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1. |
Title Page |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 117-117
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ISSN:1660-8151
DOI:10.1159/000180440
出版商:S. Karger AG
年代:1975
数据来源: Karger
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2. |
Table of Contents |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 118-118
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PDF (57KB)
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ISSN:1660-8151
DOI:10.1159/000180441
出版商:S. Karger AG
年代:1975
数据来源: Karger
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3. |
An Outline of the Uremic Syndrome |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 119-122
S. Giovannetti,
G.M. Berlyne,
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PDF (438KB)
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ISSN:1660-8151
DOI:10.1159/000180442
出版商:S. Karger AG
年代:1975
数据来源: Karger
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4. |
Uremic Intoxication |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 123-133
Sergio Giovannetti,
Giuliano Barsotti,
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摘要:
The toxic effects of metabolites that are known to accumulate in renal failure are described and the role that they may play in causing uremic symptoms is considered. The opinion of the Authors is that all they are likely to take a lesser or greater part in uremic intoxication. Methylguanidine seems to be very important in this context while for some others (like amines) nothing can be stated for studies on their chronic toxicity are lacking. The hypothesis is also considered of the accumulation of unidentified toxic metabolites with a middle molecular weight. It is stated, as to this problem, that the clinical evidence apparently supporting univocally their existence, is instead also consistent with the hypothesis of toxins (like methylguanidine) having a preferential distribution in the intracellular fluid compartment.
ISSN:1660-8151
DOI:10.1159/000180443
出版商:S. Karger AG
年代:1975
数据来源: Karger
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5. |
Protein Metabolism in Uraemia |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 134-152
Peter Richards,
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摘要:
Protein metabolism in uraemia is reviewed. Very few, if any, disorders of amino acid metabolism can at present confidently be attributed to uraemia per se rather than to protein/energy deprivation. Retained urea nitrogen is recycled to the liver as ammonia; a proportion is reutilized for synthesis of non-essential amino acids and, if their carbon skeletons are supplied, for synthesis of essential amino acids. Practical applications of the reutilization of non-amino nitrogen in advanced chronic renal failure are being explored. Nevertheless, uraemic individuals readily become undernourished, and they should receive as much protein as their symptoms will permit.
ISSN:1660-8151
DOI:10.1159/000180444
出版商:S. Karger AG
年代:1975
数据来源: Karger
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6. |
Disorders of Carbohydrate and Lipid Metabolism in Uremia |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 153-162
J.D. Bagdade,
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摘要:
Glucose intolerance and hypertriglyceridemia appear to be frequent metabolic concomitants of chronic uremia. Both these abnormalities are ameliorated but not eliminated by intensive hemodialysis and aggressive treatment of the uremic state. The plasma lipid alteration appears to result principally from disturbances in both the production and catabolism of the triglyceride-rich lipoproteins. The persistence of these well-recognized cardiovascular risk factors may contribute to the accelerated premature cardiovascular disease that appears to devastate chronic dialysis patients.
ISSN:1660-8151
DOI:10.1159/000180445
出版商:S. Karger AG
年代:1975
数据来源: Karger
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7. |
Calcium and Phosphorus Metabolism in Chronic Uremia |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 163-180
E. Fiaschi,
G. Mioni,
G. Maschio,
A. D’Angelo,
E. Ossi,
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摘要:
In chronic uremia, the clinical disorders of calcium and phosphorus metabolism are nfluenced by the following factors: (1) intestinal absorption of calcium and phosphate, resulting in a negative calcium and phosphate balance at normal dietary intakes; (2) renal handling of calcium and phosphate: the fractional transport of calcium (the isoosmotic reabsorption taking place in the proximal tubule) is not affected by GFR modifications, whereas the Tm-limited reabsorption is severely impaired; the external phosphate balance is kept, even in the presence of a reduced nephron population, by means of a proportional reduction in Tmpo4 values; physicochemical state and turnover of body calcium and phosphate: in uremic patients, the distribution spaces, turnover rate of calcium, and accretion rate of bones are increased in comparison with the controls; the calcium infusion test in patients with renal osteomalacia is followed by a regular increase in plasma [PO4], whereas a significant decrease is observed in patients with renal osteitis fibrosa, due to the extreme ‘avidity’ of bones for calcium phosphate; the role of hyperphosphatemia is critical in keeping the plasma [Ca] lower than the expected values for a given metabolic set; moreover, an increased cell uptake of phosphate could counteract to some extent the reduced renal clearance of phosphate; structural and biochemical modifications of bone tissue: uremic osteodystrophy consists mainly of two components: (a) osteomalacia, with osteoid excess, disappearance of the calcification front, and diffuse pathologic mineralization, and (b) osteitis fibrosa, with severe resorption of normally mineralized bone, slight osteoid excess, and almost normal calcification front; (5) hormonal factors: chronic stimulation of parathyroid glands may result in suppressible or even autonomous hyperparathyroidism. As to vitamin D, it has been suggested that the uremic kidney is not able to synthesize the 1,25-di-OH-cholecalciferol, the active metabolite of vitamin D: this results in an impaired intestinal absorption of calcium. On the contrary, the role of calcitonin in chronic uremia is still uncertain, since low values of plasma [Ca] are usually obser
ISSN:1660-8151
DOI:10.1159/000180446
出版商:S. Karger AG
年代:1975
数据来源: Karger
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8. |
Hematologic Disorders in Renal Failure |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 181-194
J.P. Naets,
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摘要:
Anemia is a frequent complication of renal failure. As in anemias of other origin, the resulting tissular hypoxia is partially compensated by an increased production of 2,3-diphosphoglycerate in red cells and a shift to the right of the oxygen hemoglobin dissociation curve. Two mechanisms are implicated in this anemia: increased hemolysis and depressed production of red cells. Decreased production of erythropoietin is probably the cause of reduced erythropoiesis, but the role of uremic intoxication has not been unequivocally excluded. In the course of chronic hemodialysis, iron deficiency anemia and occasionally hypersplenism develop. It is noteworthy that blood requirements in anephric patients are two to three times greater than those of nonanephric hemodialyzed patients. Accordingly, bilateral nephrectomy should be restricted to carefully selected cases. At the present time, androgens seem to be the best treatment of renal anemia. Qualitative anomalies of platelets are the main factor responsible for uremic bleeding and are corrected by hemodialysis.
ISSN:1660-8151
DOI:10.1159/000180447
出版商:S. Karger AG
年代:1975
数据来源: Karger
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9. |
T-Lymphocytes and Serum Inhibitors of Cell-Mediated Immunity in Renal Insufficiency |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 195-208
J.L. Touraine,
F. Touraine,
J.P. Revillard,
J. Brochier,
J. Traeger,
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摘要:
In acute as well as chronic renal insufficiency significant immunological abnormalities were found: diminution of delayed hypersensitivity skin reactions, lymphopenia, reduction of the absolute but not relative number of peripheral blood T-lymphocytes. Responses of lymphocytes from uremic patients to PHA, allogeneic cells, or antigens were normal when lymphocyte cultures were performed in allologous serum from a healthy individual. Sera from uremic patients had an inhibitory or toxic effect on stimulation of normal lymphocytes. Such an in vitro inhibitory activity was found not only in the whole serum but alsowhen certain substances retained in renal failure (methylguanidine, larger molecules, etc.)were added in the lymphocyte cultures.
ISSN:1660-8151
DOI:10.1159/000180448
出版商:S. Karger AG
年代:1975
数据来源: Karger
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10. |
Adequate Dialysis |
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Nephron,
Volume 14,
Issue 2,
1975,
Page 209-227
S. Barber,
D.R. Appleton,
D.N.S. Kerr,
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摘要:
Regular haemodialysis with the Kiil dialyser for 8–10 h three times a week is the present standard of adequate dialysis. In 100 patients treated by this regime there was no positive correlation between plasma urea and creatinine before or after dialysis and any of the symptoms of which these patients still complained. There are no grounds for believing that a further increase in dialysis would relieve residual symptoms. However, any reduction in current standards of dialysis should be justified by prolonged clinical trial of large groups of patients before they are accepted as equivalent in view of the infrequency of some uraemic manifestations such as pericarditis. The implications of the middle molecular hypothesis are discusse
ISSN:1660-8151
DOI:10.1159/000180449
出版商:S. Karger AG
年代:1975
数据来源: Karger
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