Renal tubular ferritin-uptake, a consequence of the increased glomerular permeability, during the benign and malignant course of renal hypertension in rats.
Tubular uptake of ferritin given intravenously was studied in the right and left kidneys of 74 Goldblatt-hypertensive rats. Previous observations pointed out the pathologically enhanced permeability of glomerular barrier as the cause of the phenomenon. It was assumed, that the extent of tubular areas taking up ferritin, refers to the number of damaged glomeruli. The process was characterized semiquantitatively by planimetric measurements and determination of the non-hemin iron concentration in the renal cortical tissue. A more frequent and extensive tubular ferritin-uptake (and glomerular damage) was bilaterally recorded in the kidneys of malignant hypertensive rats in comparison to the benign ones. The development of the phenomenon in the clamped kidneys, being defended from high blood pressure, suggests a humoral factor behind the enhanced glomerular permeability. Saline intake has a beneficial effect on the glomerular damage similar to the hypertensive angiopathy.
D000818:Animals; D005293:Ferritins / Q000378:metabolism; D006977:Hypertension, Renal / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000503:physiopathology*; D007684:Kidney Tubules / Q000378:metabolism; D008297:Male; D010539:Permeability; D051381:Rats
D005293:Ferritins