A 55-year-old male with history of end stage diabetic nephropathy with deceased donor kidney transplant on immunosuppression with tacrolimus and mycophenolate, presented with nausea, vomiting, and diarrhea. His labs showed anemia with peripheral blood schistocytosis, thrombocytopenia, low haptoglobin, elevated lactate dehydrogenase, and elevated creatinine. Stool cultures were positive for shiga toxin. He was diagnosed with STEC-HUS and managed conservatively, leading to an improvement in diarrhea and stabilization of hemoglobin and platelet count. However, kidney function continued to decline prompting a transplanted kidney biopsy confirming the diagnosis of TMA. Acute kidney injury eventually led to volume overload and uremic encephalopathy prompting initiation of hemodialysis. TMA laboratory results continued to decline, broadening the differential to atypical HUS versus refractory STEC-HUS. He was started on plasma exchange therapy while awaiting eculizumab procurement and then switched to eculizumab. There was marked improvement in kidney function and hemolysis parameters, and eventually was able to stop hemodialysis.

Keyword: Thrombotic microangiopathy; Atypical hemolytic uremic syndrome; Shiga-toxin; Eculizumab