Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Immunoglobulin A nephropathy (IgAN) is the most prevalent form of glomerulonephritis worldwide. Prediction of disease progression in IgAN can help to provide individualized treatment based on accurate risk stratification. Methods: We performed proton nuclear magnetic resonance-based metabolomics analyses of serum and urine samples from healthy controls, non-progressor (NP), and progressor (P) groups to identify metabolic profiles of IgAN disease progression. Metabolites that were significantly different between the NP and P groups were selected for pathway analysis. Subsequently, we analyzed multivariate area under the receiver operating characteristic (ROC) curves to evaluate the predictive power of metabolites associated with IgAN progression. Results: We observed several distinct metabolic fingerprints of the P group involving the following metabolic pathways: glycolipid metabolism; valine, leucine, and isoleucine biosynthesis; aminoacyl-transfer RNA biosynthesis; glycine, serine, and threonine metabolism; and glyoxylate and dicarboxylate metabolism. In multivariate ROC analyses, the combinations of serum glycerol, threonine, and proteinuria (area under the curve [AUC], 0.923; 95% confidence interval [CI], 0.667–1.000) and of urinary leucine, valine, and proteinuria (AUC, 0.912; 95% CI, 0.667–1.000) showed the highest discriminatory ability to predict IgAN disease progression. Conclusion: This study identified serum and urine metabolites profiles that can aid in the identification of progressive IgAN and proposed perturbed metabolic pathways associated with the identified metabolites.

Background: Asthma and chronic obstructive pulmonary disease (COPD) are airway diseases with similar clinical manifestations, despite differences in pathophysiology. AsthmaCOPD overlap (ACO) is a condition characterized by overlapping clinical features of both diseases. There have been few reports regarding the prevalence of ACO in COPD and severe asthma cohorts. ACO is heterogeneous; patients can be classified on the basis of phenotype differences. This study was performed to analyze the prevalence of ACO in COPD and severe asthma cohorts. In addition, this study compared baseline characteristics among ACO patients according to phenotype. Methods: Patients with COPD were prospectively enrolled into the Korean COPD subgroup study (KOCOSS) cohort. Patients with severe asthma were prospectively enrolled into the Korean Severe Asthma Registry (KoSAR). ACO was defined in accordance with the updated Spanish criteria. In the COPD cohort, ACO was defined as bronchodilator response (BDR) ≥ 15% and ≥ 400 mL from baseline or blood eosinophil count (BEC) ≥ 300 cells/μL. In the severe asthma cohort, ACO was defined as age ≥ 35 years, smoking ≥ 10 pack-years, and postbronchodilator forced expiratory volume in 1 s/forced vital capacity < 0.7. Patients with ACO were divided into four groups according to smoking history (threshold: 20 pack-years) and BEC (threshold: 300 cells/μL). Results: The prevalence of ACO significantly differed between the COPD and severe asthma cohorts (19.8% [365/1,839] vs. 12.5% [104/832], respectively; P < 0.001). The percentage of patients in each group was as follows: group A (light smoker with high BEC) – 9.1%; group B (light smoker with low BEC) – 3.7%; group C (moderate to heavy smoker with high BEC) – 73.8%; and group D (moderate to heavy smoker with low BEC) – 13.4%. Moderate to heavy smoker with high BEC group was oldest, and showed weak BDR response. Age, sex, BDR, comorbidities, and medications significantly differed among the four groups. Conclusion The prevalence of ACO differed between COPD and severe asthma cohorts. ACO patients can be classified into four phenotype groups, such that each phenotype exhibits distinct characteristics.

Background: To evaluate the effects of teneligliptin on glycosylated hemoglobin (HbA1c) levels, continuous glucose monitoring (CGM)-derived time in range, and glycemic variability in elderly type 2 diabetes mellitus patients. Methods: This randomized, double-blinded, placebo-controlled study was conducted in eight centers in Korea (clinical trial registration number: NCT03508323). Sixty-five participants aged ≥65 years, who were treatment-naïve or had been treated with stable doses of metformin, were randomized at a 1:1 ratio to receive 20 mg of teneligliptin (n=35) or placebo (n=30) for 12 weeks. The main endpoints were the changes in HbA1c levels from baseline to week 12, CGM metrics-derived time in range, and glycemic variability. Results: After 12 weeks, a significant reduction (by 0.84%) in HbA1c levels was observed in the teneligliptin group compared to that in the placebo group (by 0.08%), with a between-group least squares mean difference of –0.76% (95% confidence interval [CI], –1.08 to –0.44). The coefficient of variation, standard deviation, and mean amplitude of glycemic excursion significantly decreased in participants treated with teneligliptin as compared to those in the placebo group. Teneligliptin treatment significantly decreased the time spent above 180 or 250 mg/dL, respectively, without increasing the time spent below 70 mg/dL. The mean percentage of time for which glucose levels remained in the 70 to 180 mg/dL time in range (TIR70–180) at week 12 was 82.0%±16.0% in the teneligliptin group, and placebo-adjusted change in TIR70–180 from baseline was 13.3% (95% CI, 6.0 to 20.6). Conclusion Teneligliptin effectively reduced HbA1c levels, time spent above the target range, and glycemic variability, without increasing hypoglycemia in our study population.

Background: Neonatal porcine pancreatic cell clusters (NPCCs) have been proposed as an alternative source of β cells for islet transplantation because of their low cost and growth potential after transplantation. However, the delayed glucose lowering effect due to the immaturity of NPCCs and immunologic rejection remain as a barrier to NPCC’s clinical application. Here, we demonstrate accelerated differentiation and immune-tolerant NPCCs by in vitro chemical treatment and microencapsulation. Methods: NPCCs isolated from 3-day-old piglets were cultured in F-10 media and then microencapsulated with alginate on day 5. Differentiation of NPCCs is facilitated by media supplemented with activin receptor-like kinase 5 inhibitor II, triiodothyronine and exendin-4 for 2 weeks. Marginal number of microencapsulated NPCCs to cure diabetes with and without differentiation were transplanted into diabetic mice and observed for 8 weeks. Results: The proportion of insulin-positive cells and insulin mRNA levels of NPCCs were significantly increased in vitro in the differentiated group compared with the undifferentiated group. Blood glucose levels decreased eventually after transplantation of microencapsulated NPCCs in diabetic mice and normalized after 7 weeks in the differentiated group. In addition, the differentiated group showed nearly normal glucose tolerance at 8 weeks after transplantation. In contrast, neither blood glucose levels nor glucose tolerance were improved in the undifferentiated group. Retrieved graft in the differentiated group showed greater insulin response to high glucose compared with the undifferentiated group. Conclusion in vitro differentiation of microencapsulated immature NPCCs increased the proportion of insulin-positive cells and improved transplant efficacy in diabetic mice without immune rejection.

Background: The microencapsulation is an ideal solution to overcome immune rejection without immunosuppressive treatment. Poor biocompatibility and small molecular antigens secreted from encapsulated islets induce fibrosis infiltration. Therefore, the aims of this study were to improve the biocompatibility of microcapsules by dexamethasone coating and to verify its effect after xenogeneic transplantation in a streptozotocin-induced diabetes mice. Methods: Dexamethasone 21-phosphate (Dexa) was dissolved in 1% chitosan and was cross-linked with the alginate microcapsule surface. Insulin secretion and viability assays were performed 14 days after microencapsulation. Dexa-containing chitosan-coated alginate (Dexa-chitosan) or alginate microencapsulated porcine islets were transplanted into diabetic mice. The fibrosis infiltration score was calculated from the harvested microcapsules. The harvested microcapsules were stained with trichrome and for insulin and macrophages. Results: No significant differences in glucose-stimulated insulin secretion and islet viability were noted among naked, alginate, and Dexa-chitosan microencapsulated islets. After transplantation of microencapsulated porcine islets, nonfasting blood glucose were normalized in both the Dexa-chitosan and alginate groups until 231 days. The average glucose after transplantation were lower in the Dexa-chitosan group than the alginate group. Pericapsular fibrosis and inflammatory cell infiltration of microcapsules were significantly reduced in Dexa-chitosan compared with alginate microcapsules. Dithizone and insulin were positive in Dexa-chitosan capsules. Although fibrosis and macrophage infiltration was noted on the surface, some alginate microcapsules were stained with insulin. Conclusion Dexa coating on microcapsules significantly suppressed the fibrotic reaction on the capsule surface after transplantation of xenogenic islets containing microcapsules without any harmful effects on the function and survival of the islets.

Background: Data on liver cirrhosis (LC) patients undergoing continuous renal replacement therapy (CRRT) are lacking despite the dismal prognosis. We therefore evaluated clinical characteristics and predictive factors related to mortality in LC patients undergoing CRRT. Methods: We performed a retrospective observational study at two tertiary hospitals in Korea. A total of 229 LC patients who underwent CRRT were analyzed. Patients were classified into survivor and non-survivor groups. We used multivariable Cox regression analyses to identify factors predictive of in-hospital mortality. Results: During a median follow-up of 5 days (interquartile range, 1–19 days), in-hospital mortality rate was 66.4%. In multivariable analysis, the Acute Physiology and Chronic Health Evaluation II (APACHE II) score (hazard ratio [HR], 1.03; 95% confidence interval [CI], 1.01–1.06; p = 0.02), Model for End-Stage Liver Disease (MELD) score (HR, 1.08; 95% CI, 1.04–1.11; p <0.001), and delivered CRRT dose (HR, 0.95; 95% CI, 0.92¬–0.98; p = 0.002) were significant risk factors for in-hospital mortality. Patients with a CRRT delivered dose < 25 mL/kg/hr had a higher mortality rate than those with a delivered dose > 35 mL/kg/hr (HR, 3.13; 95% CI, 1.62–6.05; p = 0.001). Subgroup analysis revealed that a CRRT delivered dose < 25 mL/kg/hr was a significant risk factor for in-hospital mortality among LC patients with a MELD score ≥ 30. Conclusion High APACHE II score, high MELD score, and low delivered CRRT dose were significant risk factors for in-hospital mortality. CRRT delivered dose impacted mortality significantly, especially in patients with a MELD score ≥ 30.