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Related Concept Videos

Toxic Reactions: Overview01:26

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When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
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Acute Kidney Injury II: Pathophysiology01:29

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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
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Renal Failure: Dose Adjustments01:11

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In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
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Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

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Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
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Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

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Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
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Chronic Kidney Disease II: Clinical Manifestations01:24

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Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
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Updated: Oct 8, 2025

Removal of Trace Elements by Cupric Oxide Nanoparticles from Uranium In Situ Recovery Bleed Water and Its Effect on Cell Viability
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Renal Toxicity.

Maen Abdelrahim1, Ala Abudayyeh2

  • 1Institute of Academic Medicine and Weill Cornell Medical College, Houston Methodist Cancer Center, Houston Methodist Cancer Center, Houston, TX, USA.

Advances in Experimental Medicine and Biology
|January 1, 2022
PubMed
Summary
This summary is machine-generated.

Checkpoint inhibitors (CPI) improve cancer survival but cause kidney toxicities like nephritis and glomerulonephritis. This review covers CPI-related renal issues, autoimmune disease reactivation, and transplant rejection, offering insights into mechanisms and treatments.

Keywords:
Acute interstitial nephritisAutoimmune disease inductionImmune-related adverse eventsOrgan transplant rejectionRenal cell cancer

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Area of Science:

  • Nephrology
  • Oncology
  • Immunology

Background:

  • Immunotherapy, specifically checkpoint inhibitors (CPI), has improved cancer survival rates.
  • CPI use is associated with significant organ-specific toxicities, particularly affecting the kidneys.
  • Understanding these renal toxicities is crucial for managing cancer patients undergoing immunotherapy.

Purpose of the Study:

  • To review the spectrum of renal toxicities associated with checkpoint inhibitors (CPI).
  • To discuss proposed mechanisms, diagnostic approaches, and treatment strategies for CPI-induced nephrotoxicity.
  • To explore the implications of CPI use in patients with pre-existing autoimmune diseases and chronic kidney disease (CKD), including renal cell cancer, and evaluate transplant rejection risks.

Main Methods:

  • Literature review of studies on checkpoint inhibitor-related renal toxicities.
  • Analysis of proposed mechanisms for various nephropathies (e.g., tubulointerstitial nephritis, glomerulonephritis).
  • Evaluation of data from single-center and multicenter retrospective studies on transplant rejection and autoimmune disease reactivation.

Main Results:

  • Checkpoint inhibitors can induce a range of renal pathologies, including acute tubulointerstitial nephritis and glomerulonephritis.
  • CPI use may trigger reactivation of pre-existing autoimmune conditions, especially in the context of renal cell cancer and CKD.
  • Available data suggest an increased risk of transplant rejection in patients treated with CPI.

Conclusions:

  • Checkpoint inhibitor therapy, while beneficial for cancer treatment, necessitates careful monitoring for renal adverse events.
  • Further research is needed to elucidate mechanisms and optimize management of CPI-induced nephrotoxicity and related complications.
  • Clinicians must consider the risks of autoimmune reactivation and transplant rejection when prescribing CPIs.