Plasma renin activity in folic acid induced acute renal failure

1972 ◽  
Vol 50 (16) ◽  
pp. 797-798 ◽  
Author(s):  
U. Helmchen ◽  
Ursula Kneissler ◽  
Heide Fischbach ◽  
P. Reifferscheid ◽  
U. Schmidt
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Folic Acid ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity

Plasma renin activity and plasma aldosterone in acute renal failure

1980 ◽  
Vol 12 (1) ◽  
pp. 83-90
Author(s):  
M. Mydlík ◽  
K. Horký ◽  
P. Jonáš ◽  
I. Gregorová ◽  
I. Macháňová ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity

Failure of Loading with Sodium Bicarbonate to Protect against Acute Renal Failure Induced by Mercuric Chloride in the Rat

1977 ◽  
Vol 53 (2) ◽  
pp. 149-154 ◽  
Author(s):  
J. E. Beaumont ◽  
T. A. Kotchen ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance ◽  
Control Group ◽  
Sprague Dawley ◽  
Urinary Volume ◽  
Sprague Dawley Rats

1. To investigate the mechanism by which sodium loading protects against acute renal failure we compared the effects of prior chronic loading with NaCl, or with NaHCO3, on renal function after injection of HgCl2. 2. Twenty-four male Sprague-Dawley rats were divided into three groups of eight rats. One group drank isotonic NaCl solution, a second drank isotonic NaHCO3 solution and the third control group drank deionized water. Acute renal failure was induced by HgCl2 on day 9, and the rats were killed 48 h after injection. 3. Net sodium balances and plasma volumes were similar in both groups of sodium-loaded rats. After HgCl2 serum creatinine was significantly less and urinary volume was greater in NaCl-loaded than in both NaHCO3-loaded and water-drinking animals. 4. Plasma renin activity of both NaCl- and NaHCO3-loaded animals was less than that of control rats. However, renal renin content was suppressed by NaCl but not by NaHCO3 loading. 5. Loading with NaCl afforded greater protection against HgCl2-induced acute renal failure than NaHCO3. Since this difference was not related to changes in sodium balance or plasma volume before HgCl2, or plasma renin activity after HgCl2, the results support the hypothesis that intrarenal renin plays a role in the pathogenesis of HgCl2-induced acute renal failure in the rat.

Protective effect of renal denervation on normotensive endotoxemia-induced acute renal failure in mice

2002 ◽  
Vol 283 (3) ◽  
pp. F583-F587 ◽  
Author(s):  
Wei Wang ◽  
Sandor A. Falk ◽  
Suparoek Jittikanont ◽  
Patricia E. Gengaro ◽  
Charles L. Edelstein ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Plasma Renin

Acute renal failure (ARF) contributes substantially to the high morbidity and mortality observed during endotoxemia. We hypothesized that selective blockade of the renal nerves would be protective against ARF during the early (16 h) stage of endotoxemia [5 mg lipopolysaccharide (LPS)/kg ip in mice]. At 16 h after LPS, there was no change in mean arterial pressure, but plasma epinephrine (4,604 ± 719 vs. 490 ± 152 pg/ml, P < 0.001), norepinephrine (2,176 ± 306 vs. 1,224 ± 218 pg/ml, P < 0.05), and plasma renin activity (40 ± 5 vs. 27 ± 2 ng · ml−1 · h−1, P < 0.05) were higher in the LPS-treated vs. control mice. The high plasma renin activity level decreased to the control level with renal denervation in endotoxemic mice. After intravenous injection of phentolamine (200 μg/kg), the decrement in mean arterial pressure was significantly greater in LPS-treated vs. control mice (19.4 ± 3.5 vs. 8.1 ± 1.5 mmHg, P < 0.01). Sixteen hours after LPS administration, there were significant decreases in glomerular filtration rate (52 ± 18 vs. 212 ± 23 μl/min, P < 0.01) and renal blood flow (0.58 ± 0.08 vs. 0.85 ± 0.06 ml/min, P < 0.01) in sham-operated mice. The decrement in glomerular filtration rate during endotoxemia was significantly attenuated in mice with denervated kidneys (32 vs. 79%). Moreover, there was no change in renal blood flow during endotoxemia in mice with renal denervation. The present results therefore demonstrate a protective role of renal denervation during normotensive endotoxemia-related ARF in mice, an effect that may be, at least in part, due to a diminished activation of the renin-angiotensin system.

Atrial natriuretic factor and changes in dietary sodium intake in patients with chronic renal failure

1990 ◽  
Vol 78 (3) ◽  
pp. 327-334 ◽  
Author(s):  
J. C. Dussaule ◽  
C. Michel ◽  
J. P. Wolf ◽  
S. Czekalski ◽  
F. Mignon ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Renin Activity ◽  
Atrial Natriuretic Factor ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Renin Activity ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

1. In order to examine the potential role of atrial natriuretic factor in modulating the increased sodium excretion per nephron in chronic renal failure, we studied 12 uraemic patients on the last day of two successive 7 day periods during which their sodium intake was 100 and 20 mmol of sodium/day, respectively. 2. There was a parallel decrease from 6.31 ± 0.75 to 2.17 ± 0.32% in the fractional excretion of filtered sodium and from 234.4 ± 74.9 to 80.6 ± 20.3 pg/ml (supine position) or 140.1 ± 43.6 to 60.7 ± 14.6 pg/ml (upright position) in plasma atrial natriuretic factor. Both parameters were significantly correlated during the two periods of different sodium intake (P <0.05). The ratio of plasma guanosine 3′:5′-cyclic monophosphate to plasma creatinine changed proportionally to plasma atrial natriuretic factor. Plasma aldosterone and plasma renin activity increased during the sodium-depleted period but only plasma renin activity was significantly correlated with fractional excretion of filtered sodium. 3. The predominant role of atrial natriuretic factor compared with that of aldosterone in the renal response to varying sodium intake is suggested both by regression analysis and by the effect of 5 day's treatment with a converting enzyme inhibitor (enalapril) in six other uraemic patients on a normal (100 mmol/day) sodium intake. Such treatment, although resulting in a significant increase in plasma renin activity and a significant decrease in plasma aldosterone, at least in the supine position, did not modify the fractional excretion of sodium and plasma atrial natriuretic factor. 4. Taken together, these results suggest a role for plasma atrial natriuretic factor in promoting the adaptation of sodium excretion on chronic changes of sodium intake in patients with chronic renal failure.

Indomethacin-Induced Acute Renal Failure: Report of a Case and Review of the Literature

1980 ◽  
Vol 14 (10) ◽  
pp. 711-714 ◽  
Author(s):  
James F. Koren ◽  
James R. Brown ◽  
Jane K. Alissandratos ◽  
Larry B. Hudgins
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Plasma Renin Activity ◽  
Black Male ◽  
Plasma Renin ◽  
Underlying Disease ◽  
Renin Activity ◽  
Review Of The Literature ◽  
Disease States ◽  
Indomethacin Treatment

An 84-year-old black male with hypertensive cardiovascular disease and arthritis suffered deterioration in renal function when placed on indomethacin for an acute monoarticular arthritis. Renal function improved after discontinuing the indomethacin. The patient received indomethacin again, and there was a rapid increase in both the serum creatinine and blood urea nitrogen, which declined a second time when the drug was stopped. The plasma renin activity after indomethacin treatment was found to be markedly elevated. The counterbalancing effect of prostaglandins and plasma renin activity in preserving renal function in patients with underlying disease states is stressed. A review of the literature is provided and some rationalizations made as to what type of patient would be most susceptible to renal failure with indomethacin therapy.

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