Glomerular disease after renal transplantation: a multi-center protocol biopsy study in an Iberoamerican population.

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Rodolfo Torres, Maricely Reina, Camilo Montero, David Andrade, and 7 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-2094781/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Renal transplantation is the treatment of choice in end-stage renal disease (ESRD)( 1 , 2 ), nonetheless; there are still limitations in improving long-term renal graft survival in a significant way, post-transplant glomerular disease being one of the main causes of renal graft loss ( 3 , 4 ). Methods A retrospective cohort study, with renal transplant patients in 3 centers in the city of Bogota D.C Results 399 patients were included, 61.15% predominantly male, with a median age of 44.3 years, interquartile range (IQR) (32.9–55.9). Post-transplant glomerular Urology & Nephrology kidney transplantation Recurrence Glomerulonephritis Figures Figure 1 Figure 2 Figure 3 Introduction The glomerular disease accounts for approximately 30% of the etiologies of end-stage chronic kidney disease (ESRD) and its recurrence as well as its development after transplantation leads to a decrease in renal allograft function and loss of the kidney allograft. ( 2 , 5 ). The prevalence of the post-transplant glomerular disease varies according to the different series reported. ( 3 , 4 ). This depends on the underlying etiology, population diversity, follow-up time, and biopsies per protocol, being found in approximately 4 to 50% of the cases. ( 6 , 7 ). This wide margin is also explained by the limitation of performing recurrence studies of the disease due to the fact that most patients do not have a renal biopsy before transplantation, or the result is inconclusive, thus underestimating the real incidence and prevalence of this entity ( 8 , 9 ). The most frequent post-transplantation glomerulopathy is the IgAN ( 5 ); it recurs in approximately 25% of patients and its incidence increases up to 53% under the protocol biopsy strategy; up to 60% of which occurs within three years after transplantation ( 10 ); MPGN occurs in 20–30% of patients ( 2 ) and graft loss due to this entity has been reported in up to 30–50% of cases. ( 11 ). So far, in Latin America, there is no series in which the incidence of post-transplantation glomerular disease is evaluated; this information is vitally Important in order to plan the treatment strategy in future transplantations, especially in a region where the severity of glomerulopathies in native kidneys is high. Methods: A retrospective cohort study was carried out on renal transplant recipients in 3 transplant centers in the city of Bogotá D.C. Patients older than 15 years who underwent renal transplantation between 2007 and 2017 and who completed clinical follow-up within 5 years after renal transplantation were included. The information was gathered from the clinical histories recorded in the database of the renal transplant programs of 3 institutions in the city of Bogota. The clinical, analytical (proteinuria and creatinine), and histological data obtained from the medical records were recorded in a database, coded, and managed anonymously only by the research group. Biopsies per protocol performed were analyzed in the first 6 months, second and fifth-year post-transplantation. The analysis of the information was carried out through an analysis where quantitative variables were described with measures of central tendency; in the case of qualitative variables, calculations of frequencies and percentage distribution were made. Subsequently, a bivariate analysis was performed where, according to the fulfillment of assumptions and verification of normal distribution, t student and Mann Whitney U tests were performed. In the case of categorical variables, X2 and fisher's exact test were performed. Similarly, the probability of survival was estimated by applying the log-rank test to establish whether there was a difference in the probability of survival. All the tests were considered statistically significant with a p < 0.05. The information was analyzed in the statistical software R Studio version 4.2 and Jamovi version 2.2.5. The study was conducted in line with the principles of the Declaration of Helsinki (1964) and subsequent amendments, updated in 2013. All study documents were evaluated and approved by the Institutional Ethics Committee of the centers, thus being classified as safe research. Results: 399 renal transplant recipients between the years 2007 to 2017 in three transplant centers who met the inclusion criteria were included. 244 patients were male (61.15%), with a median age of 44.3 years (RIQ 32.9-55.9 years); 84.71% were cadaveric donor recipients and 15.29% were living donors. In regard to the etiologies of native kidney loss, unknown etiology predominated in 171 patients (42.86%) followed by glomerular disease in 104 patients (26%). Of the 399 patients, the glomerular disease was documented in 167 patients (41.85%) in post renal transplantation; of this subpopulation of patients, 76 (45.51%) had no etiology of native kidney damage, and 51 patients (30.53%) had the glomerular disease (GD) as etiology of renal damage. The subgroup of patients with the glomerular disease was predominantly male and the median age was 42.91 (RIQ 31.1-53.4). Table 1 shows the clinical profile of the cohort studied. In this study, the diagnosis of PTGD was made in most patients by biopsies by protocol in 123 patients (73.65%) and by clinical indication in 44 patients (26.35%). Incidence of post-transplant glomerular disease: Of the 167 patients who presented PTGD, in 88 patients (52.69%) biopsy confirmed IgAN, 37 patients (22.16%) had immune complex glomerulonephritis (CIGN) without established etiology, 30 patients (17.96%) had MPGN, 7 patients (4.19%) had FSGS, and 5 patients (2.99%) had membranous nephropathy (MN). Of this subpopulation of patients, recurrence of PTGD was documented in 21 patients (12.57%) in whom the etiology of glomerular disease prior to renal transplantation was known. Algorithm 1, Table 2 Graft loss due to GD occurred in 4 patients (6.9%) at 5 years, being the fourth cause of graft loss and the third cause censored for death. The first and the second cause of graft loss were death from another cause with functioning graft in 35 patients (60.3%) and rejection in 6 patients respectively (10.3%) Table 3. Graft survival in post-transplant glomerular disease Regarding the time of presentation of PTGD, in this study, it was found that FSGS was presented with a mean of 151.4 days Standard deviation (SD ±310.6), followed by membranous nephropathy 359 days (SD ±338.9), IgAN 712 days (SD ±692.9), MPGN with 745 days (SD ±696.3), and finally CIGN without established etiology with a mean of 852.5 days (SD ±702.5). Figure 1. The overall survival in time until the presentation of primary post-transplant glomerular disease was 1846 days (Figure 2) . Survival by subtypes of glomerular disease post-transplantation was estimated through Kaplan Meier curves; finding a median survival of 41 days for FSGS, 145 days for membranous nephropathy, and 551 days for IgAN, 579 days for MPGN, and 737 days for CIGN without established etiology. Observing a lower median survival for FSGS with respect to the other subtypes of glomerular disease with a statistically significant difference Log-rank p:< 0.001. ( Figure 3) Renal Function and Proteinuria in post-transplant glomerular disease Concerning the renal function in patients with PTGD, the mean glomerular filtration rate calculated by MDRD was 60.63 ml/min/m2 (SD±20.83) without statistical differences with respect to the population without glomerular disease, a mean of 59.12 ml/min/m2 (SD±21.55) p: 0.4. The compromise of renal function measured by GFR by MDRD and C&G evidenced that the worst renal function was for patients with MPGN and 63.6% of patients with IgAN at 5 years preserved GFR > 60 ml/min/m2, followed by immune complex glomerulonephritis without established etiology 19.5%. The mean of proteinuria for patients who presented glomerular disease was 407 mg/24 hours (SD±704), without finding statistically significant differences with respect to patients who did not present glomerular disease mean of 367 mg/24 hours (SD±515) p: 0.57. Regarding the subtypes of post-transplant glomerular disease and the range of proteinuria, in 24 hours, it was found for FSGS a mean of proteinuria of 2218 (SD±3071), and the lowest range was for IgAN with a mean of proteinuria of 251 mg/24 hours (SD±235). Risk factors associated with post-transplant glomerular disease In the 5-year follow-up, 41.85% of patients with PTGD were treated with steroids and the most commonly utilized immunosuppression maintenance regimens were calcineurin inhibitor/mycophenolate 26.35% and mycophenolate/mammalian Target of Rapamycin (mTOR) inhibitor in 30.54%; no statistical association was found in relation to the type of immunosuppression and the development of PTGD. Patients with PTGD had PRA class I and class II positivity of 9.05% and 7.76% respectively; likewise, it was found that most of this population had a low immunological risk 125 patients (74.85) and 25.1% (n=42) were considered as high immunological risk. In both, bivariate and multivariate analyses, no statistically significant differences were found in the independent variables: living or cadaveric donor, age, gender, human leukocyte antigen (HLA) mismatch compatibility, the donor with expanded criteria, and the presentation of post-transplant glomerular disease. Discussion PTGD is a problem in the young kidney transplant recipient. This study describes the clinical characteristics, outcomes, and relationship of glomerulopathies to the graft outcome in a large cohort of patients from 3 centers in Bogota (Colombia). There are several important findings in this study; first of all, this project is the first investigation that aims to explore the incidence of PTGD under a per protocol biopsy scheme at 6 months, 2 and 5 years post-transplantation in Latin America. Among the 399 patients in this cohort, it was found that 30.53% of the population had glomerular disease as a cause of renal failure prior to transplantation, similar to what other studies have shown. ( 2 , 5 ). The incidence of PTGD was 41.85%, and in 12.57%, it was documented that the glomerular disease was recurrent. Secondly, PTGD might be caused by recurrent or de novo disease. Nevertheless, a considerable number of cases of PTGD could not be classified into these categories and a third category PTGD with the unknown primary disease is required. ( 4 , 9 , 12 ). In 42.9% of this study’s patients, the cause of renal failure prior to transplantation was unknown, thus being striking the finding that about half of the patients diagnosed with PTGD (45.51%) were part of this group. These findings highlight the importance of establishing the etiology of the pathology in the native kidney prior to renal transplantation and the need to perform protocol biopsies of the renal graft in recipients with nephropathy of the unknown cause prior to transplantation. PTGD does not behave as a single entity in its presentation, the progression and the results vary substantially depending on the subtypes, in some cases very insidious, which leads to a late histologic confirmation, the most representative data of the post-transplant glomerular disease derive from clinical studies that determine the survival and risk factors associated according to histologic subtypes. ( 13 ). However, these studies are not performed under a protocol biopsy strategy and there is a lack of these types of studies. ( 12 , 14 – 16 ). As an important finding, it was found that 73.65% of patients with a diagnosis of post-transplant glomerular disease were diagnosed by protocol biopsy. Thirdly, this study confirmed that PTGD was the fourth cause of graft loss at 5 years and the third cause censored by death; different reports describe that the glomerular disease is the third most common cause of allograft loss after chronic rejection and death with functioning graft ( 3 , 4 ) and represents the second most common cause of graft failure censored by death ( 7 , 17 ). All types of glomerulonephritis can potentially recur after renal transplantation, with a reported prevalence between 3% and 15%; likewise, that incidence, with clinically evident manifestations, increases with the time of transplantation ( 5 – 7 , 9 , 13 ). This reveals that the incidence of PTGD during follow-up with biopsies by protocol is higher than the incidence reported in analyses based on biopsy diagnoses under clinical indication; the report of PTGD recurrence from the Australian and New Zealand dialysis and transplant registry among 7968 kidney transplant recipients diagnosed with the glomerular disease as a cause of end-stage renal disease, found an overall 5-year incidence of 11.8% of post-transplant glomerular disease and 2.82%, 0.76%, and 0.61% for IgAN, MPGN, and MN respectively ( 13 ); On the contrary, in this experience under biopsies by protocol, a global incidence in 5 years of 41.8% of PTGD and 52.69%, 17.96%, and 2.99% for IgAN, MPGN, MN respectively was found, thus presenting PTGN with a much higher frequency in this study overall, and in the different subtypes except for FSGS in a 5-year follow-up; the incidence of FSGS confirms the predominance of clinical manifestations in early stages of renal transplantation in this entity( 10 , 13 ). Similar findings to this study were published in follow-up studies with biopsies by protocol among 1965 renal transplant recipients, finding a cumulative incidence of PTGD of 5.2%, 18.2%, 21.7%, 35.8%, and 42.3% in 1,3,5,8 and 10 years respectively ( 15 ); these data confirm that the incidence of PTGD is underestimated. The difference between recurrent and de novo glomerular disease in this study was difficult to evaluate, mainly due to the absence of diagnosis of etiology of renal function loss prior to transplantation in the vast majority of cases, and of course, to a very low number of biopsy-confirmed diagnoses. Fourthly, this study confirms differences in the time of onset and severity between the different types of glomerular disease in the post-transplant period. FSGS showed earlier in the post-transplant period with a mean of 151.4 days, followed by membranous nephropathy for 359 days, IgA nephropathy for 712 days, MPGN with 745 days, and finally immune complex glomerulonephritis without established etiology with a mean of 852.5 days. It is important to emphasize that the time from transplantation to the diagnosis of IgAN was about 2 years post-transplantation; although this entity has been described as a time-dependent event and rarely found before 3 years post-transplantation ( 18 ). Similarly, the risk of recurrence is usually related to a greater post-transplant time; although early recurrences are frequent in patients with FSGS and some types of MPGN, these results are another important finding, evidencing that the clinical diagnosis of PTGD is frequently carried out late. It seems to be important to analyze the differences in histological findings between early cases without clinical manifestations and progression to the presence of these, a separate analysis aims to evaluate the findings during follow-up in patients with positive immunofluorescence for IgA without the presence of immune complex deposits in electron microscopy; concerning MPGN, recurrence has been frequently documented and in most cases occurs in the first 2 years post- transplantation ( 5 , 13 , 19 – 21 ). In this study, researchers were careful to discard cases associated with the presence of donor-specific anti-human leukocyte antigen antibodies (HLA); protocol biopsy findings suggestive of antibody-mediated rejection and history of antibody-mediated rejection confirmed by biopsy; moreover, the introduction of a new classification of this entity makes difficult a precise analysis of post-transplant outcomes; the major proportion of cases with MPGN found in this series presented a pattern of glomerular C3 deposits in absence of immunoglobulin deposits; thus suggesting a high probability of post-transplant recurrence that cannot be demonstrated because no case had a confirmed diagnosis prior to transplantation; regardless, recurrence of this disease has been reported in up to 50% of cases with an adverse clinical course in about half of them. ( 22 , 23 ) This adverse outcome was not found in this study probably explained by the diagnosis not being associated with clinical manifestations and by early changes in immunosuppression schemes mainly withdrawal of calcineurin inhibitors in replacement by co-stimulation inhibitors, analysis that is still going on process; as well as the use of eculizumab, a terminal complement inhibitor in a case with the presence of thrombotic microangiopathy of the renal graft in the presence of mutations in factor H of unknown significance. In regard to the MN, patients with anti-phospholipase A2 receptor (Anti PLA2R) antibody titers prior to transplantation have a higher risk of recurrence compared to those with negative anti PLA2R. ( 24 – 27 ); histological findings of membranous nephropathy may be found early, even 1 to 2 weeks post-transplant; probably secondary to deposits of circulating antibodies present at the time of transplantation. ( 15 , 24 ); late recurrence might be secondary to the presence of new recurrent or de novo anti PLA2R, different opinions suggest monitoring the behavior of anti PLA2R antibodies during transplantation as it is a factor that increases early recurrence and progression of the disease in the post-transplant up to 60–76% ( 24 , 25 ); nonetheless, it is still difficult to measure these titers in this environment. The presence of late focal and segmental sclerosis changes in renal transplantation are relatively frequent due to different associated factors such as lower renal mass, sequelae of glomerular and interstitial diseases, medications, and others; for this reason, it is difficult to state about recurrence in late stages, reason why only cases with diagnosis prior to transplantation, diagnosed in the first 3 months with clinical manifestations, were taken into account for the comparative analysis with other types of glomerular disease. Concerning the presence of immune complex deposits in electron microscopy without an established histologic pattern, it was found that it was diagnosed later than any of the other entities with a benign clinical course; analyses are in progress in order to rule out unknown pre-renal transplant glomerular diseases and secondary causes. It should be highlighted that in this experience only one case of ANCAS-associated vasculitis was found; the incidence of this disease in the general population in Latin America has been described in Peru with 5.6/1,000,000 inhabitants and a prevalence between 7.4 and 9/1,000,000 inhabitants in Argentina ( 28 ); the progression to end-stage renal disease in 5 years is between 8% and 20% ( 29 – 31 ); in comparison, the Dutch registry with more than 20 years of follow-up with biopsies by clinical indication showed a recurrence rate of 2.8%, occurring mainly in the first 5 years after transplantation; in other reports of case series, the frequency of recurrence can be up to 5% at 10 years. ( 32 – 34 ). In regard to the post-transplant glomerular disease-free survival by subtypes, a lower median survival for FSGS with respect to the other subtypes of glomerular disease with a statistically significant difference was observed, results that are comparable with other reported series. ( 10 , 13 ). Additionally, it was found that the worst renal function was for patients with MPGN similar to that reported in other series where FSGS and MPGN have the most aggressive natural history ( 20 , 35 ). Likewise, it was revealed that 63.6% of patients with IgAN at 5 years retained GFR > 60 ml/min/m2, which is in relation to analyses that show that the recurrence of this entity in the post-transplant has little impact on survival at 10 years, thus finding better survival rates and renal function of this entity ( 18 , 36 ); furthermore, in this study, the glomerular disease-free survival of the histologic finding in biopsies of immune complexes without a specific pattern of glomerular disease was analyzed, finding good survival rates in this entity; it was not found analyses of these data in other studies that are comparable with what was found in this study; nevertheless, this finding was not associated with deterioration of renal function at 5 years, in comparison with those who did not have the glomerular disease; finding that requires additional analysis of this entity. Regarding the outcome of proteinuria, in this study, a higher incidence of proteinuria compared with patients without post-transplant glomerular disease was not found, which may be related to the early diagnosis of PTGD by protocol biopsies. When examining the variables that may contribute to the presentation of post-transplant glomerular disease, this study did not show that age, gender, type of donor, and the presence of expanded criteria are associated with increased risk of PTGD, unlike what other series show where younger transplant recipients, male gender, and related living donor are associated with increased risk of recurrence of post-transplant glomerular disease ( 4 , 10 ). Concerning induction therapy, some studies have described that patients who received antithymocyte immunoglobulin had lower clinical recurrence rates of glomerular disease specifically in IgA nephropathy as opposed to other induction schemes, which differs from what was found in other studies ( 37 ); this differs from what was found in this series where a risk factor was observed between the induction scheme with thymoglobulin and the presentation of post-transplant glomerular disease, data that should be validated in a prospective randomized trial. Conclusions: Protocol biopsy studies show that the clinical diagnosis of DPT is made late, the importance of performing this type of intervention is to improve efforts for timely diagnosis, especially relevant at a time when treatments are increasingly available more specific to improve renal outcomes in post-transplant glomerular disease. References 1. Menn-Josephy H, Beck LH. Recurrent glomerular disease in the kidney allograft. 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Renal transplantation in patients with primary immunoglobulin A nephropathy. Nephrol Dial Transplant. 2003;18(11):2399–404. 37. Berthoux F, El Deeb S, Mariat C, Diconne E, Laurent B, Thibaudin L. Antithymocyte globulin (ATG) induction therapy and disease recurrence in renal transplant recipients with primary iga nephropathy. Transplantation. 2008;85(10):1505–7. Tables Tables 1-3 are available in the supplementary files. Supplementary Files Tables.docx Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-2094781","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":138936432,"identity":"f1eb1c6a-77c7-4911-8d60-c647aaf2d6fb","order_by":0,"name":"Rodolfo Torres","email":"","orcid":"","institution":"Renal Transplant Service - Colombia Keralty University clinic, Bogotá -Colombia","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Rodolfo","middleName":"","lastName":"Torres","suffix":""},{"id":138936433,"identity":"4964d957-6419-43b0-bdba-f3fee88c40af","order_by":1,"name":"Maricely Reina","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA70lEQVRIiWNgGAWjYLCCBAYGOfYGEKuAgRFIGxClxZjnAIhlQKwWIEjsIVqLbnvvwwcPd9il90gkP/7ww+CwbAN78zYJhhobnFrMzhw3Nkg8k5zbI5FmJtljcNi4gedYmQTDsTTcWm6ksUkktjHn7pfIYWPgMTic2CCRYybB2HAYt5b7z9h/JLbVp/NI5DB//APSIv+GgJYbbGwMiW2HE4BaGKQhtvAQ0HImjRnosOOGPTzPzKRlDNKN23jSii0S8Pnl+DHGjz/bquV52JMff3xTYS3bz354440PeEIME7CBiAQSNIyCUTAKRsEowAQAtu5QNrLkVLcAAAAASUVORK5CYII=","orcid":"https://orcid.org/0000-0002-1262-1555","institution":"Fundación Universitaria Ciencias de la Salud (FUCS), Bogotá - Colombia","correspondingAuthor":true,"submittingAuthor":false,"prefix":"","firstName":"Maricely","middleName":"","lastName":"Reina","suffix":""},{"id":138936434,"identity":"a2f3fc70-c79f-4a87-8d28-84cb8238f2cd","order_by":2,"name":"Camilo Montero","email":"","orcid":"","institution":"Renal Transplant Service - Colombia Keralty University clinic, Bogotá -Colombia","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Camilo","middleName":"","lastName":"Montero","suffix":""},{"id":138936435,"identity":"d3da1fed-dc54-4111-8d61-93681e57ed25","order_by":3,"name":"David Andrade","email":"","orcid":"","institution":"Fundación Universitaria Ciencias de la Salud (FUCS), Bogot","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"David","middleName":"","lastName":"Andrade","suffix":""},{"id":138936436,"identity":"4a44b677-4ab4-4c6b-a7f6-9804e3d356d2","order_by":4,"name":"Carlos Rosselli","email":"","orcid":"","institution":"Fundación Universitaria Ciencias de la Salud (FUCS), Bogot","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Carlos","middleName":"","lastName":"Rosselli","suffix":""},{"id":138936437,"identity":"e808d45f-d1b7-45df-8dfa-80c1e4725be2","order_by":5,"name":"Estefy Agudelo","email":"","orcid":"","institution":"Fundación Universitaria Ciencias de la Salud (FUCS), Bogot","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Estefy","middleName":"","lastName":"Agudelo","suffix":""},{"id":138936438,"identity":"09046e87-f541-496b-8346-a4fe52389657","order_by":6,"name":"Jonth Flechas","email":"","orcid":"","institution":"Fundación Universitaria Ciencias de la Salud (FUCS), Bogot","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Jonth","middleName":"","lastName":"Flechas","suffix":""},{"id":138936439,"identity":"143b6e18-d191-48ee-a96f-a683f66ec8b3","order_by":7,"name":"Laura Rodriguez","email":"","orcid":"","institution":"Fundación Universitaria Ciencias de la Salud (FUCS), Bogot","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Laura","middleName":"","lastName":"Rodriguez","suffix":""},{"id":138936440,"identity":"1a50b496-cc9f-4ed2-8a11-e0d3298aa125","order_by":8,"name":"Ana Trujillo","email":"","orcid":"","institution":"Fundación Universitaria Ciencias de la Salud (FUCS), Bogot","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Ana","middleName":"","lastName":"Trujillo","suffix":""},{"id":138936441,"identity":"338073f6-b168-4545-a5aa-505f0e3ae4fe","order_by":9,"name":"Nancy yomayusa","email":"","orcid":"","institution":"Translational research group, Fundación universitaria Sánitas, Bogotá - Colombia","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Nancy","middleName":"","lastName":"yomayusa","suffix":""},{"id":138936442,"identity":"d7915591-ca2a-4bcb-99cb-93667de77027","order_by":10,"name":"Luis Fernando Quintana","email":"","orcid":"","institution":"Nephrology and Renal Transplant Department Hospital Clinic Barcelona","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Luis","middleName":"Fernando","lastName":"Quintana","suffix":""}],"badges":[],"createdAt":"2022-09-23 05:01:19","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-2094781/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-2094781/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":26892787,"identity":"8c5f9568-688d-44e0-98c1-1f36274cbdb0","added_by":"auto","created_at":"2022-09-23 16:42:27","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":34212,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eTime until the presentation of post-transplant glomerular disease.\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"f1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-2094781/v1/de59d2caf36266e994084658.jpg"},{"id":26892785,"identity":"ccff6ee9-e0ce-4ed0-b892-d9283c94c685","added_by":"auto","created_at":"2022-09-23 16:42:27","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":23589,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eOverall survival free of glomerular disease post-transplantation\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"f2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-2094781/v1/e780f47731b7afcd450063f7.jpg"},{"id":26893112,"identity":"44bf5ff3-e567-4685-b91b-0c88d567254b","added_by":"auto","created_at":"2022-09-23 16:47:27","extension":"jpg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":51091,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eProbability of survival of glomerular disease, stratified by type of glomerulonephritis.\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"f3.jpg","url":"https://assets-eu.researchsquare.com/files/rs-2094781/v1/217946b664e97fab25b5fb3d.jpg"},{"id":26893113,"identity":"fb84a248-e998-4491-a53d-9ee1c3f2ec9d","added_by":"auto","created_at":"2022-09-23 16:47:31","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":389101,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-2094781/v1/002f895b-7033-40c3-a577-40a073fad916.pdf"},{"id":26893111,"identity":"a86a0638-d7d7-4989-8a49-213bc4e08b91","added_by":"auto","created_at":"2022-09-23 16:47:27","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":71310,"visible":true,"origin":"","legend":"","description":"","filename":"Tables.docx","url":"https://assets-eu.researchsquare.com/files/rs-2094781/v1/02e83c8f5c97814393e45eb3.docx"}],"financialInterests":"","formattedTitle":"\u003cp\u003e\u003cstrong\u003eGlomerular disease after renal transplantation: a multi-center protocol biopsy study in an Iberoamerican population.\u003c/strong\u003e\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eThe glomerular disease accounts for approximately 30% of the etiologies of end-stage chronic kidney disease (ESRD) and its recurrence as well as its development after transplantation leads to a decrease in renal allograft function and loss of the kidney allograft. (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). The prevalence of the post-transplant glomerular disease varies according to the different series reported. (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). This depends on the underlying etiology, population diversity, follow-up time, and biopsies per protocol, being found in approximately 4 to 50% of the cases. (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). This wide margin is also explained by the limitation of performing recurrence studies of the disease due to the fact that most patients do not have a renal biopsy before transplantation, or the result is inconclusive, thus underestimating the real incidence and prevalence of this entity (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe most frequent post-transplantation glomerulopathy is the IgAN (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e); it recurs in approximately 25% of patients and its incidence increases up to 53% under the protocol biopsy strategy; up to 60% of which occurs within three years after transplantation (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e); MPGN occurs in 20\u0026ndash;30% of patients (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e) and graft loss due to this entity has been reported in up to 30\u0026ndash;50% of cases. (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eSo far, in Latin America, there is no series in which the incidence of post-transplantation glomerular disease is evaluated; this information is vitally\u003c/p\u003e \u003cp\u003eImportant in order to plan the treatment strategy in future transplantations, especially in a region where the severity of glomerulopathies in native kidneys is high.\u003c/p\u003e"},{"header":"Methods:","content":"\u003cp\u003eA retrospective cohort study was carried out on renal transplant recipients in 3 transplant centers in the city of Bogot\u0026aacute; D.C. Patients older than 15 years who underwent renal transplantation between 2007 and 2017 and who completed clinical follow-up within 5 years after renal transplantation were included.\u003c/p\u003e \u003cp\u003eThe information was gathered from the clinical histories recorded in the database of\u003c/p\u003e \u003cp\u003ethe renal transplant programs of 3 institutions in the city of Bogota. The clinical, analytical (proteinuria and creatinine), and histological data obtained from the medical records were recorded in a database, coded, and managed anonymously only by the research group. Biopsies per protocol performed were analyzed in the first 6 months, second and fifth-year post-transplantation.\u003c/p\u003e \u003cp\u003eThe analysis of the information was carried out through an analysis where\u003c/p\u003e \u003cp\u003equantitative variables were described with measures of central tendency; in the case of qualitative variables, calculations of frequencies and percentage distribution\u003c/p\u003e \u003cp\u003ewere made. Subsequently, a bivariate analysis was performed where, according to\u003c/p\u003e \u003cp\u003ethe fulfillment of assumptions and verification of normal distribution, t student and\u003c/p\u003e \u003cp\u003eMann Whitney U tests were performed. In the case of categorical variables, X2 and fisher's exact test were performed. Similarly, the probability of survival was estimated\u003c/p\u003e \u003cp\u003eby applying the log-rank test to establish whether there was a difference in the\u003c/p\u003e \u003cp\u003eprobability of survival. All the tests were considered statistically significant with a p \u0026lt;\u003c/p\u003e \u003cp\u003e0.05. The information was analyzed in the statistical software R Studio version 4.2 and Jamovi version 2.2.5.\u003c/p\u003e \u003cp\u003e The study was conducted in line with the principles of the Declaration of\u003c/p\u003e \u003cp\u003eHelsinki (1964) and subsequent amendments, updated in 2013. All study documents\u003c/p\u003e \u003cp\u003ewere evaluated and approved by the Institutional Ethics Committee of the centers, thus being classified as safe research.\u003c/p\u003e"},{"header":"Results:","content":"\u003cp\u003e399 renal transplant recipients between the years 2007 to 2017 in three transplant centers who met the inclusion criteria were included. 244 patients were male (61.15%), with a median age of 44.3 years (RIQ 32.9-55.9 years); 84.71% were cadaveric donor recipients and 15.29% were living donors. In regard to the etiologies of native kidney loss, unknown etiology predominated in 171 patients (42.86%) followed by glomerular disease in 104 patients (26%).\u003c/p\u003e\n\u003cp\u003eOf the 399 patients, the glomerular disease was documented in 167 patients (41.85%) in post renal transplantation; of this subpopulation of patients, 76 (45.51%) had no etiology of native kidney damage, and 51 patients (30.53%) had the glomerular disease (GD) as etiology of renal damage. The subgroup of patients with the glomerular disease was predominantly male and the median age was 42.91 (RIQ\u003c/p\u003e\n\u003cp\u003e31.1-53.4). \u003cstrong\u003eTable 1\u003c/strong\u003e shows the clinical profile of the cohort studied.\u003c/p\u003e\n\u003cp\u003eIn this study, the diagnosis of \u0026nbsp;PTGD\u0026nbsp;was made in most patients by biopsies by protocol in 123 patients (73.65%) and by clinical indication in 44 patients (26.35%).\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eIncidence of post-transplant glomerular disease:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOf the 167 patients who presented\u0026nbsp;PTGD, in 88 patients (52.69%) biopsy confirmed IgAN, 37 patients (22.16%) had immune complex glomerulonephritis (CIGN) without\u003c/p\u003e\n\u003cp\u003eestablished etiology, 30 patients (17.96%) had MPGN, 7 patients (4.19%) had FSGS, and 5 patients (2.99%) had membranous nephropathy (MN). Of this subpopulation of patients, recurrence of\u0026nbsp;PTGD\u0026nbsp;was documented in 21 patients (12.57%) in whom the etiology of glomerular disease prior to renal transplantation was known. \u003cstrong\u003eAlgorithm 1, Table 2\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eGraft loss due to GD\u0026nbsp;occurred in 4 patients (6.9%) at 5 years, being\u003cbr\u003e\u0026nbsp;the fourth cause of graft loss and the third cause censored for death. The first and\u003cbr\u003e\u0026nbsp;the second cause of graft loss were death from another cause with functioning graft in\u0026nbsp;35 patients (60.3%) and rejection in 6 patients respectively (10.3%)\u0026nbsp;\u003cstrong\u003eTable 3.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cbr\u003e\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eGraft survival in post-transplant glomerular disease\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cbr\u003e\u0026nbsp;\u003c/strong\u003eRegarding the time of presentation of PTGD,\u0026nbsp;in this study, it was found that FSGS\u003cbr\u003e\u0026nbsp;was presented with a mean of 151.4 days Standard deviation (SD\u0026nbsp;\u0026plusmn;310.6), followed by\u0026nbsp;membranous nephropathy 359\u0026nbsp;days (SD\u0026nbsp;\u0026plusmn;338.9), IgAN 712 days\u0026nbsp;(SD\u003cbr\u003e\u0026nbsp;\u0026plusmn;692.9),\u0026nbsp;MPGN with 745 days\u0026nbsp;(SD\u0026nbsp;\u0026plusmn;696.3),\u0026nbsp;and finally\u0026nbsp;CIGN without established etiology\u0026nbsp;with a mean of 852.5 days\u0026nbsp;(SD\u0026nbsp;\u0026plusmn;702.5).\u0026nbsp;\u003cstrong\u003eFigure 1.\u003c/strong\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe overall survival in time until the presentation of primary post-transplant\u0026nbsp;glomerular disease was 1846 days\u0026nbsp;\u003cstrong\u003e(Figure 2)\u003c/strong\u003e. Survival by subtypes of glomerular\u0026nbsp;disease post-transplantation was estimated through Kaplan Meier curves; finding a\u0026nbsp;median survival of 41 days for FSGS, 145 days for membranous nephropathy, and 551\u0026nbsp;days for IgAN, 579 days for MPGN, and 737 days for\u0026nbsp;CIGN without established etiology. Observing a lower median survival for FSGS with respect to\u0026nbsp;the other subtypes of glomerular disease with a statistically significant difference\u0026nbsp;Log-rank p:\u0026lt; 0.001. \u0026nbsp;\u003cstrong\u003e(\u003c/strong\u003e\u003cstrong\u003eFigure 3)\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cbr\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eRenal Function and Proteinuria in post-transplant glomerular disease\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cbr\u003e\u0026nbsp;\u003c/strong\u003eConcerning the renal function in patients with PTGD, the mean glomerular filtration\u003cbr\u003e\u0026nbsp;rate calculated by MDRD was 60.63 ml/min/m2 (SD\u0026plusmn;20.83) without statistical\u003cbr\u003e\u0026nbsp;differences with respect to the population without glomerular disease, a mean of 59.12\u0026nbsp;ml/min/m2 (SD\u0026plusmn;21.55) p: 0.4.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe compromise of renal function measured by GFR by MDRD and C\u0026amp;G evidenced\u0026nbsp;\u003cbr\u003e\u0026nbsp;that the worst renal function was for patients with MPGN and 63.6% of patients with\u003cbr\u003e\u0026nbsp;IgAN at 5 years preserved GFR \u0026gt; 60 ml/min/m2, followed by\u0026nbsp;immune complex glomerulonephritis without established etiology\u0026nbsp;19.5%.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe mean of proteinuria for patients who presented glomerular disease was 407 mg/24\u0026nbsp;hours (SD\u0026plusmn;704), without finding statistically significant differences with respect to\u0026nbsp;patients who did not present glomerular disease mean of 367 mg/24 hours (SD\u0026plusmn;515)\u0026nbsp;p: 0.57. Regarding the subtypes of post-transplant glomerular disease and the range\u0026nbsp;of proteinuria, in 24 hours, it was found for FSGS a mean of proteinuria of 2218 (SD\u0026plusmn;3071),\u0026nbsp;and the lowest range was for IgAN with a mean of proteinuria of 251 mg/24 hours\u0026nbsp;(SD\u0026plusmn;235).\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eRisk factors associated with post-transplant glomerular disease\u003c/p\u003e\n\u003cp\u003eIn the 5-year follow-up, 41.85% of patients with PTGD were treated with steroids and\u003cbr\u003e\u0026nbsp;the most commonly utilized immunosuppression maintenance regimens were\u003cbr\u003e\u0026nbsp;calcineurin inhibitor/mycophenolate 26.35% and mycophenolate/mammalian Target\u003cbr\u003e\u0026nbsp;of Rapamycin (mTOR) inhibitor in 30.54%; no statistical association was found in\u003cbr\u003e\u0026nbsp;relation to the type of immunosuppression and the development of PTGD.\u0026nbsp;Patients with PTGD had PRA class I and class II positivity of 9.05% and 7.76%\u003cbr\u003e\u0026nbsp;respectively; likewise, it was found that most of this population had a low\u003cbr\u003e\u0026nbsp;immunological risk 125 patients (74.85) and 25.1% (n=42) were considered as high\u003cbr\u003e\u0026nbsp;immunological risk. In both, bivariate and multivariate analyses, no statistically significant differences were found in the independent variables: living or cadaveric donor, age, gender, human leukocyte antigen (HLA) mismatch compatibility, the donor with expanded criteria, and the presentation of post-transplant glomerular disease.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003ePTGD is a problem in the young kidney transplant\u003c/p\u003e \u003cp\u003erecipient. This study describes the clinical characteristics, outcomes, and relationship of glomerulopathies to the graft outcome in a large cohort of patients from 3 centers in Bogota (Colombia). There are several important findings in this study; first of all, this project is the first investigation that aims to explore the incidence of PTGD under a per protocol biopsy scheme at 6 months, 2 and 5 years post-transplantation in Latin America. Among the 399 patients in this cohort, it was found that 30.53% of the population had glomerular disease as a cause of renal failure prior to transplantation, similar to what other studies have shown. (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). The incidence of PTGD was 41.85%, and in 12.57%, it was documented that the glomerular disease was recurrent.\u003c/p\u003e \u003cp\u003eSecondly, PTGD might be caused by recurrent or de novo disease. Nevertheless, a considerable number of cases of PTGD could not be classified into these categories\u003c/p\u003e \u003cp\u003eand a third category PTGD with the unknown primary disease is required. (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e). In 42.9% of this study\u0026rsquo;s patients, the cause of renal failure prior to transplantation was unknown, thus being striking the finding that about half of the patients diagnosed with PTGD (45.51%) were part of this group. These findings highlight the importance of establishing the etiology of the pathology in the native kidney prior to renal\u003c/p\u003e \u003cp\u003etransplantation and the need to perform protocol biopsies of the renal graft in\u003c/p\u003e \u003cp\u003erecipients with nephropathy of the unknown cause prior to transplantation.\u003c/p\u003e \u003cp\u003ePTGD does not behave as a single entity in its presentation, the progression and the results vary substantially depending on the subtypes, in some cases very insidious, which leads to a late histologic confirmation, the most representative data of the post-transplant glomerular disease derive from clinical studies that determine the survival and risk factors associated according to histologic subtypes. (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). However, these studies are not performed under a protocol biopsy strategy and there is a lack of these types of studies. (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan additionalcitationids=\"CR15\" citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). As an important finding, it was found that 73.65% of patients with a diagnosis of post-transplant glomerular disease were diagnosed by protocol biopsy.\u003c/p\u003e \u003cp\u003eThirdly, this study confirmed that PTGD was the fourth cause of graft loss at 5 years\u003c/p\u003e \u003cp\u003eand the third cause censored by death; different reports describe that the glomerular disease is the third most common cause of allograft loss after chronic rejection and death with functioning graft (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e) and represents the second most common cause of graft failure censored by death (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eAll types of glomerulonephritis can potentially recur after renal transplantation, with\u003c/p\u003e \u003cp\u003ea reported prevalence between 3% and 15%; likewise, that incidence, with clinically\u003c/p\u003e \u003cp\u003eevident manifestations, increases with the time of transplantation (\u003cspan additionalcitationids=\"CR6\" citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). This\u003c/p\u003e \u003cp\u003ereveals that the incidence of PTGD during follow-up with biopsies by\u003c/p\u003e \u003cp\u003eprotocol is higher than the incidence reported in analyses based on biopsy\u003c/p\u003e \u003cp\u003ediagnoses under clinical indication; the report of PTGD recurrence from the\u003c/p\u003e \u003cp\u003eAustralian and New Zealand dialysis and transplant registry among 7968 kidney\u003c/p\u003e \u003cp\u003etransplant recipients diagnosed with the glomerular disease as a cause of end-stage\u003c/p\u003e \u003cp\u003erenal disease, found an overall 5-year incidence of 11.8% of post-transplant glomerular disease and 2.82%, 0.76%, and 0.61% for IgAN, MPGN, and MN\u003c/p\u003e \u003cp\u003erespectively (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e); On the contrary, in this experience under biopsies by protocol, a global incidence in 5 years of 41.8% of PTGD and 52.69%, 17.96%, and 2.99% for\u003c/p\u003e \u003cp\u003eIgAN, MPGN, MN respectively was found, thus presenting PTGN with a much higher frequency in this study overall, and in the different subtypes except for FSGS in a 5-year follow-up; the incidence of FSGS confirms the predominance of clinical manifestations in early stages of renal transplantation in this entity(\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Similar findings to this study were published in follow-up studies with biopsies by protocol among 1965 renal transplant recipients, finding a cumulative incidence of PTGD of 5.2%, 18.2%, 21.7%, 35.8%, and 42.3% in 1,3,5,8 and 10 years respectively (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e); these data confirm that the incidence of PTGD is underestimated.\u003c/p\u003e \u003cp\u003eThe difference between recurrent and de novo glomerular disease in this study was\u003c/p\u003e \u003cp\u003edifficult to evaluate, mainly due to the absence of diagnosis of etiology of renal\u003c/p\u003e \u003cp\u003efunction loss prior to transplantation in the vast majority of cases, and of course, to a very low number of biopsy-confirmed diagnoses.\u003c/p\u003e \u003cp\u003eFourthly, this study confirms differences in the time of onset and severity between\u003c/p\u003e \u003cp\u003ethe different types of glomerular disease in the post-transplant period. FSGS\u003c/p\u003e \u003cp\u003eshowed earlier in the post-transplant period with a mean of 151.4 days, followed\u003c/p\u003e \u003cp\u003eby membranous nephropathy for 359 days, IgA nephropathy for 712 days, MPGN with 745 days, and finally immune complex glomerulonephritis without established etiology with a mean of 852.5 days. It is important to emphasize that the time from transplantation to the diagnosis of IgAN was about 2 years post-transplantation; although this entity has been described as a time-dependent event and rarely found before 3 years post-transplantation (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). Similarly, the risk of recurrence is usually related to a greater post-transplant time; although early recurrences are frequent in patients with FSGS and some types of MPGN, these results are another important finding, evidencing that the clinical diagnosis of PTGD is frequently carried out late.\u003c/p\u003e \u003cp\u003eIt seems to be important to analyze the differences in histological findings between early cases without clinical manifestations and progression to the presence of these, a separate analysis aims to evaluate the findings during follow-up in patients with\u003c/p\u003e \u003cp\u003epositive immunofluorescence for IgA without the presence of immune complex deposits in electron microscopy; concerning MPGN, recurrence has been frequently documented and in most cases occurs in the first 2 years post- transplantation (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan additionalcitationids=\"CR20\" citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn this study, researchers were careful to discard cases associated with the presence of donor-specific anti-human leukocyte antigen antibodies (HLA); protocol biopsy findings suggestive of antibody-mediated rejection and history of antibody-mediated rejection confirmed by biopsy; moreover, the introduction of a new classification of this entity makes difficult a precise analysis of post-transplant outcomes; the major\u003c/p\u003e \u003cp\u003eproportion of cases with MPGN found in this series presented a pattern of glomerular C3 deposits in absence of immunoglobulin deposits; thus suggesting a high probability of post-transplant recurrence that cannot be demonstrated because no case had a confirmed diagnosis prior to transplantation; regardless, recurrence of this disease has been reported in up to 50% of cases with an adverse clinical course in about half of them. (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e, \u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e) This adverse outcome was not found in this study probably explained by the diagnosis not being associated with clinical manifestations and by early changes in immunosuppression schemes mainly withdrawal of calcineurin inhibitors in replacement by co-stimulation inhibitors, analysis that is still going on process; as well as the use of eculizumab, a terminal complement inhibitor in a case with the presence of thrombotic microangiopathy of the renal graft in the presence of mutations in factor H of unknown significance.\u003c/p\u003e \u003cp\u003eIn regard to the MN, patients with anti-phospholipase A2 receptor (Anti PLA2R) antibody titers prior to transplantation have a higher risk of recurrence compared to those with negative anti PLA2R. (\u003cspan additionalcitationids=\"CR25 CR26\" citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e); histological findings of membranous nephropathy may be found early, even 1 to 2 weeks post-transplant; probably secondary to deposits of circulating antibodies present at the time of transplantation. (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e); late recurrence might be secondary to the presence of new recurrent or de novo anti PLA2R, different opinions suggest monitoring the behavior of anti PLA2R antibodies during transplantation as it is a factor that increases early recurrence and progression of the disease in the post-transplant up to 60\u0026ndash;76% (\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e, \u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e); nonetheless, it is still difficult to measure these titers in this environment.\u003c/p\u003e \u003cp\u003eThe presence of late focal and segmental sclerosis changes in renal transplantation\u003c/p\u003e \u003cp\u003eare relatively frequent due to different associated factors such as lower renal mass, sequelae of glomerular and interstitial diseases, medications, and others; for this reason, it is difficult to state about recurrence in late stages, reason why only cases with diagnosis prior to transplantation, diagnosed in the first 3 months with clinical manifestations, were taken into account for the comparative analysis with other types of glomerular disease.\u003c/p\u003e \u003cp\u003eConcerning the presence of immune complex deposits in electron microscopy without an established histologic pattern, it was found that it was diagnosed later than any of the other entities with a benign clinical course; analyses are in progress in order to rule out unknown pre-renal transplant glomerular diseases and secondary causes.\u003c/p\u003e \u003cp\u003eIt should be highlighted that in this experience only one case of ANCAS-associated\u003c/p\u003e \u003cp\u003evasculitis was found; the incidence of this disease in the general population in Latin\u003c/p\u003e \u003cp\u003eAmerica has been described in Peru with 5.6/1,000,000 inhabitants and a\u003c/p\u003e \u003cp\u003eprevalence between 7.4 and 9/1,000,000 inhabitants in Argentina (\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e); the\u003c/p\u003e \u003cp\u003eprogression to end-stage renal disease in 5 years is between 8% and 20% (\u003cspan additionalcitationids=\"CR30\" citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e); in comparison, the Dutch registry with more than 20 years of follow-up with biopsies by clinical indication showed a recurrence rate of 2.8%, occurring mainly in the first 5 years after transplantation; in other reports of case series, the frequency of recurrence can be up to 5% at 10 years. (\u003cspan additionalcitationids=\"CR33\" citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn regard to the post-transplant glomerular disease-free survival by subtypes, a lower median survival for FSGS with respect to the other subtypes of\u003c/p\u003e \u003cp\u003eglomerular disease with a statistically significant difference was observed, results that are comparable with other reported series. (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Additionally, it was found that the worst renal function was for patients with MPGN similar to that reported in other series where FSGS and MPGN have the most aggressive natural history (\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e, \u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e). Likewise, it was revealed that 63.6% of patients with IgAN at 5 years retained GFR\u0026thinsp;\u0026gt;\u0026thinsp;60 ml/min/m2, which is in relation to analyses that show that the recurrence of this entity in the post-transplant has little impact on survival at 10 years, thus finding better survival rates and renal function of this entity (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e, \u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e); furthermore, in this study, the glomerular disease-free survival of the histologic finding in biopsies of immune complexes without a specific pattern of glomerular disease was analyzed, finding good survival rates in this entity; it was not found analyses of these data in other studies that are comparable with what was found in this study; nevertheless, this finding was not associated with deterioration of renal function at 5 years, in comparison with those who did not have the glomerular disease; finding that requires additional analysis of this entity. Regarding the outcome of proteinuria, in this study, a higher incidence of proteinuria compared with patients without post-transplant glomerular disease was not found, which may be related to the early diagnosis of PTGD by protocol biopsies.\u003c/p\u003e \u003cp\u003eWhen examining the variables that may contribute to the presentation of post-transplant glomerular disease, this study did not show that age, gender, type of\u003c/p\u003e \u003cp\u003edonor, and the presence of expanded criteria are associated with increased risk of PTGD, unlike what other series show where younger transplant recipients, male gender, and related living donor are associated with increased risk of recurrence of post-transplant glomerular disease (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). Concerning induction therapy, some studies have described that patients who received antithymocyte immunoglobulin had lower clinical recurrence rates of glomerular disease specifically in IgA nephropathy as opposed to other induction schemes, which differs from what was found in other studies (\u003cspan citationid=\"CR37\" class=\"CitationRef\"\u003e37\u003c/span\u003e); this differs from what was found in this series where a risk factor was observed between the induction scheme with thymoglobulin and the presentation of post-transplant glomerular disease, data that should be validated in a prospective randomized trial.\u003c/p\u003e"},{"header":"Conclusions:","content":"\u003cp\u003eProtocol biopsy studies show that the clinical diagnosis of DPT is made late, the importance of performing this type of intervention is to improve efforts for timely diagnosis, especially relevant at a time when treatments are increasingly available more specific to improve renal outcomes in post-transplant glomerular disease.\u003c/p\u003e"},{"header":"References","content":"\u003cp\u003e1. \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Menn-Josephy H, Beck LH. 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Nephrology (Carlton). 2014;19:6\u0026ndash;10.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e5. \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Briganti EM, Russ GR, McNeil JJ, Atkins RC, Chadban SJ. Risk of Renal Allograft Loss from Recurrent Glomerulonephritis. N Engl J Med. 2002;347(2):103\u0026ndash;9.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e6. \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Cosio FG, Cattran DC. Recent advances in our understanding of recurrent primary glomerulonephritis after kidney transplantation. Kidney Int [Internet]. 2017;91(2):304\u0026ndash;14. Available from: http://dx.doi.org/10.1016/j.kint.2016.08.030\u003c/p\u003e\n\u003cp\u003e7. \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Hariharan S, Savin VJ. Recurrent and de novo disease after renal transplantation: A report from the Renal Allograft Disease Registry. 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Am J Transplant.\u0026nbsp;2015;15(5):1349\u0026ndash;59.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e27. \u0026nbsp; \u0026nbsp;\u0026nbsp;Seitz-Polski B, Payr\u0026eacute; C, Ambrosetti D, Albano L, Cassuto-Viguier E, Berguignat M, et al.\u0026nbsp;Prediction of membranous nephropathy recurrence after transplantation by monitoring of anti-PLA2R1 (M-type phospholipase A2 receptor) autoantibodies: A case series of 15 patients. Nephrol Dial Transplant. 2014;29(12):2334\u0026ndash;42.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e28. \u0026nbsp; \u0026nbsp;\u0026nbsp;Pimentel-Quiroz VR, Sattui SE, Ugarte-Gil MF, Alarc\u0026oacute;n GS. ANCA-Associated Vasculitis in Latin America A Systematic Literature Review: About Their Epidemiology and Their Clinical Features. J Clin Rheumatol. 2022;28(1):44\u0026ndash;51.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e29. \u0026nbsp; \u0026nbsp;\u0026nbsp;Robson J, Doll H, Suppiah R, Flossmann O, Harper L, H\u0026ouml;glund P, et al. Damage in the ANCA-associated vasculitides: Long-term data from the European Vasculitis Study Group (EUVAS) therapeutic trials. Ann Rheum Dis. 2015;74(1):177\u0026ndash;84.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e30. \u0026nbsp; \u0026nbsp;\u0026nbsp;Mohammad AJ, Segelmark M. A population-based study showing better renal prognosis for proteinase 3 antineutrophil cytoplasmic antibody (ANCA)-associated nephritis versus myeloperoxidase ANCA-associated nephritis. J Rheumatol. 2014;41(7):1366\u0026ndash;73.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e31. \u0026nbsp; \u0026nbsp;\u0026nbsp;Lionaki S, Hogan SL, Jennette CE, Hu Y, Hamra JB, Jennette JC, et al. The clinical course of ANCA small-vessel vasculitis on chronic dialysis. Kidney Int [Internet]. 2009;76(6):644\u0026ndash;51. Available from: http://dx.doi.org/10.1038/ki.2009.218\u003c/p\u003e\n\u003cp\u003e32. \u0026nbsp; \u0026nbsp;\u0026nbsp;G\u0026ouml;\u0026ccedil;eroglu A, Rahmattulla C, Berden AE, Reinders MEJ, Wolterbeek R, Steenbergen EJ, et al. The Dutch transplantation in vasculitis (DUTRAVAS) study: Outcome of renal transplantation in antineutrophil cytoplasmic antibody-associated glomerulonephritis.\u0026nbsp;Transplantation. 2016;100(4):916\u0026ndash;24.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e33. \u0026nbsp; \u0026nbsp;\u0026nbsp;Marco H, Mirapeix E, Arcos E, Comas J, Ara J, Gil-Vernet S, et al.\u0026nbsp;Long-term outcome of antineutrophil cytoplasmic antibody-associated small vessel vasculitis after renal transplantation. Clin Transplant. 2013;27(3):338\u0026ndash;47.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e34. \u0026nbsp; \u0026nbsp;\u0026nbsp;Gera M, Griffin MD, Specks U, Leung N, Stegall MD, Fervenza FC. Recurrence of ANCA-associated vasculitis following renal transplantation in the modern era of immunosupression. Kidney Int [Internet]. 2007;71(12):1296\u0026ndash;301. Available from: http://dx.doi.org/10.1038/sj.ki.5002244\u003c/p\u003e\n\u003cp\u003e35. \u0026nbsp; \u0026nbsp;\u0026nbsp;O\u0026rsquo;Shaughnessy MM, Liu S, Montez-Rath ME, Lenihan CR, Lafayette RA, Winkelmayer WC. Kidney transplantation outcomes across GN subtypes in the United States. J Am Soc Nephrol. 2017;28(2):632\u0026ndash;44.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e36. \u0026nbsp; \u0026nbsp;\u0026nbsp;Choy BY, Chan TM, Lo SK, Lo WK, Lai KN. Renal transplantation in patients with primary immunoglobulin A nephropathy. Nephrol Dial Transplant. 2003;18(11):2399\u0026ndash;404.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e37. \u0026nbsp; \u0026nbsp; \u0026nbsp;Berthoux F, El Deeb S, Mariat C, Diconne E, Laurent B, Thibaudin L. Antithymocyte globulin (ATG) induction therapy and disease recurrence in renal transplant recipients with primary iga nephropathy. Transplantation. 2008;85(10):1505\u0026ndash;7. \u003c/p\u003e"},{"header":"Tables","content":"\u003cp\u003eTables 1-3 are available in the supplementary files.\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"Fundación Universitaria de Ciencias de la Salud","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"kidney transplantation, Recurrence, Glomerulonephritis","lastPublishedDoi":"10.21203/rs.3.rs-2094781/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-2094781/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eRenal transplantation is the treatment of choice in end-stage renal disease (ESRD)(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e), nonetheless; there are still limitations in improving long-term renal graft survival in a significant way, post-transplant glomerular disease being one of the main causes of renal graft loss (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e).\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eA retrospective cohort study, with renal transplant patients in 3 centers in the city of Bogota D.C\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003e399 patients were included, 61.15% predominantly male, with a median age of 44.3 years, interquartile range (IQR) (32.9\u0026ndash;55.9). Post-transplant glomerular\u003c/p\u003e","manuscriptTitle":"Glomerular disease after renal transplantation: a multi-center protocol biopsy study in an Iberoamerican population.","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2022-09-23 16:42:25","doi":"10.21203/rs.3.rs-2094781/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"17493f51-2b6f-4f00-b51f-8b06ae31dd9a","owner":[],"postedDate":"September 23rd, 2022","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":15737992,"name":"Urology \u0026 Nephrology"}],"tags":[],"updatedAt":"2022-09-23T16:42:25+00:00","versionOfRecord":[],"versionCreatedAt":"2022-09-23 16:42:25","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-2094781","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-2094781","identity":"rs-2094781","version":["v1"]},"buildId":"7rjqhiLT3MXkJMwkYKINL","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}