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PubMed1988

Sural nerve morphology in asymptomatic uremia.

This study evaluates morphologically the sural nerves of two patients with acute and another pair with chronic uremia, both of whom had neither clinical nor electrophysiologic evidence of neuropathy. Morphometric changes indicative of myelin repair were noted in the chronic uremic case who had a shorter duration of renal failure but required dialysis. Also, changes suggestive of axonal degeneration were found in the case who had chronic uremia of long duration. Both cases of acute uremia did not reveal significant abnormalities. Structural changes in the sural nerves may precede clinical and nerve conduction derangements in uremia, specifically in chronic cases.

Acute Disease↗
PubMed1991

Regulation of hypothalamic gonadotropin-releasing hormone secretion in experimental uremia: in vitro studies.

Defective regulation of hypothalamic gonadotropin-releasing hormone (GnRH) secretion is the primary defect leading to the inhibition of pituitary gonadotropin secretion and its consequences such as androgen deficiency and infertility in experimental uremia. Previous studies using indirect methods to study presumptive GnRH release and the function of GnRH-secreting neurons have suggested functional disturbances of GnRH neurosecretion; however, the precise biochemical mechanisms involved were not defined. Therefore, in order to clarify the mechanisms of aberrant regulation of hypothalamic GnRH secretion in experimental uremia, we examined basal secretion of GnRH from mediobasal hypothalamus (MBH) in vitro and the GnRH-secretory responses to naloxone, an opiate receptor antagonist in experimental uremia. Using a static incubation system, adult male rats, either intact or castrate, with subtotal nephrectomy demonstrated a significant reduction of GnRH secretion by 25% in intact and by 40% in castrate uremic male rats compared with their nonuremic controls. In contrast, hypothalamic GnRH content of uremic animals was increased significantly (6% in intact and 14% in castrate uremic rats). Despite the fall in basal GnRH release from MBH, the MBH GnRH release response to in vitro stimulation by an opioid blocker (naloxone) and a membrane-depolarizing agent (veratrine) were not diminished in uremic male rats. These findings suggest that the inhibition of pituitary gonadotropin secretion in experimental uremia is likely to be due to a functional defect in suprahypothalamic regulation of GnRH secretion rather than an intrinsic defect in the GnRH-secreting neurons. Further studies are required to clarify the nature of the neuromodulator interactions involved.

Animals↗
PubMed1984

The immunosuppressive effect of experimentally induced uremia.

Isogeneic BN rats were made uremic by subtotal renal resections. After different periods of uremia the possibility of an immunodeficiency was evaluated by (WF X BN) F1----BN heterotopic heart transplantations. A prolongation of transplant survival was found that was not related to the duration of uremia. In some rats the uremia was reversed by isogeneic BN----BN kidney transplantation before cardiac grafting. An immediate reversal of the immunodeficiency occurred. Thus an immunosuppressive effect by uremia can be documented, and to some extent quantitated, by heterotopic heart transplantation between rats of different isogeneic strains.

Animals↗
PubMed1986

Delayed-type hypersensitivity skin reaction in the chronically uremic mouse: influence of severity and duration of uremia on the development of response.

A technique of delayed-type hypersensitivity (DTH) skin reaction to a contact sensitizing agent, oxazolone, was used to assess the effects of uremia on cell-mediated immunity in chronically uremic mice and, for comparison, sham-operated and normal controls. The first objective was to establish that DTH responses are reduced in animals with renal failure. To do this, mice were made uremic by a combination of electrocoagulation of the entire surface of one kidney and subsequent contralateral nephrectomy; studies included biochemical and hematological evaluation using blood urea nitrogen level and hemoglobin concentration as routine indices to assess the degree and consequence of uremia, respectively. The second objective was to apply the technique to observe and compare changes during uremic states of varying severity and duration. A modest, although significant, decrease in both the induction and maintenance of DTH responses was observed in the mice with severe renal failure only (BUN above 100 mg/dl). This immunosuppressive effect was manifest early and persisted unchanged throughout the entire observation period (3-9 weeks). This study presents new evidence that severe uremia readily produces in the mouse sustained, albeit mild, changes in cell-mediated immunity. Furthermore the ability to elicit DTH skin reaction in the chronically uremic mouse offers a versatile system for studying changes in cell-mediated immunity occurring during uremia with a broad range of potential applicability.

Animals↗
PubMed1969

Studies on the control of sodium excretion in experimental uremia.

A study of the mechanisms governing the high rate of sodium excretion per nephron characteristic of patients with chronic renal disease has been made in dogs. A "remnant kidney" was produced by 85% infarction of the left kidney while the right kidney was left intact. A bladder-splitting procedure allowed simultaneous measurement of glomerular filtration rate and the rate of sodium excretion by each kidney. The animals were fed a constant known amount of sodium chloride and 0.1 mg of 9 alpha-fluorohydrocortisone twice daily throughout the study. In a group of dogs fed 3 or 5 g of salt per day, sodium excretion by the remnant kidney averaged 6.5 muEq/min while the intact kidney was present and 53.7 muEq/min when the animals became uremic after the intact kidney was removed. The increased sodium excretion per nephron by the remnant organ often occurred within 18 hr after contralateral nephrectomy and persisted despite experimentally induced acute reductions in the glomerular filtration rate to below prenephrectomy levels. A second group of animals studied in the same manner but receiving 1 g of salt per day or less failed to develop a natriuresis after contralateral nephrectomy despite high grade uremia. Thus an increased impermeable solute load per nephron was not a regulatory factor in the production of the natriuresis. The increased rate of sodium excretion per nephron in uremia resembles that after saline loading in that it may occur without an increase in glomerular filtration rate or a reduction in mineralocorticoid stimulation. It follows that an additional factor or factors must be involved in the genesis of the natriuresis. In contrast to the natriuresis that is seen in normal animals subjected to saline loading, these uremic animals were found not to have a detectable increase in extracellular fluid volume or blood volume in the presence of high fractional sodium excretion rates. Sodium excretion in response to a small salt load by the remnant organ in uremia was 30% greater than the response of both kidneys in the preuremic state despite a markedly reduced total GFR. These data are consistent with the view that the volume control mechanism becomes more responsive in uremia.

Animals↗
PubMed1995

Impaired cation transport in thymocytes of rats with chronic uremia includes the Na+/H+ antiporter.

To examine how uremia changes sodium, potassium, and proton transport, thymocytes from chronic renal failure (CRF) rats were studied. If alterations in cation transport associated with chronic uremia (CRF) extend to intracellular pH regulation, the susceptibility to the catabolic effects of acidosis might be increased. To evaluate the influence of acidosis, cation transport in thymocytes from normal rats with NH4Cl-induced acidosis was also studied. Ouabain-sensitive 86Rb influx in thymocytes from acidotic CRF rats was 32% lower than in control cells (P < 0.05), but intracellular sodium concentration was unchanged. This may be related to a 47 +/- 22% reduction in 22Na influx. In thymocytes from nonuremic, acidotic rats, ouabain-sensitive 86Rb influx was decreased 39% (P < 0.025), similar to the change in CRF. In CRF thymocytes, Na(+)-H+ antiporter activity in response to cell acidification (7.13 +/- 0.8 versus 9.42 +/- 0.8 mmol of H+/L per min; CRF versus control), or to osmotic shrinkage (0.43 +/- 0.09 versus 0.82 +/- 0.11 mmol of H+/L per min; CRF versus control), was significantly (P < 0.01) reduced. Buffering capacity at resting and acidic intracellular pH was unchanged by uremia, but Na+/H+ antiporter activity in response to acid loading or osmotic shrinkage was unchanged in thymocytes of nonuremic rats with metabolic acidosis. Thus, CRF reduces both Na/K-ATPase and Na+/H+ antiporter activities in rat thymocytes. The former may be secondary to reduced sodium influx. Impaired Na+/H+ antiporter activity is not caused by metabolic acidosis alone, whereas reduced Na/K-ATPase activity is found in both acidosis and uremia.

Animals↗
PubMed2000

[Clinical effect of Xinqingning combined low dose continuous gastrointestinal dialysis in treating uremia].

OBJECTIVE: To investigate the clinical effect of Xinqingning (XQN), a preparation of rhubarb, combined with low dose continuous gastrointestinal dialysis in treating uremia. METHODS: Patients of uremia were divided into three groups at random, eighteen patients in the group A were treated with 1000 ml gastrointestinal dialysate (non-absorbed mannitol solution) orally 2-3 times a day, twenty patients in the group B treated with the same therapy as that in the group A, but combined with XQN 5-10 tablets 3 times per day and 19 patients in the group C treated by orally taken coated aldehyde oxystarch 5-10 g, 3 times a day. The therapeutic course for the three groups were 11 months. The changes in clinical manifestation, renal function, nutritional condition, and electrolytes before and after treatment were observed. RESULTS: After treatment, significant improvement was revealed in aspects of uremic symptoms, quality of life, nutritional condition, serum creatinine, urea nitrogen, serum phosphate, uric acid, CO2 combining power, creatine clearance, body weight and arm muscular circumference in the group A and B, as compared with those in the group C. In comparison of the group A and B, the group B showed a lower serum triglyceride and slower progression of chronic renal failure (CRF). All the criteria were not improved in the group C and with serum creatinine raised significantly. CONCLUSION: XQN combined low dose continuous gastrointestinal dialysis therapy was effective in definitely treating uremia, it provides a new therapeutic means of non-replacement therapy for CRF with uremia.

Adult↗
PubMed1975

Effect of uremia on rates of ethanol disappearance from the blood and on the activities of the ethanol-oxidizing enzymes.

The effect of uremia on ethanol metabolism was investigated. Uremia was induced in male Spraque-Dawley rats by removal of approximately 85 per cent of the renal mass. Control animals had a sham operation. The mean activity of alcohol dehydrogenase was markedly increased in the uremic rats to 2.12 +/- 0.13 (S.E.M.) mumoles per milligram of protein per hours as compared with a control value of 1.39 +/- 0.13 mumoles per milligram of protein per hour (p less than 0.001). There were no changes in the activity of the microsomal ethanol oxidizing system, in catalase activity present in the microsomes, or in the rates of ethanol disappearance from the blood. Uremia resulted in decreases in microsomal cytochrome -450, but no changes in cytochrome b5, NADPH-cytochrome c reductase, or in the activities of aniline hydroxylase and aminopyrine demethylase. The increase in alcohol dehydrogenase activity could not be reproduced by incubation of liver from a normal rat with uremic rat plasma, uremic human serum, or urea. Also, the increase in the enzyme activity was not associated with changes in leucocyte ascorbic acid levels. The cause and physiologic significance of the increase in alcohol dehydrogenase activity in uremia remain to be elucidated.

Alcohol Oxidoreductases↗
PubMed2001

[Measurement of central respiratory drive and inspiratory muscles strength in patients with uremia].

OBJECTIVE: To investigate the changes of central respiratory drive and inspiratory muscles function in patients with uremia. METHODS: We performed the measurement of forced vital capacity (FVC), maximal voluntary ventilation (MBC), forced expiratory volume in one second (FEV1), peak expiratory flow (PEF), maximal midexpiratory flow (MMEF), expiratory flow of 25 per cent of FVC (V25), lung carbon monoxide diffusing capacity (DLco), maximal inspiratory mouth pressure (MIP) and airway occlusion pressure (P0.1) in 25 patients with uremia and 20 normal subjects. RESULTS: In patients with uremia, the FVC, MBC, FEV1, PEF, MMEF and V25 which reflect the lung ventilatory function and the DLco which reflects the lung diffusing function were significantly lower than those in normal subjects. The patients' MIP which reflects inspiratory muscles strength was significantly lower and their P0.1 which reflects the central respiratory drive was significantly higher, compared with the normal subjects'. CONCLUSION: Our findings suggest that on the basis of the disorder of ventilation and diffusing function of the lungs, the inspiratory muscles function of the patients with uremia is significantly decreased and the central respiratory drive of the patients is increased.

Aged↗
PubMed1992

Mechanisms for protein catabolism in uremia: metabolic acidosis and activation of proteolytic pathways.

Accelerated protein catabolism in uremia occurs in animals and patients with acute (ARF) and chronic renal failure (CRF). Possible causes include resistance to both insulin-induced inhibition of protein-degradation and insulin-induced stimulation of protein synthesis. The mechanisms for these effects are unknown. However, metabolic acidosis has been shown to increase proteolysis in rat skeletal muscle even in the presence of insulin and this effect is absent in adrenalectomized rats. Similarly, metabolic acidosis accounts for increased muscle proteolysis in rats with CRF. Metabolic acidosis also stimulates branched-chain amino acid (BCAA) breakdown by increasing the activity of branched-chain keto acid decarboxylase. Uremia causes high corticosterone levels in ARF and CRF and this hormone could contribute significantly to increased proteolysis, BCAA-breakdown and possibly, the inhibition of protein synthesis. Besides changing glucocorticoids, uremia could inhibit the activity of transporters which regulate intracellular pH and ultimately, the metabolism of protein and amino acids. For example, uremia inhibits ion transporters including Na/H exchange in a variety of tissues and therefore, could increase the susceptibility to metabolic acidosis. Research directed at identifying specific, proteolytic pathways stimulated by metabolic acidosis has excluded a major role for Ca2+ activated and lysosomal proteases and suggests activation of an ATP- and ubiquitin-dependent proteolytic pathway.

Acidosis↗
PubMed1986

Platelet dysfunction in uremia. II. Correction by arachidonic acid of the impaired exposure of fibrinogen receptors by adenosine diphosphate or collagen.

Previous studies showed that platelets from patients with uremia have a marked decrease in their aggregation response to adenosine diphosphate (ADP) and collagen as single agents or as a pair. It is known that small amounts of arachidonic acid can enhance the sensitivity of platelets to concentrations of ADP or collagen that do not cause aggregation when used singly. Stimulation of platelets by certain agonists induces the formation of fibrinogen receptors on the platelet surface. The binding of fibrinogen that follows is essential for platelet aggregation. The platelet membrane glycoprotein IIb-IIIa complex appears to be the site of the fibrinogen receptor. Therefore, we investigated the binding of iodine 125-labeled fibrinogen to uremic platelets exposed to ADP, collagen, or arachidonic acid as single agents and as pairs. When aggregation and binding were studied in response to ADP, collagen, or the combination of ADP with collagen, uremic platelets had reduced aggregation and bound abnormally low amounts of fibrinogen. In contrast, platelets from patients with uremia bound as much 125I-fibrinogen and aggregated as well as controls when ADP or collagen were used in combination with low concentrations of arachidonic acid. Studies with a monoclonal antibody (B 79.7) suggested that the number of glycoprotein IIb-IIa molecules is the same in uremic and normal platelets. We conclude that uremia impairs the exposure of fibrinogen receptors on platelets in response to ADP or collagen without affecting the glycoprotein IIb-IIa complex quantitatively. Correction by arachidonic acid of the impaired aggregation and exposure of fibrinogen receptors by ADP or collagen suggests that abnormal release of endogenous arachidonic acid plays a role in the dysfunction of platelets in uremia.

Adenosine Diphosphate↗
PubMed1985

Evoked potentials in uremia: basal and follow-up data.

Various EPs have been employed to disclose even early-stage central and peripheral nervous system damage in uremia. This approach also gives the possibility to follow up alterations of many sensory functions during the sequential stages of uremia. Fifty-three subjects (35 male and 18 female, mean age 42.20 +/- 5.50 yrs, conventionally low nitrogen diet treated, on dialysis or transplanted) were followed-up by recording the EPs every year for seven years. The P100 wave latency and amplitude of VEPs were recorded and found abnormal in about 70% of the examined visual systems. The auditory EPs were abnormal in 53% of the cases for the peak latencies, interpeak times and peak ratios. The somatosensory EPs showed in 75% of the cases an altered latency and morphology of the waves registered in the lumbar, cervical and cranial loci. There is evidence suggesting that evoked cerebral biorhythms may provide sensitive and objective indexes of cerebral function in uremia. The persistence of abnormalities disclosed by EPs follow-up confirm the reliability of this technique in evaluating neuro-pathologic uremic situations and in supplying optimal uremia therapies.

Adult↗
PubMed1983

Muscle protein turnover in uremia.

Abnormalities of muscle protein stores in uremia result from changes in the components of protein turnover. In vivo measurements of protein synthesis and degradation in uremia are subject to several errors. There may be incomplete equilibration of the infused labeled amino acid with the precursor pool for protein synthesis because of abnormal amino acid transport into muscle and increased catabolism of the infused amino acid. The infusion technique for measuring protein degradation cannot differentiate between rates occurring in different tissues. Moreover, measurement of 3-methylhistidine as an estimate of muscle protein degradation is invalid in uremia because its renal clearance is impaired. In vitro studies using radiolabeled amino acids should give more reliable estimates of the components of muscle protein turnover. Estimation of the rate of protein synthesis with a labeled amino acid still requires measurements of its specific activity in the precursor pool for protein synthesis, but this can be accomplished more easily in vitro. The factors known to affect protein synthesis and degradation in normal muscle, which are most likely to affect protein turnover in uremic muscle, are insulin-resistance and maladaptation to fasting. Few studies of the components of protein turnover in uremia have examined the effect of these or other factors.

Amino Acids↗
PubMed1981

Partial purification and characterization of the drug-binding-defect inducer in uremia.

The chemical basis of drug-binding defects in uremia was investigated by studying the effects of extraction of uremic sera with an organic solvent (n-butyl chloride). Extraction of uremic sera at acidic pH (3.0) with n-Butyl chloride fully corrected the binding defects for three acidic drugs (nafcillin, sulfamethoxazole, and salicylate), whereas binding of two basic drugs (trimethoprim and quinidine) was unaffected by similar treatment. When added to normal human serum or purified human serum albumin, the organic solvent layer was capable of inducing binding defects similar to those seen in uremia. Further fractionation of the organic solvent layer with purified human serum albumin at physiologic pH (7.4), followed by reacidification and extraction of the acidified albumin layer with the same solvent, gave a homogeneous fraction on thin-layer chromatography. This homogeneous fraction could induce the binding defects observed in uremia when added to normal human sera. This factor(s) is apparently a dialyzable and weakly acidic compound. It is lipid-soluble and tightly bound to albumin at physiologic pH, but extractable at acidic pH. Its molecular weight is approximately 500 or less. These findings strongly support the hypothesis that the drug-binding defect in uremia is due to accumulation of endogenous metabolic products rather than to an intrinsic structural abnormality in serum albumin.

Biological Products↗
PubMed1976

The roles of renal catabolism and uremia in modifying the clearance of fibrinogen and its degradative fragments D and E.

Elevated levels of fibrinogen/fibrin degradation products (FDP) occur in uremia, and have been thought to be in part related to intravascular coagulation in the kidney. More recent data indicated that delayed catabolism of fibrinogen fragment D occurred in anephric animals. To further evaluate FDP catabolism in the kidney, turnover studies of purified dog 131I-Fg-D and 125I-Fg-E were performed on dogs before and after acute subtotal nephrectomies, and later during chronic uremia. 131I-fibrinogen clearances were also perfomed. Slowed catabolism of Fg-D and Fg-E was observed in both the acute and chronic uremic stages. Altered urinary excretion was not a factor as only minimal amounts of Fg-D and Fg-E were excreted in the urine of the control animals. In the 131I-fibrinogen studies, there were significant changes in plasma volume, fibrinogen t 1/2, and intravascular/extravascular distribution, but not in fractional catabolic rate. To differentiate fully, the effects of uremia from those of loss of catabolic renal tissue, the Fg-D and Fg-E turnover studies were repeated on other animals with intact kidneys whose ureters were diverted into the peritoneum and compared to subsequent studies after total nephrectomy. The control and ureter-severed studies had the same clearance pattern, whereas decreased catabolism occurred in the nephrectomized dogs. The results demonstrate uremia per se does not have a major effect upon the catabolism of fibrinogen, Fg-D, and Fg-E. Loss of renal tissue does impair the clearance of Fg-D and Fg-E, indicating these proteins are normally catabolized in part by the kidneys. Thus elevated plasma FRA in uremic patients may reflect decreased Fg-D and Fg-E catabolism rather than increased FDP production from primary or secondary fibrinolysis.

Animals↗
PubMed1977

Alteration of plasma albumin in relation to decreased drug binding in uremia.

The binding of sulfadiazine in the plasma of normal and uremic subjects was measured by means of an ultrafiltration technique. Patients with uremia had reduced binding of sulfadiazine due to decreased albumin-binding capacity. No conclusive evidence was found to suggest that reduced drug binding in uremia is caused by competing metabolites. Studies of purified normal and uremic albumin revealed differences in amino acid composition and variations in the protein content of the two albumin bands found on isoelectric focusing. It is suggested that decreased drug binding in uremia may be at least partly due to altered albumin composition.

Adult↗
PubMed1991

Pentosidine: a molecular marker for the cumulative damage to proteins in diabetes, aging, and uremia.

Collagen undergoes progressive browning with age and diabetes characterized by yellowing, fluorescence, and cross-linking. The present research was undertaken in order to investigate the nature of the collagen-linked fluorescence. Human collagen was exhaustively cleaved into peptides by enzymatic digestion. Upon purification, a highly fluorescent chromophore was identified and purified from old human collagen. Structure elucidation revealed the presence of an imidazo [4,5-b] pyridinium-type structure acting as a cross-link between arginine, lysine, and a pentose. This advanced glycosylation end-product and protein cross-link results from the reaction of pentoses with proteins and was named pentosidine. Further work indicated that long-term glycosylation of proteins with hexoses also leads to pentosidine formation through sugar fragmentation. The proposed mechanism of pentosidine formation involves the dehydration of the pentose-derived Amadori compound to form an intermediate which is attacked under base catalysis by the guanido group of arginine. The strict requirement for the Amadori rearrangement is uncertain. However, oxidation is definitely involved since pentosidine is not formed in the absence of oxygen. Five-carbon sugars contributing to pentosidine formation could be formed from larger sugars by oxidative fragmentation or from trioses, tetroses, and ketoses by condensation and/or reverse aldol reactions. Pentosidine increases exponentially in human skin at autopsy. Mean age-adjusted skin levels were significantly increased in subjects with uremia and especially in type 1 diabetics with uremia vs. controls. In skin biopsy, levels were significantly elevated in all diabetic (type 1) vs. control subjects. The highest degree of association was with the cumulative grade of diabetic complication (retinopathy, nephropathy, arterial stiffness, and joint stiffness). Pentosidine also forms in various proteins other than collagen, although to a much lesser extent. In blood, pentosidine is mainly associated with plasma proteins and is highly elevated during uremia. In the lens, it is associated with both water-soluble and -insoluble protein fractions and is especially elevated during brunescent cataract formation. The origin of pentosidine in vivo is uncertain. Evidence suggests that the pentoses are the most reactive sugars in pentosidine formation in vitro; however, the origin and importance of free pentoses in vivo, especially during the diabetic state, are not certain. Possible origins include hemolysis and/or a defect in the primary pentose metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1987

Polyamines and uremia.

PAs are intracellular regulators of growth and anabolic processes. Toxic properties of PAs are conferred according to the increasing number of cationic charges. In uremia, PA accumulation occurs both in and outside the cell. Decreased PA synthesis and blunted PA pathway responses suggest PAs may participate in cellular down regulation. This would explain the lack of tissue responses to elevated plasma hormones, a feature of uremia. Such homeostatic control could prevent life-threatening PA toxicity due to an imbalance between production, degradation and excretion. The concurrent rise in plasma PA oxidative activity, while adversely influencing behavior of lymphocytes and neutrophils reduces the likelihood of direct PA toxicity. In addition, preliminary observation of increased glomerular size and capillary area of intact kidneys in PA treated mice suggest there could be a PA dependent adaptive enhancement of renal excretion in circumstances of decreased renal mass due to disease, thus, compensatory renal hypertrophy. It is important to further inspect the non-uremic chronic hyperpolyaminemias as they occur in man. The continued search for parallel adverse systemic and local effects will be useful in strengthening the base for understanding homeostatic consequences of PA accumulation unobserved by the complex mixture of uremic metabolites. In conclusion, we have examined some known regulatory and toxic properties of PAs and related these to features of the uremic syndrome. Available information on the various ramifications of PA dysmetabolism in uremia, as with other suspect toxins, is in part circumscribed and indirect. Caution is to be exercised in evaluating the new and provisional PA related cause and effect relationships suggested here.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗