Lipopolysaccharide (LPS) or endotoxin, the major cell wall component of Gram-negative bacteria, plays a pivotal role in the pathogenesis of sepsis. It is able to activate the host defense system through interaction with Toll-like receptor 4, thus triggering pro-inflammatory mechanisms. A large amount of LPS induces inappropriate activation of the immune system, triggering an exaggerated inflammatory response and consequent extensive organ injury, providing the basis of sepsis damage. In this review, we will briefly describe endotoxin’s molecular structure and its main pathogenetic action during sepsis. In addition, we will summarize the main different available methods for endotoxin detection with a special focus on the wider spectrum offered by omics technologies (genomics, transcriptomics, proteomics, and metabolomics) and promising applications of these in the identification of specific biomarkers for sepsis.

Eryptosis is the stress-induced RBC (red blood cell) death mechanism. It is known that eryptosis is largely influenced by plasma and blood composition, and that it is accelerated in patients affected by chronic kidney disease (CKD). The aim of this study is to evaluate the eryptosis rate in healthy RBCs treated with different concentration of IL-6, IL-1β, urea and p-cresol, comparable to plasmatic level of CKD patients, at different time points. We exposed healthy RBCs to increasing concentrations of IL-6, IL-1β, urea and p-cresol. Morphological markers of eryptosis (cell membrane scrambling, cell shrinkage and PS exposure at RBC surface) were evaluated by flow cytometric analyses. The cytotoxic effect of cytokines and uremic toxins were analyzed in vitro on healthy RBCs at 4, 8 and 24 h. Morphology of treated RBCs was dramatically deranged, and the average cell volume was significantly higher in RBCs exposed to higher concentration of all molecules (all, p < 0.001). Furthermore, healthy RBCs incubated with each molecules demonstrated a significant increase in eryptosis. Cytofluorimetric analysis of eryptosis highlighted significantly higher cell death rate in RBCs incubated with a higher concentration of both cytokines compared with RBCs incubated with a lower concentration (all, p < 0.05). In conclusion, our data show that cytokines and uremic toxins have a harmful effect on RBCs viability and trigger eryptosis. Further studies are necessary to validate these results in vivo and to associate abnormal eryptosis with cytokine levels in CKD patients. The eryptosis pathway could, moreover, become a new promising target for anemia management in CKD patients.

Purpose: Anastomotic pseudoaneurysms of transplanted kidneys are a very rare complication encountered in less than 1% of cases. They may be devastating, leading to functional impairment, kidney transplantectomy, or death. Treatment has not been standardized, with open surgical repair considered the safest procedure even if it is often complicated by bleeding and graft loss. The purpose of this case report is to describe an endovascular treatment of this condition, consisting of the combination of coil embolization and arterial stenting. Case report: A 61-year-old woman developed an anastomotic pseudoaneurysm 2 months after kidney transplantation, causing acute kidney injury related to ab-extrinsic stenosis of the transplant renal artery (TRA) and external iliac artery. The pseudoaneurysm was successfully treated by coil embolization, and the arterial patency was restored by the stenting of TRA and external iliac artery. The patient completely recovered kidney function, and after a 6-month-follow-up, creatinine values were stable with normal renal perfusion. Conclusion: Endovascular repair through coil embolization and TRA stenting can be a safe and effective option to treat anastomotic pseudoaneurysm in kidney transplant.

Objectives: Diabetic kidney disease (DKD) is the leading cause of kidney failure worldwide. Different phenotypes of DKD are emerging, partially attributable to a better glycemic control, partially to concomitant risk factors for kidney disease. Diabetes belongs to Non-Communicable Diseases (NCDs), but poor data about DKD in Low–Middle Income Countries are currently available. In the present paper we compare two cohorts of patients affected by DKD from Tanzania and from Italy. Study design: Retrospective observational study conducted by NCDs Clinic of Tosamaganga Regional Referral Hospital (Tanzania) and from the Multidisciplinary Diabetological-Nephrological Clinic of Bologna (Italy). Methods: Included patients’ data were analyzed for demographical features, diabetes complications, laboratory findings, and pharmacological therapy at the time of enrollment and after 6-month follow-up. Results: Tanzanian patients were younger (56.65 vs. 67.66 years, p < 0.001), with a higher prevalence of women (66.9% vs. 25.5%, p < 0.001), and showed lower level of BMI (26.39 vs. 30.18 kg/m², p < 0.001). Worsened glycemic control could be observed in the Tanzanian cohort (HbA1c 83.71 vs. 56.92 mmol/mol, p < 0.001) and higher eGFR (70.13 ± 31.93 vs. 52.31 ± 23.37 mL/min, p < 0.001). A sharp reduction in albuminuria was observed in both cohorts with an increase in nephroprotective drugs and better glycemic control. Conclusions: Two phenotypes of diabetic patients have emerged from comparison between two cohorts. Tanzanian patients are mostly female, younger, and with a normal BMI, whereas Italian patients are mainly male, older, and affected by metabolic syndrome and vascular complications. Therapy implementation is associated with a delayed decline of eGFR and downgrading of albuminuria at 6-month follow-up.

Kidney diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), represent a general, public health urgency, causing a heavy burden to global health care systems. Moreover, AKI is a frequent complication of hospitalization, and it is associated with short-term morbidity and mortality rate greater than 50%, as a result of its relationship with other severe complications. Furthermore, multiple pathophysiologic processes are involved in AKI, such as cellular death, apoptosis, mesenchymal transition, cellular infiltration, inflammation, cytokines release, coagulation, and complement activation. Since increasing evidence highlighted the central role of the immune system in AKI pathophysiology, several efforts have been made to delineate the link between this disease and the different population of immune cells. This narrative review aims to describe the role played by dendritic cells (DCs) in AKI, with a special focus on recent findings suggesting DCs suppression as a promising strategy to prevent AKI negative side effects and ameliorate renal injury and dysfunction. Furthermore, we briefly summarize the main characteristics of innovative high-throughput techniques, including as genomics, transcriptomics, proteomics, and metabolomics in the context of AKI.

Objectives: Diabetic kidney disease (DKD) is the leading cause of kidney failure worldwide. Different phenotypes of DKD are emerging, partially attributable to a better glycemic control, partially to concomitant risk factors for kidney disease. Diabetes belongs to Non-Communicable Diseases (NCD), but poor data about DKD in Low-Middle Income Countries are currently available. In the present paper we compare two cohorts of patients affected by DKD from Tanzania and from Italy. Study design: Retrospective observational study conducted by NCDs Clinic of Tosamaganga Regional Referral Hospital (Tanzania) and from the Multidisciplinary Diabetological-Nephrological Clinic of Bologna (Italy) Methods: Included patients’data were analyzed for demographical features, diabetes complications, laboratory findings and pharmacological therapy at the time of enrollment and after 6-month follow up. Results: Tanzanian patients were younger (56.65 vs 67.66 years, p< 0.001), with a higher prevalence of women (66.9% vs 25.5%, p< 0.001) and showed lower level of BMI (26.39 vs 30.18 kg/m2, p< 0.001). A worsen glycemic control could be observed in Tanzanian cohort (HbA1c 83.71 vs 56.92 mmol/mol, p< 0.001) and higher eGFR (70.13±31.93 vs 52.31±23.37 ml/min, p< 0.001). A sharp reduction of albuminuria was observed in both cohorts with an increase in nephroprotective drugs a better glycemic control. Conclusions: Two phenotypes of diabetic patients have emerged from comparison between two cohorts. Tanzanian patients are mostly female, younger and with normal BMI; whereas Italian patients are mainly male, older and affected by metabolic syndrome and vascular complications. Therapy implementation is associated with a delayed decline of eGFR and downgrading of albuminuria at 6 months follow up.