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.

If STEC infection is strongly suspected, the hemoglobin level, hematocrit, platelet count, and urea, creatinine, and electrolyte levels, along with a blood smear, should be assessed on initial evaluation and monitored during the illness. Baseline values are useful because they aid interpretation of repeat tests obtained 1 or 2 days later.^[1]

Early progression toward HUS may be reflected by decreasing platelet count, decreasing hemoglobin level, or increasing creatinine level. Elevated lactate dehydrogenase may also be an early marker. Hemoglobinuria reflects intravascular hemolysis, depletion of circulating haptoglobin, and plasma hemoglobin levels that exceed renal reabsorptive capacity.^[2]

Following Lab findings are seen in HUS:^[3][4]

• 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
  • Laboratory approaches for stool detection of STEC include agar-based isolation, Shiga toxin antigen detection, and nucleic acid amplification of Shiga toxin genes.^[5] The ideal diagnostic approach combines methods that rapidly identify whether a high-risk pathogen is present. Because the ability to identify STEC in stool diminishes daily after the onset of diarrhea, specimens should be obtained promptly. If bulk stool is not immediately available, a rectal swab specimen should be obtained and processed; stool should also be tested when it becomes available if clinical suspicion remains high.
  • Shiga toxin antigen detection should not be used as the sole screening method. Detection of E. coli O157 generally implies high risk because O157 almost always produces Shiga toxin 2; however, in non-O157 STEC infection, toxin genotype is more clinically useful than serogrouping for estimating HUS risk.
• 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
  • In most cases of STEC-associated HUS, routine screening for complement regulatory gene mutations is not warranted on the basis of current data.^[6]
• Cultures
  • Blood, spinal, organ/tissue cultures may be needed in case of suspicion of other sources of HUS for example pnemococcal infection.