Nephrotoxicity
Nephrotoxicity - Related Videos
04:18
Intravenous Microinjection of Nephrotoxins into Zebrafish Embryo: A Technique to Deliver Nephrotoxic Agents into the Bloodstream of Zebrafish Embryo
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2023
This video demonstrates the intravenous microinjection of nephrotoxins into the tail vein of a zebrafish embryo to study their chemical effects on renal function.
07:06
Isolation of Primary Human Proximal Tubule Epithelial Cells and Their Use in Creating a Microphysiological Model of the Renal Proximal Tubule
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Cited by 3 •
2025
We present an optimized protocol for processing whole human kidneys to isolate and culture primary renal proximal tubule epithelial cells and the application of these cells in a three-dimensional, microfluidic, microphysiological platform to recapitulate the renal proximal tubule.
15:55
Intravenous Microinjections of Zebrafish Larvae to Study Acute Kidney Injury
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Cited by 83 •
2010
We describe a technique of microinjecting the aminoglycoside, gentamicin, into 2 days post-fetilization (dpf) zebrafish larvae to induce acute kidney injury (AKI). We also describe a method for whole mount immunohistochemistry, plastic embedding and sectioning of zebrafish larvae to visualize the AKI mediated damage.
07:27
Laser Ablation of the Zebrafish Pronephros to Study Renal Epithelial Regeneration
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Cited by 43 •
2011
Acute kidney injury (AKI) in humans is a common clinical problem caused by damage to the epithelial cells that comprise kidney nephrons, and AKI is associated with high mortality rates of 50-70%1. Following epithelial cell destruction, nephrons have a limited ability to regenerate, though the mechanisms and limitations that guide this phenomenon remain poorly understood. In this video article, we describe our technique for targeted laser ablation of kidney nephron cells in the zebrafish...
06:38
Early Detection of Drug-Induced Renal Hemodynamic Dysfunction Using Sonographic Technology in Rats
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Cited by 14 •
2016
Early stage hemodynamic dysfunction is critical to the development of kidney disease. Yet, detection methodologies are limited. Recent advances in sonography provide a noninvasive, accurate option for early detection of kidney injury. This study outlines a step-by-step, sonographic methodology for detecting kidney dysfunction using a drug-induced nephrotoxicity rat model.
FAQs
Nephrotoxic agents can impair the kidneys through several distinct pathways. They may directly injure tubular epithelial cells, reduce renal blood flow, obstruct urine flow, or initiate inflammation and oxidative stress. Because these mechanisms affect different parts of renal function, evaluating the likely pathway can help clinicians interpret kidney injury and select appropriate monitoring or preventive measures.
Tubular epithelial cells are vulnerable targets because direct injury can interfere with renal processes that support waste removal and fluid balance. Reduced renal blood flow creates a separate mechanism by limiting kidney perfusion, while urine-flow obstruction can impair elimination. Recognizing which process is involved helps explain changes in renal function and informs clinical assessment.
Inflammation and oxidative stress are additional mechanisms through which toxic exposures can disrupt kidney tissue. Rather than acting only through direct cellular damage, these processes can amplify renal injury and contribute to either acute or chronic kidney impairment. Their involvement explains why nephrotoxicity may persist beyond the initial exposure and why mechanism-based research matters.
Clinical assessment commonly combines serum creatinine, estimated glomerular filtration rate, and urinary biomarkers. Serum creatinine and estimated filtration provide information about renal function, while urinary biomarkers can add evidence of kidney injury. Using these measures supports recognition of harmful effects, guides medication dose adjustment, and helps clinicians monitor patients receiving potentially nephrotoxic therapies.
Monitoring is particularly relevant when patients receive antibiotics, chemotherapy, analgesics, or radiographic contrast agents. These clinical contexts create a need to evaluate renal function and consider dose adjustment to reduce harm. Applying the same assessment principles across different therapies helps clinicians balance the intended treatment benefit with the possibility of impaired medication clearance or kidney injury.
A practical approach links exposure with renal monitoring and dose adjustment. Clinicians can track serum creatinine, estimated glomerular filtration rate, and urinary biomarkers while using the results to support safer treatment decisions. At the research level, understanding pathways such as tubular injury, reduced blood flow, inflammation, and oxidative stress guides development of less harmful therapies.