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Nefrología (Madrid)

versão On-line ISSN 1989-2284versão impressa ISSN 0211-6995

Resumo

PECES, Ramón et al. Medical therapy with tranexamic acid in autosomal dominant polycystic kidney disease patients with severe haematuria. Nefrología (Madr.) [online]. 2012, vol.32, n.2, pp.160-165. ISSN 1989-2284.

Background: Gross haematuria is a common manifestation of autosomal dominant polycystic kidney disease (ADPKD). It can be spontaneous or can result from trauma, renal calculi, tumour, or infection. Spontaneous cyst bleeding is important to consider in this particular group of patients, since it can be prolonged by local activation of fibrinolysis by urokinase. The management of haematuria in ADPKD is usually conservative, including bed rest, blood transfusion, correction of coagulopathies, and use of DDAVP, and erythropoietin stimulating agents. In some patients, the management of gross or life-threatening haematuria may require embolization and/or nephrectomy. Nonetheless, other modalities have been tried to avoid prolonged hospitalization and nephrectomy and to preserve kidney function. These include the use of anti-fibrinolytics. Tranexamic acid was recently suggested as a tool to treat gross haematuria in ADPKD, in single isolated cases. Objective: The aim of this study was to evaluate prospectively the response to tranexamic acid administration in a group of 8 patients with ADPKD and gross haematuria unresponsive to conventional treatment. Results: The massive bleeding promptly stopped within 2 to 5 days in all patients. The haemoglobin level and renal function subsequently stabilized. There were not side effects including thromboembolic events. In this case series, the largest prospective one study so far published and the only one including different degrees of renal function, tranexamic acid is confirmed as a promising tool for treating haematuria due to intracystic bleeding in ADPKD. Conclusions: In summary, tranexamic acid can be used safely in some ADPKD patients with chronic renal impairment or preserved renal function to treat severe haematuria poorly responsive to conventional therapy. Tranexamic acid can be administered orally or IV; and dose adjustment for renal impairment is important. Tranexamic acid therapy may preserve renal function in ADPKD, directly, by stopping haematuria episodes, or indirectly, by avoidance of embolization and/or nephrectomy. The major limitation of this study is the small sample size and the lack of an untreated control group. We suggest a prospective, randomized controlled study to confirm the efficacy of this treatment, its long-term safety, and the optimal dosage. Further larger and multicenter studies are needed to evaluate the cost-benefit ratio and the limits of this therapy in the clinical setting.

Palavras-chave : Tranexamic acid; Antifibrinolytic; Renal function; Haematuria; Cyst bleeding; ADPKD.

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