#3140 THE WEST OF SCOTLAND AND THROMBOTIC MICROANGIOPATHY

Abstract Background and Aims Thrombotic microangiopathy (TMA) is a diagnosis made on tissue biopsy manifesting as acute organ dysfunction. It has variety of causes broadly categorised as: primary hereditary/genetic, acquired, secondary, infection-related [1]. On blood testing there evidence microangiopathic haemolytic anaemia (MAHA) –, thrombocytopenia, raised lactate dehydrogenase (LDH), reduced haptoglobin fragments film. Renal involvement with injury evidenced by an elevation in creatinine; together MAHA this uraemic syndrome (HUS). We sought to examine the TMA/MAHA population it presented nephrology West Scotland evaluate if was differences presentation between TMA without MAHA. Method This retrospective case series adult patients. extracted health data from west renal electronic patient records database Strathclyde Electronic Patient Record (“SERPR”) provided VitalDataClient. ran query identify patients whom and/or HUS inputted diagnosis. 363 were identified. Each manually inspected. Patients excluded who not suitable for inclusion (e.g. paediatric data, incomplete records, relevant diagnoses). Non-parametric Kruskal Wallis used via R statistical software. Results 134 The underlying diagnoses were: hypertension (n = 34), atypical (aHUS, n 22), drug-induced 17), autoimmune 12,), thrombotic thrombocytopenic purpura 12), malignancy 10), inflammatory peri-partum 9). Others included: transplant-related, unknown, Ecoli 0157, diarrhoea-related, IgA, AAV, MPGN, essential thrombocythaemia. Note: many had multiple possible contributors their average biochemical levels at creatinine 591umol/L; haemoglobin 82; platelet count 98.7; LDH 1674.2; bilirubin 34.5. recovery observed 27 (19%); CKD3 32 (24%); CKD4 10(7%); CKD5 7(5%); those have progressed ESRF (requiring replacement therapy) 40(31%); persisting transplant function 5(4%). 15 died (10%). into 3 groups. 1 – presence 28). 2 plus 41). And biopsied 62). did biopsy. Those group lower serum 331umol/L compared (634 umol/L) (666 umol/L). result significant p <0.05. Hypertension leading cause groups 2. aHUS present - all All i.e. biopsied. Conclusion evident dataset that major contributor chronic impairment. With contributing number cases, given advances therapeutics, early liaison national services complement disorders paramount protecting kidneys. 19% regaining eGFR >60ml/min prompt investigation crucial reducing burden disease. Long term follow-up should be offered. 21% no –we wary excluding process absence