Complement activation in wasp venom-induced acute kidney injury.

Previous studies have highlighted the significant role of complement activation in kidney injuries induced by rhabdomyolysis, intravascular hemolysis, sepsis, and ischemia-reperfusion. Nevertheless, the specific role and mechanism of complement activation in acute kidney injury (AKI) caused by wasp venom remain unclear. The aim of this study was to elucidate the specific complement pathway activated and investigate complement activation in AKI induced by wasp venom. In this study, a complement-depleted mouse model was used to investigate the role of complement in wasp venom-induced AKI. Mice were randomly categorized into control, cobra venom factor (CVF), AKI, and CVF + AKI groups. Compared to the AKI group, the CVF + AKI group showed improved pathological changes in kidneys and reduced blood urea nitrogen (BUN) levels. The expression levels of renal complement 3 (C3), complement 5 (C5), complement 1q (C1q), factor B (FB), mannose-binding lectin (MBL), and C5b-9 in AKI group were upregulated compared with the control group. Conversely, the renal tissue expression levels of C3, C5, C1q, FB, MBL, and C5b-9 were decreased in the CVF + AKI group compared to those in the AKI group. Complement activation occurs through all three pathways in AKI induced by wasp venom. Furthermore, complement depletion by CVF attenuates wasp venom-induced nephrotoxicity, suggesting that complement activation plays a primary role in the pathogenesis of wasp venom-induced AKI.

Design of a 140 GHz waveguide notch filter for millimeter-wave receiver module protection in fusion plasma diagnostics.

A carefully designed waveguide-based millimeter-wave notch filter, operating at 140 GHz, safeguards plasma diagnostic instruments from gyrotron leakage. Utilizing cylindrical cavity resonators with aperture coupling, the filter efficiently resonates 140 GHz wave-power into the TE11p mode, optimizing various geometrical parameters for practical fabrication and high-yield production. Thorough thermal analysis ensures its ability to handle power. The filter achieves outstanding performance with over 90 dB rejection at 140 GHz while providing low insertion loss over the passband (110-138 GHz), which is ideally suited for system-on-chip approach F-band diagnostic system applications.

The role and mechanism of NLRP3 in wasp venom-induced acute kidney injury.

BACKGROUND: Inflammation and pyroptosis have crucial impacts on the development of acute kidney injury (AKI) and have been validated in a variety of existing AKI animal models. However, the mechanisms underlying wasp venom-induced AKI are still unclear. The involvement of nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) in some mouse models of AKI has been extensively documented, and its crucial function in controlling inflammation and pyroptosis has been highlighted. The objective of our study was to investigate the role and mechanism of NLRP3 in inflammation and pyroptosis associated with wasp venom-induced AKI. METHODS: A mouse model of AKI induced by wasp venom pre-injected with an NLRP3 inhibitor was used to study the role and mechanism of NLRP3. To verify the importance of NLRP3, western blotting was performed to assess the expression of NLRP3, caspase-1 p20, and gasdermin D (GSDMD)-N. Additionally, quantitative real-time polymerase was used to determine the expression of NLRP3, caspase-1, and GSDMD. Furthermore, enzyme-linked immunosorbent assay was utilized to measure the levels of interleukin (IL)-1ß and IL-18. RESULTS: NLRP3 was found to be the downstream signal of the stimulator of interferon genes in the wasp sting venom-induced AKI model. The administration of wasp venom in mice significantly upregulated the expression of NLRP3, leading to renal dysfunction, inflammation, and pyroptosis. Treatment with an NLRP3 inhibitor reversed the renal damage induced by wasp venom and attenuated pathological injury, inflammatory response, and pyroptosis. CONCLUSION: NLRP3 activation is associated with renal failure, inflammatory response and pyroptosis in the hyper early phase of wasp venom-induced AKI. The inhibition of NLRP3 significantly weakened this phenomenon. These findings could potentially offer a viable therapeutic approach for AKI triggered by wasp venom.

STING deficiency protects against wasp venom-induced acute kidney injury.

OBJECTIVE: Recent evidence suggests a key role of the inflammatory responses in wasp venom-induced acute kidney injury (AKI). However, the potential regulatory mechanisms underlying the inflammatory responses in wasp venom-induced AKI remain unclear. STING reportedly plays a critical role in other AKI types and is associated with inflammatory responses and diseases. We aimed to investigate the involvement of STING in inflammatory responses associated with wasp venom-induced AKI. METHODS: The role of the STING signaling pathway in wasp venom-induced AKI was studied in vivo using a mouse model of wasp venom-induced AKI with STING knockout or pharmacological inhibition and in vitro using human HK2 cells with STING knockdown. RESULTS: STING deficiency or pharmacological inhibition markedly ameliorated renal dysfunction, inflammatory responses, necroptosis, and apoptosis in wasp venom-induced AKI in mice. Moreover, STING knockdown in cultured HK2 cells attenuated the inflammatory response, necroptosis, and apoptosis induced by myoglobin, the major pathogenic factor in wasp venom-induced AKI. Urinary mitochondrial DNA upregulation has also been observed in patients with wasp venom-induced AKI. CONCLUSIONS: STING activation mediates the inflammatory response in wasp venom-induced AKI. This may offer a potential therapeutic target for the management of wasp venom-induced AKI.

Wasp venom-induced acute kidney injury: current progress and prospects.

Wasp venom can trigger local and systemic reactions, with the kidneys being commonly affected, potentially causing acute kidney injury (AKI). Despite of the recent advances, our knowledge on the underlying mechanisms of toxicity and targeted therapies remain poor. AKI can result from direct nephrotoxic effects of the wasp venom or secondary rhabdomyolysis and intravascular hemolysis, which will release myoglobin and free hemoglobin. Inflammatory responses play a central role in these pathological mechanisms. Noteworthily, the successful establishment of a suitable experimental model can assist in basic research and clinical advancements related to wasp venom-induced AKI. The combination of therapeutic plasma exchange and continuous renal replacement therapy appears to be the preferred treatment for wasp venom-induced AKI. In addition, studies on cilastatin and varespladib for wasp venom-induced AKI treatment have shown their potential as therapeutic agents. This review summarizes the available evidence on the mechanisms and treatment of wasp venom-induced AKI, with a particular focus on the role of inflammatory responses and potential targets for therapeutic drugs, and, therefore, aiming to support the development of clinical treatment against wasp venom-induced AKI.

Impact of enhanced recovery after surgery program for hungry bone syndrome in patients on maintenance hemodialysis undergoing parathyroidectomy for secondary hyperparathyroidism.

Purpose: Hungry bone syndrome after parathyroidectomy is an important clinical problem in patients on maintenance hemodialysis. We examined the effect of an enhanced recovery after surgery (ERAS) program on the incidence of hungry bone syndrome after parathyroidectomy in this population. Methods: This single-institution, retrospective study analyzed 108 patients on hemodialysis who underwent parathyroidectomy for secondary hyperparathyroidism. Patients were classified into the pre-ERAS (n = 52) and post-ERAS (n = 56) groups. The ERAS program identified high-risk patients and enforced aggressive measures to normalize calcium levels following parathyroidectomy. Results: There was no significant difference in age, sex, body weight, presenting symptoms, preoperative calcium and alkaline phosphatase levels, postoperative intact parathyroid levels, postoperative calcium levels at 1 and 24 hours after parathyroidectomy, and 30-day readmission rates between the groups. The post-ERAS group had significantly higher levels of postoperative calcium at 48 and 72 hours after parathyroidectomy, but a lower incidence of hungry bone syndrome and shorter postoperative length of stay. Patients with hungry bone syndrome had higher preoperative levels of alkaline phosphatase and intact parathyroid, longer postoperative length of stay, and were less likely to have been part of the ERAS program. High preoperative alkaline phosphatase levels and absence of the ERAS program were independent risk factors for hungry bone syndrome after parathyroidectomy. Conclusion: The ERAS program reduced the incidence of hungry bone syndrome and shortened the postoperative length of stay in patients on maintenance hemodialysis who underwent parathyroidectomy for secondary hyperparathyroidism.

Megalin blockade with cilastatin ameliorates multiple wasp sting-induced acute kidney injury in rats.

Cilastatin has been shown to prevent various drug-induced nephrotoxicities and confer renoprotection in a mouse model of glycerol-mediated rhabdomyolysis-induced acute kidney injury (AKI). The present study aimed to investigate whether cilastatin attenuates wasp sting-induced AKI in rats. Male Wistar rats were divided into the control, cilastatin, AKI, and AKI + cilastatin groups. Nephrotoxicity was assessed using renal function, rhabdomyolysis (creatine kinase, CK) and intravascular hemolysis (lactate dehydrogenase, LDH) markers, and histological changes. In addition, tubular injury biomarkers, apoptosis, oxidative stress markers, complement C3 expression, and urine and blood myoglobin levels were examined. Compared with the control or cilastatin group, the AKI group showed significant histological damage, increased levels of CK, LDH, and creatinine, and increased mRNA expression of tubular injury biomarkers. Cilastatin ameliorated wasp venom-induced kidney injury by attenuating oxidative stress and apoptosis. Cilastatin also reduced C3 expression in the renal tubular cells. In addition, cilastatin reduced serum myoglobin levels and increased urine myoglobin concentrations. Therefore, megalin blockade with cilastatin attenuates wasp venom-induced AKI owing to its antioxidative and antiapoptotic properties.

Phospholipase A2 inhibitor varespladib prevents wasp sting-induced nephrotoxicity in rats.

This study aimed to clarify whether varespladib, a phospholipase A2 (PLA2) inhibitor, can be used as a therapeutic agent for wasp sting-induced acute kidney injury (AKI). Rats were divided into control, AKI, and AKI + varespladib groups. The AKI model was established by subcutaneously injecting wasp venom at five different sites in rats. Varespladib treatment showed a significant inhibitory effect on wasp venom PLA2in vitro and in vivo. Moreover, we observed that varespladib decreased the levels of rhabdomyolysis and hemolysis markers compared with that in the AKI group. Histopathological changes in the kidney decreased significantly, and rat serum creatinine levels were reduced after varespladib administration. The significantly regulated genes in the kidney of the AKI group were mostly involved in inflammatory response pathway, and the administration of varespladib remarkably attenuated the expression of these genes. Therefore, varespladib inhibited wasp sting-induced functional and pathological damage to the kidneys. We propose that the PLA2 inhibitor varespladib protects the kidney tissue in a wasp sting-induced AKI model by inhibiting PLA2 activity.

A retrospective observational study of patients on maintenance hemodialysis receiving parathyroidectomy by ultrasonic scalpel.

BACKGROUND: Secondary hyperparathyroidism (SHPT) remains a common complication in many patients on maintenance hemodialysis. Kidney Disease Improve Global Outcomes (KDIGO) 2017 guidelines suggest that parathyroidectomy (PTX) should be performed in severe SHPT patients with chronic kidney disease stage 3a-stage 5D. In the present study, we observed the efficacy of ultrasonic scalpel for PTX in SHPT patients on maintenance hemodialysis. METHODS: A total of 74 patients on maintenance hemodialysis who underwent PTX (34 with traditional electrocautery and 40 with an ultrasonic scalpel) were observed between August 2020 and August 2021 at Xiangyang Central Hospital (Hubei University of Arts and Science). Baseline demographic and clinic characteristics were collected pre- and post-PTX. Moreover, the postoperative complications and operation time were assessed between the two groups. RESULTS: The univariate analysis showed that there was no statistical significance in weight, dialysis duration, serum potassium, serum calcium, serum magnesium, alkaline phosphate, triglyceride, and intact parathyroid hormone (iPTH) before and after PTX between the two groups (P > 0.05). The operation time in the ultrasonic scalpel group was significantly decreased compared with the traditional electrocautery group (P < 0.05). Compared with the traditional electrocautery group, the drainage amount was significantly reduced in the ultrasonic scalpel group, and the number of days with drain and postoperative hospital stay were also remarkably decreased (P < 0.05). CONCLUSIONS: The use of ultrasonic scalpel significantly reduced the operation time and postoperative hospital stay in patients on maintenance hemodialysis undergoing PTX.

A rat model of acute kidney injury caused by multiple subcutaneous injections of Asian giant hornet (Vespa mandarina Smith) venom.

A model of acute kidney injury (AKI) caused by multiple subcutaneous injections of Asian giant hornet (Vespa mandarina Smith) venom was developed in male Wistar rats. The rats were injected subcutaneously at multiple sites in the dorsal region with a total venom dose of 5 mg/kg. Blood samples were obtained 8, 24 and 48 h after venom injection for the quantification of various biochemical parameters and assessment of renal function. Wasp venom caused significant increases in all biochemical parameters (aspartate aminotransferase, creatine kinase, free hemoglobin, lactate dehydrogenase, myoglobin, and plasma creatinine) within 8 h of venom administration, as well as marked alterations in renal function (a decrease in glomerular filtration rate leading to oliguria). The biochemical parameters showed varying degrees of recovery but remained elevated to varying degrees after 48 h, whereas the glomerular filtration rate showed no recovery during this period. The histopathological alterations consisted primarily of acute tubular necrosis, with tubular epithelial cell sloughing and loss of tubule brush border. This profile of biochemical and functional alterations was similar to that seen in human envenomations by this species, suggesting that this animal model may be useful for understanding the pathophysiology of AKI caused by this wasp venom.

An integrative proteomics metabolomics based strategy reveals the mechanisms involved in wasp sting induced acute kidney injury.

The pathophysiological mechanisms involved in wasp-sting-induced acute kidney injury (AKI) remain largely unknown. Here, we combined proteomics and metabolomics to investigate the mechanisms behind multiple wasp sting-induced AKI. Interestingly, we found many differentially abundant proteins in the serum of AKI group compared with that of the non-AKI and control groups, involved in several metabolic pathways and the regulation of cellular processes. In addition, we also detected differentially abundant metabolites in the AKI group; among them many were involved in the glycerophospholipid metabolic pathway (the key pathway in the context of AKI): 50 metabolites, all downregulated in the AKI group. Importantly, the convergent analysis of metabolomics and proteomics data revealed that biomarkers of rhabdomyolysis (CA 3, MYL3, and LDH) and hemolysis (ALT and LDH) were integrated into a regulatory network with phospholipid metabolism products in the AKI group, indicating that wasp sting-induced AKI is secondary to rhabdomyolysis and intravascular hemolysis. Of note, such a phenotype suggests the disruption of the membrane of skeletal muscle cells and red blood cells mediated by the phospholipase A1 (PLA1), PLA2, and mastoparan in the wasp venom, via the disruption of membrane glycerophospholipids. Overall, our results highlight a potential new mechanism behind wasp sting-induced AKI and suggest that PLA inhibitors may be potential agents for the treatment of this condition.

A retrospective cohort study comparing high and low balloon inflation pressure on technical success and patency for treating central venous lesions in patients on chronic hemodialysis.

BACKGROUND: We aimed to analyze the success rates and the access patency rates at 12 months between patients on chronic hemodialysis with symptomatic central venous stenosis (CVS) or occlusion (CVO), receiving high or low balloon inflation pressure for treatment. METHODS: We performed a retrospective study in which angioplasty balloons were inflated using a low-pressure or a high-pressure for the management of hemodialysis patients with CVS/CVO. The outcomes of this study were the success rate and the access patency rates at 12 months after balloon angioplasty, and the differences between groups were compared. RESULTS: We included a total of 74 patients on hemodialysis and assigned them to the low-pressure or the high-pressure groups. Success rates in patients of the high-pressure group (94.12%) were higher than those in patients of the low-pressure group (67.50%) (p = 0.005). With a total of 59 patients with technical success, at 6 and 12 months after angioplasty, the rates of access patency in the low-pressure group were 68 and 48%, respectively; on the other hand, the primary patency rates in the high-pressure group were 86.67% (6-months) and 76.67% (12-months). The 6 and 12 months post-interventional patency rates were higher in patients of the high-pressure group than those in patients of the low-pressure group (p = 0.10 at 6 months and p = 0.03 at 12 months). CONCLUSIONS: Compared to balloon angioplasty using a low inflation pressure, hemodialysis patients with CVS/CVO receiving angioplasty using a high inflation pressure have significantly higher technical success and 12-month patency rates.

Clinical Features and Outcomes of Acute Kidney Injury in Patients Infected with COVID-19 in Xiangyang, China.

BACKGROUND: In December 2019, pneumonia associated with COVID-19 has spread from Wuhan to other areas in China. In the present study, we aimed to further clarify the clinical features and outcomes of acute kidney injury (AKI) in patients infected with COVID-19 in Xiangyang, Hubei, China. METHODS: All confirmed cases of COVID-19 with AKI in Xiangyang Central Hospital from January 22 to May 31, 2020, were included in this retrospective study. Data of epidemiological, clinical, laboratory, radiological tests, treatment, complication, and outcomes were collected and analyzed. Patients were divided into intensive care unit (ICU) group and isolation ward (non-ICU) group. RESULTS: Of the total patients, 33.3% in the non-ICU group and 85.7% in the ICU group had chronic diseases. In addition, 85.7% of patients in the ICU group died. The most common symptoms were fever, cough, and fatigue. The lymphocyte count in the ICU group was significantly reduced compared with the non-ICU group. The chest computed tomography (CT) images appeared showed multiple mottles and ground-glass opacity. Strip shadow could be found in chest CT images of some recovered patients. All patients received antiviral treatment. Most patients in the ICU group were given methylprednisolone, immunoglobulin, antibiotics, and mechanical ventilation and 35.7% of patients in the ICU group received continuous renal replacement therapy. CONCLUSIONS: Elderly with chronic comorbidities were more susceptible to COVID-19, showing a higher mortality rate due to multiple organ damage, and 35.7% of patients with AKI in ICU received renal replacement therapy. Moreover, part of the cured patients might need additional time to recover for poor lung function.

Role of collectin-11 in innate defence against uropathogenic Escherichia coli infection.

Classical collectins (surfactant protein A and D) play a significant role in innate immunity and host defence in uropathogenic Escherichia coli (UPEC)-induced urinary tract infection (UTI). However, the functions of collectin-11 (CL-11) with respect to UPEC and UTI remain largely unexplored. This study aimed to investigate the effect of CL-11 on UPEC and its role in UTI. We further examined its modulatory effect on inflammatory reactions in proximal tubular epithelial cells (PTECs). The present study provides evidence for the effect of CL-11 on the growth, agglutination, binding, epithelial adhesion and invasion of UPEC. We found increased basal levels of phosphorylated p38 MAPK and human cytokine homologue (keratinocyte-derived chemokine) expression in CL-11 knockdown PTECs. Furthermore, signal regulatory protein α blockade reversed the increased basal levels of inflammation associated with CL-11 knockdown in PTECs. Additionally, CL-11 knockdown effectively inhibited UPEC-induced p38 MAPK phosphorylation and cytokine production in PTECs. These were further inhibited by CD91 blockade. We conclude that CL-11 functions as a mediator of innate immunity via direct antibacterial roles as well as dual modulatory roles in UPEC-induced inflammatory responses during UTI. Thus, the study findings suggest a possible function for CL-11 in defence against UTI.

Plasma exchange for treating anti-Yo-associated paraneoplastic cerebellar degeneration: Case report and literature review.

RATIONALE: Paraneoplastic cerebellar degeneration (PCD) is a rare neurodegenerative syndrome associated with antibodies targeting the Purkinje cells of the cerebellum. Most cases of anti-Yo-associated PCD occur in females, with <20 cases reported in males. Herein, we report a male patient with anti-Yo-associated PCD who was treated with plasma exchange and achieved a favorable outcome. PATIENT CONCERNS: A 64-year-old man presented with progressive ataxia, gait instability, and dysuria. Electroencephalography, electromyography, brain and spinal neuroimaging, and routine laboratory examinations were all normal. The anti-neuronal antibody Anti-Yo was detected in the serum but not in the cerebrospinal fluid (CSF). DIAGNOSIS: The patient was diagnosed with definite anti-Yo-associated PCD based on the clinical manifestations, anti-Yo was detected in the serum and response to treatment. INTERVENTIONS: At beginning, the patient was treated with dexamethasone (10 mg/day for 10 days). Then, plasma exchange was performed. OUTCOMES: After treated with dexamethasone, no clinical improvement was noted in this patient. In the following month, his condition deteriorated. However, after two courses of plasma exchange, neurological examination showed marked improvement in gait. After four courses of plasma exchange, the patient could walk independently, the Romberg test was negative, and anti-Yo antibodies were undetectable. At the 6-month follow-up, the patients' symptoms were relieved, and tests for anti-Yo antibodies remained negative. LESSONS SUBSECTIONS: Treatment with plasma exchange for anti-Yo-associated male PCD patients without a concomitant tumor are recommend and need more studies.

Risk factors of acute kidney injury induced by multiple wasp stings.

In Asia, acute kidney injury (AKI) induced by wasp stings is common; however, the pathophysiological mechanisms involved remain unclear. To evaluate the mechanisms associated with AKI induced by wasp stings, we conducted a retrospective cohort study that assessed blood and urinary samples from 112 patients with hospital admissions resulting from wasp stings. These samples were divided into those with AKI and without AKI as described in the Kidney Disease Improving Global Outcomes (KDIGO) database. Of the patients, 48.2% presented with an elevated number of leukocytes (median 19.9 vs. 15.8 × 109/L), serum creatinine (median 122.0 vs. 66.0 µmol/L), alanine aminotransferase (ALT) (median 176 vs. 32 U/L), aspartate aminotransferase (AST) (median 402 vs. 37 U/L), lactate dehydrogenase (LDH) (median 3076.0 vs. 300.0 U/L), creatine kinase (CK) (median 9990.0 vs. 261.0 U/L), creatine kinase myocardial band (CK-mb) (median 200.0 vs. 29.5 U/L), activated partial thromboplastin time (APTT) (median 70.0 vs. 42.5s), prothrombin time (PT) (median 15.0 vs. 12.5s), myoglobin (median 2200.0 vs. 78.0 ng/mL), proteinuria (51.9% vs. 17.2% ≥ 1+), and urinary monocyte chemotactic protein-1 (MCP-1) (median 432.0 vs. 177.0 pg/mL), and subsequently developed AKI. As determined by multivariate logistic regression analysis, elevated leukocytes (>10 × 109/L) [OR 1.12 (95% CI 1.02-1.23)], high myoglobin (>1200 ng/mL) [OR 18.51 (95% CI 1.51-132.27)], and high urinary MCP-1 (>200 pg/mL) [OR 5.42 (95% CI 1.27-30.39)] on admission were independent risk factors for AKI. At admission, baseline values for ALT, aspartate aminotransferase (AST), LDH, CK-mb, APTT, PT, and proteinuria were higher for those who later died as well as for those who developed end-stage renal disease (ESRD). No patients without AKI died or developed ESRD. The present study explored the pathophysiology of AKI induced by wasp stings based on the findings of risk factors as well as factors related to outcomes. An understanding of AKI induced by wasp stings allows better treatment options and clinical management for wasp stings patients.

Coronavirus Disease 2019 in a Hemodialysis Patient.

There has been a global outbreak of the coronavirus disease 2019 (COVID-19) since December 2019. Here, we describe the case of a 49-year-old male undergoing maintenance hemodialysis (HD) who got infected with COVID-19 and our experience in performing HD for him. The patient's symptoms and lung imaging changes were atypical. However, his lymphocyte range decreased upon admission and the polymerase chain reaction of the pharyngeal swab for the -COVID-19 nucleic acid was positive. The patient developed respiratory failure and required mechanical ventilation 8 days after admission. In the end, he died from multiple organ dysfunction syndrome. The difficulties in diagnosis, infection control, and treatment of COVID-19 in maintenance HD patients are discussed in this report.

Wasp venom and acute kidney injury: The mechanisms and therapeutic role of renal replacement therapy.

Stinging accidents involving wasp venom are a notable cause of acute kidney injury (AKI) in Asia. However, very little attention has been paid to the understanding of the mechanisms involved in this type of AKI. The aims of this review are to explore the evidence for the mechanisms and the therapeutic role of renal replacement therapy of wasp venom and AKI. A systematic literature search was conducted using PubMed for the association among wasp venom and AKI. Wasp venom is a complex mixture of biologically active components, including enzymes, amines, and peptides. Wasp venom may induce local anaphylaxis reactions as well as systemic reactions such as AKI. AKI may develop as a result of direct nephrotoxic effects of the venom or secondary intravascular hemolysis and/or rhabdomyolysis. Histopathological features of renal biopsies predominantly include acute tubular necrosis and acute interstitial nephritis. Renal replacement therapy, which includes intermittent hemodialysis, hemoperfusion, plasmapheresis, continuous renal replacement therapy, and peritoneal dialysis, has been used to treat severe AKI cases induced by wasp stings. Continuous renal replacement therapy appears to provide more benefit than intermittent hemodialysis in the treatment of wasp sting-induced AKI. In this review, we summarize the existing evidence of the mechanisms and treatment for venom-induced AKI, with a particular emphasis on the role of renal replacement therapy in the management of severe AKI following massive wasp stings.

Surfactant protein D attenuates acute lung and kidney injuries in pneumonia-induced sepsis through modulating apoptosis, inflammation and NF-κB signaling.

Pneumonia and sepsis are major risk factors for acute kidney injury (AKI). Patients with pneumonia and AKI are at increased risk for morbidity and mortality. Surfactant protein D (SP-D) expressed in lung and kidney plays important roles in innate immunity. However, little is known about the role of organ-specific SP-D in the sepsis. The current study uses wild type (WT), SP-D knockout (KO), and humanized SP-D transgenic (hTG, lung-specific SP-D expression) mice to study organ-specific role of SP-D in pneumonia-induced sepsis. Analyses demonstrated differential lung and kidney injury among three-type mice infected with Pseudomonas aeruginosa. After infection, KO mice showed higher injurious scores in both lung and kidney, and decreased renal function than WT and hTG mice. hTG mice exhibited comparable lung injury but more severe kidney injury compared to WT mice. Increased renal tubular apoptosis, NF-κB activation and proinflammatory cytokines in the kidney of KO mice were found when compared with WT and hTG mice. Furthermore, in vitro primary proximal tubular epithelial cells from KO mice showed more apoptosis with higher level of activated caspase-3 than those from WT mice after LPS treatment. Collectively, SP-D attenuates AKI in the sepsis by modulating renal apoptosis, inflammation and NF-κB signaling.

Collectins in urinary tract and kidney diseases.

The innate immune system serves as the frontline defense against invading pathogens and initiates an inflammatory response to microorganisms. Collectins are C-type lectins that are structurally characterized by a collagen-like sequence and a carbohydrate recognition domain. Moreover, they are widely expressed throughout the body and are involved in the innate immunity against a variety of pathogens, regulating inflammation, and protecting the lungs from pathogens. Recently, two classical collectins, surfactant protein A (SP-A) and surfactant protein D (SP-D), as well as novel collectin 11, were found present in urinary tract tissues. They are increasingly recognized as key players in activating the humoral arm of innate immunity and host defense in urinary tract and kidney diseases, although their biological features, functions, and mechanisms in this regard remain largely unclear. In this review, we aim to integrate results reported by ourselves and others to summarize and gain a better understanding of the functions of collectins (SP-A, SP-D, and collectin 11) in urinary tract and kidney diseases.