Aims: Acute kidney injury (AKI) is highly prevalent during hospitalization of patients with type 2 diabetes (T2D). We aimed to assess the impact of AKI and its severity and duration on the risk of hypoglycaemia in hospitalized patients with T2D. Methods: Retrospective cohort analysis of patients with T2D, admitted at a University Hospital in 2018–2019. AKI was defined as an increase in serum creatinine by ≥ 0.3 mg/dl (48 h) or ≥ 1.5 times baseline (7 days), and hypoglycaemia as blood glucose concentration < 70 mg/dl. Patients with chronic kidney disease stage ≥ 4 were excluded. We registered 239 hospitalizations with AKI and randomly selected 239 without AKI (control). Multiple logistic regression was used to adjust for confounding factors and ROC curve analysis to determine a cutoff for AKI duration. Results: The risk of hypoglycaemia was higher in the AKI group (crude OR 3.6, 95%CI 1.8–9.6), even after adjusting for covariates (OR 4.2, 95%CI 1.8–9.6). Each day of AKI duration was associated with a 14% increase in the risk of hypoglycaemia (95%CI 1.1–1.2), and a cutoff of 5.5 days of AKI duration was obtained for increased risk of hypoglycaemia and mortality. AKI severity was also associated with mortality, but showed no significant association with hypoglycaemia. Patients with hypoglycaemia had 4.4 times greater risk of mortality (95%CI 2.4–8.2). Conclusions: AKI increased the risk of hypoglycaemia during hospitalization of patients with T2D, and its duration was the main risk factor. These results highlight the need for specific protocols to avoid hypoglycaemia and its burden in patients with AKI.

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Granulomatosis with polyangiitis is a necrotising small vessel vasculitis characterised by granulomatous inflammation that can involve the eyes, ear-nose-throat region, and lungs, often refractory to standard immunosuppressive therapies such as glucocorticoids, rituximab, and cyclophosphamide. The complex immunopathogenesis of granulomatous lesions, involving neutrophil swarming, macrophage activation, T-cell responses, and complement activation through the C5a receptor, contributes to treatment challenges. Avacopan, an oral C5a receptor antagonist, has demonstrated efficacy in antineutrophil cytoplasmic antibody-associated vasculitis, particularly in kidney involvement, with evidence of glucocorticoid-sparing benefits from the ADVOCATE trial. However, data on its role in granulomatous manifestations remain limited. We report two cases of severe, refractory granulomatosis with polyangiitis with ocular, ear-nose-throat, and pulmonary granulomatous disease unresponsive to standard therapies but achieving complete clinical and immunological remission with avacopan. Both patients successfully discontinued glucocorticoids and showed marked clinical improvement and radiological resolution of lesions. These cases, supported by recent trial sub-analyses, suggest that avacopan may be an effective therapeutic option for granulomatous granulomatosis with polyangiitis manifestations, enabling glucocorticoid reduction and improved disease control.

A 56-year-old male with a poorly controlled human immunodeficiency virus infection presents to the emergency room due to anorexia and weight loss. The patient was emaciated, hypertensive and his laboratory tests showed thrombocytopenia, anaemia, an elevated lactate dehydrogenase and an acute kidney injury. The patient was admitted to the Infecciology ward and by the fourth day, as the kidney function did not improve, a Nephrology consultation was requested. We collected a full auto-immune and serological panel and a urinalysis to rule out glomerular pathologies. Two days later, the patient developed a hypertensive emergency associated with an acute respiratory distress, responsive to furosemide and anti-hypertensive medications. The complementary study showed a high LDH, unmeasurable haptoglobin, thrombocytopenia and schizocytes on peripheral blood smear. These findings suggested a thrombotic microangiopathy associated with human immunodeficiency virus infection and so, he restarted antiretroviral therapy. The kidney function deteriorated and, despite starting haemodialysis, the patient died shortly after.

We admitted a 21 -year -old female to the Nephrology ward due to proteinuria and generalized oedema, which started soon after consuming clonixin 300mg thrice a day for two weeks. Her initial blood work showed nephrotic -range proteinuria, hypoalbuminaemia, hypercholesterolaemia and normal kidney function. We conducted a full auto -immune and serological study: there were no signs of infection, complement consumption or underlying auto -immune diseases. Suspecting minimal change disease, we started prednisolone 1mg/kg/day, with good clinical response and a reduction of urinary protein losses. By the third day, a kidney biopsy was performed: the glomeruli were morphologically normal and no immune deposits were found, which suggested minimal change disease. After seven days, the patient was discharged from the hospital with a corticoid taper until her Nephrology consultation. In the following weeks she maintained clinical and laboratorial remission and prednisolone was stopped after six months. Two months after, the patient noticed a growing bilateral cervical mass and went to the emergency room. The diagnostic workup was inconclusive, so an ultrasound -guided biopsy was requested. The biopsy revealed lymphoid cell proliferation, positive for CD30, CD15, MUM -1 and BCl6. These findings confirmed a Hodgkin’s Lymphoma diagnosis and the patient started radiotherapy and chemotherapy (ABVD -doxorubicin, bleomycin, vinblastin, dacarbazine). In the following months her clinical status improved and the cervical mass had a significant size reduction. The kidney disease remained in remission, without therapeutic adjustments. A post- -treatment PET scan was requested, showing only a residual mediastinal mass.