Related Experiment Video
Updated: Jul 20, 2026

Laser Ablation of the Zebrafish Pronephros to Study Renal Epithelial Regeneration
Published on: August 29, 2011
Renal tubular damage without glomerular damage after cytotoxic drugs and aminoglycosides
Abstract:
Cytotoxic agents and aminoglycosides when given for a maximum of eleven days damaged the renal tubules as indicated by an increased urinary beta 2-microglobulin (beta 2-m), N-acetyl-beta-D-glucosaminidase (NAG) and total protein. Methotrexate (MTX) caused the greatest changes among the cytotoxic agents studied. Prophylactic doses of aminoglycosides in surgical patients also caused tubuloproteinuria. The tubular damage was greatest when aminoglycosides were given to treat septicaemia complicating haematological malignancies in patients who had previously had cytotoxic drugs. However, even in these patients there was no evidence of glomerular failure or increased glomerular permeability seven days after beginning chemotherapy.
Insights
Cytotoxic drugs and aminoglycosides can cause kidney damage, indicated by elevated urinary biomarkers. Methotrexate showed the most significant effects, while aminoglycosides also caused protein in urine, especially in vulnerable patients.
Area of Science:
- Nephrology
- Oncology
- Pharmacology
Background:
- Cytotoxic agents and aminoglycosides are commonly used in cancer therapy and for treating infections.
- Renal toxicity is a known side effect of these drug classes.
- Early detection of kidney damage is crucial for patient management.
Purpose of the Study:
- To evaluate the impact of cytotoxic agents and aminoglycosides on renal tubular function.
- To identify specific drugs causing the most significant tubular damage.
- To assess the risk factors for drug-induced kidney injury in vulnerable patient populations.
Main Methods:
- Monitoring urinary biomarkers: beta 2-microglobulin (beta 2-m), N-acetyl-beta-D-glucosaminidase (NAG), and total protein.
- Assessing renal function in patients receiving cytotoxic drugs and/or aminoglycosides for up to eleven days.
- Comparing the degree of tubular damage across different drug regimens and patient groups.
Main Results:
- Both cytotoxic agents and aminoglycosides led to increased urinary beta 2-m, NAG, and total protein, indicating renal tubular damage.
- Methotrexate (MTX) induced the most pronounced tubular changes among the cytotoxic agents studied.
- Aminoglycosides, even at prophylactic doses, caused tubuloproteinuria, with the most severe damage observed in patients with hematological malignancies receiving them for sepsis post-chemotherapy.
- No evidence of glomerular damage or increased glomerular permeability was found seven days after chemotherapy initiation.
Conclusions:
- Short-term administration of cytotoxic agents and aminoglycosides can cause significant renal tubular injury.
- Methotrexate and aminoglycosides are key agents associated with this toxicity.
- Vulnerable patient groups, such as those with hematological malignancies undergoing chemotherapy and treated for sepsis, are at higher risk for aminoglycoside-induced nephrotoxicity.
Related Concept Videos
Nephrons
Kidney Transplant II: Surgical Procedure
Acute Kidney Injury I: Introduction
Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury III: Clinical Manifestations
Acute Kidney Injury IV: Diagnostic Studies and Prevention

