Higher excretion of urinary bound amino acids in infants: probably related to protein-anabolic effect of growth hormone.

Concentrations of bound amino acids in urine were found to be markedly higher in infants than in children over 4 years of age. And it was also found that bound amino acid levels in plasma were increased in infants and young children than in adults. Urinary excretion of bound amino acids was increased in hypopituitary dwarf after one day of intramuscular injection of human growth hormone. A possibility was advanced that an increased excretion of bound amino acids of the overflow type observed in infants was due to active protein biosynthesis stimulated by growth hormone of which plasma levels have been reported to be high in infancy.

Morphological changes in an early phase of norepinephrine-induced acute renal failure in unilaterally nephrectomized dogs.

The morphological factors contributing to the reduction GFR in an early phase of NE-induced ARF (0.75 microgram/kg/min) were evaluated by comparing renal morphology at the end of NE infusion with that 2 hr later in unilaterally nephrectomized dogs. GFR 2 hr after NE infusion was reduced to 50% of the preinfusion level in a 30 min infusion group (N = 6), to 13% in a 60 min infusion group (N = 7), and to 2% in a 120 min infusin group (N = 5). On the other hand, simultaneous RBF was not significantly reduced in any group. Dilated PT lumina filled with eosinophilic granular materials in paraffin sections fixed in Zenker-Formol or with impacted swollen blebs in Epon sections fixed in diluted Karnovsky's solution and osmium were found diffusely immediately following 60 and 120 min NE infusion, but patchily after 30 min infusion. Similar changes were found 2 hr after the infusion, except that some PTs came to have dilated but transparent lumina in the 60 and 120 min NE infusion groups. Electron microscopic studies revealed that a part of the membrane-bounded cytoplasm of PT cells extruded into the tubular lumen and became impacted swollen blebs during NE-induced ischemia. There was no prominent foot process fusion in any group. It is concluded that the tubular obstruction by impacted swollen blebs generated in PT during ischemia is a major factor responsible for the reduction in GFR in the early phase of NE-induced ARF.

Plasma renin activity in acute renal failure induced by norepinephrine infusion in unilaterally nephrectomized dogs.

Plasma renin activity was determined by bioassay prior to, during and following a 2-hour infusion of norepinephrine into the renal artery in unilaterally nephrectomized dogs in order to examine the role of renin-angiotensin system in norepinephrine-induced ARF. ARF was induced in 5 of 8 dogs receiving 0.75 microgram/kg/min of norepinephrine, but not in the remaining 3 dogs and 2 dogs infused with 0.6 and 0.4 microgram/kg/min of norepinephrine. There proved no difference in plasma renin activity in renal venous blood between the dogs with and without ARF when followed up to 2 h after the discontinuation of the infusion. The same results were obtained when the plasma renin activity in the foreleg vein was followed at 24, 48 and 72 h after the infusion. The renin-angiotensin system does not seem to contribute to the reduction of renal function in norepinephrine-induced ARF in dogs.

Effect of oral administration of calcium carbonate, aluminum hydroxide gel and dihydrotachysterol on renal acidosis.

The effects of oral administration of calcium carbonate, aluminum hydroxide gel, dihydrotachysterol (DHT) and sodium bicarbonate on metabolic acidosis and plasma calcium and phosphate were studied in 7 patients with chronic renal failure. Single administration of calcium carbonate alleviated the acidosis and increased the urinary bicarbonate excretion. These effects were potentiated when aluminum hydroxide gel was administered in combination with calcium carbonate. The plasma calcium was increased by this combination therapy. The effects of these two agents on acidosis and plasma calcium were further enhanced by the additional administration of DHT. Urinary bicarbonate excretion was less during the treatment with aluminum hydroxide gel and calcium carbonate than with aluminum hydroxide gel and sodium bicarbonate, when the excretions were compared at the similar concentrations of plasma bicarbonate. Aluminum hydroxide gel and DHT are likely to enhance the effect of calcium carbonate, which works as an alkalinizing salt on acidosis, probably through increasing calcium absorption in the intestine. And the three agents suppress the leak of bicarbonate into the urine contributing to the improvement of acidosis.

Cadmium-induced proximal tubular dysfunction in a cadmium-polluted area.

Health examinations were performed in 147 people living in a cadmium-polluted area, Kosaka Town, Japan. 33 of 147 residents had some indications of proximal tubular dysfunction, such as renal glucosuria, tubular proteinuria, and aminoaciduria, and 10 of them were diagnosed as having multiple proximal tubular dysfunctions. Detailed examinations revealed that none of the cases had any causal diseases other than chronic cadmium poisoning. Residents' mean cadmium intake and mean urinary cadmium concentration were over 3 times as high as those in control areas. From these findings, renal lesions identified in these residents were concluded as chronic cadmium poisoning induced by environmental cadmium pollution.

Circulating plasma volume and renal function.

The relationships of circulating plasma volume (PV) to effective renal plasma flow and glomerular filtration rate (GFR) were investigated in reference to their interrelated changes induced by upright posture in normal subjects and patients with chronic glomerulonephritis. The following relation was obtained: (percentage change in GFR) = k(percentage change in PV). The values of k were 3.4 for the normal and 3.1 for the patients. There was no statistically significant difference between the two. On account of the above relation the recumbent level of glomerular filtration rate (GFR)r was derived from the recumbent level of circulating plasma volume (PV)r as follows: (GFR)r = Kp [(PV)r]k, where Kp is a constant. On the other hand, the decreases (percentage) in effective renal plasma flow were biphasically related to those in PV. Mean arterial pressure rose in upright posture in many cases, but its changes (percentage) showed no correlation with the changes (percentage) in GFR. These results suggest that in a small decrease in PV, GFR does not decrease with the fall in mean arterial pressure, but with the power function of PV. The possible mechanisms of these changes in renal function are examined with special reference to the structure of renal arterial system.

Renal impairment in patients with paroxysmal nocturnal hemoglobinuria.

Three patients with paroxysmal nocturnal hemoglobinuria accompanied by chronic renal lesions were studied. All the cases had histories of severe hemolytic anemia and repeated hemoglobinuria. The biopsy specimen of the kidney of two patients (Case 1 and Case 2) showed interstitial nephritis. Renal glucosuria, tubular proteinuria, increased urate clearance (Case 2) and reduced tubular reabsorption of phosphate (Case 3) were revealed in Case 2 and Case 3, suggesting renal tubular impairment. From the nephrological point of view, hemodynamic alteration resulting from intravascular hemolysis and severe persistent chronic anemia may primarily be responsible for the renal impairment.