Bleeding time in Uremia: A useful test to assess clinical bleeding

Steiner, Robert W.; Coggins, Cecil H.; Carvalho, Angelina C. A.

doi:10.1002/ajh.2830070203

Cited by 193 publications

(64 citation statements)

References 21 publications

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“…The modem management of renal failure has reduced the incidence of severe hemorrhages, but bleeding still presents a problem for uremic patients, particularly during surgery or invasive procedures. There is ample evidence that the laboratory test most greatly altered in uremia is the skin bleeding time (2,4). It has been convincingly documented that the defect underlying the prolonged bleeding time of uremia involves the complex process of primary hemostasis (3), but the precise mediator(s) are still undefined.…”

Section: Introductionmentioning

confidence: 99%

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Role of endothelium-derived nitric oxide in the bleeding tendency of uremia.

Remuzzi¹,

Perico²,

Zoja³

et al. 1990

J. Clin. Invest.

116

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Endothelium-derived relaxing factor, now identified as nitric oxide (NO), is a labile humoral agent formed by vascular endothelial cells from L-arginine. NO mediates the action of substances that induce endothelium-dependent relaxation and plays a role in regulating blood pressure. In this study we investigated whether NO is involved in the pathogenesis of the bleeding tendency associated with renal failure. Rats with extensive surgical ablation of renal mass develop renal insufficiency due to progressive glomerulosclerosis. Like uremic humans, rats with renal mass reduction and uremia have a bleeding tendency that manifests itself by a prolonged bleeding time. We found that N-monomethyl-L-arginine (L-NMMA), a specific inhibitor of NO formation from L-arginine, completely normalized bleeding time when given to uremic rats. L-NMMA injection also increased ex vivo platelet adhesion but did not affect ex vivo platelet aggregation induced by adenosine diphosphate, arachidonic acid, and calcium ionophore A23187. The shortening effect of L-NMMA on bleeding time was completely reversed by giving the animals the NO precursor L-arginine, but not D-arginine, which is not a precursor of NO. It thus appears that NO is a mediator of the bleeding tendency of

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Section: Introductionmentioning

confidence: 99%

“…To assess the role of NO in the bleeding tendency of uremia, we used L-NMMA, a specific inhibitor of NO formation from L-arginine. 4 thetized rats using the tail-cuff method ( 16).…”

Section: Introductionmentioning

confidence: 99%

Role of endothelium-derived nitric oxide in the bleeding tendency of uremia.

Remuzzi¹,

Perico²,

Zoja³

et al. 1990

J. Clin. Invest.

116

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“…Cutaneous BT is an overall test of platelet function, and compelling evidence now suggests that BT is the best marker of clinical bleeding in uremia (6,17,18). To assess the mechanism(s) by which ASA inhibits platelet function in uremia, we measured BT in relation to different plasma ASA concentrations in uremic patients and normal subjects.…”

Section: Resultsmentioning

confidence: 99%

“…Serum was assayed at a final dilution of 1:150 to 1:15,000. 5,000 dpm of [3H]TxB2, and sufficient specific rabbit antibodies to bind 40% ofthe tritiated compound were incubated [16][17][18][19][20][21][22][23][24] h at 4°C in a final volume of 1.5 ml in each assay tube. Anti-TxB2 was used at a final dilution of 1:250,000.…”

Section: Methodsmentioning

confidence: 99%

Aspirin prolongs bleeding time in uremia by a mechanism distinct from platelet cyclooxygenase inhibition.

Gaspari¹,

Viganò²,

Orisio³

et al. 1987

J. Clin. Invest.

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We reported that aspirin (ASA) abnormally prolongs bleeding time (BT) in uremia. The present study was designed to investigate whether (a) the abnormally prolonged post-ASA BT in uremia is due to different ASA pharmacokinetics and bioavailability that might be a consequence of uremic condition, (b) platelet cyclooxygenase is peculiarly sensitive to ASA in uremia, and (c) ASA affects primary hemostasis in uremia by a mechanism independent of cyclooxygenase inhibition. Our results showed that in patients with uremia, but not in normal subjects, ASA markedly prolongs the BT. This effect is transient and depends on the presence of ASA in the blood. The observed differences in ASA kinetic parameters are not an explanation of the exaggerated effect of ASA on primary hemostasis in uremia. The sensitivity of platelet cyclooxygenase to ASA inhibition is comparable in uremics and in normal subjects. The temporal dissociation between ASA-induced prolongation of BT and the effect on platelet thromboxane A2 generation suggests that ASA inhibits platelet function in uremia by a mechanism distinct from cyclooxygenase blocking. This possibility is strengthened by the observation that ibuprofen at a dose that fully inhibits platelet cyclooxygenase activity does not significantly prolong BT.

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“…Platelet dysfunction, prolonged bleeding time is the other vascular dysfunctions associated with hyperureamic status of CKD [2]. Thrombosis in glomerular arteries and alterations in platelet count are often observed in CKD.…”

Section: Introductionmentioning

confidence: 99%