Medical expert of the article
New publications
Diagnosis of hemolytic uremic syndrome
Last reviewed: 04.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The clinical blood test data depend on the period of the disease and the compensatory capabilities of the body. During the peak period, normochromic hyperregenerative anemia of varying severity is observed, morphologically, pronounced anisocytosis of erythrocytes (micro- and macrocytosis) is noted, erythrocytes acquire distorted fragmented shapes in the form of rods, triangles, eggshell discs with scalloped edges (fragmentocytosis). One of the most important signs is thrombocytopenia, the severity of which coincides with the severity of the hemolytic crisis; in most patients, the decrease in the number of platelets can be significant. Leukocytosis is noted (20-60 x 109/l) with a shift to the left up to metamyelocytes, promyelocytes, blast cells. Leukopenia has been described in a number of observations. Sometimes eosinophilia is observed (up to 8-25%).
The hemolytic nature of anemia is confirmed by an increase in total serum bilirubin (due to indirect bilirubin), a decrease in haptoglobin content, a significant increase in the level of free hemoglobin in plasma, and hemoglobinuria.
According to the severity of renal failure, high levels of residual nitrogen, urea and creatinine in the blood are detected. The rate of increase in the blood urea level depends on the intensity of catabolic processes. Most often, the daily increase in urea fluctuates within 4.89-9.99 mmol/l, and creatinine 0.088-0.132 mmol/l. An increase in urea over 6.6 mmol/l is an indication for extracorporeal detoxification.
Hypoalbuminemia (30.0-17.6 g/l) is often observed; hypoalbuminemia below 25 g/l is an unfavorable prognostic factor in young children with hemolytic uremic syndrome against the background of intestinal infection.
Disturbances in water and electrolyte metabolism are manifested by an increase in the concentration of intracellular electrolytes (potassium, magnesium, phosphates) in the blood and a decrease in the concentration of extracellular electrolytes (sodium and chlorine), which usually corresponds to the severity of dehydration as a result of profuse vomiting and diarrhea.
Hemocoagulation changes depend on the phase of DIC syndrome. Hypercoagulation is accompanied by a shortening of the venous blood clotting time, recalcification time, an increase in the degree of thrombotest, normal or slightly increased levels of prothrombin complex factors. Fibrin degradation products are determined in the blood and urine; anticoagulant and fibrinolytic activity of the blood increases compensatorily.
In the hypocoagulation phase, which is usually observed in the terminal period of the disease, due to the consumption of coagulation factors, there is an increase in coagulation time, recalcification time, a decrease in the degree of thrombotest, a decrease in factors involved in the formation of active blood thromboplastin, prothrombin complex factors and fibrinogen levels. These changes are usually accompanied by extensive hemorrhages at the injection site and severe bleeding from the respiratory or gastrointestinal tract.
Urine analysis reveals proteinuria, macro- or microhematuria. In hemolytic anemia, urine takes on the color of dark beer due to hemoglobin. Very characteristic of hemolytic uremic syndrome is the detection of fibrin lumps in the urine. A loose mucous lump the size of a corn kernel to a hazelnut, white or slightly pink, floating in the urine, is of great diagnostic value, since it indicates the process of intravascular coagulation with fibrin deposition on the endothelium of the glomerular capillary loops.
Pathological examinations of patients who died from hemolytic uremic syndrome reveal varying degrees of kidney damage, from acute microthrombotic glomerulonephritis to bilateral necrosis of the renal cortex. Along with changes in the kidneys, a picture of disseminated thrombosis of vessels (mainly small caliber) of many internal organs is revealed, accompanied by hemorrhagic or ischemic infarctions. The severity of damage to the same organs varies in different patients with identical clinical pictures.
[