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At least 19 recordsLinked to original sources
PubMed1979

Hypomagnesemia. Suppression of secondary hyperparathyroidism in chronic renal failure.

Chronic renal failure is accompanied by secondary hyperparathyroidism. Inhibition of parathyroid hormone secretion has been reported to be induced by hypomagnesemia in conditions other than chronic renal failure, since severe hypomagnesemia is rare in chronic renal failure. In the case reported here, the patient had chronic renal failure and malabsorption-induced hypomagnesemia; she exhibited hypoparathyroidism while hypomagnesemic, and hyperparathyroidism after magnesium was replaced. Hypomagnesemia induced parathyroid hormone suppression in this patient with chronic renal failure, despite the presence of chronic hyperfunctioning parathyroid cells.

Female↗
PubMed1989

Vestibular functions in conservatively treated chronic renal failure.

Chronic renal failure can produce malfunction of multiple organs, including auditory and vestibular apparatus. Twelve patients of chronic renal failure of varying etiologies treated conservatively were subjected to vestibular function tests. Only 33% of the patients had normal ENG data. Fifty-eight per cent of the patients had canal paresis and 8% showed hyperactive response. Ototoxic drugs like furosemide may be most important factor in aetiology of vestibular dysfunction in chronic renal failure.

Adult↗
PubMed1985

Atriopeptin III. A potent natriuretic, diuretic, and hypotensive agent in rats with chronic renal failure.

Chronic renal failure is frequently associated with volume overload, resulting in hypertension and, in some cases, congestive heart failure. Atriopeptin III (AP III), a 24-amino acid atrial peptide, is a potent vasodilator and natriuretic/diuretic agent in normal rats. An infusion of AP III at 0.2 microgram/kg per min for 60 min produced dramatic responses in animals with chronic renal failure (5/6 nephrectomy 4 wk before study). Systemic blood pressure fell 20% by the end of infusion. A pronounced rise in glomerular filtration rate (24%) was maintained during the infusion period when urine flow rate was stable (35-60 min), even though renal blood flow was unchanged from base line. Urinary volume increased 4.4-fold and sodium excretion increased 9 to 12-fold during the infusion. Fractional excretion of sodium ranged between 9 and 15% in those animals whose initial GFR values were lower than 0.5 ml/min. We conclude that AP III is a potent natriuretic/diuretic agent in rats with reduced renal mass, presumably exerting that effect predominantly through increases in GFR. This agent may well be useful in the treatment of volume overload in patients with chronic renal failure.

Animals↗
PubMed1991

Disturbances of cerebral purine and pyrimidine metabolism in young children with chronic renal failure.

Chronic renal failure during childhood may be associated with delayed cognitive development. From 10 children with chronic renal failure, aged 2-59 months, plasma and cerebrospinal fluid (CSF) purines and pyrimidines have been determined. A marked increase of pseudouridine and cytidine was demonstrated in CSF of 10 and 8 children, respectively. The plasma concentration of pseudouridine was increased in a varying degree to a maximal value of more than 10 times the upper limit of normal. The plasma concentration of cytidine showed only moderately elevated values. In 3 children the study of CSF and plasma was repeated 6 weeks after the start of continuous ambulatory peritoneal dialysis. The abnormal concentrations of pseudouridine and cytidine were still present in CSF and plasma. Further studies are necessary to elucidate the cause of this unknown biochemical aberration of the central nervous system.

Cerebral Cortex↗
PubMedDate not supplied

[Enoxaparin in the prevention of thrombosis of extracorporeal circulation during dialysis of patients with chronic renal failure].

Chronic renal failure patients under haemodialysis are exposed to two dangers: haemorrhage and clotting of the extracorporeal circulation circuit. This problem can be solved by using low molecular weight heparins. Two studies were conducted to evaluate the effectiveness and safety of a low molecular weight heparin: enoxaparin. The first study, which involved 42 chronic renal failure patients under haemodialysis without any particular risk, enabled the optimum dosage (1 mg/kg bodyweight) to be determined. The second study, which concerned 46 patients at high risk of haemorrhage who received enoxaparin 0.5 mg/kg or 0.75 mg/kg depending on the vascular approach, confirmed that enoxaparin was highly effective (clotting of the extracorporeal circuit in only 0.6 p. 100 of the cases) and well tolerated (bleeding in only 0.2 p. 100 of the cases).

Adult↗
PubMed1986

Effects of tertatolol in hypertensive patients with chronic renal failure.

Chronic renal failure (CRF) is often associated with hypertension, as a cause or a consequence. We studied the changes in blood pressure (BP), heart rate (HR), renal function (as measured by creatinine clearance), and plasma renin activity (PRA) in 19 hypertensive patients with CRF before, during and after oral administration once a day for at least 30 days of 5 mg tertatolol, a new beta-blocker. All patients were free of any antihypertensive medication for at least 1 month before administration of tertatolol. The dose of tertatolol given in this study was the same as that commonly used in patients with normal renal function. From day 0 to day 30 of tertatolol, measurements in the supine position were as follows: systolic BP (SBP) decreased from 168.4 +/- 4.6 to 145.3 +/- 4.3 mm Hg (p less than 0.01); diastolic BP (DBP) decreased from 106.1 +/- 2.4 to 87.1 +/- 2.0 mm Hg (p less than 0.01); HR decreased from 77.9 +/- 1.6 to 63.2 +/- 1.7 b.p.m. (p less than 0.01); PRA decreased from 1.816 +/- 0.521 to 1.052 +/- 0.323 ng/ml/h (p less than 0.01). Creatinine clearance remained stable: 37.1 +/- 4.1 versus 37.1 +/- 4.7 ml/min/1.73 m2 (not significant). Similar results (for SBP, DBP, HR and PRA) were obtained in the erect position. It is concluded that tertatolol in hypertensive patients with CRF: significantly lowers BP and HR without excessive bradycardia, significantly lowers PRA, the most important decrease being observed for the highest initial PRA, does not alter renal function, and has a good clinical acceptability.

Adrenergic beta-Antagonists↗
PubMed1992

Effect of growth hormone therapy on IGF-I, bone GLA-protein and bone mineral content in short children with and without chronic renal failure.

Chronic renal failure (CRF) in the young is complicated by, among other conditions, growth retardation, hyperparathyroidism and uremic osteodystrophy. Many children with CRF are now being treated with growth hormone (GH). Since GH has a direct mitogenic effect on osteoblasts in culture, we studied the effects of GH therapy on osteoblastic activity, such as serum alkaline phosphatase (AP), bone GLA-protein (BGP) and bone mass density (BMD) in poorly growing children with and without CRF. Fifteen (4 girls, 11 boys) healthy children with short stature (SS) and 10 (3 girls, 7 boys) children with end-stage renal failure (CRF) 4.5-12.4 years of age were treated with daily subcutaneous injections of GH in a dose of 0.1-0.125 IU/kg/day for 1 year. IGF-I, BGP and BMD of the spine were determined before and after the year of treatment. During GH therapy, a similar increase in height velocity and IGF-I were noted in SS and CRF groups: 3.8 +/- 0.77 to 8.38 +/- 1.25 (p < 0.001) vs. 4.0 +/- 0.6 to 7.14 +/- 1.3 cm/year (p < 0.001) and 7.8 +/- 2.6 to 21.8 +/- 7.5 (p < 0.01) vs. 7.9 +/- 1.3 to 21.5 +/- 5.6 nmol/l (p < 0.01), respectively. AP increased from 205 +/- 27 to 274 +/- 50 IU/l (p < 0.01) in the SS group but not in CRF patients (223 +/- 58 pre- 218 +/- 51 IU/l post-GH therapy).(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMed1985

Biochemical changes in the pancreas of rats with chronic renal failure.

Chronic renal failure (CRF) was produced in female Sprague-Dawley rats by 7/8 nephrectomy. Creatinine clearance was depressed significantly (P less than 0.005) and blood urea nitrogen (BUN) increased in CRF rats when compared with the sham-operated (S) controls. CRF caused no apparent change in body weight but significantly increased pancreatic weight as well as increased DNA, RNA, and protein content. Pancreatic protein-to-DNA and RNA-to-DNA ratios were also found to be significantly higher in CRF rats than in the S controls. Trypsin-like activity and immunoreactive cationic trypsinogen levels were both increased in the pancreas of CRF rats, but not in their serum. On the other hand, protease inhibitory activity in the pancreas and serum was significantly decreased by CRF. The ability of the dispersed pancreatic acini isolated from CRF rats to incorporate [3H]-leucine into protein, in the absence and presence of 0.25 nM cholecystokinin octapeptide (CCK-8), was found to be lower than in the controls. Furthermore, discharge of both trypsinogen and chymotrypsinogen induced by CCK-8 was markedly reduced from acini of CRF rats as compared with the S controls. In contrast, lactate dehydrogenase (LDH) was released more readily from pancreatic acini of CRF. It is concluded that mild CRF produces hyperplasia and hypertrophy of the pancreas and lowers the responsiveness of acini to CCK-8 with respect to synthesis and secretion of proteins.

Animals↗
PubMed1991

Atrial natriuretic peptide concentration in dogs with congestive heart failure, chronic renal failure, and hyperadrenocorticism.

The function of atrial natriuretic peptide (ANP) is claimed to be control of salt and water homeostasis, and thus, the hormone may be involved in the pathogenesis of certain diseases with impaired volume regulation. We, therefore, studied plasma ANP concentration in dogs with chronic renal failure, congestive heart failure, and hyperadrenocorticism. Dogs with chronic renal failure had twofold higher plasma ANP concentration (16.2 +/- 5.8 fmol/ml), compared with healthy dogs (8.3 +/- 3.5 fmol/ml). An even more distinct increase (sixfold) of plasma ANP concentration was found in dogs with congestive heart failure (52.9 +/- 29.7 fmol/ml). In contrast, dogs with hyperadrenocorticism did not have high ANP plasma concentration (5.5 +/- 2.0 fmol/ml). High-performance liquid chromatographic analysis of plasma from dogs with congestive heart failure indicated that, in addition to the normal circulating form of ANP (99-126), the unprocessed precursor ANP (1-126) is detectable in the circulation. These qualitative and quantitative alterations of plasma ANP concentration in dogs further suggest involvement of this peptide in the development and/or maintenance of diseases associated with impaired volume regulation.

Adrenocortical Hyperfunction↗
PubMed1990

[Equivalence values of the antioxidative capacity in serum of children with chronic renal failure, chronic hemodialysis and kidney transplantation].

It is reported on the results of measurements of the antitoxydative capacity (AC) in the serum of children suffering from chronic renal failure, during hemodialysis and after kidney Transplantation. The results show in comparison with healthy children (19.95 +/- 5.22 mm, n = 19) that children suffering from chronic renal failure may develop an increased AC (66.18 +/- 29.14 mm, n = 24). In dialyzed children different values are found previous and after hemodialysis (58.11 +/- 9.25 vs. 17 +/- 3.6 mm). Children show after transplantation the highest values (78.9 +/- 26.04 mm, n = 13). If the increase of the AC is a compensatory and regulatory mechanism or the result of accumulation of antioxydative substances should realized in further investigations. The measurements of vitamin-E-supplemented sera may show that an oral application of vitamin E increase the AC in vivo.

Antioxidants↗
PubMed1990

[Malondialdehyde concentration in the serum of children with chronic renal failure, chronic hemodialysis and kidney transplantation].

The malondialdehyde equivalent (MDE) was measured by the thiobarbiturate method quantitatively in serum of healthy children, children suffering from chronic renal failure and after kidney transplantation. In the reference group (n = 19) a serum concentration of 3.98 +/- 0.84 nmol/ml was found. Elevated MDE serum concentrations were measured in all groups suffering from renal disease: groups with various degree of diminished renal function (7.05 +/- 2.12 nmol/ml; n = 24), children treated by chronic hemodialysis (6.38 +/- 0.98 nmol/ml; previous dialysis and 6.27 +/- 0.63 nmol/ml after dialysis, n = 9) and children after renal transplantation (6.59 +/- 1.14 nmol/ml; n = 13). In the hemodialysis group the MDE concentration was not affected by a single dialysis nor by sixth months dialysis course. A cell-damaging lipid peroxidation in children suffering from renal diseases is reflected by the investigations.

Adolescent↗
PubMed1985

Bromocriptine and the hypothalamic hypophyseal function in patients with chronic renal failure on chronic hemodialysis.

Ten patients with chronic renal failure on chronic hemodialysis had the following tests to evaluate the integrity of the hypothalamic hypophyseal axis: (A) glucose tolerance test, (B) thyrotropin releasing hormone stimulation test, (C) clonidine stimulation test, (D) insulin induced hypoglycemia, and (E) LH/RH stimulation test. The majority of those tests were abnormal and prolactin values were found to be moderately elevated in all the patients. Bromocriptine (1.25 mg twice a day) was given to all the patients for 1 month and then, while on bromocriptine, the tests were repeated. Although there is a decrement in the concentration of serum prolactin level, none of the hypothalamic hypophyseal abnormalities were corrected. However, five of the ten patients reported an improvement of their impotence with bromocriptine. The patients who responded had high levels of FSH and LH with levels of testosterone above 1 mg/mL. The nonresponders had low FSH and LH levels and very low testosterone levels. Therefore, bromocriptine, although possibly beneficial in some dialysis patients, is not a drug that can normalize abnormal functioning of hormones in the dialysis population.

Adult↗
PubMed1990

[Glycosylated plasma proteins in chronic renal failure].

In chronic renal failure HbA1c values and plasma fructosamine concentrations are difficult to interpret owing to anaemia (for HbA1c) and analytical interferences (for fructosamine test). Plasma proteins glycation was measured more specifically by affinity chromatography. Glycated albumin, glycated immunoglobulins G and glycated proteins were determined in 30 control patients, 30 diabetics and 28 patients with chronic renal failure divided into 17 non diabetics and 11 diabetics. Glycated albumin, glycated IgG and glycated total proteins were not modified by chronic renal failure in non diabetic patients on the contrary of HbA1c and fructosamine test.

Adolescent↗
PubMed1991

Altered growth hormone response after growth hormone releasing hormone administration in chronic renal failure.

Eleven chronic renal failure patients and 11 matched controls, received growth hormone GHRH (1 microgram/kg iv) or TRH (400 microgram iv) on separate occasions, immediately before undergoing hemodialysis. GHRH-induced GH peak in uremics (22.7 +/- 5.2 micrograms/l) was not different from that obtained in control subjects (16.0 +/- 4.3 micrograms/l). However, the uremic patients did not show the habitual post-peak fall, remaining GH levels over 10 micrograms/l till the end of the test. Differences between the two groups were significant (p less than 0.05). Uremic patients showed PRL values higher than in controls, however their TRH-induced PRL peak (20.6 +/- 6.6 micrograms/l) was not different from that of controls (26.5 +/- 3.0 micrograms/l). Again chronic renal failure patients showed PRL plasma values abnormally elevated till the end of the test. Differences between the two groups were significant (p less than 0.05). Administration of placebo to a different group of seven uremic patients did not alter GH and PRL plasma levels. This sustained secretion of both GH and PRL in uremia could be attributed to reduced kidney clearance. However, when subjects were examined individually both the GHRH- and the TRH-induced hormonal peaks and the subsequent fall were not different in both groups. Unlike with controls, in uremic patients GHRH-stimulated GH and TRH-stimulated PRL/GH peaks were dispersed throughout the 120 min period. In controls GH and PRL peaks clustered around 15-30 min. The peak dispersion created a false impression of flattened curves or sustained hypersecretion in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Exogenous calcitonin protects against renal bone disease in rats with early renal failure.

Chronic renal failure was induced in four groups of male Sprague-Dawley rats by unilateral nephrectomy followed by removal of the outer poles and cautery of the remnant kidney. The four groups of animals received isocaloric diets with normal (groups 1 and 4) or low (groups 2 and 3) phosphate contents and variable amounts of calcium. In addition, rats in group 4 were given salmon calcitonin. After 90-160 days the 4 groups of rats had developed comparable levels of chronic renal failure. The serum phosphate values were significantly lower in rats on low phosphate intake than in those on normal phosphate diet. Bone histology was evaluated on tibiae, lumbar vertebrae and ribs. The rats kept on low phosphate diet (groups 2 and 3) had significantly lower frequency of osteomalacia and bone resorption than those fed a normal phosphate diet. Rats treated with calcitonin (group 4) had the lowest frequency of osteomalacia and virtually no association with bone resorption, despite normal phosphate intake. The serum levels of parathyroid hormone were not significantly different in rats in groups 1 and 4 as compared to controls. Serum 1,25-dihydroxycholecalciferol levels were significantly lower in group 1 than in controls and were significantly higher in group 4 than in group 1. These data show that calcitonin effectively prevents bone lesions in rats with early chronic renal failure.

Animals↗
PubMed1987

Verapamil protects against progression of experimental chronic renal failure.

Chronic administration of verapamil (Ver) decreases nephrocalcinosis and tubular ultrastructural abnormalities in the remnant model of chronic renal disease. In the present study, the effect of chronic Ver administration on renal function, renal histology and mortality after subtotal nephrectomy was examined. Fourteen days after staged subtotal nephrectomy rats were paired according to renal functional impairment, mean arterial pressure (MAP), and body weight. Rats were pair fed and received either Ver (0.1 micrograms/g sc bid, N = 10) or saline (0.1 ml sc bid, N = 10) for up to 23 weeks. Both members of each pair were sacrificed shortly before the uremic death of controls. At sacrifice, rats treated with Ver had a lower serum creatinine (2.29 vs. 2.99 mg/dl, P less than 0.05) and a higher creatinine clearance (318 vs. 164 microliters/min, P less than 0.05) than controls. In a second experiment, survival was superior in rats treated with Ver than in controls from week seven (P less than 0.0025 by week 14). Serum creatinine was higher at week 10 in control rats (1.68 vs. 1.10 mg/dl, P less than 0.05). MAP was no different between the two groups, irrespective of the time between Ver administration and the measurement of MAP. Histological damage and nephrocalcinosis were worse, and renal and myocardial calcium content was higher in controls. In conclusion, independent of any effect on systematic MAP, chronic administration of Ver protects against renal dysfunction, histological damage, nephrocalcinosis and myocardial calcification, and improves survival in the remnant model of chronic renal disease.

Animals↗