Case Report on Hemolytic Uremic Syndrome
Authors: Manmode Nilima , Tembhare Vaishali , Singh Seema , Sharma Ranjana , Ankar Ruchira , Pohekar Savita , Waghamare Usha 
Published: February 2022

Background: In the United States, the hemolytic–uremic syndrome of childhood typically follows gastrointestinal infection with Escherichia coli O157:H7. It is presumed that the absorption from the gastrointestinal tract of Shiga toxins 1, 2, or both (formerly called Shiga-like toxins) produced by E. coli O157:H7 causes microangiopathic hemolytic anemia as a result of endothelial-cell injury. Shiga-toxin–producing E. coli belonging to serotypes other than O157:H7 can also cause the hemolytic–uremic syndrome. However, even though such organisms have been implicated as causes of sporadic cases or outbreaks of gastroenteritis, they are not believed to be important causes of the hemolytic–uremic syndrome in this country. Hemolytic uremic syndrome (HUS) is a kidney disease characterized by damaged and inflamed small blood vessels. As a result of the damage, clots in the vessels may form. Clots impede the filtration function of the kidneys, causing renal failure, which can be deadly.
Clinical Finding: Hemolytic uremic syndrome, nephropathy and thrombocytopenia, pallor, jaundice, edema. After eight hours of stomach and left-flank pain, vomiting, and dysuria, a previously healthy six-year-old girl was seen. The day before, an enema had been used to alleviate constipation. The child had not had diarrhoea during the two weeks before evaluation. On examination, the patient had an oral temperature of 39.8°C, a pulse rate of 120 per minute, and a blood pressure of 111/59 mm Hg. There was tenderness of the suprapubic area and left costovertebral angle. The white-cell count was 23,400 per cubic millimeter (58 percent neutrophils, 23 percent band forms, 9 percent lymphocytes, and 10 percent monocytes), the hematocrit was 40 percent, and the platelet count was 293,000 per cubic millimeter. Urine obtained by catheterization had a specific gravity of 1.028 and a ph of 5, and dipstick analysis was positive for leukocyte esterase (++), protein (++), ketones (++), and blood (+++). The urinary sediment contained 21 to 100 red cells, more than 100 white cells, 1 to 5 renal tubular cells, and 1 to 5 granular casts per high-power field. Many bacteria were observed by microscopy. The left kidney showed attenuation of fat and a possible collection of fluid on abdominal ultrasonography; the right kidney was normal. Before starting ceftriaxone medication, blood was taken for culture.
Diagnostic Evaluation: HB-5.7 g/dL, total protein-7.4 g/dL, total Alcaline phosphatase -123 U/L , total platelet count-2,93,000 per cubic millimeter, total bilirubin-3.2 mg/dl, WBC 23400 per cubic meter, CRP 5.58 mg/L, Sodium level 136 mg/dl, potassium level 3.92mg/dl.
Therapeutic Intervention: Tab Amlodepin 10 mg BD, Tab Prednisolone 10 mg TDS, Tab Envas 2.5 mg OD, Metropenum 340 mg BD, Inj. Pantop 20 mg OD.
Outcome: The medication has started for thrombocytopenia, the patient is on dialysis and If is given to patient for movement of body because of patient is obese. The patient was sent home after 20 days of hospitalization. Three weeks later, a voiding cystourethrogram was normal, and six weeks later, ultrasonography revealed that the focal abnormality in the left kidney had disappeared. The patient's blood urea nitrogen and serum creatinine concentrations, iothalamate clearance, and blood pressure are all normal two years later, and her urine is protein and blood-free. She has not experienced a recurrence of a urinary tract infection or hemolytic–uremic syndrome.
Conclusion: The atypical hemolytic uremic syndrome is an uncommon condition that must be diagnosed with a high index of suspicion. It's an exclusionary diagnosis. A better outcome will be achieved if the disease is detected early and treated promptly. In all patients with thrombotic microangiopathy, the atypical hemolytic uremic syndrome should be evaluated.