ABSTRACT
Epidermal growth factor (EGF), an essential factor for the proliferation and survival of renal tubular cells, is expressed by distal tubules and normally excreted via urine. Previous studies in rats demonstrated that acute tubular injury reduces urinary EGF levels. However, it is unclear whether urinary EGF is a suitable monitoring marker of tubular repair status after acute kidney injury (AKI) in humans. To address this question, we measured serum and urinary EGF in patients with AKI (n = 99) using ELISA and investigated whether urinary EGF levels were associated with the severity of tubular injury and renal prognosis. Urinary EGF was abundant in healthy controls but showed a significant decrease in AKI patients (14,522 ± 2190 pg/mL vs. 3201 ± 459.7 pg/mL, p < 0.05). The urinary EGF level in patients with renal AKI was notably lower than that in patients with pre-renal AKI. Furthermore, the urinary EGF level in patients with AKI stage 3 was significantly lower than that in patients with AKI stage 1. Urinary EGF levels were negatively correlated with urinary ß-2MG and serum creatinine levels but positively correlated with hemoglobin levels and eGFR. Urinary EGF was not significantly correlated with urinary NAG, α-1MG, L-FABP, NGAL, KIM-1, or urinary protein concentrations. No significant correlation was observed between serum and urinary EGF levels, suggesting that urinary EGF is derived from the renal tubules rather than the blood. In living renal transplantation donors, the urinary EGF/Cr ratio was approximately half the preoperative urinary EGF/Cr ratio after unilateral nephrectomy. Collectively, these data suggest that urinary EGF is a suitable noninvasive indicator of not only the volume of functional normal renal tubules but also the status of tubular repair after AKI.
ABSTRACT
BACKGROUND: Donors bravely donate their kidneys because they expect that living donor kidney transplantation (LKT) confers benefits to recipients. However, the magnitude of the survival benefit of LKT is uncertain. METHODS: This prospective cohort study used two Japanese nationwide databases for dialysis and kidney transplantation and included 862 LKT recipients and 285,242 hemodialysis (HD) patients in the main model and 5299 LKT recipients and 151,074 HD patients in the supplementary model. We employed time-dependent model in the main model and assessed the hazard ratio and the difference in the restricted mean survival time (RMST) between LKT recipients and HD patients. In the main analysis of the main model (LKT, N = 675; HD, N = 675), we matched LKT recipients with HD patients by age, sex, dialysis vintage, and cause of renal failure and excluded HD patients with dementia or performance status grades 2, 3, or 4. RESULTS: The median observational period was 8.00 (IQR 3.58-8.00) years. LKT was significantly associated with a lower risk of mortality (hazard ratios (95% confidence interval (CI)), 0.50 (0.35-0.72)) and an increase in life expectancy (7-year RMST differences (95% CI), 0.48 (0.35-0.60) years) compared with HD. In subgroup analysis, the survival benefit of LKT was greater in female patients than in male patients in the Cox model; whereas older patients gained longer life expectancy compared with younger patients. CONCLUSIONS: LKT was associated with better survival benefits than HD, and the estimated increase in life expectancy was 0.48 years for 7 years.
Subject(s)
Kidney Failure, Chronic , Kidney Transplantation , Living Donors , Female , Humans , Male , Kidney Failure, Chronic/surgery , Kidney Failure, Chronic/therapy , Prospective Studies , Renal Dialysis , Treatment Outcome , Survival AnalysisABSTRACT
INTRODUCTION AND OBJECTIVES: Both computed tomography (CT) and renal scintigraphy (RS) have been used to assess vascular anatomy, renal status, and split renal function (SRF). In this study, we used a recently developed software that facilitates renal volumetric evaluations to compare RS and automated CT volumetry for assessing residual renal function and, thus, estimating postoperative renal function after donor nephrectomy. METHODS: Fifty-one cases of donor nephrectomy were analyzed. Residual renal function was estimated based on RS and CT volumetry. The correlation between the postoperative estimated glomerular filtration rate (eGFR) and expected SRF, measured using RS and three types of CT volumetry data (ellipsoid, thin-slice, and 5-mm slice data), was determined. RESULTS: The correlation coefficient between actual eGFR and expected SRF was significantly associated at each time point and modality (p < 0.0001). At any time point, the difference in correlation coefficient between RS and 5-mm volumetry was significant (p value: 0.003-0.018), whereas the differences in correlation coefficients between RS and the triaxial volume calculation, and the triaxial volume calculation and 5-mm volumetry, were generally statistically insignificant. CONCLUSIONS: Expected SRF was estimated more accurately by CT volumetric calculations (especially 5-mm slice-based volumetry) than RS.
Subject(s)
Kidney Transplantation , Humans , Glomerular Filtration Rate , Kidney , Kidney Transplantation/methods , Living Donors , Nephrectomy/methods , Radionuclide Imaging , Retrospective Studies , Tomography, X-Ray Computed/methodsABSTRACT
Objective We studied three types of estimated glomerular filtration rate (eGFR) equations and evaluated which type was strongly associated with comorbidities in living kidney transplantation (LKT) donors. Methods We compared the Japanese modified eGFR, Modification of Diet in Renal Disease, and Chronic Kidney Disease Epidemiology Collaboration equations (Jm-eGFR, Jm-MDRD, and Jm-CKD-EPI, respectively) for Japanese LKT donors with respect to their relationships with obesity, hypertension, diabetes, cardiovascular disease, and stroke. Results Of the 8,176 enrolled Japanese LKT donors, the eGFR calculated using Jm-CKD-EPI (eGFR/Jm-CKD-EPI) detected significant differences in 4 of 5 comorbidities between the comorbidity-positive and comorbidity-negative groups, whereas the eGFR calculated using Jm-MDRD (eGFR/Jm-MDRD) and Jm-eGFR (eGFR/Jm-eGFR) detected only 3 and 1 comorbidities, respectively. The area under the receiver operating characteristic curve of Jm-CKD-EPI was larger than those of Jm-eGFR and Jm-MDRD for all five comorbidities. Conclusion We found that the eGFR/Jm-CKD-EPI correlated better with comorbidities than the eGFR/Jm-eGFR and eGFR/Jm-MDRD in Japanese LKT donors. We recommend using the eGFR/Jm-CKD-EPI for the initial assessment of the renal function in LKT donor candidates when evaluating the presence of associated comorbidities.
Subject(s)
Kidney Transplantation , Renal Insufficiency, Chronic , Comorbidity , Creatinine , Glomerular Filtration Rate , Humans , Japan/epidemiology , Renal Insufficiency, Chronic/epidemiologyABSTRACT
BACKGROUND: Urinary tract infection (UTI) is one of the most common infectious complications in kidney transplant recipients. The aims of our study were to identify possible predictive factors for UTI and advocate for the management of UTI after kidney transplantation (KT). METHODS: Between January 2013 and December 2018, 182 adult patients with end-stage kidney disease who underwent KT were retrospectively analyzed. Patients who had urinary symptoms and positive urine culture were diagnosed with UTI. The types of urinary bacteria causing UTIs were also examined. RESULTS: UTIs occurred in forty-one patients (25.1%), and the median time to UTI onset (UTI-free survival) after KT was 189 days. The Cox hazard regression analysis showed that the predictive factors for UTI onset were as follows: posttransplant urinary catheterization, including indwelling urinary catheterization and clean intermittent catheterization; a maximum bladder capacity before KT of less than 150 ml; and a low serum albumin level at 1 month after KT. The most common causative agent was Escherichia coli (56.6%), followed by Enterococcus spp. (15.6%) and Klebsiella spp. CONCLUSIONS: Kidney transplant recipients with prolonged postoperative malnutrition, posttransplant voiding dysfunction and/or urinary storage disorder had an increased risk of UTI. Bladder function tests, such as uroflowmetry, postvoid residual urine tests, and urodynamic tests, were needed to predict UTI. For patients with malnutrition, care should be taken to ensure sufficient calorie intake. Kidney transplant recipients who develop UTI should be treated as complicated UTI patients.
Subject(s)
Kidney Failure, Chronic/surgery , Kidney Transplantation/adverse effects , Postoperative Complications/etiology , Urinary Tract Infections/etiology , Adult , Aged , Female , Humans , Male , Middle Aged , Postoperative Complications/therapy , Retrospective Studies , Serum Albumin/analysis , Urinary Tract Infections/therapyABSTRACT
A transdermal patch formulation of a non-steroidal anti-inflammatory drug (NSAID) used by a 44-year-old man resulted in acute interstitial nephritis and acute tubular injury. This patient also had a history of mild kidney dysfunction and osteoporosis. The NSAID patch had been prescribed after a traffic accident. He was also receiving a vitamin D analog and taking over-the-counter calcium supplements. Two months later, renal dysfunction and hypercalcemia were discovered. A renal biopsy showed acute interstitial nephritis and acute tubular injury. Once these agents were withdrawn, the renal function recovered. This is the first reported occurrence of biopsy-proven acute interstitial nephritis attributable to NSAID patch usage.
Subject(s)
Acute Kidney Injury/chemically induced , Acute Kidney Injury/physiopathology , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Kidney Diseases/drug therapy , Nephritis, Interstitial/chemically induced , Nephritis, Interstitial/physiopathology , Phenylpropionates/adverse effects , Transdermal Patch/adverse effects , Adult , Humans , Japan , MaleABSTRACT
We retrospectively compared the post-transplantation graft survival and the donor's estimated glomerular filtration rates (eGFRs) following living donor kidney transplantations (LDKTs) involving medically complex living donors (MCLDs) (the elderly and patients with obesity, hypertension, diabetes mellitus, or reduced renal function) and standard living donors (SLDs). The clinical data on patients who underwent LDKTs at our institution from 2006-2019, including 192 SLDs and 99 MCLDs, were evaluated. Regarding recipients, the log-rank test and multivariable Cox proportional hazards analyses showed a higher incidence of overall and death-censored graft loss in the recipients who received kidneys from MCLDs (Hazard ratio = 2.16 and 3.25, P = 0.015 and 0.004, respectively), after adjusting for recipient-related variables including age, sex, duration of dialysis, ABO compatibility, and donor-specific antibody positivity. Regarding donors, a linear mixed model showed significantly lower postdonation eGFRs (-2.25 ml/min/1.73 m2 , P = 0.048) at baseline in MCLDs than SLDs, but comparable change (difference = 0.01 ml/min/1.73 m2 /year, P = 0.97). In conclusion, although kidneys from MCLDs are associated with impaired graft survival, the donation did not adversely affect the MCLDs' renal health in at least the short-term. LDKTs involving carefully selected MCLDs would be an acceptable alternative for recipients with no SLDs.
Subject(s)
Kidney Transplantation , Living Donors , Aged , Graft Rejection , Graft Survival , Humans , Registries , Retrospective StudiesABSTRACT
BACKGROUND: Sarcopenia is prevalent in patients with chronic kidney disease and is associated with increased mortality; however, limited data are available on whether kidney transplantation can improve muscle wasting. Therefore, the present study aimed to assess changes in body composition before and after kidney transplantation. METHODS: Between April 2015 and January 2018, 80 de novo consecutive adult patients with end-stage kidney disease who underwent kidney transplantation were prospectively enrolled. Muscle and fat masses were measured via bioelectrical impedance analysis using InBody 770 at - 2 and 7 days and 3, 6, and 12 months after transplantation. Presarcopenia is characterized by low muscle mass according to the skeletal muscle mass index. Changes in body composition and prevalence of presarcopenia were compared before and after transplantation. Risk factors for presarcopenia were identified using logistic regression analysis. RESULTS: Muscle mass significantly decreased at 3 months after transplantation. Consequently, the prevalence of presarcopenia was significantly higher after transplantation (3 months: 47.5%, 6 months: 42.5%, and 12 months: 38.8%) than that before transplantation (25.0%). Similarly, the body fat percentage was significantly higher at 3 months after transplantation than that before transplantation. Presarcopenia before transplantation was an independent risk factor for presarcopenia at 12 months after transplantation (odds ratio: 51.8, 95% CI 5.77-464, p < 0.001). CONCLUSIONS: Muscle wasting deteriorated and body fat percentage increased from 3 months after kidney transplantation. Presarcopenia before transplantation led to presarcopenia after transplantation, which may deteriorate with an increase in body fat percentage.
Subject(s)
Body Composition , Kidney Transplantation , Postoperative Complications/epidemiology , Sarcopenia/epidemiology , Adult , Female , Humans , Japan/epidemiology , Male , Middle Aged , Prevalence , Prospective StudiesABSTRACT
BACKGROUND: Recently, chronic hepatitis E has been reported in solid organ transplant (SOT) recipients in European countries. Previously, we clarified the prevalence of hepatitis E virus (HEV) infection in Japanese liver transplant recipients and identified 2 chronic hepatitis E patients infected by blood transfusion. However, the rate of HEV infection in recipients of SOTs other than liver in Japan remains unclear, so we conducted a nationwide survey to clarify the prevalence of chronic HEV infection in Japanese heart and kidney transplant recipients. METHODS: A total of 99 heart and 2526 kidney transplant recipients in 17 hospitals in Japan were examined for the presence of the IgG class of anti-HEV antibodies as well as for serum HEV RNA. RESULTS: The prevalence of anti-HEV IgG among heart and kidney transplant recipients was 7.07% (7/99) and 4.08% (103/2526), respectively. One heart transplant patient (1.01%) and 11 kidney transplant patients (0.44%) were found to be positive for HEV RNA. The HEV isolates from all viremic patients were typed as genotype 3. Four patients developed chronic hepatitis E after transplantation. Three patients were treated with ribavirin; their liver enzymes normalized, and HEV RNA became negative immediately. Sustained virologic response was achieved in all cases. CONCLUSIONS: This is the first nationwide survey of HEV infection in Japanese heart and kidney transplant recipients. The prevalence of anti-HEV IgG and HEV RNA in heart and kidney transplant recipients in Japan was lower than that in European countries. Of note, 42% of viremic transplant patients developed chronic hepatitis.
Subject(s)
Heart Transplantation/adverse effects , Hepatitis E virus/genetics , Hepatitis E/epidemiology , Hepatitis, Chronic/epidemiology , Kidney Transplantation/adverse effects , Population Surveillance , Transplant Recipients , Adult , Female , Hepatitis E/virology , Hepatitis, Chronic/etiology , Humans , Incidence , Japan/epidemiology , Male , Middle Aged , Prevalence , RNA, Viral/analysisABSTRACT
BACKGROUND: Rituximab is used widely for desensitization in ABO-incompatible and donor-specific antibody-positive kidney transplantation. However, data about the effects of individual differences in rituximab-induced B-cell suppression on antibody-mediated rejection (AMR) remain unknown. We aimed to assess the association between CD19-positive rate and AMR following rituximab administration after kidney transplantation. METHODS: Overall, 42 patients who underwent rituximab therapy for pretransplant desensitization in ABO-incompatible (n = 33) and donor-specific antibody-positive (n = 15) kidney transplantation were observed retrospectively. To predict AMR incidence, the peripheral blood CD19-positive rate was determined and classified into short- and long-acting groups. AMR incidence, allograft function, complications, and rituximab dose were compared. RESULTS: Eight patients (19%) had AMR within 39.2 months after transplantation. The CD19-positive rate cutoff value to predict AMR incidence was 4.4%, 6.4%, and 7.7% at 6, 12, and 18 months after transplantation, respectively. When comparing the short- and long-acting groups stratified according to the CD19-positive rate cutoff value, AMR incidence was significantly higher in the short-acting group than in the long-acting group at 6 (71.4% vs 8.6%), 12 (70.0% vs 3.1%), and 18 (58.3% vs 3.3%) months after transplantation. The CD19-positive rate for all patients with AMR exceeded the cutoff value 6, 12, or 18 months. Conversely, serum creatinine level, tacrolimus trough-level, cytomegalovirus antigenemia-positive rate, neutropenia incidence rate, and total dose of rituximab before transplantation showed no significant differences between the 2 groups. CONCLUSIONS: The risk of AMR was higher in patients with short-term B-cell suppression following rituximab administration. Additional rituximab administration after transplantation may prevent AMR in patients with a CD19-positive rate higher than the cutoff value.
ABSTRACT
BACKGROUND: Rabbit antithymocyte globulin (rATG) induction is associated with reduction in the occurrence of de novo donor-specific antibody (DSA) and antibody-mediated rejection (AMR). Therefore, rATG administration is considered as a treatment for AMR. However, only a few studies have investigated the treatment of AMR with rATG after kidney transplantation. METHODS: Between April 2013 and March 2018, 162 consecutive de novo kidney transplantations were performed with induction immunosuppressive therapy comprising tacrolimus, mycophenolate mofetil, methylprednisolone, and basiliximab. AMR was diagnosed on the basis of the presence of DSA and episode biopsy findings. For DSA-positive recipients, plasmapheresis was performed to remove DSA before rATG administration (1.5 mg/kg for 5 days). Patients treated with rATG against active AMR were retrospectively analyzed for graft function. RESULTS: A total of 13 kidney transplant recipients developed active AMR within 302 days after transplantation. After rATG administration, the mean serum creatinine and urine protein levels significantly declined from 3.03 mg/dL to 1.68 mg/dL (P = .002) within 46 days and from 3.01 g/gCr to 0.54 g/gCr (P = .006) within 106 days, respectively. The peripheral blood lymphocyte count rapidly decreased after rATG administration and remained low for 12 months. With regard to adverse events, fever (84.6%), cytomegaloviremia (84.6%), thrombocytopenia (61.5%), anemia (30.8%), and neutropenia (15.4%) occurred within 3 months after rATG administration. CONCLUSIONS: rATG improved graft function by suppressing peripheral blood lymphocytes in kidney transplant recipients with active AMR. The rATG administration as a treatment for active AMR may contribute to positive graft outcomes after kidney transplantation.
Subject(s)
Antilymphocyte Serum/therapeutic use , Graft Rejection/drug therapy , Immunosuppressive Agents/therapeutic use , Kidney Transplantation , Adult , Basiliximab/therapeutic use , Female , Graft Rejection/immunology , Humans , Kidney Transplantation/adverse effects , Male , Middle Aged , Mycophenolic Acid/therapeutic use , Plasmapheresis/methods , Retrospective Studies , Tacrolimus/therapeutic use , Treatment OutcomeABSTRACT
Post-transplant lymphoproliferative disorder (PTLD) is a fatal complication of transplantation. There is no clear consensus on the treatment of PTLD. In most cases, the pathogenetic mechanism of PTLD involves the Epstein-Barr virus (EBV). We report the case of an elderly kidney transplant recipient who developed EBV-positive monomorphic T-cell PTLD 14 years after transplantation. Conversion from conventional immunosuppressants to everolimus induced complete remission of PTLD accompanied by a decrease in blood EBV-DNA level without chemotherapy.
Subject(s)
Epstein-Barr Virus Infections/drug therapy , Everolimus/therapeutic use , Immunosuppressive Agents/therapeutic use , Kidney Transplantation/adverse effects , Lymphoproliferative Disorders/virology , Remission Induction , Aged , Herpesvirus 4, Human , Humans , Lymphoproliferative Disorders/drug therapy , Male , Postoperative Complications/drug therapy , Transplant RecipientsABSTRACT
BACKGROUND: Calcineurin inhibitors (CNIs), which remain the most important immunosuppressants in kidney transplant recipients, are a major cause of renal dysfunction due to CNI-induced nephropathy. However, a safe and effective CNI-sparing protocol is yet to be established. Herein, we report a case series of kidney transplant recipients experiencing CNI nephropathy, whose renal function is improved after conversion from CNIs to everolimus. CASES: The 3 kidney transplant recipients included in this study were diagnosed with CNI arteriolopathy by episode biopsy between 9 months and 11 years after transplantation. All patients received triple immunosuppressive therapy consisting of CNI (tacrolimus or cyclosporine), mycophenolate mofetil, and methylprednisolone. All allografts were transplanted from elderly living donors to ABO-compatible and donor-specific antibody-negative recipients. All allograft biopsy specimens exhibited CNI arteriolopathy with alternative quantitative criteria for hyaline arteriolar thickening (aah score: 2 or 3), according to the Banff classification; however, histopathologic assessment did not show any evidence of allograft rejection. Conversely, total dose and blood concentrations of CNIs were within appropriate ranges. After conversion from CNIs to everolimus (1.5 mg/day, twice daily; trough level, 3-5 ng/mL), serum creatinine levels returned to baseline levels measured before the diagnosis of CNI arteriolopathy. In all patients, renal allograft function remained stable, with no evidence of donor-specific antibodies, 1 year after conversion from CNIs to everolimus. CONCLUSION: Conversion from CNIs to everolimus can safely and effectively improve renal function in kidney transplant recipients experiencing CNI-induced nephropathy.
Subject(s)
Calcineurin Inhibitors/adverse effects , Everolimus/therapeutic use , Immunosuppressive Agents/therapeutic use , Kidney Diseases/chemically induced , Kidney Transplantation , Adult , Aged , Female , Humans , Immunosuppression Therapy/adverse effects , Immunosuppression Therapy/methods , Kidney/drug effects , Kidney Diseases/drug therapy , Male , Transplant RecipientsABSTRACT
BACKGROUND: Hypercalcemia and bone mineral density (BMD) loss are serious problems associated with post-transplant chronic kidney disease-mineral and bone disorder. The present study aimed to clarify the effects of denosumab on hypercalcemia complicated with BMD loss in kidney transplant recipients. MATERIALS AND METHODS: Among 100 consecutive adult kidney transplant recipients, 16 patients with serum corrected Ca (cCa) levels ≥ 11.0 mg/dL were included in a severe hypercalcemia group. In 14 patients (excluding 2 patients who underwent parathyroidectomy) with severe hypercalcemia and low BMD at the lumbar spine (T-score < -1.0), 60 mg of denosumab were administered by subcutaneous injection at 6-month intervals. Serum cCa and alkaline phosphatase (ALP) levels were analyzed before and after denosumab administration. Lumbar spinal BMD was compared between, before, and 12 months after denosumab administration. RESULTS: Both serum cCa (11.7 mg/dL) and ALP (525 U/L) levels declined promptly after denosumab administration, with only the cCa level showing rebound. Additionally, serum cCa and ALP levels were significantly lower after denosumab administration (all time points) than before denosumab administration. Lumbar spinal BMD increased significantly 12 months after denosumab administration when compared with the value before denosumab administration in both anterior-posterior (increase rate: 5.0%) and lateral (increase rate: 5.4%) projections. CONCLUSION: Denosumab could improve hypercalcemia and BMD loss in kidney transplant recipients. Therapeutic intervention involving denosumab should be considered for hypercalcemia and BMD loss associated with post-transplant chronic kidney disease-mineral and bone disorder.
Subject(s)
Bone Density Conservation Agents/pharmacology , Bone Density/drug effects , Denosumab/pharmacology , Hypercalcemia/blood , Hypercalcemia/drug therapy , Kidney Transplantation , Adult , Alkaline Phosphatase/blood , Calcium/blood , Female , Humans , Lumbar Vertebrae/diagnostic imaging , Male , Middle Aged , Retrospective StudiesABSTRACT
Patients who undergo kidney transplantation are at increased risk of cancer due to the long-term use of immunosuppressive treatment. Postrenal transplant cancers usually originate from recipient cells, but donor-related cancers have been rarely reported. We report the case of 49-year-old woman who developed multiple myeloma of donor origin 7 years after kidney transplantation. The donor was the mother of the recipient and also developed multiple myeloma 1 year after kidney donation. The diagnosis of multiple myeloma was based on IgG lambda monoclonal protein and the infiltration of plasma cells in bone marrow. The renal biopsy did not reveal plasmacytoma in the transplanted kidney. Epstein-Barr virus DNA load was negative in peripheral blood. The patient responded to lenalidomide and dexamethasone, and subsequently received autologous stem cell transplantation. Donor chimerism was detected in the recipient marrow by short tandem repeat analysis; however, studies of Ig gene rearrangement were inconclusive due to insufficient DNA quality. The chromosomal abnormalities in the two myelomas were different. This case suggests that donor cells with myeloma-initiating potential can be transferred to a recipient via a renal graft and can lead to the development of donor-derived multiple myeloma in the recipient under immunosuppression.
Subject(s)
Kidney Failure, Chronic/surgery , Kidney Transplantation/adverse effects , Multiple Myeloma/etiology , Nephrectomy/adverse effects , Postoperative Complications/etiology , Tissue Donors/supply & distribution , Tissue and Organ Harvesting/adverse effects , Adult , Chimerism , Female , Humans , Immunosuppressive Agents , Multiple Myeloma/pathology , Postoperative Complications/pathologyABSTRACT
Fibrosing cholestatic hepatitis (FCH) is a fatal disorder that presents as a progressive deterioration of liver function over a period of several weeks to several months. It is caused by the direct cytotoxic effect of the over-expression of viral antigens on hepatocytes in immunosuppressed patients. Our patient was a 59-year-old man with hepatitis C virus (HCV) infection of genotype 2a who had suffered from end-stage renal disease due to diabetic nephropathy and underwent kidney transplantation. His serum total bilirubin levels gradually increased to 20 mg/dl and liver atrophy progressed during several weeks after kidney transplantation, which was initially difficult to distinguish from drug-induced liver injury. We diagnosed the condition as FCH on the basis of pathological findings and increased HCV viral load, and treated the patient with Glecaprevir/Pibrentasvir. However, the patient died of refractory hemorrhagic gastric ulcer and liver failure. Currently, it is possible to treat infections of all genotypes of HCV, even with end-stage renal disease, with direct acting antivirals. Furthermore, it is preferable to treat HCV before kidney transplantation considering the risk of FCH due to immunosuppressive therapy.
Subject(s)
Cholestasis/pathology , Hepatitis C/complications , Kidney Transplantation/adverse effects , Liver Cirrhosis/pathology , Aminoisobutyric Acids , Antiviral Agents/administration & dosage , Antiviral Agents/therapeutic use , Benzimidazoles/administration & dosage , Benzimidazoles/therapeutic use , Bilirubin/blood , Cholestasis/blood , Cyclopropanes , Fatal Outcome , Hepacivirus/genetics , Hepacivirus/isolation & purification , Hepatitis C/pathology , Hepatitis C/virology , Humans , Lactams, Macrocyclic , Leucine/analogs & derivatives , Male , Middle Aged , Proline/analogs & derivatives , Pyrrolidines , Quinoxalines/administration & dosage , Quinoxalines/therapeutic use , Sulfonamides/administration & dosage , Sulfonamides/therapeutic use , Transplant Recipients , Viral LoadABSTRACT
BACKGROUND: Hepatitis E virus (HEV) infection can lead to chronic hepatitis in solid organ transplant recipients. To investigate whether HEV infection influences outcomes following kidney transplantation, we examined the prevalence of HEV infection and clinical characteristics of kidney transplant recipients in our hospital. METHODS: Our cross-sectional study included 184 kidney transplant recipients. Blood samples were obtained from all patients to detect anti-HEV immunoglobulin (Ig)A, IgM, and IgG by enzyme-linked immunosorbent assay and HEV RNA by reverse transcription polymerase chain reaction. Clinical data were collected from medical charts for all patients. RESULTS: The prevalence of anti-HEV IgG was 8/184 (4.3%). Anti-HEV IgA, anti-HEV IgM, and HEV RNA were not detected in any patients. Compared to their anti-HEV IgG-negative counterparts, anti-HEV IgG-positive patients were significantly older at the time of transplantation, and they were more likely to receive kidneys from deceased donors. No significant differences in other characteristics such as the prevalence of primary cause of end-stage renal disease, blood transfusion, and immunosuppressive therapy use; liver and renal function; and the frequencies of hepatitis B and hepatitis C virus infection were observed according to the patients' anti-HEV IgG status. CONCLUSION: HEV infection had no significant influence on the outcomes of kidney transplantation at our institution. However, HEV infection should be recognized in kidney transplant recipients similarly as hepatitis B and hepatitis C virus infection in cases of liver dysfunction.
Subject(s)
Hepatitis Antibodies/blood , Hepatitis E virus/immunology , Hepatitis E/epidemiology , Kidney Transplantation/adverse effects , Adolescent , Adult , Aged , Cross-Sectional Studies , Female , Hepatitis E/immunology , Hepatitis E virus/genetics , Humans , Immunocompromised Host , Immunoglobulin G/blood , Immunoglobulin M/blood , Japan/epidemiology , Male , Middle Aged , Prevalence , RNA, Viral/analysis , Seroepidemiologic Studies , Transplant Recipients , Young AdultABSTRACT
We report a 55-year-old man with a renal allograft that developed sarcoidosis. His autosomal dominant polycystic kidney disease (ADPKD) progressed to end-stage stage renal disease when he was 52 years old, and he underwent living-donor kidney transplantation at the age of 53 years. His proteinuria worsened at 19 months post-transplantation, and his renal function began to decline at 29 months post-transplantation. A renal allograft biopsy performed at 31 months post-transplantation revealed non-caseating granulomatous interstitial nephritis. The patient was treated with prednisolone (0.5 mg/kg/day), with gradual reduction in the dose. His proteinuria improved and renal function did not deteriorate any further. To the best of our knowledge, this is the first case of sarcoidosis in a renal allograft recipient whose primary renal disease was ADPKD.