Renal Biopsy Research Articles

Case of maternal uniparental isodisomy with autosomal recessive Alport syndrome combined with congenital myasthenia and Oguchi disease.

Uniparental isodisomy (UPiD) is a genetic condition in which an individual inherits two identical copies of a chromosome, or part of a chromosome, from one parent. UPiD can result in the development of autosomal recessive disorders if the chromosome inherited from one parent has a pathogenic variant. Herein, we present a 20year-old female patient who had no significant family history including kidney, muscular, or ocular diseases. She had muscle weakness since infancy and was suspected with congenital myasthenia. She was diagnosed with Oguchi disease, a congenital condition characterized by night blindness, by an ophthalmologist. At 3years of age, hematuria was noted, and gross hematuria was occasionally observed thereafter. Exome analysis revealed homozygous variants in the COL4A4, CHRND, and SAG genes on chromosome 2, which are the causative genes of Alport syndrome, congenital myasthenic syndrome, and Oguchi disease, respectively. Array comparative genomic hybridization analysis and microsatellite analysis revealed maternal UPiD. At approximately 18years of age, she presented with proteinuria withmild kidney impairment, and kidney biopsy was performed at 20years of age. Type IV collagen α5 chain staining showed a weak but positive image in the glomerular basement membrane. However, thinning and irregular thickening of the glomerular basement membrane and reticular changes in the dense layer were observed, which were consistent with Alport syndrome. Angiotensin II receptor blocker (candesartan) was administered, and her urinary protein levels decreased. She had a homozygous missense variant, positive α5 chain staining, and a mild phenotype.

Advances in Multitarget Therapeutic Approaches for Immune-Mediated Glomerular Diseases

Glomerulonephritis (GN) encompasses a diverse group of immune-mediated diseases that damage the glomerular component of the nephron. While kidney biopsy remains the gold standard for diagnosis, it often fails to provide adequate insight into the underlying etiology of GN. Current classification systems have limited our understanding of the disease’s pathophysiology and hinder the development of targeted therapies. Immunosuppressive treatments, such as glucocorticoids, calcineurin inhibitors, cyclophosphamide, and rituximab, remain the mainstay of therapy, though many patients fail to achieve remission or experience significant adverse effects. Moreover, the complex and multifactorial nature of GN pathogenesis calls for more refined therapeutic approaches. In recent years, multitarget therapies—combining different immunosuppressive agents targeting distinct immune pathways—have emerged as promising alternatives. Evidence suggests that multitarget therapy may offer superior outcomes compared to standard treatments. Despite early success, further studies are needed to optimize these regimens, reduce toxicity, and extend benefits to a broader range of GN patients. The development of personalized, biomarker-driven treatments, potentially leveraging innovative drug delivery systems and targeted biologics, holds promise for transforming GN care in the future.

Functional analysis of heterozygous variants in the SALL1 gene in 2 children with Townes-Brocks syndrome with FSGS

BackgroundTo investigate the functional characteristics of heterozygous variants in the SALL1 gene in two children with Townes-Brocks syndrome (TBS), as well as the underlying mechanisms leading to chronic kidney disease.MethodsWe retrospectively analyzed the clinical manifestations, laboratory findings, and genetic backgrounds of two TBS patients admitted to our hospital presenting with chronic kidney disease stage 2 and focal segmental glomerulosclerosis (FSGS). The genetic function was investigated through cultured cells transfected with variants. The Sall1 protein expression level was detected by western blotting. Immunofluorescence was also employed to detect the subcellular localization of SALL1.ResultsNovel heterozygous genetic variations (c.3175 C > T and c.694 C > T) were detected in two respective probands with distinct clinical presentations: Proband 1 presented with polydactyly, nephrotic syndrome, and stage 2 chronic kidney disease; while Proband 2 manifested renal dysplasia, progressive proteinuria, and also stage 2 chronic kidney disease. FSGS was confirmed by kidney biopsies from both probands. To assess the functional impact of these variations, we introduced mutant plasmids carrying the c.3175 C > T and c.694 C > T variants into podocytes. The expression level of variant c.3175 C > T(p.Q1059X) in podocytes showed a significant decrease compared to that of the wild-type (P < 0.05), whereas variant c.694 C > T(p.Q232X) was markedly upregulated (P < 0.01). Immunofluorescence analysis revealed aberrant localization patterns for both SALL1 variants within podocytes.ConclusionsTwo patients with Townes-Brocks syndrome (TBS) harboring novel variants presented atypical phenotypes, characterized primarily by significant and rapidly progressing renal involvement. Rare renal biopsy pathology revealed the presence of focal segmental glomerulosclerosis (FSGS) in both cases. Experimental validation demonstrated that both variants led to alterations in the molecular size, expression level, and localization of the Sall1 protein, suggesting that these SALL1 gene variants might contribute to FSGS by impacting podocyte function.

Red Blood Cell Casts on Kidney Biopsy and Progression of IgA Nephropathy.

Renal red blood cell casts (RBCC) are common in IgA nephropathy (IgAN), but their role in kidney disease progression of patients with IgAN remains unclear. 1425 patients in Peking University First Hospital IgAN (PKU-IgAN) cohort and 279 patients in TESTING trial were enrolled to test the association between RBCC and kidney outcome. RBCC was defined as positive (+) when at least one cast was identified within the renal tubules by light microscopy. Kidney endpoint was the composite of the first occurrence of a sustained 30% decrease in estimated glomerular filtration rate or end stage kidney disease or death due to kidney disease. Cox regression analysis was used. In PKU-IgAN, 529 patients (37%) had RBCC; in TESTING trial, 78 patients (28%) had RBCC. Patients with RBCC had more crescentic lesions, and less segmental sclerosis compared with patients without RBCC. In PKU-IgAN, after a median follow-up of 54 months, 119 patients (22%) with RBCC and 260 patients (29%) without RBCC reached the composite kidney endpoint (P=0.009). In multivariable analysis, RBCC was independently associated with composite kidney endpoint (HR 0.79; 95%CI 0.63 - 0.99; P=0.038). RBCC and immunosuppressive therapy (IST) had an interaction (P=0.001). RBCC was independently associated with composite kidney endpoint in patients who received IST (HR 0.56; 95%CI 0.40 - 0.77; P<0.001). In TESTING trial, after a median follow-up of 57 months, 26 patients (33%) with RBCC and 96 patients (48%) without RBCC reached the composite kidney endpoint (P=0.041). In univariate analysis, RBCC was associated with composite kidney endpoint (HR 0.64; 95%CI 0.42 - 0.99; P=0.047). Renal RBCC was frequent in IgAN and was associated with a higher incidence of acute active lesions and better renal prognosis, especially in those who received IST, warranting particular attention.

Identification of Fatty Acid-Binding Protein 4 as a Potential Biomarker and Therapeutic Target for ANCA-Associated Glomerulonephritis

Introduction: Fatty acid-binding protein 4 (FABP4) is a novel adipokine that is critically involved in many inflammatory and immune diseases. However, the role of FABP4 in anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (ANCA-GN) remains unclear. The current study aimed to investigate the role of FABP4 in patients with ANCA-GN. Methods: Plasma and urine samples from 37 patients with active ANCA-GN and kidney biopsy specimens from another group of 56 patients with ANCA-GN were collected. The plasma and urinary level of FABP4 were measured by enzyme-linked immunosorbent assay and the kidney FABP4 expression was determined by immunohistochemistry and immunofluorescence staining. Associations between FABP4 levels with clinical and pathologic parameters were analyzed. To further elucidate the role of FABP4 in ANCA-GN, a novel FABP4 inhibitor BMS309403 was employed in a recognized rat model of experimental autoimmune vasculitis (EAV). Results: Plasma and urinary levels of FABP4 in active ANCA-GN patients were significantly higher than those in normal controls (52.8 ± 23.6 ng/ml vs. 16.9 ± 8.8 ng/ml, P&lt;0.01; median 126.6 [interquartile range (IQR) 28.4-311.2] ng/g Cr vs. median 0.0 [IQR 0.0-0.0] ng/g Cr, P&lt;0.01, respectively). Immunohistochemical analysis revealed higher glomerular and tubular expression of FABP4 in the kidneys of ANCA-GN patients than those in normal controls (0.015 ± 0.012 vs. 0.004 ± 0.003, P&lt;0.001; 0.053 ± 0.026 vs. 0.011 ± 0.010, P&lt;0.001, respectively). Moreover, for ANCA-GN patients, urinary FABP4 levels were significantly higher in active ANCA than those in remission (184.3 ± 187.0 ng/g Cr vs. 9.4 ± 23.9 ng/g Cr, P&lt;0.01). Correlation analysis showed that urinary levels of FABP4 correlated with serum creatinine (r=0.596, P&lt;0.0001), urinary albumin/Cr (r=0.523, P=0.001), blood neutrophil ratio (r=0.386, P=0.018), PT (r=0.583, P=0.001), APTT (r=0.364, P=0.034), hemoglobin level (r=-0.398, P=0.015), eGFR (r=-0.680, P&lt;0.0001), crescent proportion (r=0.661, P=0.032) and all-cause death of ANCA-GN patients (HR 2.93, 95%CI (1.05-8.19)). Furthermore, FABP4 inhibition by BMS309403 ameliorated renal injury in a rat mole of ANCA-GN. Conclusions: Urinary FABP4 levels might reflect the disease activity and renal involvement of ANCA-associated vasculitis, and FABP4 might act as a promising therapeutic target against ANCA-GN.

Non-Invasive Biomarkers for Early Diagnosis of Kidney Allograft Dysfunction: Current and Future Applications in the Era of Precision Medicine

Kidney transplantation stands as the preferred treatment for end-stage kidney disease, significantly improving both the quality and longevity of life compared to dialysis. In recent years, the survival rates for patients and grafts have markedly increased thanks to innovative strategies in desensitization protocols for incompatible transplants and advancements in immunosuppressive therapies. For kidney transplant recipients, preventing allograft rejection is of paramount importance, necessitating the use of immunosuppressive medications. Regular follow-up appointments are essential, as monitoring the function of the kidney allograft is critical. Currently, established biomarkers such as serum creatinine, estimated Glomerular Filtration Rate (eGFR), proteinuria, and albuminuria are commonly employed to assess allograft function. However, these biomarkers have limitations, as elevated levels often indicate significant allograft damage only after it has occurred, thereby constraining treatment options and the potential for restoring graft function. Additionally, kidney biopsies, while considered the gold standard for diagnosing rejection, are invasive and carry associated risks. Consequently, the identification and development of new, sensitive, and specific biomarkers like dd-cfDNA, microRNAs (e.g., miR-21, miR-155), and sCD30 for allograft rejection are crucial. To tackle this challenge, intensive ongoing research employing cutting-edge technologies, including “omics” approaches, like genomic techniques, proteomics, or metabolomics, is uncovering a variety of promising new biomarkers.

Molecular Review of Suspected Alport Syndrome Patients—A Single-Centre Experience

Background: Alport syndrome (AS) is a clinically and genetically heterogeneous glomerulopathy resulting from pathogenic variants in COL4A3, COL4A4, and COL4A5. Genetic diagnosis is increasingly being conducted using next-generation sequencing (NGS). Methods: Within eight years, we examined a group of 247 Polish individuals and found in total 138 unrelated probands suspected with AS based on clinical course, laboratory findings, and/or family history, as well as the total of 109 family members. We applied a targeted NGS panel to identify the genetic spectrum of AS. Known and novel variants were revealed, and detailed evaluation was performed according to ACMG/AMP guidelines to classify them as pathogenic/likely pathogenic/VUS changes. Identified genotypes were compared with clinical manifestations: hematuria, proteinuria, chronic kidney disease, sensorineural hearing impairment, ocular abnormalities, and hypertension. Results: The molecular background was established in 109/138 probands. Overall, 79 different COL4A3-COL4A5 changes (56 known and 23 novel) were revealed. About 97% were SNVs, and only two COL4A5 CNVs were identified. In total, 11 recurrent COL4A3-COL4A5 variants were observed, including the most frequent COL4A5:p.Gly624Asp, accounting for 31% of X-linked AS. Conclusions: The use of NGS panel has shown considerable promise in the field of AS, increasing diagnostic rate to 79% and reducing time to diagnosis. The phenotype-driven gene panel, specific for genetic diseases in the pediatric population, is an affordable alternative to WGS and WES, offering comparable diagnostic efficacy and supporting its implementation as a first-line genetic test in rare diseases, including AS. Based on the obtained genotype–phenotype correlation, we assessed that NGS allows us to avoid invasive renal biopsy in AS diagnosis. It provides AS confirmation/exclusion, atypical AS identification, symptomatic/asymptomatic monoallelic COL4A3-COL4A5 carrier (especially COL4A5 females) determination, and inheritance pattern establishment. AS diagnosis confirmation enables clinical course prediction and is crucial for the early introduction of renoprotective treatment with renin–angiotensin–aldosterone system blockade, aimed at slowing the disease progression and estimating the risk in family members, which is important for genetic counselling.

CircRNA-0013747 Promotes Mesangial Cell Proliferation in Immunoglobulin A Nephropathy through Modulation of the Warburg Effect.

Immunoglobulin A nephropathy (IgAN) is characterized by aberrant mesangial cell (MC) proliferation, which is a critical determinant of glomerular sclerosis and renal dysfunction. Previous studies have highlighted the role of pyruvate kinase M2 (PKM2)- mediated aerobic glycolysis in promoting MC growth and the progression of kidney diseases. However, the precise mechanisms underlying PKM2 dysregulation in IgAN remain unclear. Circular RNAs (circRNAs), a class of noncoding RNAs, have emerged as pivotal regulators in various diseases, yet their role in IgAN has not been fully elucidated. In this study, we investigated the expression and functional significance of circRNA_0013747 in IgAN, focusing on its interaction with microRNA-330-3p (miR-330-3p) and its downstream effects on PKM2-mediated aerobic glycolysis. Our results demonstrated a significant upregulation of circRNA_0013747 in kidney biopsy samples from IgAN patients. Functional analyses revealed that circRNA_0013747 promoted MC proliferation and activated PKM2-mediated aerobic glycolysis. Importantly, these effects were attenuated by the upregulation of miR-330-3p, which was found to physically interact with circRNA_0013747, thereby inhibiting its function. Mechanistically, circRNA_0013747 acted as a sponge for miR-330-3p, relieving its suppressive effects on PKM2 expression. These findings suggest that circRNA_0013747 enhances glycolysis and proliferation in MCs through modulation of the miR-330-3p/PKM2 signaling axis. These results offer novel insights into the pathogenesis of IgAN and could contribute to new therapeutic approaches for this disease. Specifically, targeting circRNA_0013747 or modulating its interaction with miR-330-3p may provide a means to inhibit MC proliferation and aerobic glycolysis, thereby slowing the progression of IgAN and preserving renal function. Such therapeutic strategies hold the promise of substantial benefits for patients with IgAN and could pave the path toward developing more potent treatments for a wider range of renal diseases.

Comment on: Renal Arteriosclerosis in kidney biopsies associated with higher 10-year atherosclerotic cardiovascular disease in lupus nephritis: Reply.

Comment on: Renal Arteriosclerosis in kidney biopsies associated with higher 10-year atherosclerotic cardiovascular disease in lupus nephritis: Reply.

Comment on: Renal Arteriosclerosis in kidney biopsies associated with higher 10-year atherosclerotic cardiovascular disease in lupus nephritis.

Comment on: Renal Arteriosclerosis in kidney biopsies associated with higher 10-year atherosclerotic cardiovascular disease in lupus nephritis.

Acute Tubular Necrosis Attributed to High-Dose Everolimus with High-Potency Bisphosphonates for Advanced Breast Cancer – A Case Report

Introduction: Everolimus (EVR)-induced kidney injury is rarely reported. Conversely, acute tubular necrosis (ATN) is a recognized complication of high-dose bisphosphonate therapy. Case presentation: SM, a 69-year-old female patient with advanced breast cancer, who developed severe kidney injury necessitating renal replacement therapy (RRT) shortly after initiating EVR treatment, while concurrently receiving chronic high-potency bisphosphonate therapy. Kidney biopsy confirmed ATN. Upon discontinuation of both EVR and bisphosphonates, her renal function gradually improved over several months, leading to the cessation of RRT. At a two-year follow-up, her kidney function has returned to baseline. Conclusion: In this case report, we outline the patient's clinical course and provide a pathophysiological rationale for the synergistic effect of EVR and bisphosphonates in promoting ATN. With the increasing use of EVR in various oncologic indications, we emphasize the reversible nature of this kidney injury and stress the importance of timely recognition and intervention.

Kidney Biopsy-Proven Diabetic and Non-Diabetic Kidney Diseases and Outcomes in Patients With Type 2 Diabetes Receiving Dialysis: The REIN Registry.

Chronic kidney disease (CKD) in patients with diabetes does not always equate to diabetic kidney disease (DKD). This study aims to delineate and compare the clinical characteristics, survival rates, and access to kidney transplantation among patients with type 2 diabetes commencing dialysis, who were classified by kidney biopsy as having either DKD or non-diabetic kidney disease (non-DKD). We used the comprehensive French Renal Epidemiology and Information Network registry to analyze baseline clinical characteristics at dialysis inception and outcomes defined as death and access to kidney transplantation. We employed a multivariate Cox proportional hazards model and the Fine-Gray competing risk model to assess the probabilities of mortality and transplantation. Adults in the Renal Epidemiology and Information Network registry in France with a diagnosis of type 2 diabetes who initiated kidney replacement therapy from January 2009 to December 2015 and had a previous native kidney biopsy. We analyzed data from 2,869 patients with diabetes, 45% of whom had a biopsy-confirmed diagnosis of DKD. Among these patients, half presented additional histopathological findings indicative of nephroangiosclerosis and focal segmental glomerulosclerosis. The clinical profiles of patients with DKD and non-DKD were largely comparable. There were no significant differences in dialysis survival rates or kidney transplantation access between the groups, even after adjusting for confounding variables and considering competing risks. At the 6-year mark, the mortality rate was 60.3% (95% CI: 55.5-64.5) for the DKD group and 60.3% (95%CI: 55.9-64.3) for the non-DKD group. Multivariable Cox analysis revealed no significant difference in mortality risk between the DKD and non-DKD groups. The study limitations include potential residual confounders, lack of predialysis data, kidney biopsies possibly outdated, nonrandom biopsy indications, and survival bias because of analysis at dialysis inception. In patients with diabetes initiating dialysis, clinical characteristics and outcomes following dialysis initiation were similar in biopsy-proven DKD versus non-DKD. Our results suggest that the diabetic milieu has a more significant impact on outcomes in patients with diabetes treated with dialysis than the underlying pathological kidney diagnosis.

Quantification of globotriaosylceramide (GL3) in peritubular capillary endothelial cells (PTCEC) in kidney biopsies from patients with Fabry disease using machine learning

Quantification of globotriaosylceramide (GL3) in peritubular capillary endothelial cells (PTCEC) in kidney biopsies from patients with Fabry disease using machine learning

Epidemiological profile of kidney transplant patients with lupus nephritis.

Lupus nephritis (LN) affects up to 50% of patients with systemic lupus erythematosus (SLE) and may lead to kidney failure and require kidney transplantation (KT). Results compared to KT from other causes are controversial, and we aimed to assess the clinical course, complications, and survival of LN patients undergoing KT. Retrospective cohort of 99 KT due to LN from 1977 to 2023 at a single center, divided into two groups according to the immunosuppression period: G1 (before 2009) and G2 (from 2009 onwards). Clinical and demographic characteristics, as well as clinical evolution, were compared. Patients were predominantly white (65.9%), female (86.9%), in their first KT (83.8%). The median age was 20.0 (11.5-25.0) years at SLE diagnosis, and 30.0 (23.0-40.0) years at KT. Renal graft biopsy was indicated in 46% of patients, with rejection observed in 23%, and LN recurrence in 5%. When assessing the two distinct periods of standard immunosuppression, there was no difference in median glomerular filtration rate and proteinuria at 1 and 5 years, nor in 5-year survival. Throughout follow-up, 37.4% of patients lost their graft, and 13% died with a functioning graft. No graft loss was attributed to LN recurrence. KT is a successful treatment for LN, with graft survival rates similar to those of transplants from other causes. LN recurrence was not associated with renal graft loss.

Editorial comment on “Tailoring Renal Mass Biopsy: Optimal Core Number and Location Based on Tumor Size for Enhanced Diagnostic Accuracy- A Prospective Ex-Vivo Study”

Editorial comment on “Tailoring Renal Mass Biopsy: Optimal Core Number and Location Based on Tumor Size for Enhanced Diagnostic Accuracy- A Prospective Ex-Vivo Study”

WCN25-1057 Implementation of Immunohistochemistry for Renal Biopsies at the Pathology and Cytology Laboratory of Cheikh Anta Diop University in Dakar: A Study of 117 Cases

WCN25-1057 Implementation of Immunohistochemistry for Renal Biopsies at the Pathology and Cytology Laboratory of Cheikh Anta Diop University in Dakar: A Study of 117 Cases

Clinicopathological characteristics of patients with low titer anti-phospholipase A2 receptor antibodies verified by indirect immunofluorescence assay

ObjectiveLaboratory extensively applied enzyme-linked immunosorbent assay (ELISA) to measure anti-phospholipase A2 receptor antibodies (PLA2R-abs) since its diagnostic significance on PLA2R related primary membranous nephropathy (PLA2R-related pMN) was discovered. However, PLA2R-abs determined by ELISA (PLA2R-ELISA) could infrequently yield inconclusive results, specifically a grey-zone defined as PLA2R-abs ranging from 2 to 20 RU/mL. Recently, researchers suggested that double-check grey-zone PLA2R-abs by indirect immunofluorescence (IIF) could improve diagnostic accuracy. We evaluated the diagnostic performance of PLA2R-IIF in assessing PLA2R-related pMN and summarized clinicopathological characteristics of grey-zone population to provide more evidence for clinical practice. MethodsData on demographics, serology and pathology of patients with PLA2R-ELISA grey-zone results and a native kidney biopsy at Peking Union Medical College Hospital from September 2020 to April 2023 were reviewed. Grey-zone samples were analyzed using PLA2R-IIF. Negative results were defined as no fluorescence and positive results were graded according to fluorescence intensity. ResultsThis study included a total of 52 grey-zone patients divided into pMN group (n = 36, 69 %) and non-pMN group (n = 16, 31 %) according to renal pathology reports. pMN patients had higher PLA2R-abs and lower serum creatinine compared to the non-pMN patients (P = 0.003, P < 0.001). No statistically significant differences were observed in 24-hour urine protein and albumin between the two groups. Multiple pathological types were identified in the non-pMN group. The sensitivity and specificity of PLA2R-IIF in PLA2R-ELISA grey-zone population were 72 % and 88 %, respectively, with a total consistent rate of 77 % and a positive predictive value of 93 %. ConclusionBoth pMN and non-pMN patients presented grey-zone PLA2R-ELISA results. It was necessary to perform PLA2R-IIF to assist in the diagnosis of patients with PLA2R-ELISA grey-zone results.

WCN25-4473 An Insight into the clinico-pathological pattern of Native Kidney Biopsies:A Tertiary Care Centre Study From North India

WCN25-4473 An Insight into the clinico-pathological pattern of Native Kidney Biopsies:A Tertiary Care Centre Study From North India

WCN25-1083 The Role of Donor Factors and Procurement Kidney Biopsy Findings in Predicting Deceased Donor Renal Transplant Outcomes

WCN25-1083 The Role of Donor Factors and Procurement Kidney Biopsy Findings in Predicting Deceased Donor Renal Transplant Outcomes

Role of vesicoureteral reflux on pediatric kidney allograft function.

Vesicoureteral reflux (VUR) is a common urologic complication of pediatric kidney transplant, though there is little data on the effect of VUR on histologic graft changes or graft survival. All pediatric patients who received a kidney transplant from 2007 to 2020 were selected for retrospective chart review. All participants underwent a voiding cystourethrogram (VCUG) at a 6-month post-transplant. Patients were then categorized into two groups based on vesicoureteral reflux grade: no/low-grade VUR (grades 0-2) and high-grade VUR (grades 3-5). Outcomes collected included graft failure rates, graft function, urinary tract infections(UTIs), proteinuria, and Banff scores at 3- and 12-month post-transplant surveillance kidney biopsies. There were 74 pediatric patients who received a kidney transplant in the designated time-period, and of those 39 had no/low-grade VUR and 35 had high-grade VUR. There was no difference in graft failure among the two groups over time when stratified for age (p = 0.389, CI 0.53-5.08). Patients with high grade VUR had a higher risk of UTI development overall (RR 1.89, 95%CI 1-3.6, p = 0.041), mostly accounted for from increased development of febrile UTI (RR 1.66, 95%CI 1.1-2.6, p = 0.038). Unselected pediatric kidney transplant recipients with high-grade vesicoureteral reflux on VCUG at a 6-month post-kidney transplant are more likely to have febrile UTI compared to those in the low-grade VUR group. There is no difference in graft survival among the two groups.