Hemolytic-uremic syndrome laboratory findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2], Anila Hussain, MD [3]

Overview

The classic laboratory findings in hemolytic uremic syndrome (HUS) include anemia, thrombocytopenia and acute renal injury. Anemia is microangiopathic hemolytic anemia which low hemoglobin often < 8g/dl, high reticulocyte count and LDH, low haptoglobin level as well as fragmanted RBC's and schistiocytes on peripheral blood smear (PBS). Platelets are frequently less than 60,000 without active bleeding usually and renal damage is seen in form of high creatinine, BUN, and electrolyte abnormalities.

Laboratory Findings

Following Lab findings are seen in HUS:

• Microangiopathic hemolytic anemia with features as follows:
  • Low hemoglobin level typically < 10g/dl
  • High reticulocyte count
  • Increased LDH level
  • Low haptoglobin level
  • Negative Coombs test
  • Peripheral blood smear shows fragmented RBC's (Schistiocytes, Helmet, and Burr cells)
  • PT and aPTT are normal (differentiating feature from Disseminated Intravascular Coagulation)
• Thrombocytopenia
  • Below 150,000 although typically less than 60,000. In spite of low platelet count, active bleeding is rarely seen
• Serum chemistry abnormalities
  • High BUN
  • High creatinine
  • Electrolyte abnormalities may include hyponatremia, hyperkalemia, hyperphosphatemia, hypocalcemia, and acidosis (resulting from diarrhea, dehydration and renal failure)
  • Increased Bilirubin and aminotransferases
  • High uric acid levels
• Urinalysis-may show any of following
  • Blood / Red blood cells
  • Protein
  • Bilirubin
  • WBC
  • Casts
• Stool Testing
  • Stool culture on Sorbitol MacConkey's agar or detection of Shiga toxin with serological testing
• Genetic Testing
  • Done if suspicion of genetic or complement-mediated HUS/ recurrent HUS. However, results take weeks-month thus have no role in the acute management of disease and treatment should not be delayed while awaiting results
  • Low C3 and C4 may indicate complement mediated HUS
  • Genetic testing/screening for cobalamine metabolic defects in neonates presenting with HUS
• Cultures
  • Blood, spinal, organ/tissue cultures may be needed in case of suspicion of other sources of HUS for example pnemococcal infection.