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.

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.

Background/Aims: The neutrophil-to-lymphocyte ratio (NLR) has a prognostic value in cardiovascular disease, infection, inflammatory disease, and several malignancies. Therefore, the NLR has a possible predictive value in patients with chronic kidney disease (CKD), but this predictive value has not been validated. Here, we aimed to investigate the possibility of NLR as a predictor of CKD progression. Methods: This retrospective observational study included 141 patients with non-dialysis CKD. The participants were divided into terciles (T1, T2, and T3) according to NLR. The primary outcome was defined as a composite kidney event, which included a decline in the estimated glomerular filtration rate (eGFR) of at least 50% or initiation of renal replacement therapy during the follow-up period. Results: The mean follow-up duration was 5.45 ± 2.11 years. The mean NLRs were 1.35 ± 0.05 in T1 (n = 47), 2.16 ± 0.04 in T2 (n = 47), and 4.29 ± 0.73 in T3 (n = 47). The group with the highest NLR (T3) had higher baseline CKD and serum creatinine and lower eGFR levels than the group with the lowest NLR (T1). The cumulative incidence rate of composite kidney events was significantly higher in T3 compared with T1 (p < 0.001, log-rank test). Cox regression analysis revealed that high NLR was associated with the risk of composite kidney events (adjusted hazard ratio, 3.33; 95% confidence interval, 1.43–7.76). Conclusions A higher NLR reflects the more advanced stage of CKD and suggests a role for NLR as a biomarker for predicting CKD progression.

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.

Methods: Ambulatory patients who underwent single-level PVP for thoracolumbar OVF with a follow-up of at least 24 months were retrospectively reviewed. The patients were divided into two groups depending on the presence of symptomatic recollapse at the cemented vertebra: (1) recollapsed (RC) group and (2) noncollapsed (NC) group. The patient characteristics and radiographic measurements associated with sagittal imbalance were analyzed at each follow-up visit. Results: Overall, 134 patients (RC group, n=28; NC group, n=106) were enrolled. The mean fracture-free interval was 3.2 months (range, 1.2–25.1 months). The multivariate binary logistic regression analysis identified low bone mineral density (p =0.047), degree of dynamic mobility within the vertebra (p =0.025), and sagittal imbalance as significant risk factors for recollapse (p =0.013; odds ratio, 5.405). The progression of sagittal imbalance and thoracolumbar kyphosis (T10–L2) was more significant in the RC and sagittal imbalance groups than in the NC group (both p =0.000). Conclusions Sagittal imbalance, lower bone mineral density, and dynamic mobility within the vertebra are associated with the recollapse of cemented vertebrae following PVP. Sagittal imbalance, rather than local kyphosis or thoracolumbar kyphosis, is particularly significant in that it results in more progressive collapse and sagittal deformity and is accompanied by substantial back pain and neurological deficits. Therefore, a stricter and more active management, including anti-osteoporosis medication, is required for the treatment of OVF with sagittal imbalance of the spine.

We report a case of severe hyperphosphatemia in advanced CKD with poor compliance. A 55-year-old male patient with underlying type 2 diabetes mellitus, hypertension, and chronic kidney disease presented emergently with general weakness and altered mental status. The creatinine level was 14 mg/dL (normal range: 0.5-1.3 mg/dL) 2 months prior to consultation, and he was advised initiation of hemodialysis, which he refused. Subsequently, the patient stopped taking all prescribed medications and self-medicated with honey and persimmon vinegar with the false belief it was detoxifying. At the time of admission, he was delirious, and his laboratory results showed blood urea nitrogen level of 183.4 mg/dL (8-23 mg/dL), serum creatinine level of 26.61 mg/dL (0.5-1.3 mg/dL), serum phosphate level of 19.3 mg/dL (2.5-5.5 mg/dL), total calcium level of 4.3 mg/dL (8.4-10.2 mg/dL), vitamin D (25(OH)D) level of 5.71 ng/mL (30-100 ng/mL) and parathyroid hormone level of 401 pg/ml (9-55 pg/mL). Brain computed tomography revealed non-traumatic spontaneous subdural hemorrhage, presumably due to uremic bleeding.Emergent hemodialysis was initiated, and hyperphosphatemia and hypocalcemia were rectified; calcium acetate and cholecalciferol were administered. The patient’s general condition and laboratory results improved following dialysis. Strict dietary restrictions with patient education were implemented. Multifaceted interventions, including dietary counseling, administration of phosphate-lowering drugs, and lifestyle modifications, should be implemented when encountering patients with CKD, considering the extent of the patient’s adherence.

Purpose: This study evaluated the short-term safety of resident-performed intravitreal injections. Methods: We retrospectively reviewed the medical records of 503 patients (503 eyes) treated for the first time in our hospital from January 2018 to October 2020 via intravitreal bevacizumab, ranibizumab, aflibercept, or triamcinolone acetonide injections by residents or retina specialists. In terms of short-term ophthalmic complications, patients were followed-up 1 day, 1 week, and 1 month after injection. Results: A total of 503 eyes of 503 patients were included. Intravitreal injections were given to 211 and 292 eyes by residents (the resident group) and retina specialists (the retina specialist group), respectively. There were no between-group differences in baseline characteristics except in terms of the indications for injection. Intraocular pressure elevation >5 mmHg occurred in two eyes (0.95%) in the resident group and five (1.71%) in the retina specialist group, but the difference was not statistically significant. Subconjunctival hemorrhage occurred in 29 eyes (13.74%) of the resident group and 32 eyes (10.96%) of the retina specialist group; again, the difference was not statistically significant. No case of noninfectious endophthalmitis occurred in the resident group but two (0.68%) cases occurred in the retina specialist group; again, the difference was not significant. There were two (0.95%) cases of infectious endophthalmitis in the resident group and one (0.34%) case in the retina specialist group; again, the difference was not significant. No corneal erosion, traumatic lens damage, vitreous hemorrhage, or retinal tearing or detachment were noted in either group. Conclusions Resident-performed intravitreal injections appear to be safe.

Background: Minimal change disease (MCD) is one of the most common causes of nephrotic syndrome worldwide. Hyperuricemia increases the end-stage renal disease (ESRD) risk in glomerulonephritis. In this study, we aimed to determine the effect of high serum uric acid levels on the progression to ESRD in MCD. Methods: A total of 800 patients diagnosed with MCD by kidney biopsy were retrospectively analyzed. We determined the relationship of hyperuricemia with the progression to ESRD in MCD using the Cox proportional hazard model and Kaplan-Meier survival analysis. The primary outcome was defined as the initiation of dialysis or kidney transplantation. Results: A total of 42 patients (5.3%) progressed to ESRD during the follow-up period. In the restricted cubic spline curve, serum uric acid levels exhibited a positive correlation with ESRD progression in patients with MCD. In the fully adjusted model, the risk of MCD progression increased by 29% for every 1 mg/dL increase in the baseline serum uric acid level (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.09–1.54; p = 0.004). Falling into the high uric acid group (serum uric acid level > 7 mg/dL in men and > 6 mg/dL in women) was also a risk factor for progression of MCD to ESRD (HR, 3.40; 95% CI, 1.59–7.31; p < 0.001). Conclusion Our study shows that hyperuricemia is an independent risk factor for the progression to ESRD in patients with MCD.

Objective: This aim examined the outcomes of resuscitation and the clinical characteristics of patients with pre-hospitaltraumatic cardiac arrests (TCA). Methods: The charts of patients with pre-hospital TCA who visited the various emergency department (ED) in Gangwondofrom January 2013 to December 2017 were reviewed retrospectively. Results: TCA patients comprised 0.3% of patients transferred by 119. A total of 367 patients were enrolled in the study.Traffic accidents were the leading cause of the arrest. The initial field and ED rhythm were mostly asystole (field, 79.6%;ED, 82.3%). It took 11.24±9.95 minutes from the call to the field. From the field to ED, it took 22.87±15.37 minutes. Thetotal CPR time before ED arrival was 21.62±15.29 minutes. The causes of TCA were brain injury (35.7%), hypovolemicshock (29.2%), and severe lung injury (16.3%). Seventy TCA patients experienced at least one return of spontaneous circulation(ROSC). Twenty-six patients (7.14%) were admitted to the ward, and their average injury severity score was38.96. Eight patients expired before 12 hours after transient ROSC. Four more patients expired before 24 hours. Fourpatients were discharged alive among patients who lived for more than 24 hours. Conclusion In this study, 1.5% of patients were discharged alive. The possibility of ROSC was higher as the time to ED,and the cardiopulmonary resuscitation time of 119 was shorter. Pulseless electrical activity rather than asystole tends topromote ROSC. The survival rate increased when ROSC occurred before arriving at the ED.