Search

Quantitative and qualitative analyses of urinary proteins were carried out in order to follow permeability changes of the glomeruli during the course of hypertension. Benign and malignant hypertensive cases were separated by the presence of "salt-loosing-syndrome" in the latters. Six hours urinary protein excretion increased significantly from the 2nd postoperative week only in the malignant hypertensive group. Using sodium dodecyl sulfate gel electrophoresis glomerular proteinuria of selective type was commonly found in the benign, moderately unselective type in the malignant hypertensive group respectively. The findings are in accordance with the "double filter" theory of glomerular barrier.

Urinary proteins were studied by quantitative and electrophoretic methods in 6-month-old spontaneously hypertensive rats and normotensive controls. Protein analysis was carried out before and after adrenalectomy and during gluco- or mineralocorticoid treatment. Urinary protein excretion was significantly diminished after adrenalectomy both in the hypertensive and control groups. The original level of protein excretion was restored only by glycocorticoid treatment. Normal or pathologic electrophoretic pattern of urinary proteins was not influenced by the experimental procedure. Moderately non-selective glomerular proteinuria persisted in the spontaneously hypertensive rats referring to a definitely damaged glomerular barrier. One protein fraction of about 130,000 dalton molecular weight disappeared from the urine of hypertensive animals after adrenalectomy and reappeared after glucocorticoid treatment only. This fraction probably represents the dimeric form of albumin. Quantitative changes of urinary protein excretion can be explained by haemodynamic factors.

Ferritin deposition in the tubular epithelial cells developing after intravenous ferritin injection was investigated in the kidneys of 25 Goldblatt hypertensive rats and of 10 normotensive controls. The phenomenon was detected only in the hypertensive animals. Light microscopic and planimetric data indicate an increased permeability of the glomerular filter and contradict a degenerative damage of the tubular epithelial cells as a primary cause. Ferritin after having crossed the glomerular filter is partly reabsorbed by the tubular epithelium and partly excreted by the urine. The high iron content of the urine and the ferritin detected electrophoretically in it also proves this explanation.

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.