Hemolytic-uremic syndrome laboratory findings: Difference between revisions
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==Overview== | ==Overview== | ||
The classic laboratory findings in HUS include anemia, thrombocytopenia and acute renal damage. Anemia is Microangiopathic Hemolytic Anemia which low hemoglobin often < 8g/dl, high reticulocute count and LDH, low Haptoglobin level as well as fragmanted RBC's and Schistiocytes on peripheral blood smear. 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== | ==Laboratory Findings== | ||
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* '''Microangiopathic Hemolytic Anemia''' with features as follows: | * '''Microangiopathic Hemolytic Anemia''' with features as follows: | ||
** Low Hemoglobin level | ** Low Hemoglobin level Typically < 10g/dl | ||
** High reticulocyte count | ** High reticulocyte count | ||
** Increased LDH level | ** Increased LDH level | ||
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** Negative Coombs test | ** Negative Coombs test | ||
** Peripheral Blood smear shows fragmented RBC's (Schistiocytes, Helmet, and Burr cells) | ** Peripheral Blood smear shows fragmented RBC's (Schistiocytes, Helmet, and Burr cells) | ||
** PT and aPTT are nomal (differentiating feature from Disseminated Intravascular Coagulation) | |||
* '''Thrombocytopenia''' | * '''Thrombocytopenia''' | ||
** Below 150,000 although typically less than 60,000. In spite of low platelet count, active bleeding is rarely seen | ** Below 150,000 although typically less than 60,000. In spite of low platelet count, active bleeding is rarely seen | ||
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* '''Genetic 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 | ** 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. | |||
==References== | ==References== | ||
Revision as of 17:53, 10 August 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anila Hussain, MD [2]
Overview
The classic laboratory findings in HUS include anemia, thrombocytopenia and acute renal damage. Anemia is Microangiopathic Hemolytic Anemia which low hemoglobin often < 8g/dl, high reticulocute count and LDH, low Haptoglobin level as well as fragmanted RBC's and Schistiocytes on peripheral blood smear. 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[1][2]:
- 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 nomal (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.
References
- ↑ Canpolat N (2015). "Hemolytic uremic syndrome". Turk Pediatri Ars. 50 (2): 73–82. doi:10.5152/tpa.2015.2297. PMC 4523989. PMID 26265890.
- ↑ Marina Noris & Giuseppe Remuzzi (2005). "Hemolytic uremic syndrome". Journal of the American Society of Nephrology : JASN. 16 (4): 1035–1050. doi:10.1681/ASN.2004100861. PMID 15728781. Unknown parameter
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