Glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and humoral factors were simultaneously examined before and after a 50-gram oral protein load in 12 healthy controls and 12 nephrotic patients. The protein load led to rises in GFR with unchanged filtration fraction in both groups although the rate of increase in GFR was greater in the former. The levels of blood urea nitrogen, serum osmotic pressure, plasma glucagon and serum insulin, but not plasma angiotensin II, were significantly elevated following the protein load. The increase in GFR after the protein load appears to be mainly caused by increased ERPF and afferent arteriolar vasodilation.

Histological and ultrastructural studies of juxtaglomerular cells (JGC) were performed in a patient with pseudo-Bartter’s syndrome due to furosemide abuse. The biopsy done before the treatment revealed a large number of secretory granules and mitochondria, dilated rough endoplasmic reticulum and a well-developed Golgi apparatus in JGC. The JGC granules, some of which contained crystalloid structures showed various shapes and sizes. In the biopsy carried out after the cessation of furosemide intake, these morphological changes were markedly improved with a reduced activity of the renin-angiotensin system. The characteristic changes of JGC may be valuable in determing the functional and morphological interrelations of this disorder.

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Plasma renin activity (PRA) was determined in 20 normal young adult controls, in 50 young patients with essential hypertension, and in 96 older patients with essential hypertension. The results obtained showed that PRAwas significantly increased over the first five years following the onset of hypertension in young hypertensive patients who had afamily history of hypertension. In contrast, in the older hypertensive patients PRAwas significantly decreased when compared to normal controls and young hypertensive patients.These data may indicate that the renin-angiotensin system is enhanced during the developmental stages of human essential hypertension and suppressed afterwards.

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