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[Aminoglycoside nephropathy]
Abstract:
Aminoglycosides lead to an increase of number and size of secondary lysosomiotics in the cells of the renal size of secondary lysosomes in the cells of the renal tubuli. Myeloid bodies appear in the lysosomes. As a sequel of the aminoglycoside antibiotics accumulated in the kidney a rhythmic change of the function of the cells of the tubuli with hyperenzymuria, decreased reabsorption of low molecular weight proteins, decreased concentration of urine and decreased glomerular filtration develops. Despite continued drug exposure these deviations are reversible. Simultaneous application of cephalotin, dextran or furosemid increase the toxic effect. A summarizing hypothesis concerning the aminoglycoside-induced nephropathy is presented which takes into consideration the specific receptor binding of the aminoglycosides at the membrane of the tubulus, their accumulation in the lysosomes and their ways in the cell of the tubulus. The lysosomes are regarded as primary working point of the aminoglycosides.
Insights
Aminoglycoside antibiotics cause kidney tubule cell damage, increasing lysosomes and impairing kidney function. These effects are reversible, but co-administration with other drugs exacerbates toxicity.
Area of Science:
- Nephrology
- Cell Biology
- Pharmacology
Context:
- Aminoglycoside antibiotics are widely used but can cause nephrotoxicity.
- Kidney tubule cells are a primary target for aminoglycoside-induced damage.
- Lysosomes play a critical role in cellular response to aminoglycosides.
Purpose:
- To elucidate the cellular mechanisms underlying aminoglycoside-induced nephropathy.
- To investigate the role of lysosomes in aminoglycoside accumulation and toxicity.
- To present a hypothesis on aminoglycoside nephrotoxicity.
Summary:
- Aminoglycosides increase the number and size of secondary lysosomes in renal tubule cells, leading to myeloid body formation.
- Accumulation of aminoglycosides in the kidney results in altered tubule cell function, including hyperenzymuria, reduced protein reabsorption, and decreased urine concentration.
- Observed functional deviations are reversible upon continued drug exposure, though co-administration with cephalotin, dextran, or furosemide potentiates toxicity.
Impact:
- This research identifies lysosomes as the primary site of action for aminoglycosides in the kidney.
- Understanding these mechanisms can inform strategies to mitigate aminoglycoside nephrotoxicity.
- The findings contribute to a comprehensive hypothesis of aminoglycoside-induced kidney damage, considering cellular uptake and lysosomal accumulation.