Prevention and Treatment of Acute Renal Failure in Sepsis

Vriese, An S. De

doi:10.1097/01.asn.0000055652.37763.f7

Cited by 113 publications

(46 citation statements)

References 130 publications

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“…As LPS itself has only a very little direct effect on the kidney (38), cytokines such as TNF-␣ or IL-1␤ have been implicated in LPS-mediated leukocyte recruitment during sepsis. LPS is the most effective inducer of TNF-␣ by monocytes and can also lead to TNF-␣ secretion by lymphocytes (22,39).…”

Section: Discussionmentioning

confidence: 99%

T Cells Modulate Neutrophil-Dependent Acute Renal Failure during Endotoxemia

Singbartl

Bockhorn

Zarbock

et al. 2005

Journal of the American Society of Nephrology

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Section: Discussionmentioning

confidence: 99%

T Cells Modulate Neutrophil-Dependent Acute Renal Failure during Endotoxemia

Singbartl

Bockhorn

Zarbock

et al. 2005

Journal of the American Society of Nephrology

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“…No efficient treatment is available to reverse these deleterious characteristics of ARF; thus, ARF treatment today is more "supportive" than curative (23). Alterations in renal hemodynamics seem to be playing a major causative role because the decrease in GFR occurs without evidence of significant tubular obstruction and with only modest early kidney injuries, other than ischemia.…”

Section: Discussionmentioning

confidence: 99%

Thromboxane Receptor Mediates Renal Vasoconstriction and Contributes to Acute Renal Failure in Endotoxemic Mice

Boffa

Just²,

Coffman

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Sepsis is a major cause of acute renal failure (ARF) and death. Thromboxane A2 (TxA 2 ) may mediate decreases of renal blood flow (RBF) and/or GFR associated with LPSinduced sepsis. This study tested whether TxA 2 receptor blockade, with the use of TxA 2 receptor knockout (TP-KO) mice or a selective TP receptor antagonist (SQ29,548), would alleviate LPS-induced renal vasoconstriction and ARF. Under basal conditions, anesthetized TP-KO mice displayed a lower mean arterial pressure than wild-type (WT) mice (102 versus 94 mmHg; P Ͻ 0.05). RBF, renal vascular resistance (RVR), GFR, and urine flow did not differ among groups under basal conditions, suggesting little tonic influence of TxA 2 on renal TP receptors in health. In endotoxemic WT mice, 14 h after LPS (Escherichia coli LPS 8.5 mg/kg intraperitoneally), mean arterial pressure was reduced to 85 mmHg (P Ͻ 0.001), as were RBF (5.0 versus 9.3 ml/min per g kidney wt; P Ͻ 0.001) and GFR (0.38 versus 1.03 ml/min per g kidney wt; P Ͻ 0.001). Heart rate and RVR (71 versus 47 mmHg/ml per min; P Ͻ 0.05) increased. The decreases in RBF and GFR after LPS were attenuated in TP-KO mice versus WT mice (both P Ͻ 0.05). In both TP-KO and TP antagonist-treated mice, RVR remained stable in response to LPS versus WT mice that did not receive LPS. Delayed TP-antagonist treatment (12 h after LPS injection) ameliorated RBF and RVR but did not restore GFR. In other WT animals, TP-antagonist treatment for 2 h before intravenous LPS abolished the early renal vasoconstriction and alleviated the decrease in GFR. These results demonstrate that renal vasoconstriction during endotoxemic shock induced by LPS is mediated by TP receptors as indicated by pharmacologic blockade and genetic disruption of TP receptors.

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“…and Detry et al (120) demonstrated that continuous RRT (CRRT) is better tolerated than intermittent hemodialysis (HD) in patients with liver failure as evidenced by better cardiovascular stability, gradual correction of hyponatremia, and less fluctuation in intracranial pressure. Furthermore, CRRT has the potential advantage of removing inflammatory cytokines, including TNF-␣ and IL-6, both of which have been implicated in the development of HRS and the exacerbation of hepatic injury (66,75,(121)(122)(123). Despite these presumed advantages, in a prospective study by Witzke et al (124), CRRT did not confer a survival benefit in 30 patients who had HRS and were waiting for liver transplantation.…”

Section: Rrtmentioning

confidence: 99%