedullary junction of the kidney. However, linking their genesis to microvascular endothelial injury and dysfunction has been difficult. New diagnostic and therapeutic approaches to ischemic ARF must incorporate these finding to devise early recognition strategies and therapeutic approaches.
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Kidney international · Aug 2004
Tissue kallikrein attenuates salt-induced renal fibrosis by inhibition of oxidative stress.
High salt intake induces hypertension, cardiac hypertrophy, and progressive renal damage. Progressive renal injury is the consequence of a process of destructive fibrosis. Using gene transfer approach, we have shown that the tissue kallikrein-kinin system (KKS) plays an important role in protection against renal injury in several hypertensive rat models. In this study, we further investigated the effect and potential mechanisms mediated by kallikrein on salt-induced renal fibrosis. ⋯ These results indicate that tissue kallikrein protects against renal fibrosis in hypertensive DSS rats through increased nitric oxide bioavailability and suppression of oxidative stress and TGF-beta expression.
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Kidney international · Aug 2004
Smad3 deficiency attenuates renal fibrosis, inflammation,and apoptosis after unilateral ureteral obstruction.
Transforming growth factor-beta (TGF-beta) has been implicated in the development of renal fibrosis induced by unilateral ureteral obstruction (UUO). However, there is little information on signaling pathways mediating TGF-beta activity involved in molecular and cellular events leading to renal fibrosis induced by UUO. In this study, we sought to determine whether Smad3, a major signaling component of TGF-beta, mediated renal fibrosis induced by UUO. ⋯ Smad3 deficiency attenuated renal fibrosis, inflammation, and apoptosis after UUO, suggesting that Smad3 was a key molecule mediating TGF-beta activity leading to real fibrosis after UUO.