Functional distention of the kidney in perinephritic hypertension

One kidney of dogs was wrapped in collodion-soaked bandages and the other removed. This caused malignant hypertension, and usually, fatal uremia in about seven days. The fluids draining from the incarcerated kidneys, after the artery and vein had been simultaneously clamped, were analyzed for volumes and hematocrits a few days postoperatively. The volume draining was reduced to 18 ml. per 100 Gm. of functionally distended kidney, as compared with 31 ml. per cent for normal dogs or for dogs after uninephrectomy. Both vascular blood and interstitial fluid were involved in this reduction. A reduction to 21 ml. per cent was found compatible with life. But a reduction to 16 ml. per cent was incompatible with life, for the animals soon died in fatal uremia. Severe reduction in the volume of interstitial fluid was apparently the critical change in the latter case. It is the reduction in functional distention, it is postulated, which is the stimulus to the kidney's own feed-back mechanism of renin secretion; this usually restores functional distention to normal by inflating the kidney with a higher blood pressure. But in the present experiment, this was impossible because of the straight-jacketing effect of the incarcerating collodion hull. The failure of distention then led to malignant hypertension, and finally, when hypertension was extreme, to the inflexible behavior of the kidney which is characteristic of fatal uremia. At autopsy, the animals were found to have the massive necrotizing arteriolitis characteristic of death with malignant hypertension. However, in the kidneys there was no histopathologic change. Evidently, the renal morphologic change responsible for the hypertension, and also for the uremia, was a functional change only: it could not be visualized by conventional histopathologic techniques. The theory is proposed that the critical hemodynamic defect in the kidney that leads to renal hypertension is reduction in the kidney's natural distention. This may happen in a variety of ways: by an incarcerating hull, as in the present experiment; or by partial arterial constriction, with consequent reduction in the inflating action of the blood pressure; or by the constraining effect of cicatrization and contraction in renal inflammation; or by decline in the kidney's natural elasticity with age. All lead to the same response of formation of angiotensin (and other still obscure reactions) which induces hypertension.