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Two hemodialysis patients, one male and one female, aged 46 and 54 years, were treated with preceed respectively for refractory ascites secondary to hepatic cirrhosis and for large polycystic liver. Preceed was decided because of the rapid reappearance of effusion following repeated puncture and albumin infusion, the poor tolerance to ultrafiltration (UF) and the poor nutritional status of the patients, with severe hypoalbuminemia. Abdominal paracentesis was performed on initiation of the dialysis session. Reinjection of the ascites fluid was made into the arterial line, allowing its UF and control of its flow. The procedure was performed whenever necessary, i.e., when inter-dialysis weight gain and ascites volume were high. In both cases, improvement was quickly obtained, with less rapid and less severe reappearance of the effusion and correction of albuminemia. Dialysis sessions with UF were better tolerated. No notable side effect was observed. The first patient was treated for 2 months, when he died of an unrelated cause. The other patient was treated for 6 months and then could be transferred to a dialysis center near her home. Twenty five months after start of dialysis treatment, kidney and liver transplantation were performed in this same patient. After transplantation, reappearance of moderate ascites and oedema is attributed to e degradation of renal function, without liver dysfunction. Five weeks after transplantation, improvement of renal function and ascites regression were noted. Preceed is an effective method of treating refractory ascites in the hemodialysis patient. Compared to classical paracentesis, it has the advantage of good tolerance, patient comfort and moderate cost.

Background: The objective of this cross-sectional study in a population of 1472 dialysis patients was to identify the main factors involved in the choice of a specific option for dialysis therapy, taking into account three different types of criteria such as medical dependence (DM), nurse care requirement (SI) and independence for dialysis therapy (CA)., Methods: Each patient has been analysed, independently of present treatment modality, according to the above three criteria, namely DM, SI and CA. For each type of parameter, patients have been allocated to one of three levels, each level being established to evaluate whether dialytic treatment should be undertaken as hospital centre dialysis (HDC) or in a facility off the hospital. Level 3 of any one category corresponded to the inability of doing haemodialysis at home (HHD) or in self-care unit (AD). Level 2 included patients who could be treated in AD or by peritoneal dialysis (PD) with the assistance of a nurse. CAPD or HHD were considered as potential treatment modalities only in patients qualifying for level 1 of each criterion., Results: In the patient population as a whole, the following treatment options were observed: HHD 3.6%, CAPD 6%, PD 1.8%, AD 16.3% and HDC 72.2%. For medical dependence (DM) there was a relatively even distribution for the three levels in six centres. In contrast, two centres were characterized by a predominance of DM level 3. Differences in DM levels between centres were greatly reduced when considering separately only those patients who were actually treated by CAPD, HDC and AD. SI levels were more uniformly distributed within all centres, and this was true for HCD and AD patients. When considering CA levels in HDC patients, a large predominance of CA level 3 was observed in all centres whereas CA level 1 was nearly in existent., Conclusion: The major finding of this study was that the inability or the refusal of dialysis patients to participate at treatment, independently of medical condition and nurse care requirement, was the main factor in the choice of hospital centre dialysis.

The administration of recombinant erythropoietin (rHuEpo) to anemic chronic renal failure patients may be associated with an increase in blood pressure, possibly by direct effects on peripheral blood vessels. In the present study, experiments were designed to explore the hypothesis that rHuEpo could enhance vascular resistance through mitogenic effect on vascular smooth muscle cells (VSMCs), and that preexisting hypertension might be a predisposing condition. Cultured VSMCs from the thoracic aortae of spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats were studied for DNA synthesis, phospholipase C activity, and cell growth related proto-oncogene expression in the presence of rHuEpo. In cells from both strains, rHuEpo dose-dependently increased DNA synthesis and stimulated phospholipase C activity, as indicated by 3H-thymidine incorporation and 3H-inositol phosphate formation, respectively (EC50 approximately 4 U/ml). Exposure of VSMCs to rHuEpo for various times gradually increased the levels of c-myc and junB and transiently induced c-fos expression, as determined by Northern analysis. rHuEpo-induced DNA synthesis was markedly enhanced in VSMCs from SHR compared to those from WKY. In contrast, rHuEpo-induced phospholipase C activity and proto-oncogene expression did not differ between the two strains. Taken together, these results suggest that rHuEpo may function as a vascular smooth muscle cell growth promoting factor through activation of the phospholipase C cascade and modulation of proto-oncogene expression. It could thereby contribute to vascular hypertrophy and arterial hypertension.

Twenty men and 23 women aged from 18 to 65 years, who had been under maintenance haemodialysis for 2 to 16 years and whose haematocrit had been below 30 percent for at least 3 months received recombinant human erythropoietin intravenously at the end of each session for one year. Anaemia was corrected in all patients, the delay in response to each dosage variation being about 4 weeks. The necessary maintenance dosage ranged from 96 to 240 u/kg/week. The number of leucocytes increased significantly until the 4th month, from 5880 +/- 1760 to 6600 +/- 1920 per cubic mm (P less than 0.01). During treatment, pre-dialysis blood creatinine concentrations and potassium and phosphate levels rose, while blood calcium levels fell significantly from 2.45 +/- 0.16 to 2.36 +/- 0.19 mmol/l (P less than 0.01). A nonsignificant increase in systolic and diastolic pressures was also observed, from 129 +/- 16 to 134 +/- 18 mmHg (P = 0.06) and from 75 +/- 9 to 78 +/- 10 mmHg (P = 0.07) respectively. Eight patients (18 percent) required antihypertensive drugs or a higher dose of those previously prescribed. There were 7 cases of vascular thrombosis on pre-existing stenosis, and the dosage of heparin during dialysis had to be increased in most patients. This study confirms that erythropoietin plays a major role in the genesis of the anaemia associated with renal failure. The absence of severe complications in this series was probably due to the criteria of inclusion in the study.

Red blood cell (RBC) production has been explored in hyperparathyroid as compared to normal rats. The hyperparathyroid state was obtained by feeding the rats a calcium-deficient diet during 30 days. A significant decrease (p less than 0.001) in reticulocyte count and in erythrocyte 59Fe incorporation was observed in hyperparathyroid rats when compared to control animals. A comparable inhibition of erythrocyte 59Fe incorporation in hyperparathyroid rats was found when the study was performed after stimulating bone marrow activity by acute arterial hemorrhage. These results of decreased RBC production using a model of endogenous hyperparathyroidism could be confirmed in additional experiments using a model of exogenous hyperparathyroidism. In this model, the rats received either parathyroid extract (3 x 10 USP/day during 8 days) or vehicle only. Again, a decrease in erythrocyte 59Fe incorporation was observed in hyperparathyroid animals when compared to control animals. It is concluded that the hyperparathyroid state is accompanied by a decrease of RBC production in the rat. It is probable that a similar pathogenesis underlies the anemia of patients with primary or secondary hyperparathyroidism.

Between 1967 and 1978, among more than 1 000 patients under haemodialysis, 66 who had severe secondary hyperparathyroidism, underwent parathyroidectomy (PTx). Subtotal PTx's were performed in 57 patients and total PTx's immediately followed by autotransplantation of parathyroid gland fragments in 9 patients. The patients operated upon by these two methods since 1976 were compared. Among the 10 patients who had undergone subtotal PTx recurrence of severe biological hyperparathyroidism was observed in four cases and permanent hypoparathyroidism in two cases. Among the 9 patients with total PTx and immediate autotransplantation only one was considered as suffering from recurrent hyperparathyroidism on account of increased plasma parathyroid hormone concentrations; none of the other patients in this group had hypoparathyroidism. On follow-up, the clinical and radiological findings were comparable in both groups. At the present moment, our choice of surgical method remains arbitrary. Total PTx with immediate autotransplantation is carried out in all cases of reexploration of the neck, in patients who do not comply with the proposed medical treatment and when surgery reveals grossly enlarged parathyroid glands. In all other cases we continue to perform subtotal PTx.

Chronic renal failure is associated with a disturbance of calcium and phosphate metabolism. During the initial stage of chronic renal failure plasma calcium and phosphorus are either slightly diminished or at the lower limit of the normal range, most probably due to a decrease in renal 1-alpha-hydroxylase activity. This leads to a decrease in circulating calcitriol and a stimulation of parathyroid hormone secretion. The underlying anomaly could be an as yet hypothetical elevation of the cytoplasmic phosphorus concentration within the renal tubular epithelium. During more advanced stages of chronic renal failure, a retention of phosphate occurs which induces hyperphosphatemia and contributes, either directly or indirectly, to the progressive worsening of secondary hyperparathyroidism with its skeletal expression of renal osteodystrophy.

In 2 cases of recurrent secondary hyperparathyroidism and 4 cases of persisting secondary hyperparathyroidism observed in patients treated by chronic haemodialysis, 8 hyperplastic parathyroid masses and 1 parathyroid adenoma, all located in the lower part of the neck, were removed after percutaneous ultrasonographic detection. There were 7 true positive and 1 unexplained false positive results. In 1 out of the 2 false negative results, the mass located behind the esophagus could not be detected because of the laryngotracheal gas. Two masses located inside the thyroid gland and a 5th hyperplastic gland were correctly identified by ultrasound. Two reluctant patients accepted a new cervicotomy because of the ultrasound reports. The reports played a prominent role in the operative technique in 3 cases.

A hemodialyzed woman with radiologically and histologically proven osteomalacia presents a spontaneous fracture that is associated with aluminium intoxication. The hyperalbuminemia (16,6 mumol/1) was not caused by the aluminium contained in the dialysate fluid but by oral ingestion of aluminium gel in a patient presenting hyperabsorption of this metal. Increased absorption could be demonstrated by oral administration of aluminium hydroxide (2 x 12 g A1 (OH)3 spread over 48 hrs) whereas the same test failed to reveal hyperabsorption in two other hemodialyzed patients. The precise mechanism of increased absorption of aluminium is not known. It is concluded that increased digestive absorption of aluminium should be investigated in patients with kidney failure treated with aluminium gel and presenting high blood levels of this metal.

The authors report a case of acute lithium poisoning, of double interest by virtue of its accidental origin and the fact that the patient suffered from chronic uraemia treated by intermittent haemodialysis, without residual diuresis. Neurological involvement consisted of a succession of dysarthria, behaviour disturbance, extra-pyramidal hypertonia and finally coma with respiratory difficulties. A favourable outcome was obtained by daily haemodialysis which made possible the elimination of almost all the lithium introduced into the body.

It may sometimes be difficult to distinguish primary from secondary hyperparathyroidism when advanced renal failure coexists. We report here the case of a patient with end-stage renal failure who had severe hyperparathyroidism. Cervical exploration revealed only the presence of four parathyroid glands normal in size and histological appearance which were removed. Because the existence of severe hyperparathyroidism had been firmly established based on biochemical and radiological evidence, the diagnosis of primary hyperparathyroidism due to an ectopic adenoma became obvious. Digital angiography and computerized tomography were then carried out. The results of angiography were inconclusive but computerized tomography revealed and precisely localized a mediastinal adenoma which was subsequently removed via sternotomy. The existence of a hypoparathyroid state was confirmed over the following two months. Reimplantation of parathyroid fragments which had been cryopreserved during the first operation, was then performed with success.

Precise determination of myocardial function in chronic renal failure is difficult because of the fluctuation of parameters especially in those patients undergoing intermittent hemodialysis. Reliable methods of investigation should be used to correctly evaluate possible functional abnormalities. Results of our study and of several other publications prove that some hemodialysis patients have a congestive cardiomyopathy (non obstructive) which is likely to be in relation with uremia. Several factors have been suggested in the literature to explain the etiology and pathogenesis of uremic cardiomyopathy. Disturbed metabolism of phosphate and calcium associated with the hyperparathyroidism of renal failure has been observed both in laboratory animals and patients with uremia. Altered metabolism of lipids associated with carnitine deficiency might also play a role. More thorough methods of investigation and additional experimental studies, both in vitro and in vivo are called for in order to define myocardial dysfunction in chronic renal failure. This should provide a basis for improved prevention and treatment of uremic cardiomyopathy.

The binding characteristics of chlorophenoxyisobutyric acid (CPIB) to serum proteins has been studied in 10 chronically uremic patients and 9 healthy subjects using the technique of equilibrium dialysis. Scatchard analysis of the results indicated a significant decrease in association constants for low as well as for high affinity sites. The number of binding sites however was not diminished thus suggesting the presence of competitive inhibitors. Such inhibitors were dializable, at least in part, as demonstrated by in vivo-hemodialysis and in vitro-dialysis experiments. The in vivo administration of 50 mg heparin intravenously led to a striking increase in the unbound fraction of serum CPIB whereas the addition of 10 IU/ml heparin in vitro induced no change of protein binding which is in favor of only an indirect effect of heparin. In conclusion, CPIB binding to serum proteins of chronically uremic patients as compared to normal volunteers was decreased leading to an increase of its unbound circulating fraction. The observed change of protein binding appeared to be due to the presence of competitive inhibitors in uremic serum.

Amyloidosis in long-term haemodialysis patients mainly involves the osteo-articular system. It is held responsible for carpal tunnel syndrome, chronic arthralgia and various types of arthropathy, chronic synovitis and tenosynovitis, haemarthrosis, subacute polyarthritis and destructive arthropathies of the limbs and spine. Radiologically, amyloidosis may appear as bone cavities, particularly visible in the hips and wrists. Its frequency increases with the duration of haemodialysis. Biochemically, amyloidosis consists of beta 2-microglobulin (beta 2-M). This protein accumulates in uraemic patients under dialysis and seems to play a major role in the pathogenesis of amyloid deposits. The accumulation is due to renal impairment, being maximum in anuric patients. However, the unsatisfactory clearance of beta 2-M by dialysis methods also contributes to its retention: the production and elimination of beta 2-M seems to vary according to the extrarenal clearing technique. These data suggest that improvements in clearing techniques will eventually prevent dialysis amyloidosis.

Joint problems have been retrospectively analyzed in 10 uremic patients (mean age, 61.9 years; range, 50-70) undergoing long-term hemodialysis treatment for more than 10 years. All the patients suffered from arthralgias which were mainly localized in the shoulder region (9 patients). The arthralgias began 2-9 years after the initiation of intermittent hemodialysis. Eight out of the 10 patients had the carpal tunnel syndrome. Only three patients had evidence of marked secondary hyperparathyroidism but nine had aluminum intoxication. Juxta-articular calcium deposits were observed in 8 patients one of whom had pseudo-tumoral calcifications made of hydroxyapatite crystals. These soft tissue calcium deposits occurred 1-8 years after starting hemodialysis. Conspicuous X-ray abnormalities were found in 8 patients: destructive arthropathy in 5 cases, arthropathies of large joints in 5 cases consisting of sub-chondral lacunae and joint space narrowing or even disappearance. Prosthetic joint replacement was required in 4 patients: replacement of the hip in 3 and of the knee in 1. Massive amyloid deposits could be demonstrated in removed joints of 3 patients and in carpal tunnel of the 7 patients operated upon. They were located in the synovium, articular capsula and juxta-articular epiphyseal bone. It is probable that this is a new type of amyloidosis made of beta 2-microglobulin. The underlying pathogenetic mechanisms of these arthropathies remain to be defined by further studies.