Autoimmune diseases are life-threatening disorders that cause increasing disability over time. Systemic lupus erythematosus (SLE) and other autoimmune diseases arise when immune stimuli override mechanisms of self-tolerance. Accumulating evidence has demonstrated that protein glycosylation is substantially altered in autoimmune disease development, but the mechanisms by which glycans trigger these autoreactive immune responses are still largely unclear. In this study, we found that presence of microbial-associated mannose structures at the surface of the kidney triggers the recognition of DC-SIGN–expressing γδ T cells, inducing a pathogenic interleukin-17a (IL-17a)–mediated autoimmune response. Mice lacking Mgat5 , which have a higher abundance of mannose structures in the kidney, displayed increased γδ T cell infiltration into the kidney that was associated with spontaneous development of lupus in older mice. N -acetylglucosamine supplementation, which promoted biosynthesis of tolerogenic branched N-glycans in the kidney, was found to inhibit γδ T cell infiltration and control disease development. Together, this work reveals a mannose–γδ T cell–IL-17a axis in SLE immunopathogenesis and highlights glycometabolic reprogramming as a therapeutic strategy for autoimmune disease treatment.

Background: The development of vaccines to prevent COVID-19 breakouts came with highly positive results but some unexpected side effects. Rare side effects have been seen with the BNT162b2 SARS-CoV 2 vaccine. Case Presentation: We present the case of a 45-year-old female patient who developed an acute kidney injury needing urgent hemodialysis one week after the second administration of the BNT162b2 SARS-CoV 2 vaccine. She developed a macular rash on her lower limbs and palms as well. A kidney biopsy was performed 10 days after vaccine inoculation, diagnosing acute interstitial nephritis and acute tubular necrosis with cellular casts. The patient was treated with three corticosteroid pulses followed by daily prednisolone. We witnessed clinical improvement 4 days after the initial corticosteroid treatment with progressive recovery of kidney function and hemodialysis withdrawal. After 2 weeks, the patient had recovered her kidney function. Immunophenotyping was performed, diagnosing a hypersensitivity to the vaccine and the polyethylene glycol excipient. Conclusion: Patients may develop acute reactions to vaccines. In this case, symptoms seem to correlate significantly with its inoculation and, although this case had a favourable outcome, these side effects must be made aware for clinicians and patients.

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.

The incidence and prevalence of chronic kidney disease (CKD) are increasing worldwide. CKD is associated with high morbidity, premature mortality, and high healthcare costs. Genetic variants may influence CKD development and progression. This study aimed to identify the associations between allelic variants and CKD progression. We performed a systematic literature review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The PubMed, Embase, and Cochrane Central databases were used for data collection. Hereditary causes of CKD were excluded from the analysis. A total of 38 reports were included. The selected studies included cohort studies, case-control studies, and genome-wide association studies (GWASs). The studies involved patients of different ethnicities and with comorbid diseases. Several genetic variants were identified in genes that encode proteins related to metabolic processes, oxidative stress, immune regulation, the renin–angiotensin–aldosterone pathway, and epigenetics, among others. These genetic alterations can affect protein function and lead to renal damage, impacting CKD development and progression. Gene polymorphisms can influence CKD progression. Many of these are population-specific, and their relevance may be influenced by the presence of other diseases and environmental factors. Larger studies are needed to confirm the associations described here.