Renal handling of urea in subjects with persistent azotemia and normal renal function

Renal handling of urea in subjects with persistent axotemia and normal renal function. Fourteen subjects with persistent azotemia and normal glomerular filtration rate were studied by renal clearances and hormonal determinations to establish the nephron site of altered urea transport and the mechani...

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Bibliographic Details
Published in:Kidney international 1987-11, Vol.32 (5), p.721-727
Main Authors: Conte, Giuseppe, Dal Canton, Antonio, Terribile, Maurizio, Cianciaruso, Bruno, Di Minno, Giovanni, Pannain, Mario, Russo, Domenico, Andreucci, Vittorio E.
Format: Article
Language:English
Subjects:
6-Ketoprostaglandin F1 alpha - urine
Adult
Blood Urea Nitrogen
Dinoprostone
Female
Glomerular Filtration Rate
Humans
Kidney Concentrating Ability
Kidney Tubules - physiopathology
Male
Middle Aged
Prostaglandins E - urine
Renin - blood
Uremia - physiopathology
Vasopressins - blood
Water-Electrolyte Balance
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Summary:Renal handling of urea in subjects with persistent axotemia and normal renal function. Fourteen subjects with persistent azotemia and normal glomerular filtration rate were studied by renal clearances and hormonal determinations to establish the nephron site of altered urea transport and the mechanism(s) responsible for their azotemia. During constant alimentary protein, urea nitrogen appearance was normal and urea clearance was much lower than in 10 age–matched control subjects (23.3 ± 2.1 ml/min and 49.6 ± 2.6 ml/min per 1.73 m2, P < 0.001). Inulin and para-aminohippurate clearances, blood volume and plasma concentration of antidiuretic hormone were within normal limits. During maximal antidiuresis, in spite of greater urea filtered load, the urinary excretion of urea was less, and both the maximum urinary osmolality and the free–water reabsorption relative to osmolar clearance per unit of GFR were greater than in control subjects. After sustained water diuresis, the plasma urea concentration markedly decreased to near normal levels in azotemic subjects. The basal urinary excretion of prostaglandins E2 was significantly reduced in azotemic subjects and was directly correlated with fractional urea clearance (r = 0.857, P < 0.001). An additional group of control subjects (N = 8) showed a marked reduction of fractional clearance of urea after inhibition of prostaglandin synthesis (P < 0.01). These data suggest that azotemia is due to increased tubular reabsorption of urea in the distal part of nephron, presumably because of increased back diffusion in the papillary collecting duct, accounting for the enhanced maximum urinary osmolality and free–water reabsorption. Renal prostaglandin E2 may partecipate in the pathogenesis of azotemia by altering recycling of urea in the medulla.
ISSN:0085-2538
1523-1755
DOI:10.1038/ki.1987.266