Capsular contracture (CC) is a concerning issue for individuals undergoing postmastectomy radiation therapy (PMRT) with implant-based breast reconstruction. This study investigated whether the extent of CC and implant migration differs based on implant placement and the reconstruction stage. Insertion plane and stage of breast implants were investigated, and the presence and severe cases of CC and implant migration were analyzed. Among 195 participants, 83 were in the pre-pectoral group, and 112 were in the sub-pectoral group. Two-staged surgery was performed on 116 patients, while 79 underwent direct-to-implant (DTI).Notably, The occurrence of CC (prepectoral, 17 [20.48%] and subpectoral, 42 [37.50%];p = 0.011), CC severity (prepectoral, 4 [4.82%] and subpectoral, 17 [15.17%]; p = 0.021), and implant upward migration (prepectoral, 15 [18.07%] and subpectoral, 38 [33.92%]; p = 0.014) significantly varied between the two groups. The incidence of CC was more common in the DTI group (odds ratio [OR], 2.283; 95% confidence interval [CI], 1.164–4.478). Furthermore, subpectoral placement was an independent risk factor for occurrence (OR, 2.989; 95% CI, 1.476–6.054) and severity of CC (OR, 38.552; 95% CI, 1.855–801.186) and upward implant migration (OR, 2.531; 95% CI, 1.263–5.071). Our findings suggest that pre-pectoral reconstruction and the two-stage operation benefit patients who may undergo PMRT. These approaches can help reduce the incidence of CC and abnormal implant migration following radiation, leading to improved aesthetic outcomes and greater patient satisfaction.

Capsular contracture (CC) is a concerning issue for individuals undergoing postmastectomy radiation therapy (PMRT) with implant-based breast reconstruction. This study investigated whether the extent of CC and implant migration differs based on implant placement and the reconstruction stage. Insertion plane and stage of breast implants were investigated, and the presence and severe cases of CC and implant migration were analyzed. Among 195 participants, 83 were in the pre-pectoral group, and 112 were in the sub-pectoral group. Two-staged surgery was performed on 116 patients, while 79 underwent direct-to-implant (DTI).Notably, The occurrence of CC (prepectoral, 17 [20.48%] and subpectoral, 42 [37.50%];p = 0.011), CC severity (prepectoral, 4 [4.82%] and subpectoral, 17 [15.17%]; p = 0.021), and implant upward migration (prepectoral, 15 [18.07%] and subpectoral, 38 [33.92%]; p = 0.014) significantly varied between the two groups. The incidence of CC was more common in the DTI group (odds ratio [OR], 2.283; 95% confidence interval [CI], 1.164–4.478). Furthermore, subpectoral placement was an independent risk factor for occurrence (OR, 2.989; 95% CI, 1.476–6.054) and severity of CC (OR, 38.552; 95% CI, 1.855–801.186) and upward implant migration (OR, 2.531; 95% CI, 1.263–5.071). Our findings suggest that pre-pectoral reconstruction and the two-stage operation benefit patients who may undergo PMRT. These approaches can help reduce the incidence of CC and abnormal implant migration following radiation, leading to improved aesthetic outcomes and greater patient satisfaction.

Capsular contracture (CC) is a concerning issue for individuals undergoing postmastectomy radiation therapy (PMRT) with implant-based breast reconstruction. This study investigated whether the extent of CC and implant migration differs based on implant placement and the reconstruction stage. Insertion plane and stage of breast implants were investigated, and the presence and severe cases of CC and implant migration were analyzed. Among 195 participants, 83 were in the pre-pectoral group, and 112 were in the sub-pectoral group. Two-staged surgery was performed on 116 patients, while 79 underwent direct-to-implant (DTI).Notably, The occurrence of CC (prepectoral, 17 [20.48%] and subpectoral, 42 [37.50%];p = 0.011), CC severity (prepectoral, 4 [4.82%] and subpectoral, 17 [15.17%]; p = 0.021), and implant upward migration (prepectoral, 15 [18.07%] and subpectoral, 38 [33.92%]; p = 0.014) significantly varied between the two groups. The incidence of CC was more common in the DTI group (odds ratio [OR], 2.283; 95% confidence interval [CI], 1.164–4.478). Furthermore, subpectoral placement was an independent risk factor for occurrence (OR, 2.989; 95% CI, 1.476–6.054) and severity of CC (OR, 38.552; 95% CI, 1.855–801.186) and upward implant migration (OR, 2.531; 95% CI, 1.263–5.071). Our findings suggest that pre-pectoral reconstruction and the two-stage operation benefit patients who may undergo PMRT. These approaches can help reduce the incidence of CC and abnormal implant migration following radiation, leading to improved aesthetic outcomes and greater patient satisfaction.

Background: Factors related to the development and severity of polycystic liver disease (PLD) have not been well established. We aimed to evaluate the genetic and epidemiologic risk factors of PLD in patients with autosomal dominant polycystic kidney disease (ADPKD). Methods: Adult patients with inherited cystic kidney disease were enrolled from May 2019 to May 2021. Demographic, clinical, and laboratory data were collected at the initial study visit. The severity of PLD was graded based on the height-adjusted total liver volume: < 1,000 mL/m (Gr1), 1,000–1,800 mL/m (Gr2), and > 1,800 mL/m (Gr3). Targeted exome sequencing was done by a gene panel including 89 ciliopathy-related genes. We searched out the relative factors to the presence and the severity of PLD using logistic regression analysis. Results: Of 602 patients with typical ADPKD, 461 (76.6%) patients had PLD. The patients with PLD showed female predominance and a higher frequency of other ADPKD-related complications. The genetic variants with truncating mutation of PKD1 (PKD1-proteintruncating [PT]) or PKD2 commonly affected the development and severity of PLD. An older age, female sex, and higher kidney volume with Mayo classification 1C-1E was significantly associated with the development of PLD, but not with the severity of PLD. On the other hand, higher body mass index, lower hemoglobin, and higher alkaline phosphatase (ALP) were the significant risk factors of severe PLD (≥ Gr2). Conclusion Hepatic involvement in ADPKD could be related to kidney manifestations and genetic variants including PKD1-PT or PKD2. Monitoring hemoglobin and ALP and evaluating the genetic variants might help predict severe PLD.

Urine chloride has recently been suggested as a biomarker of renal tubule function in patients with nondialysis chronic kidney disease (CKD), as low urinary chloride concentration is associated with an increased risk of CKD progression. We investigate the association between urinary chloride excretion and the progression of coronary artery calcification (CAC). Methods: A total of 1,065 patients with nondialysis CKD were divided into tertiles by spot urine chloride-to-creatinine ratios. The 1st, 2nd, and 3rd tertiles were defined as low, moderate, and high urinary chloride excretion, respectively. The study outcome was CAC progression, which was defined as an increase in coronary artery calcium score of more than 200 Agatston units during the 4-year follow-up period. Results: Compared to moderate urinary chloride excretion, high urinary chloride excretion was associated with decreased risk of CAC progression (adjusted odds ratio, 0.379; 95% confidence interval, 0.190–0.757), whereas low urinary chloride excretion was not associated with risk of CAC progression. Restricted cubic spine depicted an inverted J-shaped curve, with a significant reduction in the risk of CAC progression in subjects with high spot urine chloride-to-creatinine ratios. Conclusion: High urinary chloride excretion is associated with decreased risk of CAC progression in patients with nondialysis CKD.

Tolvaptan reduces height-adjusted total kidney volume (htTKV) and renal function decline in autosomal dominant polycystic kidney disease (ADPKD). This study was aimed at investigating the efficacy and safety of tolvaptan in Korean patients with ADPKD during the titration period. Methods: This study is a multicenter, single-arm, open-label phase 4 study. We enrolled 108 patients with ADPKD (age, 19–50 years) with an estimated glomerular filtration rate (eGFR) of >30 mL/min/1.73 m2 and factors defined as indicative of rapid disease progression. After tolvaptan titration, we evaluated efficacy and side effects and assessed factors associated with the effects. Results: After titration for 4 weeks, eGFR and htTKV decreased by 6.4 ± 7.9 mL/min/1.73 m2 and 16 ± 45 mL/m, respectively. No serious adverse drug reactions were observed during the titration period. The greatest eGFR decline was observed in the first week, with a starting tolvaptan dose of 45 mg. Multivariate linear regression for htTKV decline showed that the greater the change in urine osmolality (Uosm), the greater the decrease in htTKV (β, 0.436; p = 0.009) in the 1D group stratified by the Mayo Clinic image classification. Higher baseline eGFR was related to a higher htTKV reduction rate in the 1E group (β, –0.642; p = 0.009). Conclusion: We observed short-term effects and safety during the tolvaptan titration period. The decline of htTKV can be predicted as a short-term effect of tolvaptan by observing Uosm changes from baseline to end of titration in 1D and baseline eGFR in 1E groups.

Identifying genetic mutations in individuals with inherited cystic kidney disease is necessary for precise treatment. We aimed to elucidate the genetic characteristics of cystic kidney disease in the Korean population. Methods: We conducted a 3-year prospective, multicenter cohort study at eight hospitals from May 2019 to May 2022. Patients with more than three renal cysts were enrolled and classified into two categories, typical autosomal dominant polycystic kidney disease (ADPKD) and atypical PKD. We identified the clinical characteristics and performed a genetic analysis using a targeted gene panel. Results: A total of 725 adult patients were included in the study, of which 560 (77.2%) were diagnosed with typical ADPKD and 165 (22.8%) had atypical PKD. Among the typical ADPKD cases, the Mayo imaging classification was as follows: 1A (55, 9.9%), 1B (149, 26.6%), 1C (198, 35.8%), 1D (90, 16.3%), and 1E (61, 11.0%). The atypical PKD cases were classified as bilateral cystic with bilateral atrophic (31, 37.3%), lopsided (27, 32.5%), unilateral (nine, 10.8%), segmental (eight, 9.6%), bilateral cystic with unilateral atrophic (seven, 8.4%), and asymmetric (one, 1.2%). Pathogenic variants were found in 64.3% of the patients using the ciliopathy-related targeted gene panel. The typical ADPKD group demonstrated a higher discovery rate (62.3%) than the atypical PKD group (41.8%). Conclusion: We present a nationwide genetic cohort’s baseline clinical and genetic characteristics for Korean cystic kidney disease.

Background/Aims: Previous studies have reported the protective effects of tauroursodeoxycholic acid (TUDCA) on gastric epithelial cells in some animal models, but the precise mechanisms are unclear. This study examined the effects of TUDCA on NF-κB signaling in gastric epithelial cells. Moreover, the protective effects of TUDCA in experimental gastritis models induced by ethanol and NSAID were evaluated and compared with ursodeoxycholic acid (UDCA). Methods: After a pretreatment with TUDCA or UDCA, human gastric epithelial MKN-45 cells were stimulated with tumor necrosis factor (TNF)-α to activate NF-κB signaling. A real-time PCR (RT-PCR) for human interleukin (IL)-1 mRNA was performed. An electrophoretic mobility shift assay (EMSA) and immunoblot analyses were carried out. In murine models, after a pretreatment with TUDCA or UDCA, ethanol and indomethacin were administered via oral gavage. Macroscopic and microscopic assessments were performed to evaluate the preventive effects of TUDCA and UDCA on murine gastritis. Results: A pretreatment with TUDCA downregulated the IL-1α mRNA levels in MKN-45 cells stimulated with TNF-α, as assessed by RT-PCR. As determined using EMSA, a pretreatment with TUDCA reduced the TNF-α-induced NF-κB DNA binding activity. A pretreatment with TUDCA inhibited IκBα phosphorylation induced by TNF-α, as assessed by immunoblot analysis. TUDCA attenuated the ethanol-induced and NSAID-induced gastritis in murine models, as determined macroscopically and microscopically. Conclusions TUDCA inhibited NF-κB signaling in gastric epithelial cells and ameliorated ethanol- and NSAID-induced gastritis in murine models. These results support the potential of TUDCA for the prevention of gastritis in humans.

Osteoprotegerin is an important regulator of bone metabolism and vascular calcification. The association between serum osteoprotegerin level and chronic kidney disease (CKD) progression has not been elucidated. We investigated the prognostic value of serum osteoprotegerin levels in nondialysis CKD patients. Methods: We analyzed 2,082 patients enrolled in the Korean Cohort Study for Outcomes in Patients with CKD between 2011 and 2016. Patients were divided into quartiles by their serum osteoprotegerin levels. The primary outcome was the occurrence of ≥1 of the following: dialysis initiation, kidney transplantation, a two-fold increase in serum creatinine level from baseline, or a 50% decrease in the estimated glomerular filtration rate (eGFR). Cox proportional hazard regression models were used to investigate the prognostic value of the serum osteoprotegerin level to CKD progression. Results: The median follow-up period was 48.9 months, and 641 patients (30.8%) experienced the primary outcome. The hazard ratio of serum osteoprotegerin for renal progression in the full extended Cox proportional hazard model was 1.064 (95% confidence interval, 1.041–1.088). Subgroup analyses by age, presence of diabetes, and eGFR showed significant results consistent with the overall analysis results. Conclusion: Serum osteoprotegerin level is independently associated with renal prognosis and could have prognostic importance in CKD progression.