Renal parenchymal malakoplakia. An unusual cause of renal failure.
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Biomedical subjects
Publications and source records attributed to F D McDonald.
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These experiments were performed to test if heparin inhibits the production of angiotensin I from rat renin substrate acted upon by either rat or hog renin. Substrate was prepared from the plasma of nephrectomized rats; commercially prepared hog renin and heparin (0-50 units/ml, final concentration) were added and angiotensin I production was measured by radioimmunoassay following incubation of the mixture at 37-38 degrees C for 30 min. Heparin had no effect on the radioimmunoassay for angiotensin I, nor on the Vmax nor the Km of the renin-renin substrate reaction. Heparin (0 and 50 units/ml, final concentration) was added to rat plasma which contained renin and renin substrate. No effect of heparin on the rate of production of angiotensin I was observed in this system. In conclusion, rat and hog renin are not inhibited by heparin within the range of concentrations used.
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This study was undertaken to evaluate the effect of dopamine (D) on renal water excretion. Intravenous (i.v.) infusion of D (7.5 microgram/kg per min) was associated with a significant, reversible increase in free water excretion (CH2O) and a decrease in urinary osmolality (Uosmol). These changes, however, were associated with significant increases in renal blood flow (RBF), glomerular filtration rate (GFR), and urinary sodium excretion (UNaV). These increases could have been responsible for the diuretic response to D. To examine whether D has a direct effect on vasopressin (ADH) release, D was infused into one common carotid artery at a dose equal to one-fourth the i.v. dose. No effects on CH2O and Uosmol were observed. To examine whether D might have an antagonistic effect on ADH a single bolus of ADH (100 mU) was given to the same hypophysectomized dogs with and without D infusion. The antidiuretic response to ADH was the same, whether or not D was given concomitantly. The net changes in Uosmol and CH2O in response to ADH were not significantly different. Taken together, the present results provide no evidence for a direct effect of D on ADH release nor do they indicate an interference with the peripheral action of ADH. The dopamine-induced diuresis is probably the result of increased solute excretion. This, in turn, is the result of the combined effects of dopamine on increasing renal blood flow, GFR, and sodium excretion.
Using conventional micropuncture techniques in 53 adult Sprague-Dawley rats anesthetized with sodium pentobarbital, single nephron GFR at proximal sites (snGFRprox) averaged 30+/-1 nl/min (76 tubules) and at distal sites (snGFRdis), 33+/-2 nl/min (90 tubules). Thus, in spite of interruption of macula densa fluid flow during its measurement, snGFRprox was not significantly greater than snGFRdis (p less than 0.05). Whole kidney GFR averaged 0.9+/-0.07 ml/min before and 1.0+/-0.05 ml/min during an intravenous infusion of SQ20,881, a substance which inhibits production of angiotensin II. Similarly, snGFRdis was unaffected by SQ20,881; the mean difference between paired snGFRdis (collection during NaCl infusion minus recollection at same sites during SQ20,881 infusion) was 6+/-4 nl/min (p less than 0.5). These results suggest that under the conditions of the experiments, tubulo-glomerular feedback is not operative and that angiotensin II plays no role in controlling filtration.
A randomized, controlled study of the effect of alternate-day prednisone therapy on renal transplant recipients was done on 53 patients followed for 610 patient months. There was no difference between the 17 recipients of related donor organs who received alternate-day prednisone (experimentals) and their 15 controls who received daily prednisone nor between the 11 experimental and 10 control recipients of cadaver donor organs as regards: rejections per patient month, change in serum creatinine, doses of azathioprine or prednisone, or weight. Likewise the controls and experimentals of the related and cadaver groups did not seem different in either their blood pressure change or their tendency to lose their Cushingoid facies. Alternate-day steroids had no obvious effect on the development of posterior subcapsular cataracts in either related or cadaver organ recipients.
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A retrospective review of 149 patients receiving 162 renal transplants showed that 83% of these patients developed one or more infections during a follow-up period averaging one year. In 32 (73%) of 44 deaths, infection was an important contributing cause. In only four (9%) of the deaths were the patients free of infection at the time of death. The Klebsiella-Enterobacter group was the most common agent causing pneumonitis and sepsis. Cryptococcus neoformans caused seven of 11 cases of meningitis. Pseudomonas was the most frequent agent associated with infections documented during postmortem examinations. In a short-term controlled study comparing daily and alternate daily therapy with prednisone, the alternate daily group had significantly (P less than .05) more infections per patient, especially in patients who had no evidence of rejection (P less than .025).
Using radioimmunoassay techniques, arteria (A) and renal venous (RV) plasma renin activities were measured in sodium pentobarbital-anesthetized dogs during clearance and stop-flow periods. Changes in RV-A renin were used to estimate changes in renin secretion. RV-A renin increased during stop flow from its average value during clearance periods, whether 10% mannitol in 0.15 M NaCl or 10% mannitol in 0.1 M Na2SO4 was being administered intravenously. However, RV-A renin during mannitol + NaCl stop-flow periods was significantly greater than during mannitol + Na2SO4 stop-flow periods. Distal tubular fluid Na concentrations as indicated by stop-flow analysis were higher during the latter. These observations suggest that a macula densa stimulus, Na concentration, and/or load, may control renin secretion during ureteral occlusion.
1. Pentobarbitone anaesthetized dogs were used to study the effects on renin secretion of ureteral occlusion and partial aortic clamping before and after intrarenal arterial administration of ouabain.2. Arterial plasma renin activity (A renin) and renal venous minus arterial plasma renin activity (RV-A renin) were both increased by either ureteral occlusion during mannitol diuresis or partial aortic clamping to reduce renal perfusion pressure. Intrarenal arterial ouabain administration blunted or abolished the effects of these manoeuvres on A and RV-A renins.3. The observations are not consistent with the hypothesis that renin secretion is uniquely controlled by afferent arteriolar transmural pressure. Both ureteral occlusion and aortic clamping reduce this pressure and increase renin secretion, yet evidence presented herein suggests that ouabain, which also decreases this pressure, decreases renin secretion.4. The observations are consistent with the hypothesis that renin secretion is controlled by tubular fluid flow and/or composition in the region of macula densa cells. Possibly changes in flow and/or composition are detected as changes in macula densa intracellular sodium concentration.
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