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As a genetic disease, there has been a long-standing effort to identify therapeutic options for autosomal dominant polycystic kidney disease (ADPKD). Following the development of tolvaptan, a vasopressin 2 receptor antagonist, the treatment strategy for ADPKD patients with rapid disease progression has been changed with a disease-targeted approach. Tolvaptan showed significant efficacy in preserving kidney function and reducing the total kidney volume (TKV) growth rate. These effects were especially pronounced in patients with more severe clinical phenotypes, such as higher TKV and rapidly declining kidney function. Despite the therapeutic effects of tolvaptan, aquaretic symptoms are unavoidable side effects related to the mechanism of the drug and are also directly related to the quality of life. A shared decision-making process could be a valuable strategy for reducing the incidence of side effects and improving medication adherence. Herein, we aimed to review overall clinical trials for applying tolvaptan and suggest important factors during the shared decision-making process.
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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.
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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.
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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: 1,800 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.
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Generally, an induction agent is chosen based on the conditions of the deceased donor and the recipient. Antithymocyte globulin (ATG) is preferred in relatively high-risk conditions. No clear evidence indicates which induction agent is safer or more efficient for deceased donor kidney transplantation (DDKT). This study compares the efficacy and safety of basiliximab (BSX) and ATG according to donor characteristics in DDKT. Methods: A total of 724 kidney transplant recipients from three transplant centers were enrolled, and propensity score matching was performed. Based on a donor age of 60 years, donor kidney with acute kidney injury (AKI), and Kidney Donor Profile Index (KDPI) score of 65%, we investigated how the choice of induction therapy agent affected the posttransplant clinical outcomes of delayed graft function (DGF), acute rejection (AR), infectious complications, and allograft and patient survival. Results: AR and DGF did not differ significantly according to induction agent in elderly/young donor, AKIon-AKI, and high-KDPI/ low-KDPI subgroups. The infection rate did not show meaningful differences. The differences in death-censored allograft survival and patient survival rates between induction agents were not statistically significant. Conclusion: Our study suggests that BSX can produce clinical outcomes similarly favorable to those of ATG even in DDKT cases with relatively poor donor conditions. Nonetheless, the donor and recipient conditions, immunological risk, and infection risk must be all taken into consideration when choosing an induction agent. Therefore, clinicians should carefully select the induction therapy agent for DDKT based on the risks and benefits in each DDKT case.
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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.
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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.
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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.
ABSTRACT
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.
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BACKGROUND: Cancer rates are increasing not only in the general population but also in patients with end-stage renal disease. We investigated the changing pattern of pretransplant malignancy in kidney transplant recipients over 5 decades.METHODS: We reviewed 3,748 kidney transplant recipients between 1969 and 2016. We divided patients into three groups (1969–1998, 1999–2006, 2007–2016) based on the era of the cancer screening system used throughout the nation. We analyzed the incidence and pattern of pretransplant malignancy among the three groups. We also evaluated recurrent and de novo malignancy in these patients compared to patients without pretransplant malignancy.RESULTS: A total of 72 patients exhibited pretransplant malignancy (1.9%). There were no cases of pretransplant cancer until 1998, but the rate of pretransplant malignancy gradually increased to 1.1% during 1999–2006 and further increased to 4.3% thereafter. The most frequent types of pretransplant malignancy changed from the bladder, liver, and stomach cancers to thyroid cancer and renal cell carcinoma. There were no de novo cases, but there were three cases of recurrent cancer in patients with pretransplant malignancy; the recurrence rate among kidney transplant recipients with pretransplant malignancy was not significantly different from the incidence rate of de novo malignancy among kidney transplant recipients without pretransplant malignancy (4.2% vs. 6.9%, P = 0.48).CONCLUSION: The incidence of pretransplant malignancy in kidney transplantation candidates is gradually increasing, and recent increases were accompanied by changes in cancer types. Pretransplant malignancy may not be a hindrance to kidney transplantation because of the low incidence of posttransplant recurrence and de novo malignancy.
Subject(s)
Humans , Carcinoma, Renal Cell , Early Detection of Cancer , Incidence , Kidney Failure, Chronic , Kidney Transplantation , Kidney , Liver , Recurrence , Stomach Neoplasms , Thyroid Neoplasms , Transplant Recipients , Urinary BladderABSTRACT
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℃ 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.
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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℃ 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.
Subject(s)
Animals , Humans , Rats , Brain , Calcineurin Inhibitors , Calcineurin , Cell Survival , Cyclosporine , Glioma , Kidney , Kidney Transplantation , Neurologic Manifestations , TacrolimusABSTRACT
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.
Subject(s)
Humans , Allografts , Biopsy , BK Virus , Diagnosis , Follow-Up Studies , Graft Survival , Incidence , Kidney Transplantation , Kidney , Medical Records , Prognosis , Retrospective Studies , Risk Factors , Survival Rate , Transplant Recipients , TransplantsABSTRACT
Renal vein thrombosis is a rare but serious cause of graft loss in kidney transplant recipients that is usually associated with early surgical complications. Here, we report a rare case of sudden development of late onset renal vein thrombosis after kidney transplantation. A 32-year-old man underwent deceased kidney transplantation 2 years prior. Oliguria and pain suddenly developed at the allograft site along with an elevated serum creatinine level. Doppler ultrasound showed absence of venous flow in the transplanted kidney. Magnetic resonance imaging showed thrombosis from the allograft vein to the anastomosis with the left common iliac vein and a swollen allograft kidney. The patient underwent anticoagulation with unfractionated heparin and warfarin. Serum creatinine normalized and renal vein thrombosis disappeared after 3 months of treatment. Late-onset renal vein thrombosis is rare; however, early detection and treatment are very important to restore renal allograft function.
Subject(s)
Adult , Humans , Allografts , Creatinine , Heparin , Iliac Vein , Kidney Transplantation , Kidney , Magnetic Resonance Imaging , Oliguria , Renal Veins , Thrombosis , Transplant Recipients , Transplants , Ultrasonography , Veins , WarfarinABSTRACT
BACKGROUND: Kidney transplantation (KT) is the treatment of choice for end-stage renal disease patients. The spouse is a major donor in living KT. Clinical outcomes of spousal donor KT are not inferior to those of living related donor KT. In this study, we compared clinical outcomes between ABO-compatible (ABOc) and ABO-incompatible (ABOi) spousal donor KTs. METHODS: Thirty-two cases of spousal donor KT performed from January 2011 to August 2013 were analyzed retrospectively. Twenty-one ABOc KTs and 11 ABOi KTs were performed. We investigated patient survival, graft survival, acute rejection, graft function, and complications. RESULTS: During follow-up, patient and graft survival rates were 100% in both groups. There were no significant differences in the incidence of delayed graft function, acute rejection, and the change in graft function between the 2 groups. Medical and surgical complications were not significantly different between the groups. CONCLUSION: The clinical outcomes of ABOc and ABOi spousal donor KTs were equivalent. In ABOi KT, an emotionally motivated spousal donor KT may be a good alternative to the problem of the absolute shortage of kidney donations.
Subject(s)
Humans , Blood Group Incompatibility , Delayed Graft Function , Follow-Up Studies , Graft Rejection , Graft Survival , Incidence , Kidney Failure, Chronic , Kidney Transplantation , Kidney , Retrospective Studies , Spouses , Tissue Donors , TransplantsABSTRACT
No abstract available.
Subject(s)
Hematuria , Hydronephrosis , Kidney , Lupus Erythematosus, Systemic , UreterABSTRACT
BACKGROUND: Thymoglobulin has been used for induction therapy to prevent acute rejection and delayed graft function (DGF) in kidney transplant patients. However, the usual dose of thymoglobulin is considered to be related with frequent infection. We compared the efficacy and safety of low-dose thymoglobulin to high-dose treatment in high risk recipients with kidney transplantation. METHODS: Twenty-one kidney transplant recipients underwent induction treatment with thymoglobulin and were divided into two groups: patients treated with low-dose (<6.0 mg/kg) and high-dose thymoglobulin (≥6.0 mg/kg). All patients showed one or more risk factors for acute rejection or DGF. The risk factors were re-transplantation, recipient or donor age over 60 years, human leukocyte antigen full mismatch, and panel-reactive antibody more than 50%. We compared incidence of acute rejection, infection, hematologic complications, and graft survival between two groups. RESULTS: The demographic characteristics of the two groups were comparable. Mean follow-up duration was 11.9±4.3 months, and cumulative thymoglobulin dosage was 6.3±1.6 mg/kg. The incidence rates of acute antibody-mediated rejection (AMR), DGF and infectious events as cytomegalovirus disease, or urinary tract infection were not significantly different between the two groups. Neutropenia occurred more frequently in the high-dose thymoglobulin group, but there was no statistically significant difference. The rate of graft loss were similar between the two groups. CONCLUSIONS: There were no differences in graft survival, infectious disease, and hematologic problems between the two groups. We suggest to lower the dose of thymoglobulin to less than 6 mg/kg for prevent acute AMR and DGF in high risk patients.
Subject(s)
Humans , Communicable Diseases , Cytomegalovirus , Delayed Graft Function , Follow-Up Studies , Graft Survival , Immunosuppressive Agents , Incidence , Kidney Transplantation , Kidney , Leukocytes , Neutropenia , Risk Factors , Tissue Donors , Transplant Recipients , Transplants , Urinary Tract InfectionsABSTRACT
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.
Subject(s)
Adult , Humans , Alkalosis , Biopsy , Blood Gas Analysis , Carrier State , Cytosine , Exons , Gitelman Syndrome , Hypokalemia , Microscopy , Microscopy, Fluorescence , Mutation, Missense , Parents , Pedigree , Siblings , Solute Carrier Family 12, Member 3 , Thorax , Threonine , UltrasonographyABSTRACT
BACKGROUND/AIMS: Kidney transplantation (KT) is the best treatment for end-stage renal disease patients. Although previous studies have demonstrated that the clinical outcome following living related (LR) KT is better than that following unrelated (LUR) KT in ABO-compatible KT recipients, recent studies showed no differences in clinical outcomes between the two treatments. In this study, we compared the clinical outcomes of LR and LUR KT in ABO-incompatible KT recipients. METHODS: From January 2011 to August 2013, 19 cases of ABO-incompatible KT were analyzed retrospectively. Eight kidneys (7 cases of parent-offspring and 1 case of siblings, Group 1) were donated from living-related donors and 11 (all spousal donors, Group 2) from living-unrelated donors. We investigated patient survival, graft survival, acute rejection, graft function, and complications. RESULTS: On Kaplan-Meier analysis, patient and graft survival during follow-up were 87.5% and 87.5% in Group 1; both were 100% in Group 2. Acute rejection, graft function, and medical and surgical complications were not significantly different between the two groups. CONCLUSIONS: The short-term clinical outcomes between LR and LUR KT in ABO-incompatible KT recipients were equivalent. Most domestic cases of LUR KT are from spousal donors and the spousal donor will be a major donor in ABO-incompatible KT patients.