Hormone receptor-positive (HR+) breast cancer is known for its potential to recur many years after initial treatment. Although most recurrences occur within the first 5–10 years, late recurrence, especially beyond 15 years of age, is rare and isolated cutaneous recurrence is even less frequently reported. However, awareness of the possibility of extremely late and subtle local recurrences in patients with HR+ breast cancer has gradually increased over time. Clinicians should remain vigilant for atypical cutaneous changes near previous surgical sites, even decades after the initial treatment, and consider biopsy in the absence of classic signs of recurrence. We report the case of a 56-year-old woman who experienced an isolated cutaneous recurrence nearly 20 years after mastectomy for HR+ breast cancer, presenting with only faint erythema.

Insulin resistance is prevalent in chronic kidney disease and may accelerate the progression of chronic kidney disease. This study aimed to investigate whether insulin resistance is associated with the development of incident chronic kidney disease in a population with normal renal function. Methods: A total of 3,331 participants from a community-based cohort with normal renal function were prospectively analyzed. We determined the relationship of insulin resistance indices with the incident chronic kidney disease using the Cox proportional hazard model and Kaplan-Meier survival analysis. Results: During a mean follow-up of 11.03 ± 4.22 years, incident chronic kidney disease occurred in 414 participants (12.4%). The high homeostasis model assessment-insulin resistance level group had an increased risk of incident chronic kidney disease (hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.13–1.74; p = 0.002) compared to the normal group after adjustment for age, sex, history of hypertension, body mass index, total cholesterol, alcohol drinking status, smoking status, and baseline estimated glomerular filtration rate. The risk of incident chronic kidney disease also increased with the lower quantitative insulin sensitivity check index level (HR, 0.62; 95% CI, 0.41–0.92; p = 0.02) and higher leptin-adiponectin ratio level (HR, 1.23; 95% CI, 1.06–1.42; p = 0.006). Conclusion: Higher insulin resistance indices are associated with the incidence of chronic kidney disease. Our data suggest that increased insulin resistance may be involved in the development of incident chronic kidney disease in a population with normal renal function.

Sepsis-associated acute kidney injury (SA-AKI) is a prominent sepsis complication, often resulting in adverse clinical outcomes. Hyperbaric oxygen therapy (HBOT), known for its anti-inflammatory characteristics, antioxidant effects, and ability to deliver high oxygen tension to hypo-perfused tissues, offers potential benefits for SA-AKI. This study investigated whether HBOT improved renal injury in sepsis and elucidated its underlying mechanisms. Methods: A lipopolysaccharide (LPS)-induced endotoxemia model was established using 8-week-old C57BL/6 mice. Thirty minutes post-LPS administration, a group of mice underwent HBOT at a 2.5 atmospheric pressure absolute with 100% oxygen for 60 minutes. After 24 hours, all mice were euthanized for measurements. Results: Our results demonstrated that HBOT effectively mitigated renal tubular cell apoptosis. Additionally, HBOT significantly reduced phosphorylated p53 proteins and cytochrome C levels, suggesting that HBOT may attenuate renal apoptosis by impeding p53 activation and cytochrome C release. Notably, HBOT preserved manganese-dependent levels of superoxide dismutase, an antioxidant enzyme, compared to the LPS group. Furthermore, transforming growth factor beta (TGF-β)/Smad4 and alpha smooth muscle actin expressions were significantly reduced in the LPS + HBOT group. Conclusion: An early single session of HBOT exhibited renoprotective effects in LPS-induced endotoxemia mice models by suppressing p53 activation and cytochrome C levels to mitigate apoptosis. The observed TGF-β decrease, downstream Smad expression reduction, and antioxidant capacity preservation following HBOT may contribute to these effects.

Fabry disease (FD) is an X-linked lysosomal disorder caused by α-galactosidase A enzyme activity deficiency. Although glycosphingolipid analogs have been identified in the plasma or urine of patients with FD, there is a limited understanding of altered metabolomics profiles beyond the globotriaosylceramide accumulation in FD. Methods: Metabolomics study was performed for monitoring of biomarker and altered metabolism related with disease progression in serum and urine from male α-galactosidase A knockout mice and age-matched wild-type mice at 20 and 40 weeks. Profiling analysis for metabolites, including organic acids, amino acids, fatty acids, kynurenine pathway metabolites, and nucleosides in the serum and urine was performed using gas chromatography-tandem mass spectrometry and liquid chromatography-tandem mass spectrometry combined with star symbol patterns and partial least squares discriminant analysis (PLS-DA). Results: A total of 27 and 23 metabolites from the serum and urine of FD mice were distinguished from those of wild-type mice, respectively, based on p-value (<0.05) and variable importance in projection scores (>1.0) of PLS-DA. In the serum, metabolites of the glutathione, glutathione disulfide, citrulline, and kynurenine pathways that are related to oxidative stress, nitric oxide biosynthesis, and inflammation were increased, whereas those involved in pyruvate and tyrosine metabolism and the tricarboxylic acid cycle were altered in the 20- and 40-week-old urine of FD model mice. Conclusion: Altered metabolic signatures associated with disease progression by oxidative stress, inflammation, nitric oxide biosynthesis, and immune regulation in the early and late stages of FD.

Background/Aims: Obesity has known to be a modifiable risk factor associated with worse outcomes in chronic kidney disease (CKD), but few studies have examined the impact of obesity on CKD incidence in the general population. The purpose of this study was to investigate the role of body mass index (BMI) and waist-to-hip ratio (WHR) as predictors of incident CKD and to evaluate the impact of weight reduction on CKD prevention. Methods: A total of 2,711 participants from a community-based cohort with normal renal function were prospectively analyzed. Among participants with obesity, we analyzed the change in WHR to evaluate the association of obesity reduction with CKD development. Results: During a mean follow-up of 11.03 ± 4.22 years, incident CKD occurred in 190 (7.0%) participants. In the fully adjusted multivariable Cox proportional hazard models, the risk of incident CKD increased with higher BMI (hazard ratio, 1.06; 95% confidence interval, 1.00–1.11; p = 0.033) and higher WHR (hazard ratio, 1.33; 95% confidence interval, 1.07–1.66; p = 0.009). In the Kaplan–Meier analysis, cumulative adverse renal events were significantly more common in the maintained obesity group than in the reduced obesity group (p = 0.001). Conclusions Both higher BMI and WHR were associated with development of CKD, but the magnitude of the effect of WHR was higher than that of BMI. Moreover, reducing obesity would be beneficial for renal prognosis.

Anti-glomerular basement membrane (GBM) antibody disease is a rare autoimmune disorder characterized by autoantibodies directed against antigens within the GBM, primarily affecting the kidneys and lungs. This severe form of glomerulonephritis has an incidence of less than two cases per million individuals with crescentic glomerulonephritis. The coexistence of immunoglobulin A (IgA) nephropathy and anti-GBM disease is rare. Here, we present a case of concurrent anti-GBM antibody disease and IgA nephropathy. A 49-year-old male presented with fever, azotemia, proteinuria, and hematuria. Biopsy of the kidney revealed crescentic glomerulonephritis with linear IgG deposition along the GBM and IgA deposition in the mesangium. Elevated serum levels of anti-GBM antibody (311 U/mL) confirmed the diagnosis of concurrent anti-GBM antibody disease and IgA nephropathy. Despite treatment with methylprednisolone, cyclophosphamide, and plasma exchange, renal function deteriorated, necessitating hemodialysis.

Anti-glomerular basement membrane (GBM) antibody disease is a rare autoimmune disorder characterized by autoantibodies directed against antigens within the GBM, primarily affecting the kidneys and lungs. This severe form of glomerulonephritis has an incidence of less than two cases per million individuals with crescentic glomerulonephritis. The coexistence of immunoglobulin A (IgA) nephropathy and anti-GBM disease is rare. Here, we present a case of concurrent anti-GBM antibody disease and IgA nephropathy. A 49-year-old male presented with fever, azotemia, proteinuria, and hematuria. Biopsy of the kidney revealed crescentic glomerulonephritis with linear IgG deposition along the GBM and IgA deposition in the mesangium. Elevated serum levels of anti-GBM antibody (311 U/mL) confirmed the diagnosis of concurrent anti-GBM antibody disease and IgA nephropathy. Despite treatment with methylprednisolone, cyclophosphamide, and plasma exchange, renal function deteriorated, necessitating hemodialysis.

Anti-glomerular basement membrane (GBM) antibody disease is a rare autoimmune disorder characterized by autoantibodies directed against antigens within the GBM, primarily affecting the kidneys and lungs. This severe form of glomerulonephritis has an incidence of less than two cases per million individuals with crescentic glomerulonephritis. The coexistence of immunoglobulin A (IgA) nephropathy and anti-GBM disease is rare. Here, we present a case of concurrent anti-GBM antibody disease and IgA nephropathy. A 49-year-old male presented with fever, azotemia, proteinuria, and hematuria. Biopsy of the kidney revealed crescentic glomerulonephritis with linear IgG deposition along the GBM and IgA deposition in the mesangium. Elevated serum levels of anti-GBM antibody (311 U/mL) confirmed the diagnosis of concurrent anti-GBM antibody disease and IgA nephropathy. Despite treatment with methylprednisolone, cyclophosphamide, and plasma exchange, renal function deteriorated, necessitating hemodialysis.

Anti-glomerular basement membrane (GBM) antibody disease is a rare autoimmune disorder characterized by autoantibodies directed against antigens within the GBM, primarily affecting the kidneys and lungs. This severe form of glomerulonephritis has an incidence of less than two cases per million individuals with crescentic glomerulonephritis. The coexistence of immunoglobulin A (IgA) nephropathy and anti-GBM disease is rare. Here, we present a case of concurrent anti-GBM antibody disease and IgA nephropathy. A 49-year-old male presented with fever, azotemia, proteinuria, and hematuria. Biopsy of the kidney revealed crescentic glomerulonephritis with linear IgG deposition along the GBM and IgA deposition in the mesangium. Elevated serum levels of anti-GBM antibody (311 U/mL) confirmed the diagnosis of concurrent anti-GBM antibody disease and IgA nephropathy. Despite treatment with methylprednisolone, cyclophosphamide, and plasma exchange, renal function deteriorated, necessitating hemodialysis.

Granular cell tumor is a rare disease, and it is even rarer in the male breast. Although it is typically a benign tumor, due to its features and image findings, it can be easily misdiagnosed and managed as a malignant tumor. Therefore, the extent of the surgery can inappropriately be expanded. To avoid misdiagnosis and overtreatment, surgeons must perform a careful evaluation. We describe a case of a granular cell tumor of the male breast treated with mastectomy.