Enhanced rectal potassium secretion in chronic renal insufficiency: Evidence for large intestinal potassium adaptation in man

1986 ◽  
Vol 71 (4) ◽  
pp. 393-401 ◽  
Author(s):  
G. I. Sandle ◽  
E. Gaiger ◽  
S. Tapster ◽  
T. H. J. Goodshep

1. The role of the large intestine in K+ excretion in chronic renal insufficiency was studied with a rectal dialysis technique in 14 normal subjects and eight normokalaemic, normotensive patients with chronic renal insufficiency. 2. At initial intraluminal K+ concentrations of 10, 20, 30 and 45 mmol/l, net K+ secretion in patients with renal insufficiency was significantly greater than in normal subjects by approximately 1.8 μmol h−1 cm−2. The increase in net K+ secretion was more marked in those patients with creatinine clearances of less than 10 ml/rnin. In contrast, there were no significant differences in net Na+ and water transport, transmucosal potential difference and plasma aldosterone concentrations between the two groups. 3. With an initial intraluminal K+ concentration of 30 mmol/l, the addition of amiloride (final concentration 1 mmol/l) to the rectal lumen decreased net Na+ absorption and transmucosal potential difference in normal subjects by 69% (P < 0.005) and 31% (P < 0.005) respectively, and in patients with renal insufficiency by 75% (P < 0.05) and 36% (P < 0.05) respectively, but there was no change in net K+ secretion in either group. 4. These results indicate that the K+ secretory capacity of the rectal mucosa increases in chronic renal insufficiency, and the large intestine may therefore contribute to the maintenance of K+ homoeostasis as renal K+ excretion declines. Increased rectal K+ secretion in renal insufficiency occurs independently of changes in plasma K+ and aldosterone concentrations, net Na+ absorption and transmucosal potential difference, and may reflect stimulation of an active K+ secretory process.

1987 ◽  
Vol 73 (3) ◽  
pp. 247-252 ◽  
Author(s):  
G. I. Sandle ◽  
E. Gaiger ◽  
S. Tapster ◽  
T. H. J. Goodship

1. The role of the large intestine in the maintenance of K+ balance in uraemic patients established on long-term dialysis was studied with a rectal dialysis technique in 14 normal subjects, ten normokalaemic patients undergoing chronic ambulatory peritoneal dialysis (CAPD), and seven patients undergoing haemodialysis. Dietary K+ intakes in the normal subjects, CAPD patients and haemodialysis patients were 80–100 mmol/24 h, 70–80 mmol/24 h and 60–70 mmol/24 h, respectively. 2. At an initial intraluminal K+ concentration of 45 mmol/l, rectal K+ secretion in the CAPD patients (2.4 ± 0.4 μmol h−-1cm−-2) was greater than in normal subjects (1.2 ± 0.2 μmol h−-1 cm−-2, P < 0.02). Under similar conditions, rectal K+ secretion was also greater in the haemodialysis patients than in normal subjects, both pre-dialysis (3.7 ± 0.4 μmol h−-1 cm−-2, P < 0.001) and post-dialysis (2.4 ± 0.5 μmol h−-1 cm−-2, P < 0.05), even though haemodialysis decreased plasma K+ concentration from 5.3 ± 0.1 mmol/l to 3.5 ± 0.2 mmol/l (P < 0.001). 3. There were no significant differences in rectal Na+ absorption, rectal potential difference, plasma aldosterone concentration, or total body K+ content (measured by whole-body counting of 40K), between the normal subjects and either the CAPD or the haemodialysis patients. 4. These results indicate that K+ homoeostasis is maintained in uraemic patients undergoing long-term dialysis by a combination of K+ losses during dialysis, and enhanced large intestinal K+ excretion. The role of the large intestine appears to be particularly important at higher dietary K+ intakes, and the K+ secretory process is sensitive to changes in plasma K+ concentration.


1973 ◽  
Vol 45 (1) ◽  
pp. 89-97 ◽  
Author(s):  
G. A. Young ◽  
F. M. Parsons

1. Plasma tyrosine and phenylalanine were measured in patients with chronic renal failure and in normal subjects. Plasma tyrosine to phenylalanine ratio was greatly decreased in patients with creatinine clearance less than 16 ml/min, suggesting an impairment of phenylalanine hydroxylation. This ratio correlated with the percentage of essential to total amino nitrogen in the plasma. 2. Phenylalanine hydroxylase from rat liver was inhibited or inactivated (15%) by uraemic plasma but this could not be attributed to the individual effects of urea, creatinine, uric acid, oxalic acid, phenylpyruvic acid, glycine or phosphate. It is unlikely that the degree of inhibition was sufficient to account for the impairment of phenylalanine hydroxylation in chronic renal insufficiency. 3. Phenylalanine hydroxylase was present in rat kidney but at a very low activity relative to that present in liver; consequently, the loss of functional kidney tissue associated with chronic renal insufficiency is unlikely to impair phenylalanine hydroxylation. 4. Plasma tyrosine and liver phenylalanine hydroxylase activity were significantly decreased in partially nephrectomized rats when protein intake was inadequate.


1995 ◽  
Vol 5 (9) ◽  
pp. 1697-1702 ◽  
Author(s):  
R A Ward ◽  
K R McLeish

Previous reports that polymorphonuclear leukocyte (PMN) function is impaired in hemodialysis patients do not differentiate between effects of dialysis and of uremia. The hypothesis that chronic renal insufficiency impairs PMN function was tested. Phagocytosis and oxidative burst were measured in PMN from patients with varying degrees of chronic renal insufficiency impairs PMN function was tested. Phagocytosis and oxidative burst were measured in PMN from patients with varying degrees of chronic renal insufficiency (creatinine clearance, 6 to 35 mL/min per 1.73 m2) and normal subjects. The ability of tumor necrosis factor-alpha (TNF-alpha) to prime the oxidative burst was also assessed. Phagocytosis of Staphylococcus aureus and basal H2O2 and O2- release by PMN did not differ between normal subjects and patients with chronic renal insufficiency. However, the oxidative burst stimulated by S. aureus and formyl-Met-Leu-Phe, but not phorbol myristate acetate, was significantly enhanced in PMN from patients with chronic renal insufficiency. The increase in formyl-Met-Leu-Phe-stimulated oxidative burst correlated significantly with the level of renal function. TNF-alpha significantly increased S. aureus-induced H2O2 production in normal PMN, but not in PMN from patients with chronic renal insufficiency. These data indicate that chronic renal insufficiency does not impair PMN phagocytosis and oxidative burst. To the contrary, it enhances receptor-mediated oxidative burst. The inability of TNF-alpha to further enhance the oxidative burst suggests that PMN exist in a primed state in patients with chronic renal insufficiency.


2013 ◽  
Vol 10 (3) ◽  
pp. 263-268 ◽  
Author(s):  
Jin-Gang Yu ◽  
Lin-Yan Yu ◽  
Xin-Yu Jiang ◽  
Xiao-Qing Chen ◽  
Li-Jian Tao ◽  
...  

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