Impairment of Phenylalanine Hydroxylation in Chronic Renal Insufficiency

1973 ◽  
Vol 45 (1) ◽  
pp. 89-97 ◽  
Author(s):  
G. A. Young ◽  
F. M. Parsons
Keyword(s):  
Renal Insufficiency ◽  
Chronic Renal Insufficiency ◽  
Phenylalanine Hydroxylase ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Amino Nitrogen ◽  
Normal Subjects ◽  
The Individual ◽  
Plasma Tyrosine ◽  
Low Activity

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.

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
Keyword(s):  
Renal Insufficiency ◽  
Large Intestine ◽  
Chronic Renal Insufficiency ◽  
Rectal Mucosa ◽  
Normal Subjects ◽  
Potential Difference ◽  
Secretory Process ◽  
Potassium Adaptation ◽  
K Secretion ◽  
K Concentration

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.

scholarly journals Polymorphonuclear leukocyte oxidative burst is enhanced in patients with chronic renal insufficiency.

1995 ◽  
Vol 5 (9) ◽  
pp. 1697-1702 ◽  
Author(s):  
R A Ward ◽  
K R McLeish
Keyword(s):  
Renal Insufficiency ◽  
Oxidative Burst ◽  
Chronic Renal Insufficiency ◽  
Polymorphonuclear Leukocyte ◽  
Normal Subjects ◽  
Tnf Alpha ◽  
H2o2 Production ◽  
Necrosis Factor Alpha ◽  
Primed State ◽  
Factor Alpha

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.

scholarly journals Unfavorable Reduction in the Ratio of Endothelin B to A Receptors in Experimental 5/6 Nephrectomy and Adenine Models of Chronic Renal Insufficiency

2020 ◽  
Vol 21 (3) ◽  
pp. 936
Author(s):  
Suvi Törmänen ◽  
Päivi Lakkisto ◽  
Arttu Eräranta ◽  
Peeter Kööbi ◽  
Ilkka Tikkanen ◽  
...  
Keyword(s):  
Renal Insufficiency ◽  
Chronic Renal Insufficiency ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Mrna Levels ◽  
Endothelin Receptor ◽  
Protein Ratio ◽  
Protein Levels ◽  
Mrna Ratio ◽  
Endothelin B

Chronic renal insufficiency (CRI) is characterized by increased endothelin 1 (ET-1) synthesis. We studied rat kidney endothelin receptor A (ETA) and receptor B (ETB) expressions after 12 and 27 weeks of 5/6 nephrectomy, and after 12 weeks of 0.3% adenine diet, representing proteinuric and interstitial inflammation models of CRI, respectively. Uric acid and calcium-phosphate metabolism were modulated after 5/6 nephrectomy, while ETA blocker and calcimimetic were given with adenine. Endothelin receptor mRNA levels were measured using RT-qPCR and protein levels using autoradiography (5/6 nephrectomy) or ELISA (adenine model). Both 12 and 27 weeks after 5/6 nephrectomy, kidney cortex ETA protein was increased by ~60% without changes in ETB protein, and the ETB:ETA ratio was reduced. However, the ETB:ETA mRNA ratio did not change. In the adenine model, kidney ETA protein was reduced by ~70%, while ETB protein was suppressed by ~95%, and the ETB:ETA ratio was reduced by ~85%, both at the protein and mRNA levels. The additional interventions did not influence the observed reductions in the ETB:ETA ratio. To conclude, unfavorable reduction in the ETB:ETA protein ratio was observed in two different models of CRI. Therefore, ETA blockade may be beneficial in a range of diseases that cause impaired kidney function.

Electron microscopic study of the membrane glycoproteins in the rat kidney after cisplatin treatment

1989 ◽  
Vol 47 ◽  
pp. 912-913
Author(s):  
S.K. Aggarwal
Keyword(s):  
Alkaline Phosphatase ◽  
Rat Kidney ◽  
Light And Electron Microscopy ◽  
Kidney Tissue ◽  
Membrane Glycoproteins ◽  
Electron Microscopic ◽  
Before And After ◽  
Interstrand Cross Links ◽  
Cross Links

The proposed primary mechanism of action of the anticancer drug cisplatin (Cis-DDP) is through its interaction with DNA, mostly through DNA intrastrand cross-links or DNA interstrand cross-links. DNA repair mechanisms can circumvent this arrest thus permitting replication and transcription to proceed. Various membrane transport enzymes have also been demonstrated to be effected by cisplatin. Glycoprotein alkaline phosphatase was looked at in the proximal tubule cells before and after cisplatin both in vivo and in vitro for its inactivation or its removal from the membrane using light and electron microscopy.Outbred male Swiss Webster (Crl: (WI) BR) rats weighing 150-250g were given ip injections of cisplatin (7mg/kg). Animals were killed on day 3 and day 5. Thick slices (20-50.um) of kidney tissue from treated and untreated animals were fixed in 1% buffered glutaraldehyde and 1% formaldehyde (0.05 M cacodylate buffer, pH 7.3) for 30 min at 4°C. Alkaline phosphatase activity and carbohydrates were demonstrated according to methods described earlier.

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