Mannitol Osmotic Diuresis in Patients with Chronic Renal Failure

1970 ◽  
Vol 259 (3) ◽  
pp. 175-181 ◽  
Author(s):  
P. Metaxas ◽  
M. Papadimitrion ◽  
C. Papaposlolou ◽  
D. J. Valtis
1972 ◽  
Vol 43 (6) ◽  
pp. 771-778 ◽  
Author(s):  
J. D. Swales ◽  
H. Thurston ◽  
J. E. F. Pohl

1. The defect in sodium conservation shown by patients with advanced chronic renal failure has been studied during the administration of diazoxide. 2. All nine patients showed a reduction in urinary sodium concentration to levels substantially lower than those which can normally be produced in such patients even with prolonged sodium depletion. Seven patients produced a nearly sodium-free urine. In all patients this effect could be reversed by the administration of high doses of frusemide. The fall in urinary sodium concentration was associated with a sustained fall in creatinine clearance in only two cases. 3. One patient with salt-losing renal disease showed a more modest fall in sodium concentration on treatment with diazoxide. 4. It is concluded that since the defect in sodium conservation shown by patients with chronic renal failure can be corrected without diminishing the osmotic load, it cannot be solely due to the effect of the osmotic diuresis upon residual functioning nephrons. It is suggested that the distal tubular transport mechanism for sodium is saturated by the increased delivery of sodium from the proximal tubule.


1964 ◽  
Vol 206 (5) ◽  
pp. 1118-1122 ◽  
Author(s):  
Harvey C. Gonick ◽  
Jack W. Coburn ◽  
Milton E. Rubini ◽  
Morton H. Maxwell ◽  
Charles R. Kleeman

An increased solute load per remaining functioning nephron may enhance K excretion and aid in maintaining K balance in chronic renal failure. An analogous model was sought by inducing progressive osmotic diuresis with urea in a) water-loaded dogs with minimal K excretion, b) dogs receiving K infusions at intermediate rates of 207–280 µEq/min, and c) dogs receiving K infusions at maximal tolerated rates of 400–600 µEq/min. Urea diuresis significantly augmented K excretion in experiments in which basal K excreted-to-K filtered ratios (KE:KF) were minimal (.02–.03) or intermediate (.20–.73), but when control ratios approached 1.0, urea loading became progressively less effective. The slight increment in K excretion with low basal KE:KF ratios (19 µEq/min) suggested partial inhibition of proximal reabsorption; the more marked increment in K excretion at intermediate KE:KF levels (130 µEq/min) is consistent with enhancement of K secretion following increased delivery of Na to the distal exchange sites. Once distal K secretion was maximally stimulated by K loading, however, it was not further affected by solute diuresis or augmented Na excretion.


2003 ◽  
Vol 73 (3) ◽  
pp. 215-220 ◽  
Author(s):  
de Gómez Dumm ◽  
Giammona ◽  
Touceda

Dyslipidemia and increases in plasma homocysteine usually occur at end-stage renal disease; both are recognized as risk factors for atherosclerosis. Folate administration reduces homocysteine concentration. In this study we determined the effect of a high dose of folic acid (40 mg intravenous injection three times a week) on plasma and red blood cell lipid profiles in twelve chronic renal failure patients on regular hemodialysis. Fasting blood samples were taken at the beginning of the study (baseline) and after 21, 42, and 64 days of treatment. Folic acid supplementation decreased plasma homocysteine. Plasma triglyceride levels decreased whereas polyunsaturated fatty acid values increased after 21 days; then they returned to baseline levels at the end of treatment. Total cholesterol and low-density lipoprotein (LDL) cholesterol were higher than those of the baseline during all the study, whereas high-density lipoprotein (HDL) cholesterol was reduced. In erythrocyte membranes, folic acid therapy enhanced cholesterol/phospholipid ratios and the fluorescence anisotropy of diphenyl-hexatriene. We conclude that large doses of folic acid produce a favorable effect, reducing plasma homocysteine levels and protecting patients from atherosclerosis. However, as this therapy induces significant alterations in both plasma and erythrocyte membrane lipid profiles, plasma lipid values should be controlled throughout the treatment of patients with renal failure.


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