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On this basis, first a thrombotic microangiopathy could be suspected. In fact, the hellp syndrome deteriorated clinical status included alterations of hellp syndrome consciousness and obnubilation. Further examinations such as the negative Coombs test, the predominant increase of conjugated bilirubin (8 hellp syndrome mg%) the absence of reticulocytes (28%), and the slight thrombocytopenia (84000/p.h.f.) led us to exclude a postpartum haemolytic uraemic syndrome (HUS). The findings suggested rather a major hepatic injury combined with ARF. This was confirmed by the ultrasound assessments of the liver and spleen (increased dimensions), the presence of ascitic fluid, conjugated hyperbilirubinaemia, increased levels of serum transaminases, and decreased levels of serum proteins. Renal abnormalities became evident and they were corroborated by the ultrasound finding of hyperechogenicity in both the kidneys, the presence of cellular elements in the urine, and above all the progressive and disproportionate increase in levels of blood urea in comparison with serum creatinine.
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