[Arterioarterial bypass for vascular access in hemodialysis].
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Biomedical subjects
Publications and source records attributed to J Zingraff.
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Twenty-one chronic haemodialysis patients with cardiomegaly and repeated episodes of heart failure were selected for left ventricular cineangiography and haemodynamic studies. Left ventricular end-diastolic (LVED) volume was augmented in eleven, LVED pressure increased in fourteen, and ejection fraction decreased in nine patients. A decrease of maximum velocity of myocardial fibre shortening was observed in fifteen, and of normalised ventricular rigidity index in eleven. Many patients had diminished cardiac performance in the absence of demonstrable coronary heart disease, hypertension, or chronic volume overload. The diagnosis of congestive cardiomyopathy of unknown aetiology, possibly related to uraemia, was reached in ten patients.
Sulphaemoglobin production, induced by an oxidative stress (ascorbate and cyanide) has been studied in uraemic patients. Results are expressed as the ratio of optic density of sulphaemoglobin (620nm) to optic density of total haemoglobin (540nm). The mean (+/- SEM) ratio found was 0.35 +/- 0.03 in 28 controls and 0.56 +/- 0,03 in 51 uraemic subjects (p less than 0.001). Cross incubation tests demonstrated that the anomaly was caused by a plasma factor. In vitro studies - guanidinic compounds added to control erythrocyte suspensions before incubation - suggest that this factor might be guanidinic propionic acid.
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Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1alpha,25-dihydroxyvitamin D3 (1alpha25(OH)D3) or 1alpha,hydroxyvitamin D3 (1alpha(OH)D3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1alpha,25(OH)2D3 or 1alpha(OH)D3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1alpha,25(OH)2D3, play a role in regulating bone formation and/or mineralization.
The tolerance to high levels of ultrafiltration that has been observed when using a RP-6 dialyzer with polyacrylonitrile membrane and a closed batch dialysate delivery system has led the authors to put patients on a free sodium and fluid intake. Eight patients were put on such a diet for six months. They have been dialyzed four to five hours, three times per week, on a RP-6-Rhodial 75. The mean intersession weight gain was 4.29+/-0.18 Kg after three days for a mean predialytic body weight of 63.55+/-2.54 Kg. Mean predialytic blood pressure was 1.38+/-4 mmHg for systolic pressure and 82+/-5 mmHg for diastolic pressure. Mean ultrafiltrate volume was 4.86+/-0.36 liters which corresponds to a sodium output of 661.3+/-49.5 mEq. Total plasma protein and hematocrit increased 18.8+/-3.34% and 19.13+/-3.22%, respectively, when the pre and post-dialytic values were compared. No clinical sign of fluid overload (dyspnea, edema, etc.) was noted in these patients. Cardiothoracic index remained in the normal range. This tolerance is due, possibly, to the high sodium concentration (145 mEq/L) in the dialysate. The free sodium and water diet may contribute to a better rehabilitation.
Among 500 patients on maintenance hemodialysis, 6 patients (5 young women and a 49-year-old man) developed bullous dermatosis, 2-54 months after initiating dialysis treatment. The skin lesions occurred mainly in sunlight-exposed areas, and 4 out of the 6 patients showed increased cutaneous fragility in response to trauma. Skin biopsy revealed subepidermal blisters for all of them, and skin immunofluorescence studies were negative for 2 patients. No increase in fecal or red cell coproporhyrin and protoporphyrin levels was found in any of the 6 patients. The syndrome was clinically and histologically indistinguishable from porphyria cutanea tarda.
Cardiovascular accidents are the commonest cause of death in patients on intermittent haemodialysis. Our study concerns 158 adult patients in terminal renal failure who were treated by periodic dialysis; it was carried out at Necker Hospital between January 1967 and December 1970. Between these dates, 35 patients died, 17 of the deaths being due to unequivocal or probable cardiovascular complications. The diagnosis of cerebrovascular accident was made in 13 cases. The mean age of the patients who died was 38 years. Fatal cerebrovascular accidents occurred especially during the first 12 to 24 months of treatment. The incidence of fatal vascular accidents is greatest in patients who were hypertensive at the beginning of periodic dialysis, and who remained so after six months of dialysis. Our study has therefore shown that hypertension in patients on chronic haemodialysis is a major vascular risk factors; other risk factors, especially metabolic ones, may also play a part.
Purification of b4-2 sub-peak obtained on DEAE Sephadex A25 chromatography gave us the possibility of quantifying the plasma concentration of the neurotoxin present in uraemic patients with active polyneuropathy. From the purified neurotoxin isolated by kieselguhr and cellulose chromatography we calibrated analytic columns for b4-2 analysis. Plasma concentration, measured in 6 uraemic neuropathic patients, is between 13 and 19 mg/litre. In 52 uraemic patients without neuropathy, the plasma concentration is between 3 and 9 mg/litre. In 20 healthy subjects the plasma concentration is less than 1 mg/litre. The weekly neurotoxin removal in uraemic patients without neuropathy, treated by a five hours RP6 session 3 times a week, is of the same order of magnitude as the weekly urinary excretion in healthy subjects. Preliminary results of a tentative identification of this purified product indicate that it is not a polypeptide but an acid-polyol with carbohydrate structure.
Anemia has been recognized recently as a possible complication of primary hyperparathyroidism. If the hyperparathyroid state can induce anemia in patients with normal kidney function, the extremely high levels of circulating parathyroid hormone usually observed in hyperparathyroidism secondary to chronic renal failure may have an unfavorable influence on the anemia of uremic patients. We investigated the influence of subtotal parathyroidectomy on the severity of the anemia of 18 uremic subjects undergoing long-term hemodialysis therapy. Subtotal parathyroidectomy resulted in a significant increase of mean hematocrit value. RBC count, and hemoglobin level. Serial bone biopsies suggested a relationship between the amount of marrow fibrosis and the improvement of anemia after surgery, but the precise mechanism of this phenomenon is still unknown.
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Five uraemic patients who developed progressive cardiac failure with clinical evidence of congestive cardiomyopathy at the start or during haemodialysis treatment were studied. The diagnosis of cardiomyopathy, for which there was no apparent cause, was confirmed by angiocardiographic and haemodynamic studies. These showed a significant increase in left ventricular end-diastolic volume over normal values obtained in 12 patients without uraemia. The mean velocity of myocardial fibre shortening was significantly decreased, as was the index of normalised rigidity. Three of the five patients presented the complete picture of the disease. The other two also had considerable ventricular dilatation and a decreased index of normalised rigidity but normal ejection fraction and only moderately decreased myocardial contractility indices. This suggests that there may be primary involvement of normalised heart muscle rigidity followed by secondary changes in myocardial contractility in uraemic patients with congestive cardiomyopathy.
HBs antigen (HBsAg) has been followed up every month in 440 hemodialyzed patients, typed for 26 HLA alleles of the A and B loci. An abnormally high rate of the HL-A-A1, B8 association (18.6%) was found in the group of patients able to eliminate HBsAg, when compared with the normal French population (5.05%, p less than 10(-4), and with the group of patients unable to eliminate HBsAg (7.0%, less than 0.01). Chronic aggressive hepatitis was only found in the latter. This high frequency of the HLA-A1, B8 association has also been found in patients with seronegative active chronic hepatitis and suggests that this phenotype might be associated with high immune response against HBsAg.
The case is described of a patient on intermittent hemodialysis who had had a bilateral nephrectomy but had hypertension and a surprisingly mild degree of anemia. Repeated determinations showed high plasma renin activity and plasma erythropoietin activity within the detectable range. These results were thought to be related to a completely calcified renal allograft which had been inserted 8 years before and which had been rejected four years later, but left in situ. The patient had become anuric. It is suggested that chronically rejected renal allografts, even calcified, may maintain some endocrine activity in the absence of any excretory function.
The pharmacokinetics of the hypolipidemic agent, clofibrate have been studied in anuric patients on intermittent hemodialysis. In addition we have tried to determine whether the treatment of hyperlipidemia of chronic renal failure with clofibrate was safe and efficacious. Seven healthy volunteers and five uremic patients received a single dose of 25 mg/kg body weight of clofibrate. Mean peak plasma levels of clofibrate were comparable in both groups and were reached 3.5 hr after drug ingestion in the control subjects and after 6.5 hr in the uremic patients. The mean plasma half-life of clofibrate was 16.7 hr and 68.4 hr in the control subjects and in the patients, respectively (P less than 0.001). Following a short loading period a daily oral maintenance dose of 5 mg/kg body weight was given leading to a plasma clofibrate level of 75-100 microgram/100 ml. Five hyperlipidemic uremic patients received this dose for 3 months. Their plasma clofibrate and creatine kinase levels were constantly monitoried to detect clofibrate myotoxicity which we have observed in uremic patients at plasma levels generally considered safe in patients with normal renal function. Significant decreases in serum total lipid, triglyceride, and cholesterol levels were observed when compared to pretreatment values. In two of the 5 patients serum lipids remained decreased for 10 and 14 months. It is concluded that clofibrate treatment of hyperlipidemia in uremic patients, when carefully monitored, is safe and efficacious.
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