Dialysis Bath Research Articles

Safety and Efficacy of Long-Term Treatment of Secondary Hyperparathyroidism by Low-Dose Intravenous Calcitriol

To assess the safety and efficacy of low-dose intravenous (IV) calcitriol therapy for the treatment of secondary hyperparathyroidism, 21 hemodialysis patients with amino-terminal parathyroid hormone (N-PTH) levels greater than 4 times normal were treated for 12 to 24 months in a prospective trial. The initial dose was 0.50 δg, which was titrated every 3 months thereafter, as dictated by predialysis calcium, phosphorus, and N-PTH concentration. Dialysate calcium concentration was 1.5 mmol/L. Low-dose IV calcitriol decreased the N-PTH concentration to 48 ± 6% and 29 ± 5% of baseline following 12 and 24 months of therapy, respectively. The maximum dose of calcitriol was 0.92 ± 0.11 δg (0.50 to 2.25 δg). After 12 months of therapy, serum calcium increased from 2.22 ± 0.04 to 2.41 ± 0.03 mmol/L (8.9 ± 0.2 to 9.7 ± 0.1 mg/dL) without change thereafter. Baseline serum phosphorus was 1.44 ± 0.09 mmol/L (4.5 ± 0.3 mg/dL), and was unaltered by calcitriol therapy. Control of serum phosphorus was achieved with calcium-containing phosphate binders, except in three patients who were subsequently withdrawn from the study after 12 months because of persistent hyperphosphatemia due to noncompliance. We conclude that long-term, low-dose IV calcitriol is a safe and effective therapy for most hemodialysis patients with secondary hyperparathyroidism. In contrast to conventional dosing regimens, low-dose IV therapy does not necessitate the use of aluminum-containing phosphate binders and/or a low-calcium dialysate bath.

Effects of hemodialysis on activation of lymphocytes: analysis by an in vitro dialysis model.

Patients undergoing maintenance hemodialysis have impaired immune responsiveness, which appears to deteriorate progressively with the duration of the replacement treatment. It has been suggested that it is caused by a chronic preactivation state of T cells caused by hemodialysis. Each treatment session has been compared with a recurring "acute-phase" inflammatory reaction. In this study, the acute effects of hemodialysis on the activation state and functional responsiveness of normal peripheral blood mononuclear cells have been evaluated by use of an in vitro dialysis model. The dialysis was carried out with either cuprophan or polysulfone membranes, with or without sodium acetate in the dialysis fluid. It was observed that a single session of in vitro dialysis did not induce production of interleukin-2 (IL-2) and did not alter the expression of IL-2 receptor (IL-2R) on the cytoplasmic membrane and the secretion of soluble IL-2R, whereas it induced transcription of mRNA for IL-2R. The proliferative response of lymphocytes to phytohemagglutinin or IL-2 in vitro also did not change after a single dialysis session. There was only a slight decrease of the release of soluble IL-2 receptor by phytohemagglutinin-stimulated cells after dialysis. Dialysis induced an active synthesis of IL-1 by peripheral blood mononuclear cells, even in the absence of sodium acetate in the dialysate bath, but there was no release of IL-1 to the circulating medium. The results show that a single dialysis encounter can acutely prime the activation of human peripheral blood mononuclear cells.(ABSTRACT TRUNCATED AT 250 WORDS)

The Arterial Oxygen Extraction Tension and Oxygen Compensation Factor during Acetate and Bicarbonate Dialysis

Recently introduced algorithms for determination of the arterial oxygen extraction tension <i>(p_x), </i>oxygen compensation factor <i>(Q_x), </i>total oxygen concentration, <i>p </i>50 and erythrocyte 2,3-diphosphoglycerate (cDPG) concentration were applied and compared in 10 patients on acetate and bicarbonate dialysis. The oxygen extraction tension and cardiac oxygen compensation factor are new parameters for estimating the risk of peripheral tissue hypoxia. <i>p_×</i>was reduced to the same level (acetate 4.3 pKa vs. bicarbonate 4.3 pKa), whatever the mode of dialysis and changed only on acetate dialysis. The <i>Q_x</i>was at baseline within normal (acetate 1.3 vs. bicarbonate 1.8), increased in acetate dialysis, but fell in bicarbonate dialysis. During acetate dialysis tissue oxygen supply fell and was not fully compensated by increasing <i>Q_x, </i>whereas during bicarbonate dialysis <i>Q_x</i>tended to fall without change in <i>p_x</i>indicating a better oxygen delivery to peripheral tissue.Hypoxia was observed independent of the dialysate bath. Isocapnia was observed during acetate dialysis, but <i>pCO₂</i>increased significantly using bicarbonate dialysate (p < 0.001). pH increased significantly (p < 0.001) during bicarbonate dialysis. Calculated in vivo <i>p50 </i>(acetate 3.8 pKa vs. bicarbonate 3.9 pKa) was slightly elevated in acetate dialysis partly due to the metabolic acidosis and in bicarbonate dialysis due to an increased cDPG concentration. After 30 min of bicarbonate dialysis a decrease was observed in <i>p50, </i>but improved during treatment reaching baseline level at the end of dialysis. <i>p50 </i>in acetate dialysis decreased steadily during the initial 3 h of treatment regaining baseline level before the end of dialysis. The predialysis level of cDPG (acetate 5.4 mmol/l vs. bicarbonate 6.9 mmol/l) was elevated, declined in bicarbonate dialysis within 30 min, but increased to baseline level. In acetate dialysis the cDPG changes paralleled the changes in <i>p </i>50. The algorithms are based on approximations and therefore give approximate values, but they are in keeping with previously reported values of/; 50 and cDPG. They add new information about peripheral tissue hypoxia. Thus, the algorithms leave us with a useful and informative tool in getting reliable information on the state of the patient.

Metabolic Alkalosis in the Patient With Uremia

A 55-year-old man was admitted with the chief complaints of nausea, vomiting, abdominal pain, and weakness. He experienced intermittent nausea and vomiting that became progressively more severe for several weeks. During the last week he could not retain food in his stomach, and developed moderately severe epigastric pain. He became progessively weaker, which the patient attributed to lack of food. He also admitted moderate to heavy alcohol intake. He had a past history of peptic ulcer disease, gout, and 15 years of hypertension for which he took medications sporadically. About a year prior to the current admission, a physician told him that the high blood pressure had caused kidney damage. He had had nocturia (once or twice) for many years, which became more pronounced (two or three times per night) during the last 6 months. During the last week he noticed a reduced volume of urine, with a sharp decline over the last 24 hours. Physical examination showed a well-developed, thin, anxious, pale, and somewhat confused white man. Vital signs included pulse rate, 96/min and regular; respirations, 18/min; blood pressure, 156/110 mm Hg supine and 140/100 mm Hg sitting; and a normal temperature. The skin was pale, with poor turgor in the upper part of the body, although mild pitting edema was present in his legs. Conjunctivae and oral mucosae were pale. A systolic ejection murmur was heard at the base of his heart. Scattered inspiratory rales were present at both pulmonary bases. The abdomen was soft, without distention, and moderately tender to palpation in the epigastric and umbilical areas. The prostate was slightly enlarged, but the bladder was not distended. No occult blood was present in the stool. The chest x-ray showed an enlarged heart and possibly a small amount of fluid in the costophrenic pleural space. The electrocardiogram changed consistently with left ventricular hypertrophy. Laboratory tests disclosed anemia, advanced renal in sufficiency, electrolyte disturbances, and a mixed acidbase disturbance (metabolic acidosis and metabolic alkalosis) (Table 1). An increased anion gap, common in severe renal failure and not uncommon in alkalemia, was also observed. The 8 mmollL increment in the anion gap approximately reflects the 8 mmol/L of retained acid that, in turn, consumed 8 mmollL of bicarbonate. Thus, had the renal failure acidosis not been present, the serum bicarbonate concentration would have increased from 38 mmol/L to perhaps as high as 46 mmollL. The clinical picture was initially interpreted as a vicious circle of uremia, vomiting, and worsening of the uremic syndrome by volume contraction. Persistent hypertension despite volume contraction was almost certainly related to his long history of essential hypertension and perhaps to an exaggerated release of renin that was triggered by the hypovolemia. Administration of 0.9% NaCl solution corrected the dehydration but failed to increase the urine output. The patient was dialyzed (standard acetate bath) through a subclavian catheter, with marked improvement of his blood chemical profile. However, attempts to remove the nasogastric tube were unsuccessful because of the recurrrence and persistence of vomiting. On the third day after admission, following endoscopy and x-ray examination of the stomach, a diagnosis of pyloric stenosis secondary to chronic peptic ulcer disease was determined. Treatment began with intravenous ranitidine and fluid replacement with 0.9% NaCl solution, later changed to 5% dextrose in 0.3% NaCl and 20 mmoles KCI. The dialysis bath had the standard acetate concentration and 4.0 mmollL KCI. Packed red-cell transfusions were given before surgical correction of the pyloric stenosis.

Sodium fluxes during hemodialysis.

Three sets of experiments were performed to determine the effect of the dialysate sodium concentration on the sodium balance of patients undergoing maintenance hemodialysis. First, patients were treated with three different dialysate bath sodium concentrations: 125-132 mEq/l (n = 7), 135-140 mEq/l (n = 11) and 145-150 mEq/l (n = 6). We demonstrated that the pretreatment plasma sodium concentration was independent of the sodium concentration of the dialysate used. Second, the plasma sodium concentration available for diffusion during the treatment was calculated from the plasma sodium concentration and the plasma proteins. The accuracy of this calculation was demonstrated by comparing the predicted value with the concentration of sodium measured in an ultrafiltrate obtained at minimal filtration fraction. Third, the sodium fluxes using a hypernatremic or hyponatremic dialysate were calculated for 100 ml of plasma going through the dialyzer. At steady state, no significant differences in net sodium fluxes were demonstrated between hyper- and hyponatremic dialysis.

Noninvasive diagnosis of uremic osteodystrophy: uses and limitations.

45 bone biopsies from patients with chronic uremia were reviewed to define which noninvasive investigations were of value in predicting the histological diagnosis and to quantify the spectrum of uremic bone disease at a center that has consistently used an aluminum-free dialysis bath. 17 biopsies were taken postmortem. 15 patients received conservative treatment, the rest were on maintenance dialysis. 13 patients had symptomatic bone disease. Virtually all patients with a uremia duration greater than 3 years had uremic osteodystrophy. All patients with clinical bone disease, hypercalcemia or raised alkaline phosphatase activity had osteodystrophy, but the specific histology was not indicated. Greatly raised parathyroid levels suggested secondary hyperparathyroidism, but the test was only 100% specific when 20 times normal. Total aluminum consumption was highly indicative of bone aluminum concentration (p less than 0.0001) and aluminum-related osteomalacia (5 cases), suggesting that a considerable proportion of uremic bone disease is iatrogenic. Serum aluminum was of some use in the diagnosis of aluminum-related osteomalacia, but was not wholly reliable. Bone mineral content (BMC) using both forearm measurements and total body bone mineral levels (TBBM) were assessed in 32 patients and were found to be reduced in 12, with a preponderance of secondary hyperparathyroidism. BMC and TBBM were negatively correlated to resorbing surfaces and bone formation rate, suggesting that secondary hyperparathyroidism is the uremic bone disease that represents the greatest threat to bone mass. It is concluded that while noninvasive investigations give considerable information, reliable diagnosis requires the use of histological methods.

A prostacyclin-stimulating factor from human serum: partial purification

Prostacyclin synthesis by vascular tissue is stimulated by human serum as a consequence of a heat stable. low-M, factor (serum factor, SF) (Ritter ct (11.. 1982~1, 1983). Biological activity of SF is determined by radioimmunoassay of 6-oxo-prostaglandin F,, (the stable hydrolysis product of prostacyclin) in incubations of fresh rings of rat aorta (Bunting i>t (11.. 1976; Ritter c t ul., 1982h). Bioactivity was expressed as the ratio of 6-oxo-prostaglandin F,, produced in purified serum fractions to that produced in the corresponding plasma control. We report here the partial purification of SF; volatile bufrers were used whenever possible to minimize interference with the bioassay. The purification protocol was designed both to minimize handling losses and also to niaximiie physicochemical data relevant to the structure. Blood from drug-free volunteers was collected into sodium citrate (0.31 YO. wjv, final concentration) and plasma separated ( 1 0 0 0 ~ ~ 20min). Half of the plasma was re-calcified (20rnM-Ca'' ) and allowed to clot (37 C. 3 h ) and the serum expressed with a spatula; the other half was used as the plasma control. which was sequentially purified and assayed along with the serum (Ritter C't d.. 1983). Serum/plasma were dialysed twice against 5 vol. o f water (4 C, 36 h) and the dialysis bath fluid, containing the bioactivity (Ritter i't (11.. 1983), was freeze-dried. Initial purification/structural work was undertaken with this crude preparation: ( I ) The pH dependence of S F adsorption to Sephadex A-35 was determined over a pH range 4 9. Maximum adsorption was obtained above pH 8; at pH 7 and below, SF did not adsorb t o A-25. This implies that SF is anionic at pH > 8 and neutraljcationic below this pH. (2) High-voltage paper electrophoresis of SF was undertaken on Whatman no. I paper in pyridine/acetate buffer (pH 6.5. 3 kV. 45 min). Strips of paper (2cm) were eluted with 0.1 % acetic acid bioassay. Activity was associated with both the neutral and first cationic strip (Masp = 0 0.25). Taken together with the A-25 data, the high-voltage paper electrophoresis experiment implies that SF contains cationic as well as anionic functional groups. (3) SF binds to Sephadex C-25 strong cation exchanger across the pH range 4 -8. (4) The gel filtration profile of SF on Sephadex G-25. G-15 and GI0 was determined. In each case, bioactivity eluted with the salt peak. and was associated with U . V . ( Azx , , ) absorbance. The behaviour on Sephadex G10 defines the M , o f S F < 700. Based on these initial studies, the following protocol was developed and applied to larger quantities of

The effects of passive CO2 removal on breathing pattern in humans.

To determine the effects of nonventilatory CO2 transfer on breathing pattern, we monitored breathing in 7 patients with renal failure undergoing hemodialysis. A respiratory inductance plethysmograph was used to record ventilation before and during dialysis. The duration of inspiration (TI), the duration of each breath (TTot) and the duty cycle (TI/TTot) did not differ for the pre-dialysis and the dialysis periods. In contrast, for each patient the mean tidal volume (VT) fell significantly during dialysis (p less than 0.05), accounting for the reduction in minute ventilation (p less than 0.005). The mean inspiratory flow rate (VT/TI) also fell (p less than 0.01), demonstrating that nonventilatory CO2 loss via the dialysis bath is associated with reduced respiratory drive.

Serum and dialysate aluminium concentration of dialysed patients with chronic renal failure determined by atomic absorption spectrometry with a graphite furnace

We investigated the aluminium content in water, in solutions for haemodialysis and in serum of patients, under regular haemodialysis using flameless atomic absorption spectroscopy with 1'Vov platform. The aluminium content found for tap water was 6–36 μg/l. After deionization the aluminium content was negligible. The dialysis bath, prepared with deionized water from a concentrated solution with 30 μg/l of aluminium, also showed a negligible amount of aluminium. The results obtained showed that patients who take aluminium orally have predialytic aluminium serum levels between 14 and 68 μg/l and between 10 and 66 after dialysis. For patients who do not take aluminium orally, the corresponding values were 12–27 and 12–24. No correlation was found between age, sex, years of dialysis and aluminium serum levels.

Hemodialysis. Basic principles and practice.

Hemodialysis removes uremic toxins and excess fluid from the blood by diffusion dialysis and ultrafiltration. The efficiency of this process depends on the size, shape, and type of semipermeable membrane used in the hemodialyzer. Although the hollow-fiber kidney remains popular, the parallel-plate hemodialyzer is reestablishing itself, partly because it can use newer types of membranes. With newer membranes, ultrafiltration can be performed without diffusion dialysis, which appears to have important clinical advantages. The dialysate bath used in the hemodialyzer resembles plasma water in composition, with electrolytes added to compensate for abnormalities of end-stage renal disease. Although the technical problems of hemodialysis have been largely overcome, an accurate, easy-to-use method of evaluating the adequacy of the hemodialysis prescription has yet to be devised.

Central venous blood composition and the pulmonary ventilation during hemodialysis.

The elimination of CO2 across the dialyzer has been reported as the cause of pulmonary hypoventilation during hemodialysis. There are some evidences that the venous line blood composition could influence the central venous blood and this one the pulmonary ventilation. Our purpose was to analyze (1) the influence of the changes in composition of the venous line blood on the central venous blood and (2) the possible role of the central venous blood composition on the pulmonary ventilation of 10 chronic renal failure patients during hemodialysis performed twice in the same patients in two different conditions: acetate dialysate without (condition I) and with (condition II) constant addition of 100% CO2 bubbling into the dialysis bath. During condition I the venous line blood pH was kept in a normal range, and the PCO2 was low, whereas during condition II the pH was very low and the PCO2 extremely high. The patients during condition I decreased their pulmonary ventilation and lost CO2 across the dialyzer as the central venous blood pH and HCO3- increased, and PCO2 did not change. The same patients during condition II increased their pulmonary ventilation and absorbed CO2 across the dialyser as the central venous blood pH decreased and PCO2 increased. Thus, the venous line blood has influence on the central venous blood composition, and this plays a role on the control of pulmonary ventilation of these patients.

Effects of Amino Acid Additives during Hemodialysis of Children

The intradialytic losses into the dialysate of free amino acids (AA) and alpha-amino nitrogen were determined during the dialysis of three children. Variations in plasma AA were determined pre- and postdialysis. The effect of these losses with the addition of an Abbott General Amino Acid Mixture to the dialysate in concentrations of 8.5, 17, and 34 mg/100 ml was studied. The major determinant of AA losses was the plasma concentration of the AA before beginning the dialysis treatment. Dialysance of individual AA varied inversely with their molecular weights. A zero flux of alpha-amino nitrogen occurred at a derived concentration of 22 mg/100 ml of the AA additive in the dialysate. Plasma concentrations of nonessential amino acids were little affected by the dialysate additive. In contrast, total essential amino acid nitrogen which fell during baseline dialyses showed significant improvement when the AA solution was added to the dialysate. This study suggests that the addition of AA to the dialysate bath may be effective in decreasing AA nitrogen losses during dialysis.

Pulmonary ventilation during hemodialysis.

During hemodialysis a decrease in pulmonary ventilation has been reported. The elimination of CO2 across the dialyzer has been suggested as the cause of the pulmonary hypoventilation. Our purpose was to analyze the factors that could have influenced the pulmonary ventilation of 7 patients with chronic renal failure during hemodialysis, performed against an acetate dialysate with constant addition of CO2, bubbling into the dialysis bath. In spite of the large volume of CO2 mainly as bicarbonate, eliminated across the dialyzer there was no significant decrease of ventilation. The values of pH in the venous line were extremely low and the values of PvCO2 were artificially maintained around 35.0 mm Hg. Thus, the total CO2 delivered to the lungs, but mainly the levels of pH and PCO2 in the venous line play an important role in the control of pulmonary ventilation of these patients.

Accidental Systemic Exposure to Sodium Hypochlorite (Clorox) during Hemodialysis

A case of accidental exposure of a patient undergoing hemodialysis to a sodium hypochlorite solution is reported. A 61-year-old woman was completing a hemodialysis treatment when routine cleaning of the hemodialysis machine was started. Approximately two liters of undiluted sodium hypochlorite cleaning solution (Chlorox) was added to the dialysis bath, soaking the membrane fibers. For less than two minutes the Chlorox-soaked membrane was in contact with the blood returning to the patient. This accident led to massive hemolysis, hyperkalemia, cyanosis, and cardiopulmonary arrest. Hemolysis may have been caused by the hypertonic solution, rapid exothermic protein degradation, alkaline degradation, or another mechanism. The sudden rise and fall in the concentrations of serum electrolytes and subsequent hyperkalemia was the most probable cause for the cardiac arrest. Cardiopulmonary resuscitation was started, the patient was intubated, given oxygen, sodium bicarbonate, atropine, dopamine, and isoproterenol. Sodium thiosulfate 5 g was administered by a nasogastric tube approximately 25 minutes after the cardiac arrest as a neutralizing reducing agent. The patient's condition stabilized, and she recovered after a week of hospitalization. Cleaning solutions used in the routine cleaning of hemodialysis machinery represent potentially toxic agents. Hemodialysis procedures should ensure that cleaning and sterilizing solutions cannot accidentally come into contact with a dialysis machine that is still connected to the patient.

The effect of zinc on cellular immunity in chronic uremia

Delayed hypersensitivity to mumps was examined in 25 apparently well-nourished men receiving regular hemodialysis, each of whom had a history of mumps. A positive reaction was observed in eight of nine patients already under therapy with zinc added to the dialysis bath. In contrast, 11 of 16 untreated patients were anergic. Four of the anergic patients were subsequently treated with zinc resulting in restoration of sensitivity in three patients. There were no significant differences in lymphocyte, monocyte, or T-cell counts between the two groups of patients. Consequently, zinc probably acts by improving the function of one or more of these cell types. Protracted zinc deficiency may be a major cause of impaired cellular immunity in chronic renal failure.

Hypopnea associated with acetate hemodialysis: carbon dioxide-flow-dependent ventilation.

IN patients with chronic renal failure who are undergoing hemodialysis, arterial oxygen tension (PaO2) falls when a dialysis solution containing acetate is used.1 2 3 4 It has been suggested that hypoxemia results from altered pulmonary ventilation-perfusion ratios in the lung that are consequent to pulmonary sequestration of neutrophils.3 4 5 However, Aurigemma1 and Tolchin2 and their colleagues have proposed that the major cause of the reduced PaO2 is a reduction in carbon dioxide output at the lungs, as a consequence of the carbon dioxide loss through the dialysis bath that leads to reduced ventilation. Such a reduction in ventilation has been . . .

Mechanism and prevention of cardiac arrhythmias in chronic hemodialysis patients

We monitored, by the Holter method, 23 clinically stable maintenance hemodialysis patients for 5 +/- (SEM) 2 hours before hemodialysis, 5.0 +/- 0.5 hours during hemodialysis, and 13 +/- 3 hours after hemodialysis. Of 23 patients, 9 (39%) had unexpected frequent or complex ventricular arrhythmias recorded and after hemodialysis with a potassium dialysate bath concentration of 2.0 mEq/liter. Patients with ventricular arrhythmias were more likely to be using digoxin (8/9 vs. 1/4) and to have evidence of left ventricular hypertrophy (9/9 vs. 7/4 than were those patients without arrhythmias. Of these 9 patients with arrhythmias, 6 underwent repeat Holter monitoring during multiple dialysate protocols. Of the 6 patients, 4 had a significant reduction in the frequency of ventricular ectopy when a dialysate of 3.5 mEq/liter potassium was used (P < 0.05), but of these 6, 3 still had complex arrhythmias. The use, however, of a 3.5 mEq/liter potassium dialysate plus the administration of a 400-mg dose of quinidine sulfate orally 45 min prior to hemodialysis was successful in reducing ventricular ectopic frequency and complexity in all the patients studied. Conclusion. Maintenance hemodialysis patient using digoxin and with left ventricular hypertrophy have an unexpectdly high indicence of occult, potentoial serious, ventricular arrhythmias during and after hemodialysis, revealed by Holter monitoring. There is preliminary evidence that a low-potassium bath concentration may play a role in predisoposing patients to these arrhythmias. Further prospective studies with largaer number of patients will be needed, however, to evaluate the significance of these findings.

Serum Aluminum and Continuous Ambulatory Peritoneal Dialysis

Letters and Corrections1 January 1980Serum Aluminum and Continuous Ambulatory Peritoneal DialysisA. WOLF, M.D., H. GRAF, M.D., W. F. PINGGERA, M.D., H. K. STUMMVOLL, M.D., V. MEISINGER, M.D.A. WOLF, M.D.Search for more papers by this author, H. GRAF, M.D.Search for more papers by this author, W. F. PINGGERA, M.D.Search for more papers by this author, H. K. STUMMVOLL, M.D.Search for more papers by this author, V. MEISINGER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-92-1-130_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Accumulation of aluminum in the blood and tissues of patients maintained on chronic hemodialysis may cause "dialysis dementia," frequently leading to death (1). The aluminum content of the dialysis bath fluid or the aluminum-hydroxide (Al [OH]3) gels taken by dialysis patients are responsible for the hyperalbuminemia and the high aluminum body stores (2, 3). In the past 4 years continuous ambulatory peritoneal dialysis has been established in the treatment of patients with end-stage renal disease. To our knowledge no information exists on aluminum kinetics in patients thus treated.We have measured serum aluminum and aluminum clearances in...

Hemodialysis in the Treatment of Psoriasis

We have treated seven patients with severe psoriasis with sham or true hemodialysis. Three patients received one 24-h course of true hemodialysis over 4 d followed by an identical 24-h course 4 weeks later. Four patients received one 24-h course of sham diaglysis over 4 d followed by a 24-h course of true dialysis 4 weeks later. Significant subjective improvement was noted by both groups after the first series of treatments but not after the second. No objective improvement in skin disease was found at any time. We were unable to confirm the many uncontrolled reports on the efficacy of dialysis in ameliorating severe psoriasis. Neither the heparin used for anticoagulation, the acetate present in the dialysis bath, nor the removal of a "psoriatic factor" seemed to affect the skin disease in these patients.

The metabolic effects of hemodialysis with and without glucose in the dialysate1–2

The present study compares some of the metabolic effects of hemodialysis of fasting patients with and without glucose in the dialysate bath. Unlike glucose dialysis, glucose-free dialysis caused marked decreases in blood levels of glucose, insulin, lactate, and pyruvate along with profound increases in acetoacetate and β-hydroxybutyrate. It is concluded that oxidation of fatty acids increases to meet energy demands and that the combined processes of glycogenolysis and gluconeogenesis serve to prevent critical hypoglycemia during glucose-free dialysis.