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        <title>Frontiers in Nephrology | Onconephrology section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/nephrology/sections/onconephrology</link>
        <description>RSS Feed for Onconephrology section in the Frontiers in Nephrology journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-15T20:47:51.482+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1615779</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1615779</link>
        <title><![CDATA[The safety of percutaneous renal biopsy for acute kidney injury in metastatic renal cell cancer patients with reduced nephron mass]]></title>
        <pubdate>2025-08-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tomaz Milanez</author><author>Vinay Srinivasan</author><author>Vladimir Premru</author><author>Miha Arnol</author><author>Janja Ocvirk</author><author>Edgar A. Jaimes</author>
        <description><![CDATA[BackgroundPercutaneous renal biopsy (PRB) provides valuable information to guide treatment decisions in patients with metastatic renal cell carcinoma (mRCC) who develop acute kidney injury (AKI) after systemic anticancer therapy (SACT). The rising incidence of renal cell carcinoma (RCC) and the substantial impact of SACT on overall survival suggest a higher prevalence of RCC patients with reduced nephron mass and a solitary kidney (SK) requiring PRB for AKI. However, safety data on SK biopsies are scarce, and the potential for dialysis-requiring complications may deter clinicians.MethodsThis retrospective case series reports the safety of 13 PRBs in 12 mRCC patients with reduced nephron mass who developed AKI during SACT as well as six PRBs in six patients with metastatic solid malignancies and AKI, which developed during SACT.ResultsEleven biopsies in mRCC patients and five biopsies in patients with metastatic solid malignancies were uneventful. One patient with mRCC experienced a major bleeding event due to an arteriovenous (AV) fistula seven days post-procedure, while another mRCC patient developed macrohematuria within 24 hours. In the group of patients with metastatic solid malignancies, one patient experienced a small perinephric hematoma during the observational period. Despite the small sample size, individual chart reviews and direct management of adverse events allowed assessment of the association between biopsy and complications.ConclusionUntil further data become available, a longer observation period is recommended for these patient cohorts compared to the general population. Further studies are needed to develop consensus guidelines for PRB in mRCC patients with reduced nephron mass.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2025.1585605</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2025.1585605</link>
        <title><![CDATA[Editorial: Onconephrology: evolving concepts and challenges]]></title>
        <pubdate>2025-04-04T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Rogerio Passos</author><author>Bruno Zawadzki</author><author>Etienne Macedo</author><author>Marcelino Durão</author><author>Fernanda Oliveira Coelho</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1399977</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1399977</link>
        <title><![CDATA[Triple monoclonal protein-related kidney lesions in a patient with plasma cell dyscrasia: a case report]]></title>
        <pubdate>2024-11-08T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Arsalan Alvi</author><author>Alexander J. Gallan</author><author>Nattawat Klomjit</author>
        <description><![CDATA[A toxic monoclonal protein typically results in a single kidney pathology due to the specific biophysical characteristics of monoclonal proteins. Multiple monoclonal protein lesions are rarely reported and often portend a poor prognosis. We present a 57-year-old male who developed rapidly progressive glomerulonephritis after concealed ruptured diverticulitis. A kidney biopsy showed light chain cast nephropathy, light chain proximal tubulopathy, and thrombotic microangiopathy. Laboratories showed IgG kappa with an M-spike of 0.2 g/dl and a kappa light chain of 16 mg/dl. A bone marrow biopsy showed 3% kappa-restricted plasma cells. The dramatic renal presentation despite the minimal hematological burden is suggestive of a highly toxic light chain, which is consistent with monoclonal gammopathy of renal significance (MGRS). Clone-directed therapy and a complement blockade were initiated. The patient remained dialysis-dependent despite a hematological response. This case highlights the importance of considering the toxic properties of monoclonal proteins in causing kidney diseases. Our case is the first report of an MGRS patient with three distinct kidney lesions. Triple monoclonal protein-related kidney lesions are very rare and are usually associated with multiple myeloma. Light chain cast nephropathy (LCCN) is a myeloma-defining event but his light chain (LC) (<50 mg/dl) and plasma cell (<10%) burdens were low which makes this case very unusual. Sepsis-induced low-flow stage and the toxic properties of LC may induce LCCN in this patient. Aggressive therapy is likely needed to eradicate the clone in order to achieve an organ response.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1439288</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1439288</link>
        <title><![CDATA[Unraveling monoclonal gammopathy of renal significance: a mini review on kidney complications and clinical insights]]></title>
        <pubdate>2024-09-12T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Mythri Shankar</author><author>Manjusha Yadla</author>
        <description><![CDATA[Monoclonal gammopathy of renal significance (MGRS) is where kidney injury occurs due to the accumulation or effects of abnormal monoclonal proteins. These proteins, originating from non-cancerous or pre-cancerous plasma cells or B cells, deposit in specific areas of the kidney. Mechanisms contributing to MGRS include high levels of vascular endothelial growth factor secretion, autoantibodies targeting complement components, and targeting specific receptors leading to nephropathy. Kidney lesions in monoclonal gammopathy of renal significance (MGRS) are classified based on the presence of organized or nonorganized deposits, including fibrillar, microtubular, or crystal inclusions. Kidney biopsy is essential for confirming the diagnosis of MGRS by identifying monoclonal immunoglobulin deposits. Immunofluorescence helps determine the class of light and/or heavy chain involved in MGRS. The treatment approach is clone-directed and hence it depends on the presence of B cell clone or plasma cell clone or any detectable monoclonal protein. Chemotherapy targeting plasma cell or B cell malignancies and autologous hematopoietic cell transplantation may be used to manage MGRS. Kidney outcomes in MGRS patients strongly correlate with the hematologic response to chemotherapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1400027</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1400027</link>
        <title><![CDATA[Case report: Successful treatment of renal-limited thrombotic microangiopathy secondary to chronic lymphocytic leukemia]]></title>
        <pubdate>2024-08-13T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Kristina Nasr</author><author>Sabine Karam</author><author>Marshall Mazepa</author><author>Jan Czyzyk</author><author>Nattawat Klomjit</author>
        <description><![CDATA[Thrombotic microangiopathy (TMA) is a rare renal complication of patients with chronic lymphocytic leukemia (CLL) and is often associated with peripheral features. We present the first case of CLL patients with renal-limited TMA. A 70-year-old female patient with a history of well-controlled type 2 diabetes and baseline albuminuria of 87.2 mg/g 1 year prior and CLL was on active surveillance only. Her baseline white blood cell (WBC) was 202.6 x 103/µl. She presented with nephrotic syndrome with proteinuria of 10 g/g and a subsequent unremarkable serologic work-up. A kidney biopsy revealed diabetic glomerulosclerosis and chronic TMA. Initially, she was treated conservatively with angiotensin receptor blockade and sodium glucose cotransporter-2 inhibition but progressed with increased proteinuria of 17 g/g. Complement functional panel testing was pursued and showed dysregulation of the classical and alternative complement pathways. We decided to treat CLL which was suspected to be the culprit. At 9 months post-ibrutinib initiation, there was a 90% reduction in the WBC as well as a 94% reduction in proteinuria (17 g/g to 0.97 g/g). This case emphasizes the role of complement dysregulation in the pathogenesis of TMA in CLL patients. Treatment of CLL can restore complement dysregulation and improve renal outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1436896</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1436896</link>
        <title><![CDATA[Chemotherapy-induced acute kidney injury: epidemiology, pathophysiology, and therapeutic approaches]]></title>
        <pubdate>2024-08-09T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Rafaella Maria da Cunha Lyrio</author><author>Bruna Reis Araújo Rocha</author><author>Ana Luiza Rodrigues Mascarenhas Corrêa</author><author>Maria Gabriela Santana Mascarenhas</author><author>Felipe Luz Santos</author><author>Rafael da Hora Maia</author><author>Lívia Benezath Segundo</author><author>Paulo André Abreu de Almeida</author><author>Clara Magalhães Oliveira Moreira</author><author>Rafael Hennemann Sassi</author>
        <description><![CDATA[Despite significant advancements in oncology, conventional chemotherapy remains the primary treatment for diverse malignancies. Acute kidney injury (AKI) stands out as one of the most prevalent and severe adverse effects associated with these cytotoxic agents. While platinum compounds are well-known for their nephrotoxic potential, other drugs including antimetabolites, alkylating agents, and antitumor antibiotics are also associated. The onset of AKI poses substantial risks, including heightened morbidity and mortality rates, prolonged hospital stays, treatment interruptions, and the need for renal replacement therapy, all of which impede optimal patient care. Various proactive measures, such as aggressive hydration and diuresis, have been identified as potential strategies to mitigate AKI; however, preventing its occurrence during chemotherapy remains challenging. Additionally, several factors, including intravascular volume depletion, sepsis, exposure to other nephrotoxic agents, tumor lysis syndrome, and direct damage from cancer’s pathophysiology, frequently contribute to or exacerbate kidney injury. This article aims to comprehensively review the epidemiology, mechanisms of injury, diagnosis, treatment options, and prevention strategies for AKI induced by conventional chemotherapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1389562</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1389562</link>
        <title><![CDATA[Case report: A case of pseudo-acute kidney injury due to cyclin-dependent kinase inhibitor]]></title>
        <pubdate>2024-06-10T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Praveen Errabelli</author><author>Maulik Lathiya</author><author>Devender Singh</author>
        <description><![CDATA[Various classes of targeted therapies have emerged in the last few years, which have revolutionized cancer treatment, and improved the prognosis and survival of cancer patients. Unfortunately, these agents have serious toxic effects on the kidneys. Some of the toxic effects are hypertension, acute kidney injury (AKI), and proteinuria. One interesting phenomenon that has emerged recently is pseudo-acute kidney injury due to the interference with the tubular secretion of creatinine by some of the targeted therapeutic agents. Understanding this physiology is needed to avoid unnecessary investigation and withholding of lifesaving chemo regimen. Alternative methods to assess renal function such as cystatin C-based estimated glomerular filtration rate (eGFR) can differentiate true AKI from pseudo-AKI. Here, we describe one such case of pseudo-AKI from cyclin-dependent kinase (CDK) 4/6 inhibitor, abemaciclib, which inhibits tubular secretion of creatinine. Using cystatin-C-based eGFR revealed pseudo-AKI in this case.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1378250</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1378250</link>
        <title><![CDATA[CAR T-cell therapy and the onco-nephrologist]]></title>
        <pubdate>2024-04-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Marco Aurelio Salvino</author><author>Alberto Mussetti</author><author>Marta Peña</author><author>Annalisa Paviglianiti</author><author>Abel Santos Carreira</author><author>Daniel Rizky</author><author>Anna Sureda</author>
        <description><![CDATA[Cell therapy, specifically the revolutionary chimeric antigen receptor (CAR) T-cell therapy, has transformed the landscape of oncology, making substantial strides in practical treatment approaches. Today, established guidelines for diseases such as lymphomas, myelomas, and leukemias actively advocate the utilization of these once-unconventional therapies. The practical impact of these therapies is underscored by their unparalleled efficacy, reshaping the way we approach and implement treatments in the realm of oncology. However, CAR T-cell therapy, with its performance in anti-tumor aggression through cellular action and inflammatory response, also comes with various adverse events, one of which is kidney injury. Therefore, the management of these side effects is extremely important. The integration of knowledge between oncologists and specialized nephrologists has led to the emergence of a new sub-area of expertise for onco-nephrologists specializing in managing kidney complications from immune effector therapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1384208</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1384208</link>
        <title><![CDATA[Chemotherapy-induced tubulopathy: a case report series]]></title>
        <pubdate>2024-04-11T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Mario Alamilla-Sanchez</author><author>Juan Daniel Diaz Garcia</author><author>Valeria Yanez Salguero</author><author>Fleuvier Morales Lopez</author><author>Victor Ulloa Galvan</author><author>Francisco Velasco Garcia-Lascurain</author><author>Benjamin Yama Estrella</author>
        <description><![CDATA[Acquired tubulopathies are frequently underdiagnosed. They can be characterized by the renal loss of specific electrolytes or organic solutes, suggesting the location of dysfunction. These tubulopathies phenotypically can resemble Bartter or Gitelman syndrome). These syndromes are infrequent, they may present salt loss resembling the effect of thiazides (Gitelman) or loop diuretics (Bartter). They are characterized by potentially severe hypokalemia, associated with metabolic alkalosis, secondary hyperaldosteronism, and often hypomagnesemia. Tubular dysfunction has been described as nephrotoxic effects of platinum-based chemotherapy. We present 4 cases with biochemical signs of tubular dysfunction (Bartter-like/Gitelman-like phenotype) related to chemotherapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2024.1349859</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2024.1349859</link>
        <title><![CDATA[Bioinformatics-driven identification of prognostic biomarkers in kidney renal clear cell carcinoma]]></title>
        <pubdate>2024-04-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Varinder Madhav Verma</author><author>Sanjeev Puri</author><author>Veena Puri</author>
        <description><![CDATA[Renal cell carcinoma (RCC), particularly the clear cell subtype (ccRCC), poses a significant global health concern due to its increasing prevalence and resistance to conventional therapies. Early detection of ccRCC remains challenging, resulting in poor patient survival rates. In this study, we employed a bioinformatic approach to identify potential prognostic biomarkers for kidney renal clear cell carcinoma (KIRC). By analyzing RNA sequencing data from the TCGA-KIRC project, differentially expressed genes (DEGs) associated with ccRCC were identified. Pathway analysis utilizing the Qiagen Ingenuity Pathway Analysis (IPA) tool elucidated key pathways and genes involved in ccRCC dysregulation. Prognostic value assessment was conducted through survival analysis, including Cox univariate proportional hazards (PH) modeling and Kaplan–Meier plotting. This analysis unveiled several promising biomarkers, such as MMP9, PIK3R6, IFNG, and PGF, exhibiting significant associations with overall survival and relapse-free survival in ccRCC patients. Cox multivariate PH analysis, considering gene expression and age at diagnosis, further confirmed the prognostic potential of MMP9, IFNG, and PGF genes. These findings enhance our understanding of ccRCC and provide valuable insights into potential prognostic biomarkers that can aid healthcare professionals in risk stratification and treatment decision-making. The study also establishes a foundation for future research, validation, and clinical translation of the identified prognostic biomarkers, paving the way for personalized approaches in the management of KIRC.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2023.1193494</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2023.1193494</link>
        <title><![CDATA[Early clinical indicators of acute kidney injury caused by administering high-dose methotrexate therapy to juvenile pigs]]></title>
        <pubdate>2023-09-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Randal K. Buddington</author><author>Thomas Wong</author><author>Karyl K. Buddington</author><author>Torben S. Mikkelsen</author><author>Xueyuan Cao</author><author>Scott C. Howard</author>
        <description><![CDATA[IntroductionEarly identification of compromised renal clearance caused by high-dose methotrexate (HDMTX) is essential for initiating timely interventions that can reduce acute kidney injury and MTX-induced systemic toxicity.MethodsWe induced acute kidney injury (AKI) by infusing 42 juvenile pigs with 4 g/kg (80 g/m2) of MTX over 4 hours without high-volume alkalinizing hydration therapy. Concentrations of serum creatinine and MTX were measured at 15 time points up to 148 hours, with 10 samples collected during the first 24 hours after the start of the HDMTX infusion.ResultsDuring the first 28 hours, 81% of the pigs had increases in the concentrations of serum creatinine in one or more samples indicative of AKI (i.e., > 0.3g/dL increase). A rate of plasma MTX clearance of less than 90% during the initial 4 hours after the HDMTX infusion and a total serum creatinine increase at 6 and 8 hours after starting the infusion greater than 0.3 g/dL were predictive of AKI at 28 hours (p < 0.05 and p < 0.001, respectively). At conclusion of the infusion, pigs with a creatinine concentration more than 0.3 g/dL higher than baseline or serum MTX greater than 5,000 μmol/L had an increased risk of severe AKI.ConclusionsOur findings suggest that serum samples collected at conclusion and shortly after HDMTX infusion can be used to predict impending AKI. The pig model can be used to identify biological, environmental, and iatrogenic risk factors for HDMTX-induced AKI and to evaluate interventions to preserve renal functions, minimize acute kidney injury, and reduce systemic toxicity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2023.1240195</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2023.1240195</link>
        <title><![CDATA[Editorial: Women in onconephrology: 2022]]></title>
        <pubdate>2023-08-01T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Ala Abudayyeh</author><author>Sabine Karam</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2023.1168614</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2023.1168614</link>
        <title><![CDATA[Case Report: Immune checkpoint inhibitor–induced multiorgan vasculitis successfully treated with rituximab]]></title>
        <pubdate>2023-07-20T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Sehrish Qureshi</author><author>Naszrin Arani</author><author>Vishnu Parvathareddy</author><author>Amanda Tchakarov</author><author>Maen Abdelrahim</author><author>Maria Suarez-Almazor</author><author>Jianjun Zhang</author><author>Don Lynn Gibbons</author><author>John Heymach</author><author>Mehmet Altan</author><author>Ala Abudayyeh</author>
        <description><![CDATA[Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of cancer. ICIs have a unique side effect profile, generally caused by inflammatory tissue damage, with clinical features similar to autoimmune conditions. Acute kidney injury from ICIs has been well studied; incidence ranges from 1% to 5%, with higher incidence when combination ICI therapies are used. Although the overall reported incidence of ICI-associated glomerulonephritis is less than 1%, vasculitis is the most commonly reported ICI-related glomerulonephritis. Other biopsy findings include thrombotic microangiopathy, focal segmental glomerulosclerosis, minimal change disease, and IgA nephropathy with secondary amyloidosis. We report a case in which a woman previously treated with the PD-L1 inhibitor durvalumab for locally advanced non-small cell lung cancer with pre-existing antineutrophil cytoplasmic (anti-PR3) antibody who later developed multi-organ vasculitis after ICI exposure, which was successfully treated with rituximab, with continued cancer remission for 3 years.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2023.1043874</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2023.1043874</link>
        <title><![CDATA[The need for kidney biopsy in the management of side effects of target and immunotherapy]]></title>
        <pubdate>2023-02-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Roberta Fenoglio</author><author>Martina Cozzi</author><author>Giulio Del Vecchio</author><author>Savino Sciascia</author><author>Antonella Barreca</author><author>Alessandro Comandone</author><author>Dario Roccatello</author>
        <description><![CDATA[IntroductionThe introduction of innovative therapies, resulting from revisiting cancer as a disease of the immune system, has changed the scenario of complications. These new classes of drugs, such as targeted therapies and immune checkpoint inhibitors, assure substantial advantages in cancer therapy, despite some side effects affecting various organs, including the kidney. Histological evaluations of kidney disorders induced by targeted/immunotherapy are limited.MethodIn this study we examined the histological features of patients treated with new cancer agents who underwent a kidney biopsy for new onset kidney failure and/or urinary abnormalities.ResultsThe cohort included 30 adult patients. The most frequently administered therapies were immunotherapy (30%), targeted therapy (26.7%), immunotherapy plus targeted therapy (13.3%), immunotherapy plus chemotherapy (13.3%), targeted therapy plus chemotherapy (16.7%). The most common histological finding was tubular interstitial nephritis (30%) that was associated with acute tubular necrosis in 4 cases, and thrombotic microangiopathy (23.3%). After kidney biopsy, 16 of the 30 patients were treated according to the histological diagnosis. Fourteen patients were treated with steroids. One patient with membranous nephropathy was treated with a single dose of rituximab. A patient with severe thrombotic microangiopathy requiring dialysis received a treatment with eculizumab for 3 months. Overall some renal response was obtained in all patients treated with glucocorticoids, while complete kidney response was achieved in the patient treated with rituximab. Cancer treatment was resumed without change in 21 out of 30 patients.ConclusionKidney biopsy is critical for the management of kidney toxicities and should be strongly encouraged for patients showing adverse kidney effects of novel cancer agents.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2022.1129134</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2022.1129134</link>
        <title><![CDATA[Corrigendum: Cemiplimab for advanced cutaneous squamous cell carcinoma in kidney transplant recipients]]></title>
        <pubdate>2023-01-05T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>T. Van Meerhaeghe</author><author>J.F. Baurain</author><author>O. Bechter</author><author>C. Orte Cano</author><author>V. Del Marmol</author><author>A. Devresse</author><author>P. Doubel</author><author>M. Hanssens</author><author>R. Hellemans</author><author>D. Lienard</author><author>A. Rutten</author><author>B. Sprangers</author><author>A. Le Moine</author><author>S. Aspeslagh</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2022.1041819</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2022.1041819</link>
        <title><![CDATA[Cemiplimab for advanced cutaneous squamous cell carcinoma in kidney transplant recipients]]></title>
        <pubdate>2022-10-31T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>T. Van Meerhaeghe</author><author>J.F. Baurain</author><author>O. Bechter</author><author>C. Orte Cano</author><author>V. Del Marmol</author><author>A. Devresse</author><author>P. Doubel</author><author>M. Hanssens</author><author>R. Hellemans</author><author>D. Lienard</author><author>A. Rutten</author><author>B. Sprangers</author><author>A. Le Moine</author><author>S. Aspeslagh</author>
        <description><![CDATA[BackgroundKidney transplant recipients (KTR) are at increased risk of cancer due to chronic immunosuppression. Non-melanoma skin cancer has an excess risk of approximately 250 times higher than the general population. Moreover, in solid organ transplant recipients (SOTR) these cancers have a more aggressive behavior, with an increased risk of metastasis and death. Cemiplimab, a human monoclonal IgG4 antibody against programmed cell death (PD-1) has shown considerable clinical activity in metastatic and locally advanced cutaneous squamous cell carcinoma (cSCC) in patients for whom no widely accepted standard of care exists. Cemiplimab has therefore been approved since 2018 for the treatment of advanced cSCC. However, data regarding the use of cemiplimab in SOTR and particularly in KTR are scarce and based on published case reports and small case series. In this study, we report on the real-life outcome of cemiplimab use in a Belgian cohort of seven KTR suffering from advanced cSCC.ObjectiveTo report on the overall response rate (ORR) and safety of cemiplimab in KTR in Belgium.ResultsSeven patients suffering from advanced cSCC, treated with cemiplimab, between 2018 and 2022, in Belgium were identified. Three patients were on corticosteroid monotherapy, one patient on tacrolimus monotherapy and three patients were on at least 2 immunosuppressants at start of cemiplimab. The ORR was 42.8%, stable disease was seen in 14.3% and progressive disease was found in 42.8% of the patients, respectively. The median administered number of cycles was 12, interquartile range (IQR) 25-75 [3.5 – 13.5]. All patients were treated with surgery before administration of cemiplimab, 71.4% received additional radiotherapy and only 1 patient was treated with chemotherapy prior to receiving cemiplimab. Biopsy-proven acute renal allograft rejection was observed in one patient, who eventually lost his graft function but showed a complete tumor response to treatment. Low grade skin toxicity was seen in one patient of the cohort.ConclusionThe present case series shows that the use of cemiplimab in KTR with advanced cSCC who failed to respond to previous surgery, chemo – and/or radiotherapy treatment is associated with an ORR of 42.8% with minimal risk of graft rejection (14.3%) and good tolerance.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2022.1017921</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2022.1017921</link>
        <title><![CDATA[Immune checkpoint inhibitor related nephrotoxicity: Advances in clinicopathologic features, noninvasive approaches, and therapeutic strategy and rechallenge]]></title>
        <pubdate>2022-10-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jing Miao</author><author>Meghan E. Sise</author><author>Sandra M. Herrmann</author>
        <description><![CDATA[Immune checkpoint inhibitors (ICIs) are used increasingly to treat more than 17 cancers and have shown promising therapeutic results. However, ICI use can result in a variety of immune-related adverse events (IRAEs) which can occur in any organ, including the kidneys. Acute kidney injury (AKI) is the most common nephrotoxicity, classically related to acute interstitial nephritis. Much more diverse patterns and presentations of ICI-related kidney injury can occur, and have implications for diagnostic and therapeutic management approaches. In this review, we summarize the recently approved ICIs for cancer, the incidence and risk factors for nephrotoxicity, our current understanding of the pathophysiological mechanisms and the key clinicopathological features of ICI-related AKI, and therapeutic strategies. We also explore important knowledge that require further investigation, such as the risks/benefits of ICI rechallenge in patients who recover from an episode of ICI-related AKI, and the application of liquid biopsy and microbiome to identify noninvasive biomarkers to diagnose and predict kidney injury and guide ICI therapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2022.847847</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2022.847847</link>
        <title><![CDATA[Case Report: Roxadustat in Combination With Rituximab Was Used to Treat EPO-Induced Pure Red Cell Aplasia]]></title>
        <pubdate>2022-03-24T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Xiaoe You</author><author>Baochun Guo</author><author>Zhen Wang</author><author>Hualin Ma</author><author>Ru Zhou</author><author>Lixia Liu</author><author>Xinzhou Zhang</author>
        <description><![CDATA[Recombinant human erythropoietin (rHuEPO) is a drug given to patients who have low hemoglobin related to chronic kidney disease or other anemia-related diseases. Some patients who receive rHuEPO repeatedly develop anti-rHuEPO-neutralizing antibodies, leading to the occurrence of pure red cell aplasia (PRCA). PRCA associated with rHuEPO includes severe rHuEPO resistance, blood transfusion dependence, high serum ferritin, severe reticulocytopenia, and presence of anti-rHuEPO antibody. However, the optimal treatment of erythropoietin (EPO)-induced PRCA is unclear. Therapeutic options against it remain a major clinical challenge. Herein we report on 2 male patients with PRCA during rHuEPO treatment, who received a combination therapy of roxadustat plus rituximab but had completely different clinical outcomes. The results obtained in this study show that roxadustat in combination with rituximab could be one of the treatment options for EPO-induced PRCA, but the treatment efficacy can vary from one individual to another. Additionally, we recommend starting reticulocyte monitoring and immunosuppressive agent therapy as early as possible to shorten the course of the disease and improve the outcomes of the patients.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneph.2022.875207</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneph.2022.875207</link>
        <title><![CDATA[Levels of Soluble NKG2D Ligands and Cancer History in Patients Starting Hemodialysis]]></title>
        <pubdate>2022-03-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kei Nagai</author><author>Takashi Tawara</author><author>Joichi Usui</author><author>Itaru Ebihara</author><author>Takashi Ishizu</author><author>Masaki Kobayashi</author><author>Yoshitaka Maeda</author><author>Hiroaki Kobayashi</author><author>Kunihiro Yamagata</author>
        <description><![CDATA[BackgroundImmune dysfunction in hemodialysis patients is partially due to NK cell impairment. Ligands for NK activating receptors such as NKG2D expressed on cancer cells are involved in NK cell dysfunction and can lead to cancer development.MethodsA cohort with 370 patients who started hemodialysis (HD) was investigated. Serum levels of soluble NKG2D ligands were measured. Cancer history was defined as any cancer diagnosis at induction and hospitalization and death due to cancer during 2-year follow-up.ResultsSixty-two patients with and 308 patients without a cancer history showed mostly comparable biochemical parameters and uremic status at HD induction. Soluble MICB, ULBP-1, and ULBP-2 were detected in sera from most patients starting HD rather than MICA, the most representative NKG2D ligand. Measured NKG2D ligands, except for ULBP-1, were strongly correlated with each other. Correlations between NKG2D ligands and renal function were significant but modest in patients starting HD. Cancer history did not have any impact on levels of soluble NKG2D ligands.DiscussionEven though this investigation lacked a control cohort and serial measurement of parameters, expression patterns of NKG2D ligands were comprehensively described, and the significance of cancer in patients starting HD was elucidated for the first time. Elevated levels of soluble NKG2D ligands occurred potentially due to complex mechanisms of oxidative stress, with insufficient metabolism and excretion in a uremic milieu, but they might mask the significance of elevations in serum levels of soluble NKG2DLs in patients with a cancer history.]]></description>
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