Heparin-induced thrombocytopenia (HIT) and thrombosis in a haemodialysis-dependent patient with systemic vasculitis

Autor: Jennifer Byrne, S. D. Roe, Michael J. D. Cassidy, A P Haynes
Rok vydání: 1998
Předmět:
Zdroj: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 13(12)
ISSN: 0931-0509
Popis: ature was 37.3°C, pulse 100, BP 170/98 mmHg. The Heparin is widely used for the prevention and treatjugular venous pressure was normal. There were widement of thromboembolic disorders and to prevent spread inspiratory crepitations throughout both lung clotting within the extracorporeal circuit during fields. Urine dipstick showed blood+++ and haemodialysis. Unfortunately a small but significant protein+++. Microscopy revealed red cells and redproportion of patients develop thrombocytopenia cell casts. during heparin exposure and these patients are at risk Haemoglobin was 8.9 g/dl (normochromic normoof potentially severe thromboembolic complications. cytic), white cell count 8.63×109/l, platelets The reported incidence of heparin-induced thrombocy363×109/l. CRP was elevated at 294. Renal function topenia varies widely and is not precisely known. The was severely impaired (urea 46.2 mmol/l, creatinine incidence is generally lower in patients receiving low1035 mmol/l, serum potassium 6.4 mmol/l ). Chest molecular-weight heparins (LMWH) than in those X-ray revealed widespread bilateral interstitial infilttreated with unfractionated heparin. A recent prospectrates. Arterial blood gases on 28% oxygen showed ive study reported an incidence of serologically conpH 7.38, pO2 8.28 kPa (10.0–13.3 kPa) 63 mmHg firmed heparin-induced thrombocytopenia (HIT ) and (85–100 mmHg), 2 4.24 kPa (4.67–6.00 kPa) thrombosis of 0.3% in patients with cardiac and neuro32 mmHg (36–44 mmHg). Autoantibody screening logical diseases treated with unfractionated heparin was negative, serum immunoglobulins were normal [1]. In the dialysis population Yamamato et al. [2] with no paraprotein band on electrophoresis; C4 was report an incidence of HIT of 3.9%. Exposure to normal, C3 minimally elevated at 1.8 g/l (0.8–1.7 g/l ). heparin in line flushes or thromboprophylaxis as well Antiglomerular basement membrane antibodies were as therapeutic doses has been associated with HIT. negative. ANCA was positive with a cytoplasmic patClinically two types of HIT are described; type I is a tern (titre 160) and antiproteinase 3 antibodies were mild, early-onset thrombocytopenia, often asymptodetected by EIA. Carbon monoxide transfer coefficient matic, which usually resolves (even if heparin is conwas elevated (2.91 mmol/min/kPa/l–predicted result tinued); type II is of later onset (typically 4–14 days 1.33 mmol/min/kPa/l ). after the start of heparin therapy), produces more Renal biopsy contained 30 glomeruli, one-third of severe thrombocytopenia (often below 60×109/l ), which were completely sclerosed. The rest showed a which continues until heparin is withdrawn and may segmental proliferative glomerulonephritis with necbe associated with thrombotic complications [3]. rosis and universal crescent formation. The interstitium Here we report on a patient with acute renal failure showed tubular atrophy, interstitial fibrosis and a and pulmonary haemorrhage who developed HIT chronic inflammatory cell infiltrate. There were no associated with an extensive deep venous thrombosis significant deposits on immunofluorescence or electron after commencement of haemodialysis. Management microscopy. of this uncommon though life-threatening problem is A diagnosis of ANCA associated pauci-immune discussed. cresenteric glomerulonephritis with pulmonary haem
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