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Impact of calcineurin inhibitors on rat glioma cells viability
Seong, Jeong Hun,Park, Woo Yeong,Paek, Jin Hyuk,Park, Sung Bae,Han, Seungyeup,Mun, Kyo-Cheol,Jin, Kyubok Yeungnam University College of Medicine 2019 Yeungnam University Journal of Medicine Vol.36 No.2
Background: Although kidney transplantation outcomes have improved dramatically after using calcineurin inhibitors (CNIs), CNI toxicity continues to be reported and the mechanism remains uncertain. Here, we investigated the neurotoxicity of CNIs by focusing on the viability of glioma cells. Methods: Glioma cells were treated with several concentrations of CNIs for 24 hours at $37^{\circ}C$ and their cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Results: Exposure to 0, 0.25, 0.5, 2.5, 5.0, and 10.0 mM concentrations respectively showed 100%, 64.3%, 61.3%, 68.1%, 62.4%, and 68.6% cell viability for cyclosporine and 100%, 38.6%, 40.8%, 43.7%, 37.8%, and 43.0% for tacrolimus. The direct toxic effect of tacrolimus on glioma cell viability was stronger than that of cyclosporine at the same concentration. Conclusion: CNIs can cause neurological side effects by directly exerting cytotoxic effects on brain cells. Therefore, we should carefully monitor the neurologic symptoms and level of CNIs in kidney transplant patients.
Park Woo Yeong,Kim Yaerim,Paek Jin Hyuk,Jin Kyubok,Han Seungyeup 대한이식학회 2021 Korean Journal of Transplantation Vol.35 No.1
Background: Chronic antibody-mediated rejection (CABMR) is an important cause of late graft loss. De novo donor-specific antibody (dnDSA) is an important prognostic factor for long-term allograft outcomes. However, the prognosis of CABMR based on the presence of dnDSA is uncertain. Methods: We retrospectively analyzed 35 kidney transplant recipients with CABMR between 2010 and 2018. Fourteen recipients had no detectable DSA, and 21 recipients had detectable DSA. We investigated the pathologic findings at diagnosis of CABMR, allograft function 12 months later, related factors for allograft failure, and allograft survival rate based on the presence of dnDSA. Results: The pathologic findings showed that acute and chronic changes were more severe in the dnDSA (+) group than in the dnDSA (–) group. There was no significant difference in the allograft function 12 months after the diagnosis of CABMR and in the amount of proteinuria at diagnosis between the two groups. However, the death-censored graft survival rate was lower in the high-proteinuria group than in the low-proteinuria group in both groups. The treatment rate of recipients was higher in the dnDSA (+) group than in the dnDSA (–) group; however, there was no significant difference in the death-censored graft survival rate between the two groups. Conclusions: Although the effect of dnDSA on the prognosis of CABMR is not clear, it would be important not to neglect treatment for CABMR with risk factors for allograft failure even without dnDSA. Continuous and rigorous surveillance of DSA and allograft function is needed in patients with CABMR.
( Hyuk Huh ),( Yong Soo Kim ),( Wookyung Chung ),( Yong Lim Kim ),( Yaerim Kim ),( Seungyeup Han ),( Yeonsoon Jung ),( Ki Young Na ),( Kyu Beck Lee ),( Yun Kyu Oh ),( Hyeong Cheon Park ),( Seung Hyeok 대한신장학회 2023 Kidney Research and Clinical Practice Vol.42 No.2
Background: 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 ㎡ 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 ㎡ 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.
( Woo Yeong Park ),( Yaerim Kim ),( Jin Hyuk Paek ),( Kyubok Jin ),( Seungyeup Han ) 대한신장학회 2021 Kidney Research and Clinical Practice Vol.40 No.2
Background: Recurrent glomerulonephritis (GN) is a common cause of allograft loss in kidney transplantation (KT), the most frequent of which is immunoglobulin A (IgA) nephropathy (IgAN). Galactose-deficient IgA1 (Gd-IgA1) plays a major role in the pathophysiology of IgAN, but the association between Gd-IgA1 and recurrent IgAN in kidney transplant recipients (KTRs) is uncertain. We aimed to evaluate the efficacy of Gd-IgA1 for prediction of recurrent IgAN and graft and patient survival according to Gd-IgA1 level. Methods: We enrolled 27 KTRs who underwent allograft biopsy between 2009 and 2016 and measured the serum Gd-IgA1 level of each KTR. We divided the patients into two groups: nonrecurrent IgAN (patients with IgAN prior to KT who were not diagnosed with recurrent IgAN) and recurrent IgAN (patients with IgAN prior to KT who were diagnosed with recurrent IgAN). Results: The mean serum Gd-IgA1 level was significantly higher in the recurrent IgAN group than in the nonrecurrent IgAN group (6,419 ± 3,675 ng/mL vs. 3,381 ± 2,844 ng/mL, p = 0.02). The cutoff value of serum Gd-IgA1 in receiver operating characteristic curve analysis was 4,338 ng/mL (area under the curve, 0.76; 95% confidence interval [CI], 0.57-0.95, p = 0.02). Serum Gd-IgA1 level was an independent factor for recurrent IgAN (odds ratio, 17.60; 95% CI, 1.33-233.03, p = 0.03). There was no significant difference in graft or patient survival between the two groups. Conclusion: Serum Gd-IgA1 can be used as a diagnostic biomarker for recurrent IgAN in KT.
Kim Yaerim,Park Hayne Cho,Ryu Hyunjin,Kim Yong Chul,Ahn Curie,Lee Kyu-Beck,Kim Yeong Hoon,Han Seungyeup,Bae Eun Hui,Jeong Kyungjo,Choi Jungmin,Oh Kook-Hwan,Oh Yun Kyu 대한의학회 2023 Journal of Korean medical science Vol.38 No.38
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.
( Woo Yeong Park ),( Yoon Kyung Chang ),( Young Soo Kim ),( Kyubok Jin ),( Chul Woo Yang ),( Seungyeup Han ),( Byung Ha Chung ) 대한신장학회 2021 Kidney Research and Clinical Practice Vol.40 No.1
Background: This study evaluated the impact of acute kidney injury (AKI) on posttransplant clinical outcomes for deceased donor (DD) kidney transplantation (KT) using the Kidney Donor Profile Index (KDPI) system. Methods: Overall, 657 kidney transplant recipients (KTRs) receiving kidneys from 526 DDs from four transplant centers were included. We divided them into the high and low KDPI donor groups by 65%, the KDPI score, and both groups were subdivided into the AKI-DDKT and non-AKI-DDKT subgroups according to AKI in DDs. Results: There was no significant difference in the incidence of delayed graft function (DGF) between the high and low KDPI-KTR groups; however, the AKI-DDKT subgroup showed significantly higher incidence of DGF than the non-AKI-DDKT subgroup in both groups (p = 0.001, p < 0.001, respectively). The death-censored graft survival rate was significantly lower in the high KDPI-KTR group than in the low KDPI-KTR group (p = 0.005). Only in the high KDPI-KTR group, the death-censored graft survival rate was significantly lower in the KT from DDs with AKI stage 3 than KT from DDs with non-AKI or AKI stage 1 or 2 (p = 0.040). The interaction between AKI stage 3 in DDs and high KDPI on the allograft outcome was significant (p = 0.002). Conclusion: KTs from DDs with AKI stage 3 showed an adverse impact on the allograft outcome in the high KDPI-KTR group. Therefore, DDs with a high KDPI score should be managed carefully so that severe AKI does not occur prior to KT.
Long-term prognosis of BK virus-associated nephropathy in kidney transplant recipients
( Woo Yeong Park ),( Seong Sik Kang ),( Kyubok Jin ),( Sung Bae Park ),( Misun Choe ),( Seungyeup Han ) 대한신장학회 2018 Kidney Research and Clinical Practice Vol.37 No.2
Background: The long-term prognosis of BK virus-associated nephropathy (BKVAN) in kidney transplant recipients (KTRs) is uncertain. We evaluated the long-term prognosis in KTRs with BKVAN and the clinical significance of BKVAN on post-transplant clinical outcome. Methods: We retrospectively analyzed the medical records of 582 patients who underwent kidney transplant (KT) between 2001 and 2014. We divided the patients into a BKVAN group (15 patients) diagnosed by allograft biopsy and a control group (356 patients). Results: The incidence of BKVAN was 4.0%, and the mean follow-up duration was 93.1 ± 52.3 months. Median time from KT to BKVAN diagnosis was 5.9 months (interquartile range [IQR], 4.4-8.7). In the BKVAN group, 9 (60.0%) KTRs with combined acute rejection progressed to graft failure, and the median time from BKVAN diagnosis to graft failure was 36.2 months (IQR, 9.7-65.5). Death-censored graft survival rate and patient survival rate in the BKVAN group were significantly lower than those in the control group. BKVAN and rejection were independent risk factors for graft failure. In the subgroup analysis, death-censored graft survival rate of KTRs with BKVAN with acute rejection was significantly worst in comparison with similar patients without BKVAN regardless of acute rejection (P < 0.001). Conclusion: The long-term prognosis of BKVAN with acute rejection was very poor because of graft failure caused by inadequate treatment for acute rejection considering BKVAN. Therefore, we should carefully monitor the allograft status of KTRs through regular surveillance tests after treatment for BKVAN with acute rejection.
( Yaerim Kim ),( Seong Sik Kang ),( Woo Yeong Park ),( Kyubok Jin ),( Dae Kwang Kim ),( Seungyeup Han ) 대한전해질학회 2016 Electrolytes & Blood Pressure Vol.14 No.1
A 42-year-old man came to the hospital presenting chest discomfort and general weakness. He had come to the hospital with the same symptoms 3 months ago and 12 years prior. His laboratory test showed hypokalemia, hypomagnesemia and hypocalciuria. The arterial blood gas analysis showed hypochloremic metabolic alkalosis. He had an ultrasonography guided renal biopsy, the result was normal at light microscopy and immunofluorescence microscopy. However, a special stain for Na-Cl cotransporter was weakly expressed compared with the control. The patient and his family underwent genetic sequencing about the SLC12A3 gene. He had a homozygous mutation in the 179th nucleotide of Exon 1 on the SLC12A3 gene (p.Thr60Met) and his parents and sisters were diagnosed as carrier state of Gitelman’s syndrome (GS). GS is an inherited tubular disorder which presents mild hypokalemia, hypomagnesemia and hypocalciuria. Since the symptoms and laboratory results are not severe, it can go unnoticed by physicians. Herein we present a family with GS, diagnosed by genetic sequencing.