Deadly E. coli kidney failure struck without classic blood markers, case report warns

A 47-year-old man with no medical history developed catastrophic kidney failure and a coma after eating homemade deer pâté, yet the blood tests that normally betray his condition were absent. His case, described by physicians at a French intensive care unit in a new case-based review published in Critical Care: Sepsis and Severe Infection, exposes a dangerous diagnostic trap: Shiga toxin-producing Escherichia coli hemolytic uremic syndrome, or STEC-HUS, can strike adults as overwhelming organ failure even when the classic peripheral hallmarks of thrombotic microangiopathy never appear.

The clinical story began deceptively. The patient consulted his general practitioner with fever of 39 degrees Celsius, dysuria with malodorous, burgundy-colored urine, and mild abdominal pain with transient non-bloody diarrhea. Serum creatinine was 100 micromoles per liter, and urine analysis revealed leukocyturia with a culture growing more than 100,000 colony-forming units per milliliter of E. coli. Ciprofloxacin was started for a suspected urinary tract infection. Three days later, the man was anuric and arrived at the emergency department, where blood tests showed a hemoglobin of 15 grams per deciliter, a platelet count of 110 giga per liter, a normal haptoglobin, and a blood smear with no schistocytes. Creatinine had soared to 447 micromoles per liter and serum sodium had fallen to 122 millimoles per liter.

Imaging deepened the alarm. A computed tomography scan of the abdomen and pelvis showed both kidneys of normal size with no urinary tract obstruction, but contrast injection revealed a complete absence of perfusion of the renal parenchyma on both sides. Doppler examination ruled out thrombosis of the renal arteries and veins. Stool culture and polymerase chain reaction testing for Shiga toxins Stx1 and Stx2 were both negative. The patient was transferred to the intensive care unit and hemodialysis was initiated. Three days later he developed diplopia, disorientation and seizures, and was ultimately intubated for coma.

The diagnosis finally came from an unexpected sample. The E. coli strain recovered from the urine before hospitalization was analyzed, and Shiga toxins Stx1 and Stx2 were identified by PCR. Urine culture identified an enterohemorrhagic E. coli O171 strain, and PCR detected the virulence genes ehxA and saa. A detailed interview revealed the patient had eaten homemade deer pâté eight days before the first symptoms. Following the institutional protocol for thrombotic microangiopathy, ADAMTS13 activity was not measured because the patient’s French score was zero, indicating a very low probability of thrombotic thrombocytopenic purpura. A complete complement workup, including C3, C4, Factor H, Factor I and anti-factor H antibodies, was normal, ruling out atypical HUS. The diagnosis of STEC-HUS was established, antibiotics were stopped, and supportive care continued.

A renal biopsy explained the imaging findings: cortical necrosis with glomerular capillary thrombosis, with coagulative necrosis of a glomerulus and tubules, ghost-like outlines of cells without discernible nuclei, karyorrhexis, and thrombi within capillaries. Brain MRI and lumbar puncture were normal despite the coma. Neurological symptoms improved gradually and the patient was extubated after six days of invasive mechanical ventilation. Renal function recovered enough to cease hemodialysis after one month. At nine months, serum creatinine was 115 micromoles per liter with an estimated glomerular filtration rate of 64 milliliters per minute, a follow-up contrast CT showed complete reperfusion of both renal cortices, and the patient had no neurological complaints.

The authors place this single case against a broader body of evidence assembled from international surveillance networks, the French national registry, and major adult outbreak cohorts. Their narrative review was designed to address a precise clinical question: how should clinicians diagnose and manage adult STEC-HUS when the classic peripheral markers of thrombotic microangiopathy are missing? The answer they build is that adult disease is far more heterogeneous than the pediatric archetype, and that the diagnostic playbook built around the triad of Coombs-negative hemolytic anemia, thrombocytopenia, and acute kidney injury may fail precisely in the patients who are sickest.

In a recent French nationwide study of 96 adults with STEC-HUS, nearly one-third of patients carried coexisting risk factors for other causes of thrombotic microangiopathy, such as solid organ transplantation, hematologic malignancies, or autoimmune diseases. These competing explanations can obscure the clinical picture and delay the correct diagnosis. Data from the 2011 German outbreak, which affected mostly young adults with a median age of 42 years, demonstrated that STEC-HUS in adults can manifest as severe organ failure before hematological markers of thrombotic microangiopathy become fully evident in the peripheral blood. The authors describe this as an organ-failure-first phenotype, and they argue it justifies STEC-specific polymerase chain reaction screening and culture in any unexplained acute kidney injury following mild gastrointestinal symptoms, regardless of the initial platelet count or the absence of schistocytes on the blood smear.

The case also illustrates a second diagnostic blind spot: the stool. Both stool culture and stool polymerase chain reaction for Shiga toxins were negative in this patient, plausibly because ciprofloxacin exposure reduced fecal shedding before testing. Data from the French national registry reported that 7 percent of adults with STEC-HUS had STEC-positive urine samples, and the diagnosis here rested entirely on the urine specimen collected before hospitalization. The authors advocate routine STEC polymerase chain reaction and culture across multiple biological samples, including urine and blood, in adults being evaluated for thrombotic microangiopathy.

The coagulation and inflammatory profile of the patient adds another layer. Sustained activation of coagulation, reflected in markedly elevated D-dimers that remained high for ten days, occurred alongside a high neutrophil count and elevated C-reactive protein. Such prothrombotic abnormalities have been reported in previous studies of patients with hemolytic uremic syndrome, and a high leukocyte count has been identified as a risk factor for STEC-HUS. Notably, the platelet count normalized by day two and a senior hematologist confirmed the absence of schistocytes on manual smear review, underscoring how far this case drifted from the textbook picture.

Age shapes both incidence and outcome in STEC-HUS. The age-specific incidence typically follows a U-shaped distribution: the disease predominantly affects children, but the highest morbidity and mortality are observed in the elderly, with case-fatality rates reaching up to 20 percent. Age over 65 years is a well-established risk factor for adverse outcomes, and data from FoodNet surveillance between 2000 and 2006 indicate that hemolytic uremic syndrome in people aged 65 and older is associated with high rates of hospitalization and mortality compared with younger adults. Studies comparing adult and pediatric populations found that adults often suffer more severe neurological complications and higher mortality rates, up to 20 percent. The neurological failure observed in this patient, requiring intensive care, is consistent with the severe phenotypes described in adult STEC O104:H4 and O157 outbreaks, where neurological involvement was a major reason for intensive care unit admission.

Brain imaging in adult STEC-HUS is itself an imperfect tool. Radiological abnormalities have been reported in up to 50 percent of adult patients and include signal changes in the basal ganglia, pons, and corpus callosum, and cerebral infarcts have also been documented. Yet this patient, despite diplopia, seizures, and coma, had a normal brain magnetic resonance imaging scan and a normal lumbar puncture. The mechanisms of brain injury are diverse, encompassing toxin-mediated damage, disruption of the blood-brain barrier, complement activation, microvascular occlusion, systemic inflammation, and metabolic encephalopathy, which may explain the inconsistent sensitivity of routine imaging. Interestingly, specific sequences such as susceptibility-weighted imaging with venous contrast have shown pathological changes in cerebral hemodynamics in almost all STEC-HUS patients with neurological symptoms. The authors call for more research to characterize these mechanisms and to better predict long-term neurological sequelae.

The antibiotic question remains one of the most contested areas in the field. Antibiotic administration has been shown to significantly reduce the duration of fecal shedding during the STEC O104:H4 outbreak, and the mechanism of antibiotic-induced toxin release is documented with ciprofloxacin compared with other antimicrobials, which may have contributed to the severity of the renal and neurological failure in this case. However, the authors are careful to note that a causal relationship between antibiotic treatment and the risk of hemolytic uremic syndrome has not been robustly demonstrated. Expert opinion generally discourages antibiotics, but recent data suggest the effect may be class-specific: macrolides such as azithromycin may suppress Shiga toxin expression and have been used for decolonization without worsening clinical outcomes. The results of the randomized controlled trial ZITHROSHU are expected to clarify the role of azithromycin in the management of STEC-HUS.

The renal trajectory of the patient is, in the authors’ view, the most exceptional feature. Cortical necrosis classically carries a poor prognosis for renal function and often leads to end-stage renal disease. Yet recent literature on adult STEC-HUS shows that even with dialysis requirement rates reaching up to 60 percent, long-term renal recovery is possible, and similar findings have been reported in a European registry. This patient ceased hemodialysis after one month and recovered near-normal function, which the authors interpret as evidence that aggressive supportive care in the intensive care unit can defy traditional prognostic expectations.

Finally, the review addresses eculizumab, the anti-C5 monoclonal antibody that is standard of care for atypical hemolytic uremic syndrome. Complement activation appears to play a substantial role in STEC-HUS: Shiga toxins regulate complement activation in vitro, and patients often show reduced C3 with augmented C3a, C3b, and factor Bb, changes linked to renal endothelial and podocyte injury and to central nervous system damage. A study from a French O104:H4 outbreak suggested a potential role for eculizumab in severe forms with neurological or renal involvement, though its use remains debated, and a recent randomized controlled trial in pediatric patients found that eculizumab did not improve renal outcome during the acute phase but reduced long-term kidney sequelae. The authors conclude that further research is needed to demonstrate any benefit of eculizumab in adults with severe STEC-HUS-related organ failure.

Subject of Research: An atypical adult case of Shiga toxin-producing E. coli hemolytic uremic syndrome diagnosed via urine testing despite negative stool tests and absent peripheral thrombotic microangiopathy markers

Article Title: Atypical presentation of Shiga toxin-producing Escherichia coli hemolytic and uremic syndrome (STEC-HUS): case-based discussion and literature review

Article References: Hirsinger, B., Deltombe, C., & Canet, E. (2026). Atypical presentation of Shiga toxin-producing Escherichia coli hemolytic and uremic syndrome (STEC-HUS): case-based discussion and literature review. Critical Care: Sepsis and Severe Infection, 1(1), Article 10. https://doi.org/10.1186/s44541-026-00012-8

Image Credits: AI Generated

DOI: 10.1186/s44541-026-00012-8

Keywords: STEC-HUS, Shiga toxin, Escherichia coli, acute kidney injury, cortical necrosis, thrombotic microangiopathy, urine PCR diagnosis, eculizumab, antibiotics debate, adult HUS, complement activation, intensive care