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PubMed1981

Characteristics of active sodium and potassium transport in erythrocytes in children with different stages of symptomatic uremia.

Erythrocytes from 15 uremic children aged from 7 months to 16 years were analyzed for adenosine triphosphatase (total ATPase and ouabain sensitive ATPase i.e. Na+, K+-ATPase), sodium and potassium ions and ATP concentration, in some cases before and after therapeutic measures had been undertaken. No correlation was found between the levels of Na+, K+-ATPase and serum creatinine and all uremic children had Na+, K+-ATPase levels within the range for normal children. The children with rapidly progressive uremia had higher activities of Na+, K+-ATPase at the corresponding serum creatinine concentration than those with slowly progressive uremia. Longitudinally the Na+, K+-ATPase activities fell and the erythrocyte Na+-K+ ratio increased in slowly progressive uremia. Introduction of a low-protein, high-energy diet giving accelerated growth did not change the Na+, K+-ATPase activities, the concentrations of erythrocyte sodium and potassium ions or ATP. Hemodialysis gave a slight increase of Na+, K+-ATPase and of the erythrocyte Na+-K+ ratio, whereas renal transplantation resulted in a remarkable increase of Na+, K+-ATPase activity and decrease of Na+-K+ ratio. A distinct feature of uremic children with hypertension was a low erythrocyte Na+-K+ ratio and a high Na+, K+-ATPase level.

Adenosine Triphosphatases↗
PubMed1981

Effect of uremia on lymphocyte transformation and chemiluminescence by spleen cells of normal and Cryptococcus neoformans-infected mice.

The effect of uremia on immune incompetence was studied. BALB/c mice were infected with a minimally virulent strain of Cryptococcus neoformans 6 weeks before immune assay. Uremia was induced by intramuscular injection of 0.15 ml of glycerol. Pooled spleen cells from four experimental groups (normal, uremic, infected, and infected and uremic) were assayed by lymphocyte transformation (LT) and luminol-dependent chemiluminescence (CL) 24 h after induction of uremia. A greater response to phytohemagglutinin and concanavalin A stimulation in tests of LT and CL was exhibited by uremic cells than by nonuremic cells; however, the presence of BALB/c uremic serum resulted in lower responses by both LT and CL. Infected mice showed a greater response to mitogens than did noninfected mice, but no significant stimulation in response to heat-killed whole cells of C. neoformans. Spleen cell populations of uremic mice had a lower viability and a different composition of spleen cell subpopulations than did cell preparations from nonuremic mice.

Animals↗
PubMed1982

Synergism between immunosuppressive agents and uremia?

The susceptibility of uremic patients to infectious disease has been widely reported, but the host immune factors associated with the increased incidence of infection have not been clearly defined. In this study, the possibility of synergism between biologically active components that accumulate in uremia and immunosuppressive drugs used in the course of management was investigated. An animal model of chronic stable uremia was used in these experiments to assess the effect of cyclophosphamide, methotrexate, and azathioprine on antibody response in the uremic host. Chronic uremia did not affect the immunosuppressive activity of cyclophosphamide, methotrexate, or azathioprine, and synergism between these agents and uremic components is unlikely to complicate further the immune status of the host in renal failure.

Animals↗
PubMed1986

Reduced chronotropic responsiveness of the heart in experimental uremia.

Cardiac beta-adrenoceptor responsiveness was evaluated in experimental uremia by in vivo and in vitro techniques. Uremia was induced in rats by bilateral nephrectomy for 48 h. In rats with chronic intra-arterial and intravenous catheters, cardiovascular reflexes and the renin-angiotensin system were blocked with atropine, pentolinium, and a converting-enzyme inhibitor, respectively. Blood pressure (BP) and heart rate (HR) were continuously recorded. Cumulative doses of isoproterenol were injected intravenously. In uremic rats, the dose-response curve for the HR response showed a lower maximal response (P less than 0.01) and no significant difference in 50% effective dose values compared with controls, whereas the BP decrease caused by isoproterenol was similar in control and uremic rats. When forskolin was injected intravenously to stimulate adenylate cyclase in a receptor-independent manner, the maximal HR increase was lower in uremic rats (P less than 0.01). beta-Adrenoceptor density and affinity, measured by 125I-cyanopindolol binding to sarcolemmal membranes, was not different between control and uremic rats. Also binding affinities for the agonist isoproterenol were not different between groups. Basal adenylate cyclase activity, as well as activity after maximal stimulation by isoproterenol and by forskolin were lower in uremic than in control rats (P less than 0.01). The results show that the chronotropic response of the heart is reduced in uremia. Such hyporesponsiveness may be due, at least in part, to a reduced activity of cardiac adenylate cyclase.

Adenylyl Cyclases↗
PubMed1999

Oxidative protein damage with carbohydrates and lipids in uremia: 'Carbonyl stress'.

Chronic uremia appears to be in a state of an increased oxidative stress. Under oxidative stress, proteins are modified directly by reactive oxygen species with the eventual formation of oxidised amino acids. Proteins are also modified indirectly with reactive carbonyl compounds formed by the autoxidation of carbohydrates and lipids, with the eventual formation of the advanced glycation/lipoxidation end products (AGEs/ALEs). AGEs, pentosidine and carboxymethyllysine (CML), and ALE, malondialdehyde (MDA)-lysine, are elevated in plasma and matrix proteins of uremic patients several times above normal subjects. Precursor carbonyl compounds derived from carbohydrates and lipids are indeed elevated in uremic circulation. Uremia thus appears to be in a state of carbonyl overload with potentially damaging proteins (carbonyl stress). Carbonyl stress might be relevant to long-term complications associated with chronic renal failure and dialysis, such as dialysis-related amyloidosis and atherosclerosis. Immunohistochemical studies identified carbonyl stress in long-lived amyloid deposits and vascular lesions. Proteins modified under carbonyl stress exhibit several biological activities, which might, at least in part, account for the development of joint and vascular complications in uremia.

Carbohydrate Metabolism↗
PubMedDate not supplied

Apolipoprotein C-III, hypertriglyceridemia and triglyceride-rich lipoproteins in uremia.

Apolipoprotein C-III (ApoC-III) plays an important role in the metabolism of triglyceride-rich lipoproteins and is known to be elevated in patients with uremia. To investigate the role of apoC-III in uremic dyslipidemia, we examined apoC-III, triglyceride levels and lipoprotein particles containing both apoB and apoC-III (LP-Bc) in 27 uremic patients prior to dialysis (predialysis), 30 patients on hemodialysis (HD) and 31 patients on peritoneal dialysis (PD). All three groups of patients had elevated levels of plasma apoC-III (20+/-7 mg/dl for predialysis, 18+/-5 for HD and 22+/-8 for PD, compared to 11+/-3 mg/dl for control subjects [p<0/01 for all comparisons]). ApoC-III was positively correlated with plasma triglycerides in PD patients (r = 0.86, p<0.0001), HD patients (r = 0.67, p<0.0001) and predialysis patients (r = 0.60, p<0.001) as well as in all patients combined (r = 0.75, p<0.0001). ApoC-III was also positively correlated with levels of LP-Bc in all three groups of patients, although this correlation was less strong (r = 0.46, p<0.0001 for all patients combined). In predialysis and PD patients, the majority of apoC-III was found in heparin precipitable lipoproteins, whereas the majority of apoC-III in HD patients was found in HDL, indicating less efficient lipolysis in predialysis and PD patients in comparison with HD. These data support the hypothesis that the elevation of apoC-III in uremia can alter the metabolism of triglyceride-rich lipoproteins, leading to an elevation in triglycerides and LP-Bc. Understanding the mechanism(s) of elevated apoC-III in uremia may help to clarify the causes of uremic dyslipidemia.

Adult↗
PubMed2004

Effect of dietary creatine on skeletal muscle myosin heavy chain isoform expression in an animal model of uremia.

BACKGROUND: Chronic renal failure is accompanied with muscle dysfunction and myopathy, characterized by muscle weakness and increased fatigue. Myosin heavy chain (MHC) is the principal structural protein that controls the intrinsic contractile properties of striated muscle. Creatine is widely used as an ergogenic nutritional supplement in sportsmen. This study investigates the effect of creatine supplementation on MHC expression in the setting of uremic myopathy. METHODS: Male Wistar rats were either sham operated or subtotally nephrectomized and received a control diet or creatine (2% w/w)-supplemented diet. After 4 weeks of treatment, serum creatinine, creatine, urea and creatinine clearances were determined. MHC isoforms were determined electrophoretically in the extensor digitorum longus and soleus muscles. RESULTS: Creatinine clearances were lower in nephrectomized animals, but similar in creatine-supplemented and control diet animals. Nephrectomized animals had significantly higher MHC IIb and lower MHC IIx isoform expression in the extensor digitorum longus muscle compared to sham-operated animals. In the soleus muscle, MHC IIb expression was increased in nephrectomized animals. Creatine supplementation reversed the MHC transitions observed in uremia in the soleus muscle, but not in the extensor digitorum longus muscle. CONCLUSION: We observed altered expression of MHC isoforms in uremia. In uremic animals, fast MHC IIb isoforms were increased, whereas MHC I and IIx isoforms predominate in control animals. Dietary creatine supplementation reversed the altered MHC expression during uremia in slow-twitch, but not in fast-twitch muscles.

Administration, Oral↗
PubMed1985

Parathyroid hormone and the altered vascular response to norepinephrine in uremia.

Patients with chronic renal failure manifest reduced pressor response to norepinephrine (NE); this abnormality is at least partly responsible for the autonomic nervous system dysfunction observed in these patients. Since uremia is associated with increased levels of parathyroid hormone (PTH) and since PTH blunts the pressor effect of NE most likely via activation of prostaglandins, we have studied the relationship between blood levels of PTH and the reduced pressor response to NE in 17 uremic patients and we examined the effect of treatment with indomethacin on the response to NE in 9 uremic and 5 normal subjects. There was a significant negative correlation (r = -0.63, p less than 0.01) between the changes in blood pressure and the blood levels of PTH in uremic patients. Treatment with indomethacin was followed by significant improvement or normalization of the pressor response to NE in uremic patients. These data are consistent with the notion that the decreased pressor response to NE in uremia is due to increased production of prostaglandins induced by excess PTH and provide a therapeutic tool for the treatment of some of the manifestations of autonomic nervous system dysfunction in uremia.

Adult↗
PubMed1982

Elevated thrombocyte calcium content in uremia and its correction by 1 alpha(OH) vitamin D treatment.

Intracellular calcium plays an important role in the regulation of platelet function. It has also been demonstrated that platelet functions are impaired in uremia. A rise in intracellular calcium has been shown in several tissues and has been held responsible for the impaired function of several organs seen in uremia. This study was undertaken to evaluate whether the calcium (Ca) content of thrombocytes is elevated in uremia and, if so whether treatment with an active vitamin D metabolite might correct this abnormality. In 10 patients on chronic hemodialysis, platelet Ca content was determined by a technique utilizing consecutive freezing and thawing of platelet-rich plasma. The platelet Ca content of uremic patients was found to be markedly higher (20.86 +/- 0.9 ng/200,00 platelets, p less than 0.01) than that of a group of 20 normals (12.8 +/- 1.2 ng/200,000 platelets). 1 months after treatment with 1 alpha (OH) vitamin D at a dosage of 0.5-2.5 microgram/day, the platelet Ca content of the dialysis patients decreased to 14.99 +/- 2.14 ng/200,000 platelets (p less than 0.05). The data show that in dialysis patients the platelet Ca content is markedly elevated in comparison with that of normals, and the treatment with 1 alpha (OH) vitamin D may significantly reverse this abnormality. It is suggested that elevated Ca content may play a role in the pathogenesis of uremic platelet dysfunction, and that 1 alpha (OH) vitamin D administration may be of benefit in correcting this disorder.

Adolescent↗
PubMed1983

Prolidase and prolinase activities in the erythrocytes of patients with chronic uremia.

To elucidate the nature of the iminoacidopathy in uremia, the prolidase and prolinase activities in erythrocytes from 36 normal subjects, 28 patients with chronic uremia, and 21 patients on maintenance hemodialysis were determined. A statistically significant decrease in the activities of both prolidase and prolinase was found in the uremic patients and the hemodialysis group. No difference has been observed in the enzyme activities in the pre- and postdialysis samples of the hemodialysis patients. It is suggested that decreased activities of prolidase and prolinase may contribute to the iminoacidopathy in uremia, including high contents of serum iminoacid containing peptides.

Adult↗
PubMed1986

Plasma fibronectin levels in patients with chronic uremia.

Plasma fibronectin (FN) concentration was measured in patients with idiopathic glomerulonephritis (GN) with or without impaired renal function, in uremic patients undergoing periodic hemodialysis and in renal transplant patients before and after an acute rejection crisis. Results show normal FN levels in idiopathic GN and in renal transplant patients with normal renal function, while significantly lower levels were found in GN with severe renal damage, in uremia before and after dialysis, and in renal transplant patients during acute and chronic graft rejection. Significant correlations between high serum creatinine values and low plasma FN levels were found in renal transplant patients. These findings suggest that the kidney may influence FN levels in the blood since acute (rejection crisis) and chronic renal failure (uremia) cause low concentrations of this protein, while levels tend to return to normal values in patients with uremia after renal transplantation. We hypothesize that the normal kidney removes or perhaps degrades some substances or hormones that may control the release or synthesis of FN. These substances are not dialyzed by cellophane membranes since low plasma FN levels persist after periodic hemodialysis. Only the renal graft provokes an increase of FN in the blood stream.

Adult↗
PubMed1987

Circulating hyaluronate. A potential marker of altered metabolism of the connective tissue in uremia.

Hyaluronate, a glycosaminoglycan of connective tissue matrix, was measured in serum by radioassay in patients with renal insufficiency (n = 22) and with end-stage renal failure (n = 40). The serum hyaluronate levels were significantly increased in both groups compared with the levels measured in age- and sex-matched healthy controls. Significant correlations were found between serum hyaluronate and degree of impaired renal function. None of the patients had laboratory signs indicating affection of the liver, the major elimination route for circulating hyaluronate. No significant alteration of hyaluronate levels was seen during hemodialysis. Renal transplants, previously on dialysis treatment, had normal serum hyaluronate values. Data obtained indicate either an essential role of the kidneys for the elimination of circulating hyaluronate or an increased outflow of hyaluronate to the circulation in uremia or a combination of these two possibilities. The altered metabolism of hyaluronate in uremia was not only related to the azothemic state but also to the age of the patients. The mechanism may be qualitively similar to that underlying the age-dependent increase of serum hyaluronate seen in health. The hypothesis that elevated serum hyaluronate in uremia may reflect an accelerated ageing of the connective tissue is highly speculative, but has some support by the finding that cardiovascular and other clinical symptoms were linked to particularly high serum levels of hyaluronate.

Adult↗
PubMed1989

Significant increase of IQ-type heterocyclic amines, dietary carcinogens in the plasma of patients with uremia just before induction of hemodialysis treatment.

The concentrations of 2-amino-3-methylimidazo(4,5-f) quinoline (IQ) and 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline (MeIQx), a family of mutagenic and carcinogenic heterocyclic amines, in the plasma of normal subjects (10 cases), patients with uremia receiving maintenance hemodialysis treatment (9 cases) and patients with uremia just before induction of hemodialysis treatment (5 cases) were determined by a high-performance liquid chromatography method. The plasma levels of IQ and MeIQx in uremic patients just before induction of hemodialysis treatment were 12.6 +/- 4.1 nM (mean +/- S.D., n = 5) and 10.0 +/- 2.3 nM (n = 5), respectively. In patients with uremia receiving maintenance hemodialysis treatment, IQ and MeIQx were detected in 4 and 2 out of 9 cases, respectively and the levels of those in the plasma were 4.1 nM (n = 4) and 1.7 nM (n = 2), respectively. However, IQ and MeIQx could not be detected in all normal subjects. These results indicate that uremic patients just before induction of hemodialysis treatment are actually exposed to higher levels of the carcinogenic heterocyclic amines, as compared with normal subjects and uremic patients receiving maintenance hemodialysis treatment.

Adult↗
PubMed1993

Plasma parameters of the prothrombotic state in chronic uremia.

We measured plasma parameters of the prothrombotic state, namely thrombin-antithrombin III complex (TAT), fibrinopeptide A (FPA). D-dimer (DD), von Willebrand factor (vWF), tissue-type plasminogen activator (tPA), beta-thromboglobulin (beta TG), platelet factor 4 (PF4) and serotonin (5HT) in a series of 51 adult patients with chronic uremia: 22 were on maintenance hemodialysis (MHD) and 29 on conservative dietary treatment. Serum tumor necrosis factor alpha (TNF) was determined as well. Uremics presented significantly higher levels of TAT, FPA, DD, vWF, TNF, beta TG and 5HT than normal controls. Patients on conservative treatment showed lower levels of TAT, DD, TNF and beta TG than patients on MHD. Our results provide evidence that a prothrombotic state exists in chronic uremia and that MHD patients have a higher degree of hypercoagulation. Both hemodialysis procedure and uremia-related factors are likely to contribute to the hemostatic derangement.

Adult↗
PubMed1994

Analysis of platelet abnormalities in uremia with and without Glanzmann's thrombasthenia.

Uremia causes a bleeding tendency associated with platelet dysfunction, and previous studies have shown abnormalities of platelet glycoprotein (GP) Ib or GPIIb/IIIa and a tendency for platelet activation in uremia. The present study compared the abnormalities of platelet function in uremia with (n = 1) or without (n = 18) associated Glanzmann's thrombasthenia. There was a significant difference between ristocetin-induced agglutination of platelets from the uremic patients without Glanzmann's thrombasthenia and platelets from healthy controls (n = 15). In addition, a reduction of GPIb expression by uremic platelets along with normal GPIIb/IIIa expression was confirmed using flow cytometry. Many coagulation markers were increased in the uremic patient with Glanzmann's thrombasthenia, suggesting that the coagulation was enhanced and the platelets were prone to activation. However, the thrombasthenic platelets actually showed little increase in the binding of a monoclonal anti-CD63 antibody directed against lysosomal integral membrane protein (which is expressed after platelet activation), while uremic platelets showed a marked increase. In addition, the expression of GPIb by thrombasthenic platelets was normal, while that of GPIIb/IIIa was markedly decreased. Our results suggest that thrombasthenic platelets are resistant to activation and to the degradation of GPIb under uremic condition and that this difference from 'ordinary' uremic platelets be related to the difference in GPIIb/IIIa.

Adult↗
PubMed1996

Iron absorption in patients with chronic uremia on maintenance hemodialysis and in healthy volunteers measured with a simple oral iron load test.

Gastrointestinal iron absorption was measured by an oral iron load test in patients with uremia on maintenance hemodialysis (n = 19), with iron overload (n = 9), iron deficiency (n = 10) and in healthy volunteers (n = 9). After an overnight fast, serum iron was measured before, and 1, 2, 4 and 6 h after administration of 100 mg ferrous chloride. Bone marrow iron was assessed after staining with Prussian blue. The study shows that iron absorption is impaired in uremic patients. Even uremic subjects with iron deficiency absorbed significantly less than normal subjects. Patients with iron overload and uremia absorbed even less, showing that the iron status of the patient influences absorption also in uremia.

Adult↗
PubMed1982

Lymphocyte kinetics in acute uremia: redistribution of circulating lymphocytes to the bone marrow.

The mechanism(s) responsible for the peripheral blood lymphocytopenia found in uremia was investigated. Inbred Magnum guinea pigs were made uremic by ureteral ligation, and 1 day later injected with chromium (Cr)51-labeled syngeneic lymphocytes intravenously. 1 day later, the animals were sacrificed and organs counted for radioactivity. Sham-operated animals served as controls. Radioactivity in the lung and liver was the same or greater in the sham-operated animals than in uremic animals. In the blood and spleen, radioactivity was slightly higher in the uremic animals, while in the long bones this was significantly higher. In uremia therefore, there appears to be a redistribution of circulating lymphocytes to the bone marrow. The resultant lymphocytopenia may play a role in the immunologic incompetence seen in uremia.

Animals↗
PubMed1986

Studies on therapy of metabolic alkalosis during experimental uremia. Influences of arginine-hydrochloride on the intra- and extracellular acid-base status of the rat.

Severe metabolic alkalosis, combined with acute renal failure or uremia presents a difficult problem for the clinician. The standard treatment modalities of metabolic alkalosis are then limited and infusion of arginine-HCl is often tried in these cases. It was the purpose of this investigation to study the effects of arginine-HCl on the whole-body acid-base status during experimental uremia. While the extracellular acid-base status was determined from blood-gas measurements, the intracellular pH was calculated from the distribution of 5,5-dimethyl-2,4-oxazolidinedione. It was found that administration of arginine-HCl leads to a significant increase of intracellular pH though extracellular plasma pH decreases, and that arginine-HCl causes only an insignificant reduction of the intracellular bicarbonate concentration. The observed intracellular pH increase may have adverse consequences for patients and raises objections to the further use of arginine-HCl in the treatment of metabolic alkalosis, especially during renal failure or uremia.

Acid-Base Equilibrium↗