URINE i-TXB2 IN RENAL ALLOGRAFT REJECTION

Foegh, Marie L.; Zmudka, M.; Cooley, C. O.; Winchester, J F; Helfrich, G.B.; Ramwell, Peter W.; Schreiner, G. E.

doi:10.1016/s0140-6736(81)90772-8

Cited by 95 publications

(22 citation statements)

References 14 publications

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“…Because leukocytes and various renal cells produce locally vasoactive eicosanoids, alterations in prostaglandin (PG) and thromboxane (TX) metabolism may play an important role in renal allograft rejection. For example, Foegh et al (5,6) reported that urinary immunoreactive thromboxane B2 (TXB2) increases during episodes of acute rejection in human renal allograft recipients. However, the source of the TXB2 that is excreted in urine and the physiologic significance of increased urinary TX is currently unknown (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Functional role of thromboxane production by acutely rejecting renal allografts in rats.

Coffman¹,

Yarger²,

Klotman³

1985

J. Clin. Invest.

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We investigated the role of thromboxane in mediating the reduction in renal function and renal blood flow characteristic of acute renal allograft rejection. We transplanted kidneys from Lewis rats to Brown-Norway recipients. By the third day after transplantation, histologic changes that were consistent with cellular rejection occurred in the kidney. These changes were associated with a moderate reduction in renal function. By day 6, histologic changes of rejection were advanced and included interstitial and perivascular infiltration by mononuclear cells. The clearances of inulin and para-aminohippuric acid were also markedly reduced.As renal function deteriorated, thromboxane B2 (TXB2) production by ex vivo perfused renal allografts increased progressively from 2 to 6 d after transplantation. However, prostaglandin (PG) E2 and 6-keto PGFI. production remained essentially unchanged. There was a significant inverse correlation between the in vivo clearance of inulin and the log of ex vivo TXB2 production. Infusion of the thromboxane synthetase inhibitor UK-37248-01 into the renal artery of 3-d allografts significantly decreased urinary TXB2 excretion and significantly increased renal blood flow (RBF) and glomerular filtration rate (GFR). Although renal function improved significantly after the acute administration of UK-37248-O1, GFR and RBF did not exceed 33 and 58% of native control values, respectively. In other animals, daily treatment with cyclophosphamide improved the clearances of inulin and para-aminohippuric acid and reduced thromboxane production by 6-d renal allografts. These studies demonstrate that histologic evidence of rejection is associated with increased renal thromboxane production. Inhibition of thromboxane synthetase improves renal function in 3-d allografts. Cytotoxic therapy improves renal function, reduces mononuclear cell infiltration, and decreases allograft thromboxane production. Thus, the potent vasoconstrictor thromboxane A2 may play a role in the impairment of renal function and renal blood flow during acute allograft rejection.

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Section: Introductionmentioning

confidence: 99%

Functional role of thromboxane production by acutely rejecting renal allografts in rats.

Coffman¹,

Yarger²,

Klotman³

1985

J. Clin. Invest.

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“…Re-cently, it has been reported that urinary excretion of TXB 2 was increased in patients with renal allograft rejection, systemic lupus erythematosus, or hepatorenal syndrome. 8 " 10 As TXA 2 is a vasoconstrictor, TXA 2 is thought to be involved in the modulation of vascular tone." However, the role of TXA 2 in the regulation of blood pressure and renal function has not been fully elucidated.…”

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confidence: 99%

Role of thromboxane A2 in the hypotensive effect of captopril in essential hypertension.

et al. 1988

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“…A possible role for TXA2 in human transplant rejection was first proposed by the studies of Foegh et al (34), who measured the levels of TXB2 (the stable metabolite of TXA2) in daily urine samples from 12 patients after renal transplantation and demonstrated a several-fold increase in urinary TXB2 excretion during episodes of acute rejection. In the vast majority of cases, the increase in TXB2 excretion preceded the increase in serum creatinine and the clinical diagnosis of rejection.…”

Section: Thromboxane A2 In Transplantationmentioning

confidence: 99%

Prostanoids modulate inflammation and alloimmune responses during graft rejection

Rocha

Carvalho

2005

Braz J Med Biol Res

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Acute rejection of a transplanted organ is characterized by intense inflammation within the graft. Yet, for many years transplant researchers have overlooked the role of classic mediators of inflammation such as prostaglandins and thromboxane (prostanoids) in alloimmune responses. It has been demonstrated that local production of prostanoids within the allograft is increased during an episode of acute rejection and that these molecules are able to interfere with graft function by modulating vascular tone, capillary permeability, and platelet aggregation. Experimental data also suggest that prostanoids may participate in alloimmune responses by directly modulating T lymphocyte and antigen-presenting cell function. In the present paper, we provide a brief overview of the alloimmune response, of prostanoid biology, and discuss the available evidence for the role of prostaglandin E2 and thromboxane A2 in graft rejection.

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URINE i-TXB2 IN RENAL ALLOGRAFT REJECTION

Cited by 95 publications

References 14 publications

Functional role of thromboxane production by acutely rejecting renal allografts in rats.

Functional role of thromboxane production by acutely rejecting renal allografts in rats.

Role of thromboxane A2 in the hypotensive effect of captopril in essential hypertension.

Prostanoids modulate inflammation and alloimmune responses during graft rejection

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