Journal articles: 'Rejection kidney pathology'

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Solez, Kim, Donna Battaglia, Hanan Fahmy, and Kiril Trpkov. "Pathology of kidney transplant rejection." Current Opinion in Nephrology and Hypertension 2, no. 6 (November 1993): 904–11. http://dx.doi.org/10.1097/00041552-199311000-00008.

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Kuan, Kevin, and Daniel Schwartz. "Educational Case: Kidney Transplant Rejection." Academic Pathology 8 (January 1, 2021): 237428952110068. http://dx.doi.org/10.1177/23742895211006832.

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The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040 .1

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Wood, R. "Kidney Transplant Rejection." Journal of Clinical Pathology 40, no. 5 (May 1, 1987): 590–91. http://dx.doi.org/10.1136/jcp.40.5.590-e.

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Higuchi, Haruka, Daisuke Kamimura, Jing-Jing Jiang, Toru Atsumi, Daiki Iwami, Kiyohiko Hotta, Hiroshi Harada, et al. "Orosomucoid 1 is involved in the development of chronic allograft rejection after kidney transplantation." International Immunology 32, no. 5 (January 13, 2020): 335–46. http://dx.doi.org/10.1093/intimm/dxaa003.

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Abstract Chronic allograft rejection is the most common cause of long-term allograft failure. One reason is that current diagnostics and therapeutics for chronic allograft rejection are very limited. We here show that enhanced NFκB signaling in kidney grafts contributes to chronic active antibody-mediated rejection (CAAMR), which is a major pathology of chronic kidney allograft rejections. Moreover, we found that urinary orosomucoid 1 (ORM1) is a candidate marker molecule and therapeutic target for CAAMR. Indeed, urinary ORM1 concentration was significantly higher in kidney transplant recipients pathologically diagnosed with CAAMR than in kidney transplant recipients with normal histology, calcineurin inhibitor toxicity, or interstitial fibrosis and tubular atrophy. Additionally, we found that kidney biopsy samples with CAAMR expressed more ORM1 and had higher NFκB and STAT3 activation in tubular cells than samples from non-CAAMR samples. Consistently, ORM1 production was induced after cytokine-mediated NFκB and STAT3 activation in primary kidney tubular cells. The loss- and gain-of-function of ORM1 suppressed and promoted NFκB activation, respectively. Finally, ORM1-enhanced NFκB-mediated inflammation development in vivo. These results suggest that an enhanced NFκB-dependent pathway following NFκB and STAT3 activation in the grafts is involved in the development of chronic allograft rejection after kidney transplantation and that ORM1 is a non-invasive candidate biomarker and possible therapeutic target for chronic kidney allograft rejection.

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Belkadi, Aziz, Gaurav Thareja, Darshana Dadhania, John R. Lee, Thangamani Muthukumar, Catherine Snopkowski, Carol Li, et al. "Deep sequencing of DNA from urine of kidney allograft recipients to estimate donor/recipient-specific DNA fractions." PLOS ONE 16, no. 4 (April 15, 2021): e0249930. http://dx.doi.org/10.1371/journal.pone.0249930.

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Kidney transplantation is the treatment of choice for patients with end-stage kidney failure, but transplanted allograft could be affected by viral and bacterial infections and by immune rejection. The standard test for the diagnosis of acute pathologies in kidney transplants is kidney biopsy. However, noninvasive tests would be desirable. Various methods using different techniques have been developed by the transplantation community. But these methods require improvements. We present here a cost-effective method for kidney rejection diagnosis that estimates donor/recipient-specific DNA fraction in recipient urine by sequencing urinary cell DNA. We hypothesized that in the no-pathology stage, the largest tissue types present in recipient urine are donor kidney cells, and in case of rejection, a larger number of recipient immune cells would be observed. Extensive in-silico simulation was used to tune the sequencing parameters: number of variants and depth of coverage. Sequencing of DNA mixture from 2 healthy individuals showed the method is highly predictive (maximum error < 0.04). We then demonstrated the insignificant impact of familial relationship and ethnicity using an in-house and public database. Lastly, we performed deep DNA sequencing of urinary cell pellets from 32 biopsy-matched samples representing two pathology groups: acute rejection (AR, 11 samples) and acute tubular injury (ATI, 12 samples) and 9 samples with no pathology. We found a significant association between the donor/recipient-specific DNA fraction in the two pathology groups compared to no pathology (P = 0.0064 for AR and P = 0.026 for ATI). We conclude that deep DNA sequencing of urinary cells from kidney allograft recipients offers a noninvasive means of diagnosing acute pathologies in the human kidney allograft.

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Clauss, R. P., and A. Kobryn. "The renal transplant score: A different way of evaluating renal transplant pathology." South African Journal of Radiology 2, no. 2 (June 30, 1997): 16–18. http://dx.doi.org/10.4102/sajr.v2i2.1582.

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The renal transplant is a notoriously difficult organ to assess for pathology. Radionuclide imaging can help, but, although sensitive, the evaluation is not very specific. For this reason, a different approach was used to examine renal images and results were correlated with histology. The transplant score is determined from images of perfusion and function on certain criteria such as time of appearance of the kidney after tracer injection, intensity of background, size and homogeneity of tracer uptake by the kidney. Although small, the pilot study could distinguish between hyperacute rejection, acute rejection, chronic rejection and cyclosporin toxicity.

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Andersen, CLAUS B., SØREN D. Ladefoged, and SVEND Larsen. "Acute kidney graft rejection." APMIS 102, no. 1-6 (January 1994): 23–37. http://dx.doi.org/10.1111/j.1699-0463.1994.tb04841.x.

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Burton, Robert. "Kidney Transplant Rejection — Diagnosis and Treatment." Pathology 19, no. 3 (1987): 323. http://dx.doi.org/10.1016/s0031-3025(16)36760-5.

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Goesch, Torsten R., Nancy A. Wilson, Weifeng Zeng, Bret M. Verhoven, Weixiong Zhong, Maya M. Coumbe Gitter, and William E. Fahl. "Suppression of Inflammation-Associated Kidney Damage Post-Transplant Using the New PrC-210 Free Radical Scavenger in Rats." Biomolecules 11, no. 7 (July 19, 2021): 1054. http://dx.doi.org/10.3390/biom11071054.

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Allograft kidney transplantation, which triggers host cellular- and antibody-mediated rejection of the kidney, is a major contributor to kidney damage during transplant. Here, we asked whether PrC-210 would suppress damage seen in allograft kidney transplant. Brown Norway (BN) rat kidneys were perfused in situ (UW Solution) with or without added 30 mM PrC-210, and then immediately transplanted into Lewis (LEW) rats. 20 h later, the transplanted BN kidneys and LEW rat plasma were analyzed. Kidney histology, and kidney/serum levels of several inflammation-associated cytokines, were measured to assess mismatch-related kidney pathology, and PrC-210 protective efficacy. Twenty hours after the allograft transplants: (i) significant histologic kidney tubule damage and mononuclear inflammatory cell infiltration were seen in allograft kidneys; (ii) kidney function metrics (creatinine and BUN) were significantly elevated; (iii) significant changes in key cytokines, i.e., TIMP-1, TNF-alpha and MIP-3A/CCL20, and kidney activated caspase levels were seen. In PrC-210-treated kidneys and recipient rats, (i) kidney histologic damage (Banff Scores) and mononuclear infiltration were reduced to untreated background levels; (ii) creatinine and BUN were significantly reduced; and (iii) activated caspase and cytokine changes were significantly reduced, some to background. In conclusion, the results suggest that PrC-210 could provide broadly applicable organ protection for many allograft transplantation conditions; it could protect transplanted kidneys during and after all stages of the transplantation process—from organ donation, through transportation, re-implantation and the post-operative inflammation—to minimize acute and chronic rejection.

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Nikonenko, Т. N., A. V. Trailin, V. N. Nepomnyashchy, S. V. Fen’, S. R. Vildanov, I. R. Rusanov, and A. S. Nikonenko. "LONG-TERM FUNCTIONING OF KIDNEY GRAFTS." Modern medical technologies 44, no. 1 (March 1, 2020): 4–10. http://dx.doi.org/10.34287/mmt.1(44).2020.1.

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Abstract Purpose of the study. To study the morphological changes of long-functioning kidney transplants and determine the main causes of transplant dysfunction. Materials and methods. A total of 52 recipients aged 20 to 70 years were analyzed retrospectively at different times after transplant surgery (5 to 22 years).Morphological changes in the kidney transplant are comparable according to light microscopy. The morphological changes in the graft were studied in the initial and long-term period. Morphological studies were conducted in monitoring mode. Results. In the early period after transplantation, ischemic injuries, primary graft function, and episodes of acute rejection were taken into account. In the distant period, morphological changes were evaluated in accordance with the recommendations of the Banff-classification.When analyzing long-term results, antigen- dependent (immune) and antigen-independent (visible) factors that affect the renal transplant are distinguished. The main clinical and laboratory indicators of allografts dysfunction are increased creatinine and proteinuria.In antigen-dependent forms (cellular, humoral and mixed rejection), humoral rejection is the most common (25%) allografts dysfunction.Antigen-independent forms of dysfunction (streptococcal infection 25%, inflammatory diseases 19,2%, recurrent pathology 3,8%, signs of cyclosporine nephrotoxicity in combination with other forms was found in 59,2%, nephrosclerosis 65,4%). Conclusions. The data obtained suggest that antigen-dependent (immune) factors, and in particular humoral rejection, are the most common cause of allografts dysfunction, and antigen- independent factors contribute to the progression of chronic rejection and the development of nephrosclerosis. Keywords: renal transplant, antigen-dependent, antigen-independent, dysfunction.

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Aufman, Jeffrey. "What a Nonnephropathologist Must Know About Kidney Rejection." Pathology Case Reviews 20, no. 6 (2015): 281–87. http://dx.doi.org/10.1097/pcr.0000000000000114.

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Schmidbauer, Martina, Song Rong, Marcel Gutberlet, Rongjun Chen, Jan Hinrich Bräsen, Dagmar Hartung, Martin Meier, et al. "Diffusion-Weighted Imaging and Mapping of T1 and T2 Relaxation Time for Evaluation of Chronic Renal Allograft Rejection in a Translational Mouse Model." Journal of Clinical Medicine 10, no. 19 (September 23, 2021): 4318. http://dx.doi.org/10.3390/jcm10194318.

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We hypothesized that multiparametric MRI is able to non-invasively assess, characterize and monitor renal allograft pathology in a translational mouse model of chronic allograft rejection. Chronic rejection was induced by allogenic kidney transplantation (ktx) of BALB/c-kidneys into C57BL/6-mice (n = 23). Animals after isogenic ktx (n = 18) and non-transplanted healthy animals (n = 22) served as controls. MRI sequences (7T) were acquired 3 and 6 weeks after ktx and quantitative T1, T2 and apparent diffusion coefficient (ADC) maps were calculated. In addition, in a subset of animals, histological changes after ktx were evaluated. Chronic rejection was associated with a significant prolongation of T1 time compared to isogenic ktx 3 (1965 ± 53 vs. 1457 ± 52 ms, p < 0.001) and 6 weeks after surgery (1899 ± 79 vs. 1393 ± 51 ms, p < 0.001). While mean T2 times and ADC were not significantly different between allogenic and isogenic kidney grafts, histogram-based analysis of ADC revealed significantly increased tissue heterogeneity in allografts at both time points (standard derivation/entropy/interquartile range, p < 0.05). Correspondingly, histological analysis showed severe inflammation, graft fibrosis and tissue heterogeneity in allogenic but not in isogenic kidney grafts. In conclusion, renal diffusion weighted imaging and mapping of T2 and T1 relaxation times enable detection of chronic renal allograft rejection in mice. The combined quantitative assessment of mean values and histograms provides non-invasive information of chronic changes in renal grafts and allows longitudinal monitoring.

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Mansoor, Khurram, Muhammad Osama, Muhammad Ishaque, Sohail Sabir, Hafeez Ud Din, Muhammad Asif, and Haroon Sabir. "SPECTRUM OF RENAL ALLOGRAFT BIOPSY FINDINGS IN RENAL TRANSPLANT PATIENTS AT A TERTIARY CARE CENTER IN RAWALPINDI, PAKISTAN." PAFMJ 71, no. 3 (June 30, 2021): 942–46. http://dx.doi.org/10.51253/pafmj.v71i3.4304.

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Objective: To evaluate outcome of diagnostic kidney biopsy in patients with renal allograft dysfunction at a tertiary care hospital. Study Design: Retrospective observational study. Place and Duration of Study: Armed Forces Institute of Urology, Rawalpindi, from Jan 2014 to Jan 2020. Methodology: A consolidate registry review was carried to formulate this study. The registry data exists at our center containing information about the graft dysfunction (manifesting as proteinuria, deranged urea and creatinine or urine sediment abnormalities) and other major indications which warrant probing with biopsy. The histopathological diagnosis of these biopsies is confirmed from the nephro-pathology registry before finalization of diagnosis. Results: A total of 94 diagnostic kidney biopsies were performed in patients with graft dysfunction. Out of 94 biopsies, 80 (85.1%) patients were male while 14 (14.9%) were female patients. The most frequent single cause for graft dysfunction was Cell Mediated Rejection (n 12, 24.5%) followed by Interstitial Fibrosis and Tubular Atrophy/Acute Tubular Injury. The most common cause among the glomerulonephritis was Membranoproliferative Glomerulonephritis (n 3, 6.1%) followed by others. The most common cause for mixed pathology remainedcell mediated rejection with Interstitial fibrosis and tubular atrophy (n 8, 17.8%). Conclusion: Cell mediated rejection is thecommonest pathology responsible for renal allograft dysfunction both as a single lesion as well as part of mixed pathology.

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Yang, Tiancheng, Ilia Sucholutsky, Kuang-Yu Jen, and Matthias Schonlau. "exKidneyBERT: a language model for kidney transplant pathology reports and the crucial role of extended vocabularies." PeerJ Computer Science 10 (February 28, 2024): e1888. http://dx.doi.org/10.7717/peerj-cs.1888.

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Background Pathology reports contain key information about the patient’s diagnosis as well as important gross and microscopic findings. These information-rich clinical reports offer an invaluable resource for clinical studies, but data extraction and analysis from such unstructured texts is often manual and tedious. While neural information retrieval systems (typically implemented as deep learning methods for natural language processing) are automatic and flexible, they typically require a large domain-specific text corpus for training, making them infeasible for many medical subdomains. Thus, an automated data extraction method for pathology reports that does not require a large training corpus would be of significant value and utility. Objective To develop a language model-based neural information retrieval system that can be trained on small datasets and validate it by training it on renal transplant-pathology reports to extract relevant information for two predefined questions: (1) “What kind of rejection does the patient show?”; (2) “What is the grade of interstitial fibrosis and tubular atrophy (IFTA)?” Methods Kidney BERT was developed by pre-training Clinical BERT on 3.4K renal transplant pathology reports and 1.5M words. Then, exKidneyBERT was developed by extending Clinical BERT’s tokenizer with six technical keywords and repeating the pre-training procedure. This extended the model’s vocabulary. All three models were fine-tuned with information retrieval heads. Results The model with extended vocabulary, exKidneyBERT, outperformed Clinical BERT and Kidney BERT in both questions. For rejection, exKidneyBERT achieved an 83.3% overlap ratio for antibody-mediated rejection (ABMR) and 79.2% for T-cell mediated rejection (TCMR). For IFTA, exKidneyBERT had a 95.8% exact match rate. Conclusion ExKidneyBERT is a high-performing model for extracting information from renal pathology reports. Additional pre-training of BERT language models on specialized small domains does not necessarily improve performance. Extending the BERT tokenizer’s vocabulary library is essential for specialized domains to improve performance, especially when pre-training on small corpora.

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Jafree, Daniyal J., and David A. Long. "Beyond a Passive Conduit: Implications of Lymphatic Biology for Kidney Diseases." Journal of the American Society of Nephrology 31, no. 6 (April 15, 2020): 1178–90. http://dx.doi.org/10.1681/asn.2019121320.

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The kidney contains a network of lymphatic vessels that clear fluid, small molecules, and cells from the renal interstitium. Through modulating immune responses and via crosstalk with surrounding renal cells, lymphatic vessels have been implicated in the progression and maintenance of kidney disease. In this Review, we provide an overview of the development, structure, and function of lymphatic vessels in the healthy adult kidney. We then highlight the contributions of lymphatic vessels to multiple forms of renal pathology, emphasizing CKD, transplant rejection, and polycystic kidney disease and discuss strategies to target renal lymphatics using genetic and pharmacologic approaches. Overall, we argue the case for lymphatics playing a fundamental role in renal physiology and pathology and treatments modulating these vessels having therapeutic potential across the spectrum of kidney disease.

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Mauiyyedi, Shamila, Marta Crespo, A. Bernard Collins, Eveline E. Schneeberger, Manuel A. Pascual, Susan L. Saidman, Nina E. Tolkoff-Rubin, et al. "Acute Humoral Rejection in Kidney Transplantation: II. Morphology, Immunopathology, and Pathologic Classification." Journal of the American Society of Nephrology 13, no. 3 (March 2002): 779–87. http://dx.doi.org/10.1681/asn.v133779.

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ABSTRACT. The incidence of acute humoral rejection (AHR) in renal allograft biopsies has been difficult to determine because widely accepted diagnostic criteria have not been established. C4d deposition in peritubular capillaries (PTC) of renal allografts has been proposed as a useful marker for AHR. This study was designed to test the relative value of C4d staining, histology, and serology in the diagnosis of AHR. Of 232 consecutive kidney transplants performed at a single institution from July 1995 to July 1999, all patients (n = 67) who developed acute rejection within the first 3 mo and had a renal biopsy with available frozen tissue at acute rejection onset, as well as posttransplant sera within 30 d of the biopsy, were included in this study. Hematoxylin and eosin and periodic acid-Schiff stained sections were scored for glomerular, vascular, and tubulointerstitial pathology. C4d staining of cryostat sections was done by a sensitive three-layer immunofluorescence method. Donor-specific antibodies (DSA) were detected in posttransplant recipient sera using antihuman-globulin–enhanced T cell and B cell cytotoxicity assays and/or flow cytometry. Widespread C4d staining in PTC was present in 30% (20 of 67) of all acute rejection biopsies. The initial histologic diagnoses of the C4d+ acute rejection cases were as follows: AHR only, 30%; acute cellular rejection (ACR) and AHR, 45%; ACR (CCTT types 1 or 2) alone, 15%; and acute tubular injury (ATI), 10%. The distinguishing morphologic features in C4d+versus C4d− acute rejection cases included the following: neutrophils in PTC, 65% versus 9%; neutrophilic glomerulitis, 55% versus 4%; neutrophilic tubulitis, 55% versus 9%; severe ATI, 75% versus 9%; and fibrinoid necrosis in glomeruli, 20% versus 0%, or arteries, 25% versus 0%; all P < 0.01. Mononuclear cell tubulitis was more common in the C4d− group (70% versus 100%; P < 0.01). No significant difference between C4d+ and C4d− acute rejection was noted for endarteritis, 25% versus 32%; interstitial inflammation (mean % cortex), 27.2 ± 27% versus 38 ± 21%; interstitial hemorrhage, 25% versus 15%; or infarcts, 5% versus 2%. DSA were present in 90% (18 of 20) of the C4d+ cases compared with 2% (1 of 47) in the C4d− acute rejection cases (P < 0.001). The pathology of the C4d+ but DSA− cases was not distinguishable from the C4d+, DSA+ cases. The C4d+ DSA− cases may be due to non-HLA antibodies or subthreshold levels of DSA. The sensitivity of C4d staining is 95% in the diagnosis of AHR compared with the donor-specific antibody test (90%). Overall, eight grafts were lost to acute rejection in the first year, of which 75% (6 of 8) had AHR. The 1-yr graft failure rate was 27% (4 of 15) for those AHR cases with only capillary neutrophils versus 40% (2 of 5) for those who also had fibrinoid necrosis of arteries. In comparison, the 1-yr graft failure rates were 3% and 7%, respectively, in ACR 1 (Banff/CCTT type 1) and ACR 2 (Banff/CCTT type 2) C4d− groups. A substantial fraction (30%) of biopsy-confirmed acute rejection episodes have a component of AHR as judged by C4d staining; most (90%), but not all, have detectable DSA. AHR may be overlooked in the presence of ACR or ATI by histology or negative serology, arguing for routine C4d staining of renal allograft biopsies. Because AHR has a distinct therapy and prognosis, we propose that it should be classified separately from ACR, with further sub-classification into AHR 1 (neutrophilic capillary involvement) and AHR 2 (arterial fibrinoid necrosis).

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ANDERSEN, CLAUS B. "Acute Kidney Graft Rejection Morphology and immunology." APMIS 105, S67 (January 1997): 5–35. http://dx.doi.org/10.1111/j.1600-0463.1997.tb05595.x.

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Stolyarevich, E. S., T. R. Zhilinskaya, L. Yu Artyukhina, I. G. Kim, V. A. Zaydenov, and N. A. Tomilina. "MORPHOLOGICAL STRUCTURE OF LATE RENAL GRAFT DYSFUNCTION AND ITS EFFECT FOR LONG-TERM RESULTS." Russian Journal of Transplantology and Artificial Organs 20, no. 1 (April 24, 2018): 45–54. http://dx.doi.org/10.15825/1995-1191-2018-1-45-54.

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Aim:to analyze the frequency of different histological diagnoses and it simpact on graft survival in a cohort of patients with renal allograft dysfunction, and to determine pathology features, infl uencing prognosis.Materials and methods.The data obtained from 1470 biopsies, performed by indication at different time after kidney transplantation (48.8 ± 46.1 months) were analyzed retrospectively according to the Banff 2013 classifi cation. Results.The majority of graft dysfunction episodes were attributed to fi ve causes: acute (26,8%) and chronic (12,4%) rejection; chronic nephrotoxicity of СNI (19,3%), interstitial fi brosis/tubular atrophy (15,8%) and recurrent or de novo glomerulonephritis (10,6%). T-cell-mediated acute rejection and functional disorders were the most often cause of dysfunction during the fi rst year after transplantation (40,5% and 21% respectively) but decreased over time. On the other hand, the frequency of chronic rejection, interstitial fi brosis/tubular atrophy with or without СNI nephrotoxicity and recurrent or de novo glomerulonephritis increased from 13%, 26% and 5,5% at the fi rst year to 26,4%, 35,3% and 22,8% respectively at 8 year after transplantation. Chronic rejection represented a major risk for graft loss – 8-year graft survival did not exceed 5%. The prognosis of acute rejection as well asde novoor recurrent glomerular pathologies was more favorable (38% and 42% respectively). In cases of interstitial fi brosis/tubular atrophy with or without СNI nephrotoxicity 8-year graft survival was slightly lower than in the functional disorders (62% and 76%). In acute rejection prognosis for C4d-positive forms was worse compared to C4d-negative, while in chronic rejection there was no difference between C4d-positive and C4d-negative forms. The features of СNI nephrotoxicity did not infl uence the prognosis of non-specifi c interstitial fi brosis and tubular atrophy.Conclusion.Transplant pathology in patients with allograft dysfunction is heterogeneous and changes over time. Acute and chronic rejection; interstitial fi brosis/tubular atrophy with or without СNI nephrotoxicity and recurrent/de novoglomerular pathology are the most often causes of graft dysfunction, but only rejection (mostly chronic) and glomerular pathology are associated with unfavorable prognosis.

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Tajima, Soichiro, Rao Fu, Tomohiro Shigematsu, Hiroshi Noguchi, Keizo Kaku, Akihiro Tsuchimoto, Yasuhiro Okabe, and Satohiro Masuda. "Urinary Human Epididymis Secretory Protein 4 as a Useful Biomarker for Subclinical Acute Rejection Three Months after Kidney Transplantation." International Journal of Molecular Sciences 20, no. 19 (September 22, 2019): 4699. http://dx.doi.org/10.3390/ijms20194699.

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Kidney transplantation is the treatment of choice for patients with advanced chronic kidney disease (CKD) and end stage renal disease (ESRD). However, acute rejection (AR) is a common complication in kidney transplantation and is associated with reduced graft survival. Current diagnosis of AR relies mainly on clinical monitoring including serum creatinine, proteinuria, and confirmation by histopathologic assessment in the biopsy specimen of graft kidney. Although an early protocol biopsy is indispensable for depicting the severity of pathologic lesions in subclinical acute rejection (subAR), it is not acceptable in some cases and cannot be performed because of its invasive nature. Therefore, we examined the detection of noninvasive biomarkers that are closely related to the pathology of subAR in protocol biopsies three months after kidney transplantation. In this study, the urinary level of microtubule-associated protein 1 light chain 3 (LC3), monocyte chemotactic protein-1 (MCP-1), liver-type fatty acid-binding protein (L-FABP), neutrophil gelatinase-associated lipocalin (NGAL), and human epididymis secretory protein 4 (HE4) were measured three months after kidney transplantation. Urine samples of 80 patients undergoing kidney transplantation between August 2014 to September 2016, were prospectively collected after three months. SubAR was observed in 11 patients (13.8%) in protocol biopsy. The urinary levels of LC3, MCP-1, NGAL, and HE4 were significantly higher in patients with subAR than in those without, while those of L-FABP did not differ between the two groups. Multivariate regression models, receiver-operating characteristics (ROC), and areas under ROC curves (AUC) were used to identify predicted values of subAR. Urinary HE4 levels were able to better identify subAR (AUC = 0.808) than the other four urinary biomarkers. In conclusion, urinary HE4 is increased in kidney transplant recipients of subAR three months after kidney transplantation, suggesting that HE4 has the potential to be used as a novel clinical biomarker for predicting subAR.

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Troxell, Megan L., John P. Higgins, and Neeraja Kambham. "Evaluation of C4d Staining in Liver and Small Intestine Allografts." Archives of Pathology & Laboratory Medicine 130, no. 10 (October 1, 2006): 1489–96. http://dx.doi.org/10.5858/2006-130-1489-eocsil.

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Abstract Context.—Antibody-mediated humoral rejection in kidney and heart allografts is well recognized and is often associated with poor outcome. C4d deposition in allograft biopsy specimens occurs at sites of antibody-mediated complement activation and has become one of the histopathologic criteria for diagnosis of humoral rejection in the kidney and the heart. Objective.—To study immunohistochemical C4d staining as a potential diagnostic marker in liver and small intestine allograft biopsy specimens. Design.—Thirty-six small intestine and 71 liver specimens, including native specimens, allografts with and without histologic features of acute cellular rejection, and explants, were stained with antisera to C4d using an immunohistochemical method on formalin-fixed, paraffin-embedded tissue. Results.—In small intestine, C4d labeled capillaries in 27% of cases with no evidence of rejection, 36% of cases with evidence of acute rejection, and 2 (28%) of 7 specimens of native normal small intestine. In liver allograft biopsy specimens, C4d stained endothelium of veins, arteries, and/or sinusoids in 2 (8%) of 25 cases of acute rejection with central vein involvement; C4d staining was negative in biopsy specimens with no evidence of rejection. C4d stained the endothelium in a subset of explanted liver allografts with ductopenic rejection or chronic vascular rejection and strongly stained 1 explant with features of hyperacute rejection. Conclusions.—The clinical utility of C4d staining in solid organ transplantation may vary by organ. Our data show C4d is unlikely to have utility in small intestine allograft biopsy specimens; however, further study in liver allografts, in conjunction with donor-specific antibody testing, is warranted.

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Sousa, Marcos Vinicius de, Ricardo de Lima Zollner, and Marilda Mazzali. "Renal transplant patients with preformed anti-HLA antibodies: early biopsy findings and clinical outcomes." Brazilian Journal of Nephrology 42, no. 2 (June 2020): 201–10. http://dx.doi.org/10.1590/2175-8239-jbn-2018-0244.

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Abstract Introduction: Renal fibrosis is the end point of a process that begins at transplant, with ischemia reperfusion and early inflammation, and progresses over time with immunological and non-immunological phenomena. Early identification of morphological markers and intervention could improve graft function and survival. Objective: to evaluate the correlation between intensity and specificity of pre-transplant anti-HLA antibodies and kidney allograft pathology in order to identify early risk factors or markers of allograft dysfunction. Methods: A retrospective cohort of kidney transplant recipients with pre-transplant anti-HLA antibodies who underwent graft biopsy within the first two years post-transplant was divided into two groups according to the specificity of anti-HLA antibodies: nonspecific (non-DSA, n = 29) and specific (DSA+, n = 16). Kidney graft pathology, renal function, and proteinuria were analyzed. Results: general characteristics were similar in both groups, except for the higher dose of thymoglobulin in DSA+ group (p < 0.05). The non-DSA group had higher scores for glomerulosclerosis, interstitial inflammation (i) and interstitial fibrosis (ci) (p < 0.05) and higher incidence of cell-mediated acute rejection. No statistical difference in incidence of antibody-mediated rejection, renal function, and proteinuria was observed during follow up. Discussion and conclusions: the difference in inflammation scores and interstitial fibrosis may be associated to the higher incidence of acute cell-mediated rejection and polyomavirus nephropathy in the Non-DSA group. We also should take into account the protective effect of higher doses of thymoglobulin, reducing ischemia reperfusion injury in the DSA+ group. The short follow-up might have been insufficient to detect long-term changes in allograft tissue, renal function, and proteinuria.

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Jordan, Milan, Eric P. Cohen, Allan Roza, Mark B. Adams, Christopher Johnson, Stephen L. Gluck, and Bahar Bastani. "An immunocytochemical study of H+ ATPase in kidney transplant rejection." Journal of Laboratory and Clinical Medicine 127, no. 3 (March 1996): 310–14. http://dx.doi.org/10.1016/s0022-2143(96)90100-6.

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Morozumi, Kunio, Asami Takeda, Yasuhiro Otsuka, Keiji Horike, Norihiko Gotoh, Shunji Narumi, Yoshihiko Watarai, and Takaaki Kobayashi. "Reviewing the pathogenesis of antibody-mediated rejection and renal graft pathology after kidney transplantation." Nephrology 21 (June 24, 2016): 4–8. http://dx.doi.org/10.1111/nep.12777.

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Jacquemont, Lola, Jean-Paul Soulillou, and Nicolas Degauque. "Blood biomarkers of kidney transplant rejection, an endless search?" Expert Review of Molecular Diagnostics 17, no. 7 (June 7, 2017): 687–97. http://dx.doi.org/10.1080/14737159.2017.1337512.

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Sonawane, S., E. Borys, D. Borys, and M. Picken. "Evaluation of Renal Biopsy for Transplant: The Significance of Whole Slide Imaging (WSI) in Telepathology." American Journal of Clinical Pathology 154, Supplement_1 (October 2020): S117. http://dx.doi.org/10.1093/ajcp/aqaa161.256.

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Abstract Introduction/Objective Percutaneous Renal biopsy remains a gold standard technique to provide diagnostic and prognostic information post kidney transplantation. Recently Whole slide imaging (WSI) telepathology systems have been widely used for clinical, education and research purposes. Our aim was to examine reliability and accuracy of WSI telepathology service in the pathology diagnosis of biopsy specimens from transplanted kidney. Methods At our institution we have two renal pathologists. They utilize WSI telepathology service with Aperio scanner for rapid initial assessment of the transplant renal biopsy specimens. We retrospectively reviewed reports of all transplant renal biopsies which were examined remotely utilizing WSI telepathology service and compared the results for initial versus final diagnoses. Results In period from Jan 2019 to April 2020 total 160 renal transplant biopsies were evaluated remotely utilizing the WSI scanner. The diagnosis was divided in 4 subcategories as reperfusion injury, rejection (Antibody mediated or T cell mediated), mixed inflammation-favor infection and Polyoma virus infection. There were 48 cases of reperfusion injury; 5 cases of polyoma virus infection, 37 cases of rejection and 28 cases with mixed inflammation and 42 cases with no significant histopathologic findings. There was no discrepancy between the preliminary and final diagnosis for all 160 cases. The ancillary studies including special stains and electron microscopy added to the final diagnosis or confirmed the preliminary diagnosis. Conclusion WSI telepathology is a reliable and simple method to rapidly review transplant kidney biopsies. The ability to transmit images from hospitals to pathologists with WSI scanner has the potential for not only an accurate assessment of the rejection but also for additional histopathological findings. Digital pathology enhances the clinical usefulness of immediate assessments of transplant biopsy samples and also provides a platform to share the scanned images with clinicians which also can be utilized for education of trainees.

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Voroniak, O., and R. Zograbian. "The first experience of cord blood stem cells application in kidney transplantation: A descriptive study." Ukrainian Journal of Nephrology and Dialysis, no. 3(75) (June 5, 2022): 34–42. http://dx.doi.org/10.31450/ukrjnd.3(75).2022.05.

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Abstract. Kidney transplantation is recognized as the optimal method of end-stage kidney disease treatment, but chronic renal allograft rejection remains an unresolved issue and leads to transplanted organ function loss. Recent studies show positive effects of stem cell injections in a variety of diseases, including kidney transplantation. The present study aimed to analyze the first experience of umbilical cord blood stem cells application in living-related kidney transplantation in Shalimov’s National Institute of Surgery and Transplantation, give a preliminary assessment of their effectiveness and safety, evaluate the clinical course and especially the dynamics of laboratory parameters in the recipient’s postoperative period. Methods. The study group included 6 male, adult recipients of kidney transplants, who performed the first kidney allotransplantation from a living family donor in the Shalimov’s National Institute of Surgery and Transplantology in 2020 – 2021. Before surgery, all patients received intravenous administration of a fraction of nuclear cells from human umbilical cord blood at a dose of 2-3 x 106/kg body weight in combination with standard three-component immunosuppressive therapy. Immune system studies were performed before kidney transplantation, on the first and third days of the postoperative period, at the end of the first and second week, as well as on the first, third, sixth, and twelfth months, following kidney transplantation. Renal graft function was assessed by serum creatinine and glomerular filtration rate. Monitoring of clinical and laboratory parameters of blood and urine, the concentration of calcineurin inhibitors (C0) was carried out regularly three times a week for the first month, twice a month for 2-3 months, and once a month until the end of the year. Puncture biopsy of the transplanted kidney was performed three months after surgery to diagnose the pathology of the graft, namely the manifestations of acute and chronic rejection, the nature and degree of which were determined according to the Banff classification. The state of the immune system of the recipients was characterized by indicators of cellular and humoral immunity. Statistical processing of research results was performed using the statistical package StatSoft (2010) STATISTICA 9.1 for Windows StatSoft Inc, Tusla. Results. All patients received cord blood stem cells without complications. On the first day after surgery, an average diuresis was 9415 ± 928.1 ml. Normalization of graft function was observed on the second or third day (GFR more than 90 ml/ min/1.73 m2). There were no rejections of grafts and signs of opportunistic infections in the patients during 1 year follow-up period. Morphological studies did not reveal signs of significant pathological changes in transplanted kidneys in patients who received stem cells as induction therapy. The study of the state of the immune system of recipients in the dynamics, given the insufficient number of patients, requires further research. Conclusions. The administration of cord blood stem cells to recipients prior to kidney transplantation is safe and promotes rapid recovery of renal allograft function. There were no signs of morphological proven chronic graft rejection, which allows us to predict its long-term functioning in the future. To assess the response of the recipient's immune system to the application of cord blood stem cells requires the accumulation of additional data.

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SÁNCHEZ-FRUCTUOSO, ANA I., DOLORES PRATS, JAIME TORRENTE, M. JESÚS PÉREZ-CONTÍN, CRISTINA FERNÁNDEZ, JOAQUÍN ALVAREZ, and ALBERTO BARRIENTOS. "Renal Transplantation from Non-Heart Beating Donors." Journal of the American Society of Nephrology 11, no. 2 (February 2000): 350–58. http://dx.doi.org/10.1681/asn.v112350.

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The aim of this study was to compare the survival and midterm function of kidneys from non-heart beating donors (NHBD) with those of kidneys from heart beating donors (HBD). From 1989 to 1998, 144 kidneys were procured from NHBD at the Hospital Clínico San Carlos in Madrid, of which 95 were transplanted. The kidney grafts were maintained from the moment of the diagnosis of cardiac arrest until the time of procurement by cardiopulmonary bypass. There was no significant difference in renal function and the number of rejection episodes between the NHBD and HBD transplants. The NHBD kidneys showed a 5.73-fold increase in the incidence of delayed graft function (adjusted relative risk 95% confidence interval, 2.82 to 11.62). One- and five-year survival rates for NHBD grafts were 84.6 and 82.7%, respectively, compared with 87.5 and 83.9% for HBD (P = 0.5767). Cox analysis showed that the predictive factors for worse NHBD graft survival were type of NHBD donor and the occurrence of corticoresistant rejection. Ninety of the NHBD organs were procured from subjects suffering irreversible cardiac arrest on the street who were transferred to our center for the sole purpose of donation. Fifty-four of these kidneys were transplanted and all showed primary function. When a strict protocol is adhered to, the outcome of renal transplant from NHBD compares well with that from HBD. It is believed that the high number of organs obtained from subjects undergoing irreversible cardiac arrest on the street might encourage the adoption of new criteria for the management of this type of pathology with the ultimate goal of kidney donation.

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Bedke, Jens, Eva Kiss, Carl-Ludwig Behnes, Zoran V. Popovic, Markus Heuser, Tomislav Stojanovic, Tjeerd Sijmonsma, et al. "Anti-Inflammatory Effects of αv Integrin Antagonism in Acute Kidney Allograft Rejection." American Journal of Pathology 171, no. 4 (October 2007): 1127–39. http://dx.doi.org/10.2353/ajpath.2007.070329.

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Gallan, Alexander J., Woojin James Chon, Michelle A. Josephson, Patrick N. Cunningham, Kammi J. Henriksen, and Anthony Chang. "Bowman capsulitis predicts poor kidney allograft outcome in T cell–mediated rejection." Human Pathology 76 (June 2018): 47–51. http://dx.doi.org/10.1016/j.humpath.2018.02.016.

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Simonov, Pavel A., Mikhail A. Firsov, Daria A. Dunc, Eugene A. Bezrukov, and Sergei V. Ivliev. "The role of urological pathology in the development of terminal renal failure." Consilium Medicum 24, no. 10 (December 15, 2022): 759–62. http://dx.doi.org/10.26442/20751753.2022.10.201927.

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Background. Chronic kidney disease (CKD) is one of the most serious and pressing health problems worldwide today. The end stage of CKD leads to disability and dramatically reduces the quality of life, which is caused by the need for continuous renal replacement therapy. The causes of CKD are various and are often caused by urological pathology. Materials and methods. Five hundred eighty seven case histories of patients with CKD on renal replacement therapy in the Krasnoyarsk Territory for 2022 were analyzed. Most of them were patients with chronic glomerulonephritis (38%) and urological diseases (29%). Other reasons that led to hemodialysis are diabetic nephropathy (12%), hypertensive nephropathy (8%), mixed nephropathy (5%). Systemic diseases with kidney damage, oncological diseases, rejection of a kidney transplant, genetic diseases 2% each. Results. Оne hundred and seventy patients with urological diseases are on program hemodialysis. The mean age of this group of patients was 56.2 years. The incidence of CKD varies slightly between men (48%) and women (52%). The structure of the incidence of urological pathology is as follows: all patients somehow had signs of chronic pyelonephritis. Of 170 people, only 15% had primary chronic pyelonephritis as the main cause of end-stage CKD. The remaining 81% of patients showed signs of secondary pyelonephritis. Patients with polycystic kidney disease accounted for 44%, patients with urolithiasis 13%, patients with anomalies in the development of the kidneys and urinary tract 7%, vesicoureteral reflux, with prostate adenoma 5% patients with signs of a neurogenic bladder 3% and 3% patients with ureteral structure. Patients with oncological pathology accounted for 4%. Conclusion. Over the past decade, the structure of diseases of patients on hemodialysis has changed. Due to the more accessible diagnostic service in the region, the proportion of urological pathologies in patients is increasing. At the same time, the timely use of reconstructive, minimally invasive, nephron-sparing operations can reduce the risks of progression of CKD. However, the number of end-stage patients is steadily increasing, requiring continued development of the hemodialysis service and other forms of renal replacement therapy.

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Wu, Henry H. L., Mohan Shenoy, Philip A. Kalra, and Rajkumar Chinnadurai. "Intrinsic Kidney Pathology Following COVID-19 Infection in Children and Adolescents: A Systematic Review." Children 9, no. 1 (December 22, 2021): 3. http://dx.doi.org/10.3390/children9010003.

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Introduction: COVID-19 infections resulting in pathological kidney manifestations have frequently been reported in adults since the onset of the global COVID-19 pandemic in December 2019. Gradually, there have been an increased number of COVID-19-associated intrinsic kidney pathologies in children and adolescents reported as well. The pathophysiological mechanisms between COVID-19 and the onset of kidney pathology are not fully known in children; it remains a challenge to distinguish between intrinsic kidney pathologies that were caused directly by COVID-19 viral invasion, and cases which occurred as a result of multisystem inflammatory syndrome due to the infection. This challenge is made more difficult in children, due to the ethical limitations of performing kidney biopsies to reach a biopsy-proven diagnosis. Although previous systematic reviews have summarized the various pathological kidney manifestations that have occurred in adults following acute COVID-19 infection, such reviews have not yet been published for children and adolescents. We describe the results of a systematic review for intrinsic kidney pathology following COVID-19 infection in children and adolescents. Methods: A systematic literature search of published data up until 31 October was completed through the Preferred Reporting Items for Systematic Reviews and Meta Analyses (PRISMA) guidelines. Research articles reporting new-onset or relapsed intrinsic kidney pathology in children or adolescents (≤18 years) following acute COVID-19 infection were included for qualitative review. COVID-19 infection status was defined by a positive result from a RT-PCR, or nuclear antibody testing. Only full-text articles published in the English language were selected for review. Results: Twenty-nine cases from fifteen articles were included in the qualitative synthesis of this systematic review. Nephrotic syndrome, as an umbrella condition, appeared as the most frequently observed presentation (20 cases) with disease remission noted in all cases with steroid treatment. Other cases included numerous glomerulonephritides, such as acute necrotizing glomerulonephritis, MPO vasculitis and collapsing glomerulopathy, and thrombotic microangiopathies, such as aHUS. For patients with transplanted kidneys, T-cell-mediated rejection and mild tubular interstitial infiltration were noted following testing positive for COVID-19. There were no mortalities reported in any of the included cases, although two patients remained dialysis dependent at hospital discharge. Conclusion: This systematic review highlights the various intrinsic pathological kidney manifestations in children and adolescents as a result of acute COVID-19 infection. The clinical timeline and presentation of these cases support the mechanistic hypothesis between COVID-19 infection and the onset of intrinsic kidney pathologies within this context. The progressive introduction of vaccination programs for children and adolescents may hopefully reduce the severity of COVID-19-associated illnesses, and pathological kidney manifestations in this population.

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Troxell, Megan L., and Christian Lanciault. "Practical Applications in Immunohistochemistry: Evaluation of Rejection and Infection in Organ Transplantation." Archives of Pathology & Laboratory Medicine 140, no. 9 (January 13, 2016): 910–25. http://dx.doi.org/10.5858/arpa.2015-0275-cp.

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Context.—Immunohistochemical analysis of tissue biopsy specimens is a crucial tool in diagnosis of both rejection and infection in patients with solid organ transplants. In the past 15 years, the concept of antibody-mediated rejection has been refined, and diagnostic criteria have been codified in renal, heart, pancreas, and lung allografts (with studies ongoing in liver, small intestine, and composite grafts), all of which include immunoanalysis for the complement split product C4d. Objectives.—To review the general concepts of C4d biology and immunoanalysis, followed by organ-allograft–specific data, and interpretative nuances for kidney, pancreas, and heart, with discussion of early literature for lung and liver biopsies. Additionally, practical applications and limitations of immunostains for infectious organisms (Polyomavirus, Adenoviridae [adenovirus], and the herpes virus family, including Herpes simplex virus, Cytomegalovirus, Human herpes virus 8, and Epstein-Barr virus) are reviewed in the context of transplant recipients. Data Sources.—Our experience and published primary and review literature. Conclusions.—Immunohistochemistry continues to have an important role in transplant pathology, most notably C4d staining in assessment of antibody-mediated rejection and assessment of viral pathogens in tissue. In all facets of transplant pathology, correlation of morphology with special studies and clinical data is critical, as is close communication with the transplant team.

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Rascio, Federica, Paola Pontrelli, Matteo Accetturo, Annarita Oranger, Margherita Gigante, Giuseppe Castellano, Maddalena Gigante, et al. "A type I interferon signature characterizes chronic antibody-mediated rejection in kidney transplantation." Journal of Pathology 237, no. 1 (June 4, 2015): 72–84. http://dx.doi.org/10.1002/path.4553.

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DiLillo, David, Robert Griffiths, Philip Ruiz, Thomas Coffman, and Thomas Tedder. "B cells differentially regulate acute and chronic cardiac, renal, and skin allograft rejection (145.42)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 145.42. http://dx.doi.org/10.4049/jimmunol.184.supp.145.42.

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Abstract T cells contribute to both acute and chronic allograft rejection, but the roles of B cells and alloantibody are less clear. Therefore, CD20 and CD19 mAbs were used to deplete mature or total B cells, respectively, in mice before allografting. Both CD20 and CD19 mAbs effectively depleted mature B cells, but CD19 mAb also depleted >70% of CD138+ plasma cells in flow cytometry assays, as well as >66% of Ab-secreting cells in ELISPOT assays. Consequently, CD19 mAb treatment depleted serum IgG levels by 80% in naïve mice, while CD20 mAb did not. Neither CD20 nor CD19 mAb treatment affected acute cardiac allograft rejection, with all grafts rejected within 7-9 days. However, CD19 mAb treatment prevented the generation of allo-IgG. In a second model of rejection, treatment with CD19 mAb before renal transplant significantly delayed and prevented chronic renal allograft rejection, reduced kidney pathology, and abrogated the development of allo-IgG, while CD20 mAb did not. In additional experiments, CD19 mAb treatment also depleted pre-existing allo-IgG levels in serum. In a third allograft model, pretreatment with CD20 mAb exacerbated acute skin allograft rejection and augmented the proliferation of adoptively transferred alloantigen-specific CD4+ T cells by 2-fold, indicating that B cells negatively regulate acute skin graft rejection and CD4+ T cell responses. Thus, depending on the nature of the allograft, B cells can either positively or negatively regulate allograft rejection.

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Loupy, A., M. Haas, K. Solez, L. Racusen, D. Glotz, D. Seron, B. J. Nankivell, et al. "The Banff 2015 Kidney Meeting Report: Current Challenges in Rejection Classification and Prospects for Adopting Molecular Pathology." American Journal of Transplantation 17, no. 1 (December 28, 2016): 28–41. http://dx.doi.org/10.1111/ajt.14107.

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Ramackers, Wolf, Lars Friedrich, Wolfgang Schüttler, Sabine Bergmann, Arnold Ganser, Michael Winkler, and Andreas Tiede. "An Ex Vivo Perfusion Model To Study the Treatment of Thrombotic Microangiopathy during Pig-to-Human Xenogenic Kidney Transplantation." Blood 110, no. 11 (November 16, 2007): 3190. http://dx.doi.org/10.1182/blood.v110.11.3190.3190.

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Abstract Early rejection of xenogenic organs is associated with thrombotic microangiopathy and changes of coagulation resembling disseminated intravascular coagulation (DIC). Here, we used an ex vivo perfusion circuit as a model of pig-to-human kidney transplantation to study the nature and treatment of this pathology. Porcine kidneys were obtained following in situ cold perfusion with HTK organ preservation solution and immediately connected to a perfusion circuit containing porcine (“autologous”) or human (“xenogenic”) AB blood supplemented with complement component C1 inhibitor (1 U/ml) and heparin (1 U/ml). Perfusion of porcine kidneys with autologous blood was feasible for >240 min in all experiments. In contrast, perfusion of porcine kidneys with xenogenic human blood was limited by a dramatic increase of flow resistance after 30 to 240 min. Increased concentrations of C3a as a marker for complement activation were associated with early perfusion failure. In addition, a dramatic increase of thrombin-antithrombin complex (TAT) and D Dimer (DD) was observed together with consumption of platelets, fibrinogen and antithrombin (AT). Histological examination demonstrated extensive thrombotic microangiopathy. Supplementation recombinant human activated protein C (rhAPC, 300 ug/l*h, n=3) or recombinant human antithrombin (rhAT, 3 U/ml, n=3) abolished the increase of flow resistance and allowed for a xenogenic kidney survival of >240 min in all experiments. Increase of DD was abolished and the consumption of fibrinogen was abrogated by both treatments as compared to control, whereas the increase of TAT was abolished only by rhAPC. Histological examination revealed no evidence of thrombotic microangiopathy for both treatments as compared to control. In conclusion, the perfusion model introduced here is a suitable tool for studying coagulopathy during early rejection in xenotransplantation. Thrombotic microangiopathy and DIC-like activation of coagulation is associated with an increased flow resistance and failure of perfusion in this model. Pharmacological intervention such as the supplementation of rhAPC or rhAT can be studied using this model and has been shown to prevent coagulopathy and thrombotic microangiopathy.

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Han, Jing Light, Jason M. Zimmerer, Qiang Zeng, Bryce A. Ringwald, Clarissa Cassol, Robert T. Warren, Mahmoud Abdel-Rasoul, Christopher K. Breuer, and Ginny L. Bumgardner. "Antibody-suppressor CD8+ T cells ameliorate antibody-mediated rejection following kidney transplant in mice." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 87.16. http://dx.doi.org/10.4049/jimmunol.204.supp.87.16.

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Abstract Purpose CCR5 KO kidney transplant (KT) mice produce high titer alloantibody (alloAb) associated with severe antibody-mediated rejection (AMR) that reproduces AMR histology observed in human KT recipients. We previously reported the novel alloAb suppressor activity of alloprimed CXCR5+IFNγ+CD8+ T (Tab-supp) cells following hepatocellular transplant in mice. Here, we investigated the biologic impact of alloprimed CD8+ Tab-supp cells and their capacity to suppress alloAb following adoptive cell transfer (ACT) into CCR5 KO KT mice. Methods CCR5 KO (H-2b) mice were transplanted with allogeneic A/J (H-2a) kidneys, and on postoperative day (POD) 5 underwent ACT of alloprimed CD8+ Tab-supp cells (retrieved from C57BL/6 mice alloprimed with A/J alloantigen). A second cohort received concomitant bilateral native nephrectomy, and allograft survival was monitored with serial serum creatinine (>100 μmol/L defines KT graft loss). Untreated CCR5 KO KT mice served as controls. Results CCR5 KO KT mice developed high alloAb titer compared to wild-type (WT) recipients (5,800±700 vs 1,200±100; p=0.0003). ACT significantly inhibited alloAb production by 5-fold (1,200±200; p<0.0001) and POD14 AMR pathology (peritubular capillary margination and C4d deposition, arteritis) in CCR5 KO KT mice (composite histologic score 3.6±1.5 vs 8.4±0.2 in untreated controls; p=0.006). Following ACT, alloAb remained suppressed beyond POD 30, correlating with enhanced allograft survival (MST 52 vs 14 days; p=0.006). Conclusion ACT of CD8+ Tab-supp cells effectively inhibits alloAb production and AMR not only after allogeneic hepatocellular transplant, but also after vascularized solid organ transplant such as in CCR5 KO KT recipients.

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Tabernero, Guadalupe, Moisés Pescador, Elena Ruiz Ferreras, Ana I. Morales, and Marta Prieto. "Evaluation of NAG, NGAL, and KIM-1 as Prognostic Markers of the Initial Evolution of Kidney Transplantation." Diagnostics 13, no. 11 (May 25, 2023): 1843. http://dx.doi.org/10.3390/diagnostics13111843.

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Kidney transplantation is the best option for end-stage chronic kidney disease. Transplant viability is conditioned by drugs’ nephrotoxicity, ischemia–reperfusion damage, or acute rejection. An approach to improve graft survival is the identification of post-transplant renal function prognostic biomarkers. Our objective was to study three early kidney damage biomarkers (N-acetyl-d-glucosaminidase, NAG; neutrophil gelatinase-associated lipocalin, NGAL; and kidney injury molecule-1, KIM-1) in the initial period after transplantation and to identify possible correlations with main complications. We analysed those biomarkers in urine samples from 70 kidney transplant patients. Samples were taken on days 1, 3, 5, and 7 after intervention, as well as on the day that renal function stabilised (based on serum creatinine). During the first week after transplant, renal function improved based on serum creatinine evolution. However, increasing levels of biomarkers at different times during that first week could indicate tubular damage or other renal pathology. A relationship was found between NGAL values in the first week after transplantation and delayed graft function. In addition, higher NAG and NGAL, and lower KIM-1 values predicted a longer renal function stabilisation time. Therefore, urinary NAG, NGAL, and KIM-1 could constitute a predictive tool for kidney transplant complications, contributing to improve graft survival rates.

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Mubarak, Muhammed, Amber Raza, Rahma Rashid, and Shaheera Shakeel. "Evolution of human kidney allograft pathology diagnostics through 30 years of the Banff classification process." World Journal of Transplantation 13, no. 5 (September 18, 2023): 221–38. http://dx.doi.org/10.5500/wjt.v13.i5.221.

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Type 1 diabetes mellitus (T1DM) is one of the important causes of chronic kidney disease (CKD) and end-stage renal failure (ESRF). Even with the best available treatment options, management of T1DM poses significant challenges for clinicians across the world, especially when associated with CKD and ESRF. Substantial increases in morbidity and mortality along with marked rise in treatment costs and marked reduction of quality of life are the usual consequences of onset of CKD and progression to ESRF in patients with T1DM. Simultaneous pancreas-kidney transplant (SPK) is an attractive and promising treatment option for patients with advanced CKD/ESRF and T1DM for potential cure of these diseases and possibly several complications. However, limited availability of the organs for transplantation, the need for long-term immunosuppression to prevent rejection, peri- and post-operative complications of SPK, lack of resources and the expertise for the procedure in many centers, and the cost implications related to the surgery and postoperative care of these patients are major issues faced by clinicians across the globe. This clinical update review compiles the latest evidence and current recommendations of SPK for patients with T1DM and advanced CKD/ESRF to enable clinicians to care for these diseases.

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Yi, Stephanie Grace, Dawei Zou, Yulin Dai, Zhongming Zhao, Osama Gaber, and Wenhao Chen. "Chromatin profiling of renal allograft-infiltrating cells reveals epigenetic regulation of CD8+ T cell exhaustion in chronically rejected human kidney allografts." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 175.03. http://dx.doi.org/10.4049/jimmunol.208.supp.175.03.

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Abstract Purpose Our single cell RNA sequencing (scRNA-seq) analysis found that T cells in chronically rejected kidney allografts and peripheral blood mononuclear cells (PBMCs) of the same kidney transplant recipients (KTR) exhibited a spectrum of dynamic cell states; herein, we investigate how T cell states are regulated at the epigenetic level during chronic rejection. Methods H3K27me3 and H3K27ac CUT&Tag was performed in live T cells isolated from PBMCs and allografts of 3 KTR with failed transplants. All transplants had chronic cellular and antibody mediated rejection on pathology. Results With CD8+ T cell infiltration into allografts, H3K27me3 was deposited at the gene loci associated with T cell quiescence and stemness (TCF7, BACH2, FOXP1, IL7R, etc.), whereas H3K27ac was mostly deposited at the gene loci involved in T cell effector (GZMB, ID2, ZEB2, etc) and exhaustion (TOX, TOX2, TIGIT, PDCD1, HAVCR2, etc) programs. Conclusion Our prior scRNA-seq analysis revealed that most CD8+ T cells in PBMCs maintain TCF7+ stem-like cell phenotypes. However, most CD8+ T cells infiltrated in chronically rejected allografts lose stemness, becoming either TCF7−GZMBhi effector or TCF7−PDCD1hiHAVCR2hi exhausted T cells. Herein our CUT&Tag analysis reveals that chromatin remodeling mediates such dynamic changes of T cell states. Of note, although T-cell exhaustion occurs in chronically rejected allografts, it only represents dynamic changes of T cell states. We propose that TCF7+ allogenic T cells in the periphery maintain stem-like property. Without proper epigenetic silencing of their function, TCF7+ allogenic T cells produce not only exhausted progeny but also effector cell progeny to mediate allograft rejection. Supported by internal

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Kobayashi, Akimitsu, Takamune Takahashi, Shigeru Horita, Izumi Yamamoto, Hiroyasu Yamamoto, Satoshi Teraoka, Kazunari Tanabe, Tatsuo Hosoya, and Yutaka Yamaguchi. "Activation of the transcription factor c-Jun in acute cellular and antibody-mediated rejection after kidney transplantation." Human Pathology 41, no. 12 (December 2010): 1682–93. http://dx.doi.org/10.1016/j.humpath.2010.04.016.

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Fu, Mei Sian, Soo Jin Lim, Maisarah Jalalonmuhali, Kee Seong Ng, Soo Kun Lim, and Kok Peng Ng. "Clinical Significance of Renal Allograft Protocol Biopsies: A Single Tertiary Center Experience in Malaysia." Journal of Transplantation 2019 (May 2, 2019): 1–8. http://dx.doi.org/10.1155/2019/9153875.

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Background. The role of protocol renal allograft biopsy in kidney transplantation is controversial due to the concern with procedural-related complications; however, its role is slowly evolving. Recent evidence suggests that protocol biopsy is useful in detecting subclinical renal pathology. Early recognition and treatment of renal pathologies can improve long-term outcomes of renal allografts. Methodology. A total of 362 renal allograft protocol biopsies were performed in adult recipients of kidney transplantation between 2012 and 2017. After excluding those with poor quality or those performed with a baseline serum creatinine level >200 umol/L, we analyzed 334 (92.3%) biopsies. Histology reports were reviewed and categorized into histoimmunological and nonimmunological changes. The immunological changes were subcategorized into the following: (1) no acute rejection (NR), (2) borderline changes (BC), and (3) subclinical rejection (SCR). Nonimmunological changes were subcategorized into the following: (1) chronicity including interstitial fibrosis/tubular atrophy (IFTA), chronic T-cell-mediated rejection (TCMR), unspecified chronic lesions, and arterionephrosclerosis, (2) de novo glomerulopathy/recurrence of primary disease (RP), and (3) other clinically unsuspected lesions (acute pyelonephritis, calcineurin inhibitors toxicity, postinfective glomerulonephritis, and BK virus nephropathy). Risk factors associated with SCR were assessed. Results. For the histoimmunological changes, 161 (48.2%) showed NR, 145 (43.4%) were BC, and 28 (8.4%) were SCR. These clinical events were more pronounced for the first 5 years; our data showed BC accounted for 59 (36.4%), 64 (54.2%), and 22 (40.7%) biopsies within <1 year, 1-5 years, and > 5 years, respectively (p = 0.011). Meanwhile, the incidence for SCR was 6 (3.7%) biopsies in <1 year, 18 (15.3%) in 1-5 years, and 4 (7.4%) in >5 years after transplantation (p=0.003). For the nonimmunological changes, chronicity, de novo glomerulopathy/RP, and other clinically unsuspected lesions were seen in 40 (12%), 10 (3%), and 12 (3.6%) biopsies, respectively. Living-related donor recipients were associated with decreased SCR (p=0.007). Conclusions. Despite having a stable renal function, our transplant recipients had a significant number of subclinical rejection on renal allograft biopsies.

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Degner, Kenna R., Nancy A. Wilson, Shannon R. Reese, Sandesh Parajuli, Fahad Aziz, Neetika Garg, Maha Mohamed, et al. "Short-Term Immunopathological Changes Associated with Pulse Steroids/IVIG/Rituximab Therapy in Late Kidney Allograft Antibody Mediated Rejection." Kidney360 1, no. 5 (March 19, 2020): 389–98. http://dx.doi.org/10.34067/kid.0001082019.

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BackgroundB cell depletion is a common treatment of antibody-mediated rejection (ABMR). We sought to determine the specific immunopathologic effects of this therapeutic approach in kidney transplantation.MethodsThis was a prospective observational study of recipients of kidney transplants diagnosed with late ABMR (>3 months after transplant). Patients received treatment with pulse steroids, IVIG, and rituximab. Donor-specific HLA antibodies (DSA), kidney allograft pathology, renal function, immune cell phenotypes, and 47 circulating cytokines were assessed at baseline and at 3 months.ResultsWe enrolled 23 patients in this study between April 2015 and March 2019. The majority of patients were male (74%) and white (78%) with an average age of 45.6±13.8 years. ABMR was diagnosed at 6.8±5.9 years (4 months to 25 years) post-transplant. Treatment was associated with a significant decline in circulating HLA class I (P=0.003) and class II DSA (P=0.002) and peritubular capillaritis (ptc; P=0.04) compared to baseline. Serum creatinine, BUN, eGFR, and proteinuria (UPC) remained stable. Circulating B cells were depleted to barely detectable levels (P≤0.001), whereas BAFF (P=0.0001), APRIL (P<0.001), and IL-10 (P=0.02) levels increased significantly post-treatment. Notably, there was a significant rise in circulating CD4+ (P=0.02) and CD8+ T cells (P=0.003). We also noted a significant correlation between circulating cytotoxic CD8+ T cells and BAFF (P=0.05), regulatory T cells and IL-10 (P=0.002), and regulatory T cells and HLA class I DSA (P=0.005).ConclusionsShort-term pulse steroids/IVIG/rituximab therapy was associated with inhibition of ABMR (DSA and ptc), stabilization of kidney function, and increased regulatory B cell and T cell survival cytokines. Additional studies are needed to understand the implications of B cell depletion on the crosstalk between T cells and B cells, and humoral components that regulate ABMR.

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Wu, Henry H. L., Philip A. Kalra, and Rajkumar Chinnadurai. "New-Onset and Relapsed Kidney Histopathology Following COVID-19 Vaccination: A Systematic Review." Vaccines 9, no. 11 (October 29, 2021): 1252. http://dx.doi.org/10.3390/vaccines9111252.

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Abstract:

Introduction: The introduction of COVID-19 vaccination programs has become an integral part of the major strategy to reduce COVID-19 numbers worldwide. New-onset and relapsed kidney histopathology have been reported following COVID-19 vaccination, sparking debate on whether there are causal associations. How these vaccines achieve an immune response to COVID-19 and the mechanism that this triggers kidney pathology remains unestablished. We describe the results of a systematic review for new-onset and relapsed kidney histopathology following COVID-19 vaccination. Methods: A systematic literature search of published data up until 31 August 2021 was completed through the Preferred Reporting Items for Systematic Reviews and Meta Analyses (PRISMA) guideline. Research articles reporting new onset or relapsed kidney histopathology in adult patients (>18 years) following COVID-19 vaccination were included for qualitative review. Only full-text articles published in the English language were selected for review. Results: Forty-eight cases from thirty-six articles were included in the qualitative synthesis of this systematic review. Minimal change disease (19 cases) was the most frequent pathology observed, followed by IgA nephropathy (14 cases) and vasculitis (10 cases). Other cases include relapse of membranous nephropathy, acute rejection of kidney transplant, relapse of IgG4 nephritis, new-onset renal thrombotic microangiopathy, and scleroderma renal crisis following COVID-19 vaccination. There was no mortality reported in any of the included cases. Patients in all but one case largely recovered and did not require long-term renal replacement therapy. Conclusion: This systematic review provides insight into the relationship between various kidney pathologies that may have followed COVID-19 vaccination. Despite these reported cases, the protective benefits offered by COVID-19 vaccination far outweigh its risks. It would be recommended to consider early biopsy to identify histopathology amongst patients presenting with symptoms relating to new-onset kidney disease following vaccination and to monitor symptoms for those with potential relapsed disease.

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Solez, K. i. m., Roy A. Axelsen, Hallgrimur Benediktsson, James F. Burdick, Arthur H. Cohen, Robert B. Colvin, Byron P. Croker, et al. "International standardization of criteria for the histologic diagnosis of renal allograft rejection: The Banff working classification of kidney transplant pathology." Kidney International 44, no. 2 (August 1993): 411–22. http://dx.doi.org/10.1038/ki.1993.259.

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Bellan, C., T. Amato, M. Carmellini, M. Onorati, A. D'Amuri, L. Leoncini, and M. T. del Vecchio. "Analysis of the IgVH genes in T cell-mediated and antibody-mediated rejection of the kidney graft." Journal of Clinical Pathology 64, no. 1 (November 20, 2010): 47–53. http://dx.doi.org/10.1136/jcp.2010.082024.

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Pratt, Julian R., Miriam E. Jones, Jun Dong, Wuding Zhou, Paramit Chowdhury, Richard A. G. Smith, and Steven H. Sacks. "Nontransgenic Hyperexpression of a Complement Regulator in Donor Kidney Modulates Transplant Ischemia/Reperfusion Damage, Acute Rejection, and Chronic Nephropathy." American Journal of Pathology 163, no. 4 (October 2003): 1457–65. http://dx.doi.org/10.1016/s0002-9440(10)63503-1.

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Aufman, Jeffrey. "Transplant Kidney With Acute Humoral Rejection Diagnosed by Needle Core Biopsy—A Case Report With Review of Pathological Morphology." Pathology Case Reviews 20, no. 6 (2015): 288–90. http://dx.doi.org/10.1097/pcr.0000000000000112.

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Khubutiya, M. Sh, F. M. Musaeva, T. A. Kanunova, O. N. Rzhevskaya, A. G. Balkarov, and Kh G. Alidzhanova. "Arterial hypertension in kidney transplant recipients: pathophysiology, diagnostics, treatment." Bulletin of the Medical Institute "REAVIZ" (REHABILITATION, DOCTOR AND HEALTH) 14, no. 2 (April 15, 2024): 140–49. http://dx.doi.org/10.20340/vmi-rvz.2024.2.tx.2.

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Abstract:

Relevance: Arterial hypertension (HTN) in kidney transplant recipients is a major risk factor for cardiovascular diseases, graft rejection and premature death. In the post-transplant period in 80% of cases persistent or refractory arterial hypertension develops which is difficult to correct with conventional drug therapy. Treatment difficulties include the ineffectiveness of many first-line drugs and the fact that the most common immunosuppressive drugs (cyclosporine, tacrolimus and methylprednisolone) contribute to the development of hypertension. This type of hypertension represents a significant problem in clinical practice due to the complexity of treatment and high mortality. The need to study the treatment of post-transplant hypertension is due not only to its clinical significance, but also to the potential opportunity to improve treatment results and life expectancy of kidney transplant recipients.Objective: to study the genesis, risk factors, pathophysiology, diagnosis and treatment of posttransplant hypertension.Materials and methods: 37 literary sources were analyzed.Conclusions: High blood pressure exposes the recipient of a kidney transplant to the risk of CVD and mortality as well as increased systemic hypertension which can be a cause and a consequence of renal pathology. Hypertension is a modifiable risk factor contributing to the progression of renal failure. There is no any single treatment algorithm. It is often necessary to use several antihypertensive drugs to achieve the target blood pressure.

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Liu, Peng, George Tseng, Zijie Wang, Yuchen Huang, and Parmjeet Randhawa. "Diagnosis of T-cell–mediated kidney rejection in formalin-fixed, paraffin-embedded tissues using RNA-Seq–based machine learning algorithms." Human Pathology 84 (February 2019): 283–90. http://dx.doi.org/10.1016/j.humpath.2018.09.013.

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Journal articles on the topic 'Rejection kidney pathology'

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