Biochemical and neurophysiological parameters in hemodialyzed patients with chronic renal failure

Schoots, AC Ad; Vries, de B Bauke; Thiemann, R.; Hazejager, WA; Visser, Sako; Oe, P. L.

doi:10.1016/0009-8981(89)90134-4

Cited by 34 publications

(20 citation statements)

References 18 publications

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“…HA is markedly elevated in the serum and cerebrospinal fluid of uremic patients (Porter et al, ). In addition, the serum concentration of HA in hemodialysis patients correlates positively with neurophysiological indices (Schoots et al, 1989), suggesting that HA is related to neurological symptoms in uremia. Likewise, a relationship was observed in patients between the increasing severity of abnormalities attributable to the uremic state and higher plasma concentrations of 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (Costigan et al, 1996).…”

Section: Discussionmentioning

confidence: 95%

“…HA also inhibits glucose utilization in muscles and so may be involved in development of muscular weakness in uremia (Spustova et al, 1987(Spustova et al, , 1989. Serum and cerebrospinal fluid concentrations of HA correlate positively with neurophysiological indices (Schoots et al, 1989), which suggests that HA induces neurological symptoms, perhaps via inhibition of organic anion transport at the blood-brain barrier (Ohtsuki et al, 2002) or blood-cerebrospinal fluid barrier (Porter et al, 1975). In addition, HA accelerates the renal damage associated with CRF (Satoh et al, 2003).…”

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confidence: 99%

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Renal Clearance of Endogenous Hippurate Correlates with Expression Levels of Renal Organic Anion Transporters in Uremic Rats

Deguchi

Takemoto²,

Uehara³

et al. 2005

J Pharmacol Exp Ther

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Hippurate (HA) is a harmful uremic toxin that accumulates during chronic renal failure, and failure of the excretion system for uremic toxins is thought to be responsible. Recently, we reported that rat organic anion transporter 1 (rOat1) is the primary mediator of HA uptake in the kidney, and so now we have studied the pharmacokinetics and tissue distribution of HA after a single i.v. dose of HA to normal and 5/6 nephrectomized rats (5/6Nx rats). In control rats, the renal and biliary clearances of HA were 18.1 and 0.1 ml/min/kg, respectively. Plasma clearance decreased as dosage increased from 0.1 to 5 mg/kg, which suggests that renal tubular secretion is the primary route for elimination of HA. The plasma clearance of HA was significantly decreased in 5/6 Nx rats compared with normal rats. In 5/6 Nx rats, renal clearance of endogenous HA correlated more closely with clearance of p-aminohippurate than with that of creatinine. Protein expression of rOat1 and rOat3, assessed by Western blot analysis, was decreased in 5/6 Nx rats. Furthermore, in 5/6 Nx rats, the renal secretory clearance of endogenous HA correlated closely with protein expression of renal rOats. Thus, HA is primarily eliminated from the plasma via the kidney by active tubular secretion. The renal clearance of endogenous HA seems to be a useful indicator of changes in renal secretion that accompany the reduced levels of OAT protein in chronic renal failure.

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Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

Renal Clearance of Endogenous Hippurate Correlates with Expression Levels of Renal Organic Anion Transporters in Uremic Rats

Deguchi

Takemoto²,

Uehara³

et al. 2005

J Pharmacol Exp Ther

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“…It should be stressed that many protein-bound uremic solutes have important pathophysiologic actions and might be subject to a similar enhancement of toxicity in the case of hypoalbuminemia. Candidate molecules are indoxyl sulfate (6,33,34 ), indole 3-acetic acid (35,36 ), 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid (37,38 ), phenol (39 ), advanced glycation end products (40 -42 ), leptin (43,44 ), homocysteine (45,46 ), hippuric acid (47,48 ), and p-hydroxyhippuric acid (49,50 ).…”

Section: Discussionmentioning

confidence: 99%

Toxicity of Free p-Cresol: A Prospective and Cross-Sectional Analysis

et al. 2003

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Background: Uremic syndrome is the consequence of the retention of solutes usually cleared by the healthy kidneys. p-Cresol can be considered a prototypic protein-bound uremic toxin. It is conceivable, analogous with drugs, that the non-protein-bound fraction of pcresol exerts toxicity. This aspect had never been evaluated, nor have the factors influencing the free fraction of p-cresol. Methods: In a transsectional study we evaluated the relationship between prehemodialysis free p-cresol and the ratio of free to total p-cresol (F:T) to clinical and biological factors in 44 chronic renal failure patients. The evolution of free p-cresol was assessed prospectively in 12 patients showing a change in serum albumin of at least 5 g/L over time. Hospitalization days attributable to infection and the free p-cresol concentrations were noted over a 1-year period. The impact of free p-cresol in vitro on leukocyte functional capacity was evaluated by chemiluminescence. Results: We observed a correlation between total and free p-cresol (r ‫؍‬ 0.84; P <0.001). In the multivariate analyses, free p-cresol and F:T showed a negative correlation with albumin. A shift from normal serum albumin to hypoalbumininemia in 12 patients led to an increase in free p-cresol from 5.9 ؎ 3.2 to 8.2 ؎ 4.5 mol/L (P <0.05; 0.64 ؎ 0.35 to 0.89 ؎ 0.49 mg/L). Free p-cresol (P <0.05) was higher in the patients hospitalized for infectious disease. In vitro, free p-cresol was higher in a 25 g/L than in a 50 g/L albumin solution (P <0.05). Leukocyte chemiluminescence production was more inhibited in the low albumin (high free p-cresol) solution (28% ؎ 6% vs 21% ؎ 8%; P <0.05).

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“…HA also inhibits glucose utilization in muscles and it may be involved in development of muscular weakness [35,36]. Furthermore, it can also be correlated positively with neurophysiological indices [37], which suggest that HA induces neurological symptoms, perhaps via inhibition of organic anion transport at the blood-brain barrier or bloodcerebrospinal fluid barrier [38].…”

Section: Discussionmentioning

confidence: 99%

Correlation of Age-Related Metabonomic Changes in 1H NMR Serum and Urine Profiles of Rats with Cognitive Function

Mahdi¹,

Annarao²,

Tripathi³

et al. 2008

TOMRJ

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Age related metabonomic changes in young and aged male albino rats have been investigated using Proton Nuclear Magnetic Resonance ( 1 H NMR) spectroscopy. The studies were performed using 'in vivo' behavioral and metabonomic assessment in serum and urine of the rats. Significant changes (p<0.05) were obtained in the concentration of creatinine, allantoin and hippurate in urine. Also significant (p<0.05) alterations were also discernible in acetate, pyruvate, lactate, creatine and glucose in serum. Attempts have been made to correlate these changes with the cognitive impairment and perturbed energy metabolism in aged rats. The metabonomic evaluation of age related changes in serum and urine showed altered concentrations of many Krebs cycle intermediates in old rats. Likewise it was associated with diminished mitochondrial functioning. On the basis of our results it is suggested that the observed changes may be an early clinical indication of cognitive decline related to dementia.

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Biochemical and neurophysiological parameters in hemodialyzed patients with chronic renal failure

Cited by 34 publications

References 18 publications

Renal Clearance of Endogenous Hippurate Correlates with Expression Levels of Renal Organic Anion Transporters in Uremic Rats

Renal Clearance of Endogenous Hippurate Correlates with Expression Levels of Renal Organic Anion Transporters in Uremic Rats

Toxicity of Free p-Cresol: A Prospective and Cross-Sectional Analysis

Correlation of Age-Related Metabonomic Changes in 1H NMR Serum and Urine Profiles of Rats with Cognitive Function

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