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Paraneoplastic glomerular disease (PGD) develops from tumor cell products, leading to renal dysfunction. Unlike direct tumor effects, PGD illustrates the complex association between cancer and diverse clinical presentations and outcomes. Initially detected in a Hodgkin's disease patient, current research has defined diagnostic criteria based on PGD symptoms and cancer progression. PGDs, although rare (found in <1% of adult cancer patients with overt renal manifestations), are crucial, as they can signal cancer onset and frequently resist standard glomerulonephritis treatments. The emerging field of onconephrology studies this relationship between kidney disorders and cancers. The exact cause of many PGD cases remains unknown. This review examines PGDs, their clinicopathological features, related cancers, and mechanisms, emphasizing the need for early diagnosis and tailored treatment for kidney disease and linked cancer.
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Glomerulonefritis , Síndromes Paraneoplásicos , Humanos , Síndromes Paraneoplásicos/diagnóstico , Glomerulonefritis/diagnóstico , Glomerulonefritis/patología , Glomerulonefritis/terapia , Glomérulos Renales/patología , Glomérulos Renales/fisiopatología , Neoplasias/complicaciones , Neoplasias/diagnóstico , Enfermedad de Hodgkin/diagnóstico , Enfermedad de Hodgkin/complicaciones , Enfermedad de Hodgkin/patologíaRESUMEN
Accurate assessment of GFR is crucial to guiding drug eligibility, dosing of systemic therapy, and minimizing the risks of both undertreatment and toxicity in patients with cancer. Up to 32% of patients with cancer have baseline CKD, and both malignancy and treatment may cause kidney injury and subsequent CKD. To date, there has been lack of guidance to standardize approaches to GFR estimation in the cancer population. In this two-part statement from the American Society of Onco-Nephrology, we present key messages for estimation of GFR in patients with cancer, including the choice of GFR estimating equation, use of race and body surface area adjustment, and anticancer drug dose-adjustment in the setting of CKD. These key messages are based on a systematic review of studies assessing GFR estimating equations using serum creatinine and cystatin C in patients with cancer, against a measured GFR comparator. The preponderance of current data involving validated GFR estimating equations involves the CKD Epidemiology Collaboration (CKD-EPI) equations, with 2508 patients in whom CKD-EPI using serum creatinine and cystatin C was assessed (eight studies) and 15,349 in whom CKD-EPI with serum creatinine was assessed (22 studies). The former may have improved performance metrics and be less susceptible to shortfalls of eGFR using serum creatinine alone. Since included studies were moderate quality or lower, the American Society of Onco-Nephrology Position Committee rated the certainty of evidence as low. Additional studies are needed to assess the accuracy of other validated eGFR equations in patients with cancer. Given the importance of accurate and timely eGFR assessment, we advocate for the use of validated GFR estimating equations incorporating both serum creatinine and cystatin C in patients with cancer. Measurement of GFR via exogenous filtration markers should be considered in patients with cancer for whom eGFR results in borderline eligibility for therapies or clinical trials.
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Antineoplásicos , Creatinina , Cistatina C , Tasa de Filtración Glomerular , Neoplasias , Insuficiencia Renal Crónica , Humanos , Neoplasias/complicaciones , Neoplasias/fisiopatología , Cistatina C/sangre , Insuficiencia Renal Crónica/fisiopatología , Insuficiencia Renal Crónica/diagnóstico , Insuficiencia Renal Crónica/sangre , Creatinina/sangre , Antineoplásicos/efectos adversos , Biomarcadores/sangreRESUMEN
Acute kidney injury (AKI) is a frequently occurring complication of cardiovascular interventions, and associated with adverse outcomes. Therefore, a clear definition of AKI is of paramount importance to enable timely recognition and treatment. Historically, changes in the serum creatinine and urine output have been used to define AKI, and the criteria have evolved over time with better understanding of the impact of AKI on the outcomes. However, the reliance on serum creatinine for these AKI definitions carries numerous limitations including delayed rise, inability to differentiate between hemodynamics versus structural injury and assay variability to name a few.
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Lesión Renal Aguda , Procedimientos Quirúrgicos Cardiovasculares , Terminología como Asunto , Humanos , Lesión Renal Aguda/sangre , Lesión Renal Aguda/diagnóstico , Biomarcadores/sangre , Procedimientos Quirúrgicos Cardiovasculares/efectos adversos , Creatinina/sangre , Índice de Severidad de la EnfermedadRESUMEN
Nonalcoholic fatty liver disease is a multisystem condition with effects beyond the liver. The identification of chronic kidney disease as an independent mediator of nonalcoholic fatty liver disease or associated entity with shared cardiometabolic risk factors remains controversial and continues to draw scientific interest. With increasing prevalence of nonalcoholic fatty liver disease and lack of Food and Drug Administration approved therapies, these shared cardiometabolic risk factors have drawn significant attention. In this article, we review shared pathophysiological mechanisms between nonalcoholic fatty liver disease and chronic kidney disease along with current treatment strategies that might be useful for both disease processes.
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Enfermedad del Hígado Graso no Alcohólico , Insuficiencia Renal Crónica , Estados Unidos , Humanos , Enfermedad del Hígado Graso no Alcohólico/diagnóstico , Factores de Riesgo Cardiometabólico , Fenómenos Fisiológicos Celulares , Insuficiencia Renal Crónica/epidemiologíaRESUMEN
Introduction: Percutaneous kidney biopsy is the gold standard method to reach a precise diagnosis in most medical kidney diseases, which positively impacts patient care by personalizing the treatment. Accurate diagnosis in the pathology report for medical kidney diseases requires clinicopathological correlation, and clinical data is not always reachable to the nephropathologist. This study aimed to create a standardized, paperless requisition form compatible with medical renal biopsies. Methods: An initial form was prepared for native and allograft renal biopsies according to the current classification of medical kidney diseases. We invited 33 nephropathologists working in Canadian healthcare institutions to answer survey questions about the need to include a particular aspect of clinical information. According to the responses, we modified the experimental form. Eighty nephrologists were asked to complete a clinical data-collecting form given out as PDF files. The time for completing the form and clinicians' satisfaction were assessed. Results: The experimental form survey was answered by 20 out of 33 nephropathologists (61%) from 14 Canadian healthcare centers. The agreement rate on the questions was from 38.89% to 100.00% (average 83.33% and 77.14% for the native and the allograft section, respectively). Seventeen out of 80 nephrologists and their assistants (21%) responded by completing 22 PDF forms. The time required to finish a PDF form was 10.4 min on average. Nephrologists considered the form time-consuming and suggested making it more clinically relevant. Only seven nephrologists responded to the satisfaction survey; four (57%) were satisfied. Conclusions: Medical information is critical in renal pathology diagnoses. A uniform paperless clinical data requisition form was evolved through an agreement by Canadian nephropathologists.
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Onconephrology is an upcoming and expanding subspecialty that deals with the intersections between hematology/oncology and nephrology. With the paradigm shift in the understanding of cancer immunobiology and mechanisms of oncotherapeutic drug toxicities, it is important for a nephrologist to have a sound understanding of this field. Over the last 5 years, there have been immense developments in our understanding of kidney-related adverse events from various targeted, immuno- and cellular-based therapies. Pathogenic mechanisms of electrolyte imbalance, hypertension (oncohypertension), and AKI from multiple forms of cancer therapies have been explored. Significant research has also been conducted in the field of transplant onconephrology. In this review, we have tried to assimilate the most recent updates in the last 2 years in this ever-growing and fascinating field.
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Antineoplásicos , Neoplasias , Nefrología , Humanos , Antineoplásicos/uso terapéutico , Neoplasias/tratamiento farmacológico , Oncología Médica , RiñónRESUMEN
Graphical Abstract.
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Advances in cancer therapy have significantly improved overall patient survival; however, AKI remains a common complication in patients with cancer, occurring in anywhere from 11% to 22% of patients, depending on patient-related or cancer-specific factors. Critically ill patients with cancer as well as patients with certain malignancies (e.g., leukemias, lymphomas, multiple myeloma, and renal cell carcinoma) are at highest risk of developing AKI. AKI may be a consequence of the underlying malignancy itself or from the wide array of therapies used to treat it. Cancer-associated AKI can affect virtually every compartment of the nephron and can present as subclinical AKI or as overt acute tubular injury, tubulointerstitial nephritis, or thrombotic microangiopathy, among others. AKI can have major repercussions for patients with cancer, potentially jeopardizing further eligibility for therapy and leading to greater morbidity and mortality. This review highlights the epidemiology of AKI in critically ill patients with cancer, risk factors for AKI, and common pathologies associated with certain cancer therapies, as well as the management of AKI in different clinical scenarios. It highlights gaps in our knowledge of AKI in patients with cancer, including the lack of validated biomarkers, as well as evidence-based therapies to prevent AKI and its deleterious consequences.
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Lesión Renal Aguda , Carcinoma de Células Renales , Neoplasias Renales , Humanos , Enfermedad Crítica , Lesión Renal Aguda/epidemiología , Lesión Renal Aguda/etiología , Lesión Renal Aguda/terapia , Biomarcadores , Carcinoma de Células Renales/complicaciones , Neoplasias Renales/complicacionesRESUMEN
Thrombotic microangiopathies (TMAs) represent a complex interaction of endothelial and podocyte biology, nephron physiology, complement genetics, and oncologic therapies with host immunology. The complexity of various factors, such as molecular causes, genetic expressions, and immune system mimicking, along with incomplete penetrance, make it difficult to find a straightforward solution. As a result, there may be variations in diagnosis, study, and treatment approaches, and achieving a consensus can be challenging. Here, we review the molecular biology, pharmacology, immunology, molecular genetics, and pathology of the various TMA syndromes in the setting of cancer. Controversies in etiology, nomenclature, and points requiring further clinical, translational, and bench research are discussed. Complement-mediated TMAs, chemotherapy drug-mediated TMAs, TMAs in monoclonal gammopathy, and other TMAs central to onconephrology practice are reviewed in detail. In addition, established and emerging therapies within the US Food and Drug Administration pipeline subsequently are discussed. Finally, a comprehensive review of critical areas of onconephrology clinical practice is presented as practical value to the clinical practitioner and seeds of investigation to be sown among the community of atypical hemolytic uremic syndrome researchers.
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Síndrome Hemolítico Urémico Atípico , Púrpura Trombocitopénica Trombótica , Microangiopatías Trombóticas , Humanos , Púrpura Trombocitopénica Trombótica/diagnóstico , Púrpura Trombocitopénica Trombótica/terapia , Microangiopatías Trombóticas/etiología , Microangiopatías Trombóticas/terapia , Síndrome Hemolítico Urémico Atípico/genética , Proteínas del Sistema Complemento , Diagnóstico DiferencialRESUMEN
Over the last three decades, advancements in the diagnosis, treatment, and supportive care of patients with cancer have significantly improved their overall survival. However, these advancements have also led to a higher rate of cancer-related complications. Acute kidney injury (AKI) and chronic kidney disease (CKD) are highly prevalent in patients with cancer, and they are associated with an increased risk of all-cause mortality. This bidirectional interplay between cancer and kidney, termed "the kidney-cancer connection" has become a very active area of research. This review aims to provide an overview of some of the most common causes of AKI in patients with cancer. Cancer therapy-associated AKI is beyond the scope of this review and will be discussed separately.
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Over the past 2 decades, significant research and advancements have been made in oncology and its therapeutics. Thanks to novel diagnostic methods, treatments, and supportive measures, patients with cancer live longer and have a better quality of life. However, an unforeseen consequence of this progress has been increasing medical complications, including acute kidney injury. The purpose of this review is to provide an overview of the epidemiology and most common causes of acute kidney injury in patients with cancer unrelated to oncological treatment.
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Lesión Renal Aguda , Trasplante de Células Madre Hematopoyéticas , Neoplasias , Microangiopatías Trombóticas , Lesión Renal Aguda/epidemiología , Lesión Renal Aguda/etiología , Lesión Renal Aguda/terapia , Trasplante de Células Madre Hematopoyéticas/efectos adversos , Trasplante de Células Madre Hematopoyéticas/métodos , Humanos , Neoplasias/complicaciones , Neoplasias/epidemiología , Neoplasias/terapia , Calidad de Vida , Microangiopatías Trombóticas/etiologíaRESUMEN
Cancer is one of the leading causes of death worldwide. With the introduction of newer chemotherapeutic agents, targeted therapies, and immunotherapy, the prognosis and survival of patients with cancer has remarkably improved. As a result, patients are living longer and experiencing long-term cardiovascular complications. Hypertension is an important risk factor for cardiovascular diseases. Patients with malignancy have multiple etiologies of hypertension development, worsening, or association. This is because of the complex interplay between cancer type, chemotherapeutic agent, patient age, antihypertensive agent, and preexisting comorbidities in the etiology and pathogenesis of hypertension. Management of hypertension in patients with cancer requires accurate blood pressure measurement and considering factors such as adjuvant therapy and cancer-related pain. There are no set guidelines for management of hypertension in this unique cohort, and the therapy should be individualized based on the treatment guidelines for the general population. Onco-hypertension is an emerging subspeciality and entails a multidisciplinary approach between oncology, primary care physicians, nephrology, and cardiology.
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Antineoplásicos , Cardiología , Hipertensión , Neoplasias , Antihipertensivos/uso terapéutico , Antineoplásicos/efectos adversos , Humanos , Hipertensión/complicaciones , Hipertensión/terapia , Oncología Médica , Neoplasias/tratamiento farmacológicoRESUMEN
BACKGROUND: Apolipoprotein L1 gene (APOL1) variants predispose to nondiabetic kidney disease in African American (AA) patients. Here, we share our experience with APOL1 genotyping of AA potential living kidney donors and offer a perspective on its utility and cost-effectiveness in this population. METHODS: Since May 2017, all potential AA living kidney donors at our center underwent APOL1 genotyping early in the donor evaluation process. APOL1 high-risk individuals were declined, whereas those with low-risk genotype continued with further evaluation and testing. RESULTS: One out of 26 potential donors had high-risk genotype and was therefore declined. The rest were eligible to continue the donor evaluation process and 7 of them underwent donor nephrectomy without any complications. A crude cost analysis utilizing our sample suggested probable cost-effectiveness of APOL1 genotyping as it can prevent earlier onset of chronic kidney disease in AA donors. CONCLUSION: We propose a role for systematically incorporating APOL1 genotyping in the evaluation and informed consent process of potential AA donors while acknowledging the controversial considerations associated with it.
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Apolipoproteína L1/genética , Negro o Afroamericano/genética , Selección de Donante/economía , Selección de Donante/métodos , Análisis Costo-Beneficio , Genotipo , Técnicas de Genotipaje , Humanos , Donadores VivosRESUMEN
Acute kidney injury in acute decompensated heart failure leads to increased readmissions regardless of being transient or sustained at the time of discharge. Timely identification of acute kidney injury and worsening heart failure in patients with acute decompensated heart failure is of utmost importance to optimize different components of heart failure treatment. Acute kidney injury is a strong predictor of poor outcomes and early death in patients with pulmonary artery hypertension and acute right-sided heart failure. Extracorporeal ultrafiltration should not be used as an initial or alternative to diuretic therapy. It should be reserved for diuretic-resistant individuals.