The next step in diagnosis is a peripheral blood smear. This patient has findings suggestive of Shiga toxin–associated hemolytic uremic syndrome (HUS). This is a diarrhea-associated syndrome of microangiopathic hemolytic anemia, thrombocytopenia, and kidney failure caused by Shiga toxin–producing Escherichia coli, typically with serotypes O157:H7, O104:H4, and, less commonly, Shigella dysenteriae. Shiga toxin binds to endothelial cells, triggering thrombosis and resulting in a thrombotic microangiopathy. It also binds to renal mesangial cells, podocytes, and renal tubular cells, causing direct damage. These actions lead to acute kidney injury (AKI). Although this patient has a consistent clinical history, a peripheral blood smear is essential to determine whether the anemia is caused by a microangiopathic hemolytic process as indicated by the presence of schistocytes. Stool cultures may reveal the offending organism. Treatment is primarily supportive, and many patients require dialysis.

ADAMTS13 is a metalloprotease enzyme that cleaves von Willebrand factor; low activity levels are supportive of a diagnosis of thrombotic thrombocytopenic purpura (TTP). Although this would be a reasonable study in this patient if a likely diagnosis of Shiga toxin–associated HUS were less clear to assess for the possibility of TTP, confirmation of true thrombocytopenia and microangiopathic hemolytic anemia would be an initial diagnostic step before additional testing.

Kidney biopsy would show evidence of capillary thrombosis as well as glomerular and tubular damage, but it is not necessary to establish the diagnosis of Shiga toxin–associated HUS.

Urine protein electrophoresis may be useful in evaluating AKI due to monoclonal urine immunoglobulin light chains (Bence Jones proteins). Although a plasma cell disorder may cause anemia and AKI due to precipitation of light chains in the renal tubule (myeloma kidney), it is not a cause of microangiopathic hemolytic anemia or thrombocytopenia as seen in this patient.