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.