Immunoglobulin M (IgM) nephropathy (IgMN) is characterized by the IgM deposition in the kidney’s mesangium. We assessed the impact of electron-dense deposits (EDDs) on IgMN and compared it to other kidney diseases. Methods: We enrolled 63 adult patients with IgMN who underwent renal biopsy from May 2003 to June 2017. We compared clinicopathological features of IgMN based on EDD presence; compared characteristics to 91 minimal change disease (MCD), 103 focal segmental glomerulosclerosis (FSGS), and 469 immunoglobulin A nephropathy (IgAN) patients. Renal events were defined as a >50% decrease in estimated glomerular filtration rate (eGFR), eGFR of <15 mL/min/1.73 m2, or end-stage renal disease development. Results: IgMN patients with EDDs had increased mesangial cellularity, matrix accumulation, prominent immunofluorescent staining, and more diffuse podocyte effacement than those without EDD. Clinical characteristics and renal outcomes did not differ significantly based on EDD presence. During 79.5 ± 58.8 months of follow-up, renal events developed in 46.2% and 46.0% of IgMN cases with and without EDD. IgMN (46.0%) and FSGS cases (40.8%) had similar frequencies of renal events and higher frequency than MCD (18.7%) or IgAN cases (26.4%). IgMN cases had more severe manifestations than MCD and IgAN; higher blood pressure, lower proteinuria, and eGFR levels at biopsy than MCD cases; higher blood pressure, proteinuria, frequency of acute kidney injury, and lower eGFR levels. Conclusion: Clinical characteristics of IgMN did not differ based on EDD presence. Therefore, IgMN should be defined based on IF findings. IgMN shared clinical characteristics with FSGS but had more severe than MCD and IgAN.

EW-7197, a potent oral ALK5 inhibitor, was assessed for its impact on transforming growth factor beta 1 (TGF-β1)–induced fibrosis in a three-dimensional (3D) renal fibrosis-on-a-chip and a mouse model. The evaluation included tubular epithelial- mesenchymal transition, angiogenesis, and inflammatory cytokine expression. Methods: In a 3D renal fibrosis-on-a-chip model, three cell types(kidney fibroblasts, human proximal tubular cells, and human umbilical vein endothelial cells) were cultured and treated with TGF-β1 and EW-7197. Alpha smooth muscle actin (α-SMA) and keratin 8 (KRT-8) was assessed, angiogenesis observed via confocal microscopy, and cytokine levels measured by polymerase chain reaction, immunoassay, and enzyme-linked immunosorbent assay. In a cisplatin-induced renal fibrosis mouse model, blood urea nitrogen levels, TGF-β, and Smad 2/3 were determined, and fibrosis was assessed with Masson’s trichrome stain. Results: The α-SMA expression was significantly lower in the EW-7197 group than in the TGF-β fibrosis group. TGF-β decreased the expression of the epithelial marker KRT-8, an effect that was reversed by EW-7197 and SB431542. In the TGF-β–induced fibrosis model, the length of the thick vessels was reduced, and the diameter of both thick and thin vessels was decreased, but EW-7197 reversed these effects. EW-7197 significantly reduced the messenger RNA expression of TGF-β and increased the levels of vascular endothelial growth factor receptor 2, interleukin (IL)-10, and IL-6. EW-7197 reduced the levels of secretory cytokines TGF-β1, TGF-β3, IL- 1β. In the cisplatin-induced renal fibrosis mouse model, EW-7197 reduced renal fibrosis by down-regulating TGF-β signaling. Conclusion: EW-7197 attenuated the TGF-β1–induced fibrotic cellular response in the 3D chip model and animal model. These findings indicate the potential effect of EW-7197 in attenuating renal fibrosis.

The disease burden of chronic kidney disease (CKD) and its impact on healthcare systems has been poorly studied in Asia, a socioeconomically diverse region with wide variations in availability, access, and quality of CKD care. The high CKD burden in this region is predominantly driven by an increased prevalence of risk factors including diabetes mellitus, hypertension, obesity, and use of traditional medicines and is further aggravated by challenges associated with effective implementation of population-based screening and surveillance systems in early detection and intervention of CKD. The Asian continent mostly comprised of low- and middle-income countries with resource restraints lacks robust population-based CKD registries resulting in a paucity of data on CKD incidence and prevalence, various treatment modalities, uptake of current guidelines, and the overall impact of implementation of developmental programs. There is an urgent need for a collaborative action plan between the healthcare community and governments in this region to detect CKD in its early stages and prevent its complications including kidney failure, cardiovascular disease, and death. Research- based evidence on the impact of early detection, sustainable treatment options, quality of life, delay or avoidance of dialysis, and related cost analysis is the need of the hour. We highlight successful implementation of strategic and policy-sharing programs adopted in a few countries; also, consolidate available region-specific data, quantify estimates of CKD burden and propose strategies with a multidisciplinary approach involving patients, the healthcare community and governmental bodies to combat CKD and its complications.

Background: Posttransplant diabetes mellitus (PTDM) complicates kidney transplant recipients (KTRs) in morbidity and mortality. This study aimed to predict PTDM risk in KTRs using machine learning and deep learning models. Methods: Data were obtained from the Korea Organ Transplantation Registry, a nationwide cohort study of KTRs. Four machine learning algorithms, including eXtreme Gradient Boosting (XGBoost), CatBoost, light gradient boosting machine and logistic regression, and deep learning were implemented on 41 pretransplant and 31 posttransplant variables to predict PTDM. Model performance was assessed using the area under the curve (AUC) of the receiver operating characteristic curve, accuracy, precision, recall, and F1 score. Results: Among 3,213 KTRs, 497 patients (15.5%) developed PTDM within 1 year. The PTDM group had higher age, body mass index (BMI), triglyceride level, and prevalence of hypertension and cardiovascular disease, and lower total cholesterol level at baseline than the No-PTDM group. The XGBoost model showed the highest AUC (0.738) and F1 score (0.42), and modest accuracy (0.86), while the CatBoost model exhibited the highest accuracy (0.87) and precision (0.79). Feature importance in XGBoost was highest for recipient age, followed by baseline BMI, triglyceride level at posttransplant 6 months, baseline glycated hemoglobin and high-density lipoprotein cholesterol level, white blood cell (WBC) count and serum uric acid level at 6 months, baseline WBC count, and tacrolimus trough level at discharge. Conclusion The XGBoost model demonstrated the best performance for predicting PTDM within 1 year, offering an accurate tool for early identification and personalized care of high-risk KTRs for PTDM.

Objective: Many studies have examined the July effect. However, little is known about the July effect in sepsis. We hypothesized that the July effect would result in worse outcomes for patients with sepsis. Methods: Data from patients with sepsis, collected prospectively between January 2018 and December 2021, were analyzed. In Korea, the new academic year starts on March 1, so the “July effect” appears in March. The primary outcome was 30-day mortality. Secondary outcomes included adherence to the Surviving Sepsis Campaign bundle. Outcomes in March were compared to other months. A multivariate Cox proportional hazard regression was performed to adjust for confounders. Results: We included 843 patients. There were no significant differences in sepsis severity. The 30-day mortality in March was higher (49.0% vs. 28.5%, P<0.001). However, there was no difference in bundle adherence in March (42.2% vs. 48.0%, P=0.264). The multivariate Cox proportional hazard regression showed that the July effect was associated with 30-day mortality in patients with sepsis (adjusted hazard ratio, 1.925; 95% confidence interval, 1.405–2.638; P<0.001). Conclusion The July effect was associated with 30-day mortality in patients with sepsis. However, bundle adherence did not differ. These results suggest that the increase in mortality during the turnover period might be related to unmeasured in-hospital management. Intensive supervision and education of residents caring for patients with sepsis is needed in the beginning of training.

Orthopedic surgeons treating fractures need to consider comorbidities, including chronic kidney disease (CKD), which affects millions worldwide. CKD patients are at elevated risk of fractures due to osteoporosis, especially in advanced stages. In addition, fractures in CKD patients pose challenges due to impaired bone healing and increased post-fracture complications including surgical site infection and nonunion. In this article, we will discuss factors that must be considered when treating fractures in CKD patients.Perioperative management includes careful adjustment of hemodialysis schedules, selection of anesthetic methods, and addressing bleeding tendencies. Tourniquet usage for fractures in limbs with arteriovenous fistulae should be cautious. Pain medication should be administered carefully, with opioids like hydromorphone preferred over nonsteroidal anti-inflammatory drugs. Medical management after fractures should address underlying factors and include physical rehabilitation to reduce the risk of subsequent fractures. A comprehensive approach to fracture management in CKD patients can improve outcomes.

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is a common cause of autoimmune encephalitis. The condition is difficult to diagnose or suspect in the emergency department because it usually presents with nonspecific neurological or psychiatric symptoms. It is often mistaken for viral encephalitis or psychiatric illness. This paper reports a case of anti-NMDAR encephalitis in which the patient experienced mood changes, including suicidal ideation, which led to a delayed diagnosis after three visits to the emergency department. This paper aims to raise awareness among emergency physicians about the possibility of anti-NMDAR encephalitis and to encourage them to consider it in their differential diagnosis in the emergency department.

Hyponatremia is primarily a water balance disorder associated with high morbidity and mortality. The pathophysiological mechanisms behind hyponatremia are multifactorial, and diagnosing and treating this disorder remains challenging. In this review, the classification, pathogenesis, and step-by-step management approaches for hyponatremia in patients with liver disease are described based on recent evidence. We summarize the five sequential steps of the traditional diagnostic approach: 1) confirm true hypotonic hyponatremia, 2) assess the severity of hyponatremia symptoms, 3) measure urine osmolality, 4) classify hyponatremia based on the urine sodium concentration and extracellular fluid status, and 5) rule out any coexisting endocrine disorder and renal failure. Distinct treatment strategies for hyponatremia in liver disease should be applied according to the symptoms, duration, and etiology of disease. Symptomatic hyponatremia requires immediate correction with 3% saline. Asymptomatic chronic hyponatremia in liver disease is prevalent and treatment plans should be individualized based on diagnosis. Treatment options for correcting hyponatremia in advanced liver disease may include water restriction; hypokalemia correction; and administration of vasopressin antagonists, albumin, and 3% saline. Safety concerns for patients with liver disease include a higher risk of osmotic demyelination syndrome.