Hemolytic uremic syndrome (HUS), a thrombotic microangiopathy primarily affecting the kidneys, can also involve the central nervous system (CNS), often leading to significant morbidity and mortality. Neurologic manifestations are among the most severe extra-renal complications, particularly in children and during outbreaks of Shiga toxin-producing Escherichia coli (STEC)-associated HUS (typical (tHUS)). This review explores the clinical spectrum, pathophysiology, diagnostic workup, and age-specific outcomes of neurologic involvement in both typical (tHUS) and atypical (aHUS). Neurologic complications occur in up to 11% of pediatric and over 40% of adult STEC-HUS cases in outbreak settings. Presentations include seizures, encephalopathy, focal deficits, movement disorders, and posterior reversible encephalopathy syndrome (PRES). Magnetic resonance imaging (MRI) commonly reveals basal ganglia or parieto-occipital lesions, though subtle or delayed findings may occur. Laboratory workup typically confirms microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and kidney damage, with additional markers of inflammation or metabolic dysregulation. Eculizumab is the first-line treatment for aHUS with CNS involvement, while its utility in STEC-HUS remains uncertain. Although many children recover fully, those with early CNS involvement are at greater risk of developing epilepsy, cognitive delays, or fine motor deficits. Adults may experience lingering neurocognitive symptoms despite apparent clinical recovery. Differences in presentation and imaging findings between age groups emphasize the need for tailored diagnostic and therapeutic strategies. Comprehensive neurorehabilitation and long-term follow-up are crucial for identifying residual deficits. Continued research into predictive biomarkers, neuroprotective interventions, and standardized treatment protocols is needed for improving outcomes in HUS patients with neurological complications.

Ibogaine is an indole alkaloid originally extracted from the root bark of the African rainforest shrub Tabernanthe iboga. It has been explored as a treatment for substance abuse because it interrupts drug addiction and relieves withdrawal symptoms. However, it has been shown that ibogaine treatment leads to a sharp and transient fall in cellular ATP level followed by an increase of cellular respiration and ROS production. Since contractile tissues are sensitive to changes in the levels of ATP and ROS, here we investigated an ibogaine‐mediated link between altered redox homeostasis and uterine contractile activity. We found that low concentrations of ibogaine stimulated contractile activity in spontaneously active uteri, but incremental increase of doses inhibited it. Inhibitory concentrations of ibogaine led to decreased SOD1 and elevated GSH‐Px activity, but doses that completely inhibited contractions increased CAT activity. Western blot analyses showed that changes in enzyme activities were not due to elevated enzyme protein concentrations but posttranslational modifications. Changes in antioxidant enzyme activities point to a vast concentration‐dependent increase in H₂O₂ level. Knowing that extracellular ATP stimulates isolated uterus contractility, while H₂O₂ has an inhibitory effect, this concentration‐dependent stimulation/inhibition could be linked to ibogaine‐related alterations in ATP level and redox homeostasis.

Background: Renal arteriovenous malformations (rAVMs) are rare vascular anomalies that may lead to hematuria, anemia, or acute kidney injury (AKI). Although endovascular embolization is the treatment of choice, post-procedural complications such as new-onset proteinuria may occur and require long-term management. Case Presentation: A 56-year-old man with recurrent gross hematuria and elevated serum creatinine (128 μmol/L) was diagnosed with a right rAVM and underwent successful selective embolization. Despite recovery of renal function, follow-up revealed new-onset proteinuria (2.2 g/24 h). Results: Introduction of an angiotensin-converting enzyme inhibitor (ACEi) resulted in partial improvement of proteinuria, while subsequent addition of a sodium–glucose cotransporter-2 inhibitor (SGLT2i) achieved almost complete resolution of proteinuria (0.33 g/24 h) and stable renal function (serum creatinine 93 μmol/L) after 12 months. Conclusions: This case highlights the occurrence of post-embolization proteinuria and illustrates the synergistic renoprotective effect of combined ACEi and SGLT2i therapy in a non-diabetic patient with vascular kidney disease.