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BackgroundContinuous renal replacement therapy (CRRT) is an important treatment modality for severe acute kidney injury. As such, the epidemiology of CRRT in Korea needs further investigation.MethodsWe conducted a nationwide, population-based study analyzing the claims data from National Health Insurance Service of Korea. All index intensive care unit admission cases of CRRT in government-designated tertiary referral hospitals in Korea from 2005 to 2016 were included. Patients with a history of renal replacement therapy or who were under 20 years old were not considered. In addition to baseline and treatment characteristics, patient outcomes, including all-cause mortality and renal survival rates, were investigated. We stratified the study patients according to 3-year time periods and major regions of the nation.ResultsWe included 37,337 patients who received CRRT in Korea. The overall use of CRRT increased over time, and more than 80% of cases of acute renal replacement therapy were CRRT after 2014. Seoul was the region in which the majority of CRRT (45.0%) was performed. The clinical characteristics of CRRT patients were significantly different among time-intervals and regions. Both all-cause mortality and renal survival rates after CRRT were prominently improved in the recent time periods (P < 0.001).ConclusionCRRT is a widely used treatment strategy for severe acute kidney injury in Korea. The prognosis of CRRT patients has improved compared to the past. This epidemiological study of CRRT in Korea revealed notable trends with regard to time period and geographic region.

Conflicting data have been reported on the clinical significance of contrast-induced nephropathy after CT scan (CT-CIN). In addition, the epidemiologic characteristics and clinical outcomes of CT-CIN following proper prophylactic intervention remain elusive.We examined the incidence, risk factors, and outcomes of CT-CIN in stable chronic kidney disease (CKD) patients using data collected from our outpatient CT-CIN prophylaxis program conducted between 2007 and 2014. The program recruited patients with an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 using an electronic health record-based pop-up alert system and provided an identical protocol of CIN prophylaxis to all patients.A total of 1666 subjects were included in this study, and 61 of the 1666 subjects (3.7%) developed CT-CIN. Multivariate analysis showed that baseline eGFR, diabetes mellitus, and low serum albumin were significant risk factors for CT-CIN. The generalized additive model analysis revealed a nonlinear relationship between the baseline eGFR and the risk of CT-CIN. In this analysis, the risk of CT-CIN began to increase below an eGFR threshold of 36.8 mL/min/1.73 m2. To assess the outcomes of CT-CIN, patients with and without CT-CIN were compared after propensity score-based 1:2 matching. CT-CIN did not increase the mortality rate of patients. However, patients with CT-CIN were significantly more likely to start dialysis within 6 months of follow-up, but not after those initial 6 months.CT-CIN developed in only a small number of stable CKD patients who received proper prophylactic intervention, and the risk of CT-CIN was increased in patients with more advanced CKD. Despite the low incidence, CT-CIN conferred a non-negligible risk for the initiation of dialysis in the acute period, even after prophylaxis.

BackgroundInterleukin-6 (IL6) is an important regulator of cellular hypertrophy through the gp130/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. We tested the hypothesis that IL6 and its downstream gp130/JAK2/STAT3 pathway participated in high glucose (HG)–induced podocyte hypertrophy.MethodsIL6 levels in the media and lysates of podocytes were measured by enzyme-linked immunosorbent assay. Western blots were performed to determine the protein expression levels of gp130/JAK2/STAT3 among podocytes cultured with normal glucose (NG), NG + mannitol, NG + recombinant IL6, HG, and HG + IL6-neutralizing antibodies (IL6NAb). Immunoprecipitation was examined to determine whether gp130 interacted with JAK2 in response to HG or IL6. Podocyte hypertrophy was verified using protein/cell counts and flow cytometry.ResultsIL6 levels were significantly increased in the media and lysates of podocytes cultured in HG compared with the NG groups. The nuclear phospho-STAT3/STAT3 ratio was increased by HG and NG + IL6 and was attenuated in the HG + IL6NAb groups, indicating that nuclear STAT3 was activated following JAK2 and cytosolic STAT3 activation in response to IL6 secreted by HG-stimulated podocytes. Immunoprecipitation showed increased phospho-JAK2 recruitment to gp130 in the HG and NG + IL6 groups, and the addition of IL6NAb in the HG group significantly abrogated these increases. Podocyte hypertrophy was significantly increased in the HG and NG + IL6 compared with the NG condition and was diminished by the addition of IL6NAbs to the HG group.ConclusionIL6 might play a prominent role in the local activation of JAK2/STAT3 in podocyte hypertrophy under HG conditions. In vivo studies examining this pathway are warranted.

BackgroundThe role of hyperuricemia in disease progression of autosomal dominant polycystic kidney disease (ADPKD) has not been defined well. We investigated the association of serum uric acid (sUA) with renal function and the effect of hypouricemic treatment on the rate of renal function decline.MethodsThis is a single-center, retrospective, observational cohort study. A total of 365 patients with ADPKD who had estimated glomerular filtration rate (eGFR) ≥ 15 mL/min/1.73 m2 and who were followed up for > 1 year were included in our analysis. Hyperuricemia was defined by a sUA level of ≥ 7.0 mg/dL in male and ≥ 6.0 mg/dL in female or when hypouricemic medications were prescribed.ResultsHyperuricemia was associated with reduced initial eGFR, independent of age, sex, hypertension, albuminuria, and total kidney volume. During a median follow-up period of over 6 years, patients with hyperuricemia showed a faster annual decline in eGFR (−6.3% per year vs. −0.9% per year, p = 0.008). However, after adjusting for age, sex, hypertension and initial eGFR, sUA was no longer associated with either annual eGFR decline or the development of ESRD. Among 53 patients who received hypouricemic treatment, the annual eGFR decline appeared to be attenuated after hypouricemic treatment (pretreatment vs. posttreatment: −5.3 ± 8. 2 vs. 0.2 ± 6.2 mL/min/1.73 m2 per year, p = 0.001 by Wilcoxon signed-rank test).ConclusionsAlthough hyperuricemia was associated with reduced eGFR, it was not an independent factor for renal progression in ADPKD. However, the correction of hyperuricemia may attenuate renal function decline in some patients with mild renal insufficiency.