Disequilibrium Syndrome Research Articles

Thalamic disequilibrium syndrome after thrombolytic therapy for acute myocardial infarction

Thalamic disequilibrium syndrome (TDS) refers to unsteady stance and gait resulting from unilateral thalamic lesion. Posterolateral thalamic involvement may result in disequilibrium with minimal motor or sensory deficit.1 However, this entity has received less attention in comparison with thalamic sensory, movement, and ataxic disorders. The transient nature of TDS underscores its importance for the prevention of falls in neurorehabilitation. The current report highlights development of TDS due to right thalamic hemorrhage after thrombolytic therapy for acute myocardial infarction. A 65-year-old man underwent thrombolytic therapy for acute anterior wall myocardial infarction with streptokinase followed by heparin and oral antiplatelet agents. When he tried to move 3 days later, he could not stand or walk unassisted. On assisted standing, he had truncal instability with axial lateropulsion to the left. He also required assistance for sitting up in bed. Neurologically he had normal visual fields, cranial nerve function (especially ocular movements), muscle power, and …

Molecular basis for the dialysis disequilibrium syndrome: altered aquaporin and urea transporter expression in the brain

Cerebral disorders caused by brain oedema characterize the dialysis disequilibrium syndrome, a complication of rapid haemodialysis. Brain oedema is presumably caused by the 'reverse urea effect', i.e. the significant urea gradient between blood and brain after dialysis, with, as a result, an inflow of water into the brain. To assess the molecular basis of this effect, we examined the expression of urea transporter UT-B1 and aquaporin (AQP) 4 and AQP9 in the brain of uraemic rats. Brain, kidneys and one testis were collected from four sham-operated (control) and four uraemic rats, 10 weeks after 5/6 nephrectomy (Nx). Protein abundance was measured by semi-quantitave immunoblotting using affinity-purified rabbit anti-rat antibodies applied on tissue crude homogenates. The results are expressed as means+/-SE of band density (arbitrary units). In Nx compared with control rats, the brain expression of UT-B1 was reduced by half (32+/-3 vs 62+/-8, P<0.01) whereas that of AQ4 was doubled (251+/-13 vs 135+/-5, P<0.001), and that of AQP9 increased by 65% (253+/-22 vs 154+/-10, P<0.01). UT-B1 expression was also lowered by Nx in kidney medulla (45+/-21 vs 141+/-4, P<0.01) but was unchanged in testis. The conjunction of a reduced expression of UT-B and an increased expression of AQPs in brain cells may bring a new clue to understanding the DDS mechanism. Because of low UT-B abundance, urea exit from astrocytes is most probably delayed during rapid removal of extracellular urea through fast dialysis. This creates an osmotic driving force that promotes water entry into the cells (favoured by abundant AQPs) and subsequent brain swelling.

Hospitalization for Initiation of Maintenance Hemodialysis

Background: Recent data on complications of hemodialysis (HD) is lacking. With advancement in dialysis technology the incidence of complications such as dialysis disequilibrium syndrome (DDS) has decreased. Notwithstanding these improvements many patients with end-stage renal disease (ESRD) continue to be hospitalized solely for initiation of hemodialysis. This study was undertaken to assess if such admissions are justified and also to determine incidence and predictors of complications of HD during initiation. Methods: Medical records of adult patients (>18 years) initiated on maintenance hemodialysis from January 1st, 1998 through December 31st, 2000 at our institution were reviewed. The demographics of the patients, cause of renal failure, creatinine clearance, type of vascular access, comorbidities, serum chemistries, ultrafiltration (UF) rate and indications for initiating dialysis were noted. Intradialytic complications were retrieved from the dialysis flow sheets. Results: Of the 240 patients reviewed, 18.3% developed complications during initiation of dialysis, and none was severe. Hypotension and leg cramps were the most frequent complications. The patients who developed hypotension and cramps were significantly older than those with no complications, 57.7 ± 14.9 (mean ± SD) years versus 52.3 ± 14.8 years, respectively (p = 0.02). The increment of age significantly influenced the complication rate [odds ratio (OR): 1.03, 95% confidence interval (CI) 1.01–1.05 (p = 0.03)], and so did hematocrit (HCT) (OR: 1.07, 95% CI 1.01–1.13). Multivariate analysis using age and hematocrit as continuous variables revealed that the older patients with anemia had a significantly higher risk of developing HD related complications than younger patients with anemia (OR: 1.05, 95% CI 1.01–1.09 at HCT of 24%, and OR: 1.03, 95% CI 1.00–1.06 at HCT 27%). When patients were stratified by hematocrit level, older patients with hematocrit <27% had higher risk of complications and the risk increased with increasing age [complication rate (HCT <27%): age <40 = 0%, age 40–64 = 11.7%, age >65 = 25%, p < 0.016]. Conclusion: Although very few, hypotension and muscle cramps were the main complications during initiation of HD. Older patients with anemia are prone for these complications although no physician intervention was necessary. Hospitalization solely for initiation of maintenance dialysis is not necessary and the additional cost from such admissions cannot be justified.

Optimization of dialysate sodium in sodium profiling haemodialysis.

Sodium profiling haemodialysis is a modified method of sodium gradient dialysis during which dialysate sodium follows a time-dependent profile. Sodium profiling haemodialysis has claimed to reduce intradialytic discomforts such as hypotension, muscle cramps, and disequilibrium syndrome. Having the low sodium period is an essential part of the sodium profiling haemodialysis to compensate for the sodium gain during the high sodium period. In spite of this, however, the incidence of interdialytic complications that results from the excessive sodium gain has been reported in previous literature. Making the prediction of optimal dialysate sodium concentration for isonatric dialysis is practically very difficult since too many variables influence the sodium gradient, including the initial plasma sodium and tonicity and/or dialysis dynamics that differ from patient to patient and from treatment to treatment. As for sodium profiling haemodialysis, complexities are added further since details of profile, such as type and form of profile, or initial, terminal, or time-distribution of dialysate sodium are varied considerably. We have recently reported that the intradialytic sodium balance and interdialytic weight gain are directly related to the time-averaged concentration of dialysate sodium (TACNa). The dialysate sodium can be optimized using this concept of TACNa for sodium profiling dialysis. TACNa should be approximately 0.5-0.8 mmol/L lower than patient's predialysis serum sodium concentrations to achieve a sodium balance neutral dialysis. In that study the optimal TACNa, seems to be between 137.8 and 143.5 mmol/L. Such an optimal value should be defined for the individual centres based on their profile protocols for clinical use. In the future, dialysate sodium should be optimized based on the exact prediction of the postdialysis plasma sodium levels.

Diabetic coma. Management of diabetic ketoacidosis and nonketotic hyperosmolar coma

This review describes the current guidelines of German diabetes association for the management of diabetic coma, both of diabetic ketoacidosis and hyperosmolal coma. The outline focuses on emergency treatment and the management on the intensive care unit, in particular, volume and insulin therapy, and potassium replacement. The delineation of the concept of low insulin therapy is emphasized to avoid the incidence of disequilibrium syndrome. Also, the indications for bicarbonate therapy in diabetic ketoacidosis are critically discussed, as well as phosphate and magnesium replacement. With today's therapeutic possibilities the therapeutic goal, i.e. a low mortality, may be achieved, dependent on the underlying illness.

Dialysis disequilibrium: another reversible posterior leukoencephalopathy syndrome?

Dialysis disequilibrium syndrome is a disorder of the central nervous system in patients on dialysis. The underlying etiology is thought to be primarily due to cerebral edema; however, neuroradiologic findings have not been described previously. We describe a patient who presented with new onset headaches and status epilepticus after beginning hemodialysis. Her neuroimaging studies revealed white matter changes in the posterior parietal and occipital lobes similar to those seen in patients with reversible posterior leukoencephalopathy syndrome (RPLS). This case suggests that dialysis disequilibrium syndrome and RPLS may represent a spectrum of disorders in which the underlying mechanism is vasogenic edema.

Dialysis Disequilibrium Syndrome Revisited

An aggressive dialysis in a grossly azotemic patient, especially one with severe metabolic acidosis, can lead to dialysis disequilibrium syndrome (DDS). Mild forms present as nausea, vomiting, restlessness, and headache. Severe manifestations include seizures, obtundation, coma, and even death. This clinical picture is caused by cerebral edema induced by one or more of the following mechanisms: “Reverse urea effect” - Dialysis removes urea faster from the blood than from the brain; consequently, water enters the brain. “Cerebrospinal fluid acidosis” - Correction of systemic acidosis engenders the condition due to a lowering of brain pH. “Idiogenic osmoles” - As a response to blood hyperosmolar state, osmoles are produced in the brain. As blood osmolality decreases under relatively quick dialysis, idiogenic osmoles tend to induce brain edema. Because the symptoms of DDS can be life-threatening, preventive measures in patients with severe uremia are important. The first strategy relies on raising blood osmolality by introducing solutes (osmoles) into the blood. The second approach, which is the most common, decreases the efficiency of the dialysis treatment by shortening the duration of a dialysis run to 25% – 30% of normal, by lowering dialyzer blood flow or dialysate flow rate, by using a less efficient dialyzer, or by a combination of these maneuvers. Dialysis frequency is increased instead. Anticonvulsant drugs are needed in cases where the preventive measures have not been used or have been unsuccessful.

Dialysis Disequilibrium Syndrome Revisited.

An aggressive dialysis in a grossly azotemic patient, especially one with severe metabolic acidosis, can lead to dialysis disequilibrium syndrome (DDS). Mild forms present as nausea, vomiting, restlessness, and headache. Severe manifestations include seizures, obtundation, coma, and even death. This clinical picture is caused by cerebral edema induced by one or more of the following mechanisms: "Reverse urea effect" - Dialysis removes urea faster from the blood than from the brain; consequently, water enters the brain. "Cerebrospinal fluid acidosis" - Correction of systemic acidosis engenders the condition due to a lowering of brain pH. "Idiogenic osmoles" - As a response to blood hyperosmolar state, osmoles are produced in the brain. As blood osmolality decreases under relatively quick dialysis, idiogenic osmoles tend to induce brain edema. Because the symptoms of DDS can be life-threatening, preventive measures in patients with severe uremia are important. The first strategy relies on raising blood osmolality by introducing solutes (osmoles) into the blood. The second approach, which is the most common, decreases the efficiency of the dialysis treatment by shortening the duration of a dialysis run to 25% - 30% of normal, by lowering dialyzer blood flow or dialysate flow rate, by using a less efficient dialyzer, or by a combination of these maneuvers. Dialysis frequency is increased instead. Anticonvulsant drugs are needed in cases where the preventive measures have not been used or have been unsuccessful.

Massive reduction of urea transporters in remnant kidney and brain of uremic rats

The facilitated urea transporters (UT), UT-A1, UT-A2, and UT-B1, are involved in intrarenal recycling of urea, an essential feature of the urinary concentrating mechanism, which is impaired in chronic renal failure (CRF). In this study, the expression of these UTs was examined in experimentally induced CRF. The abundance of mRNA was measured by Northern analysis and that of corresponding proteins by Western blotting in rats one and five weeks after 5/6 nephrectomy (Nx). At five weeks, urine output was enhanced threefold with a concomitant decrease in urine osmolality. The marked rise in plasma urea concentration and fall in urinary urea concentration resulted in a 30-fold decrease in the urine/plasma (U/P) urea concentration ratio, while the U/P osmoles ratio fell only fourfold. A dramatic decrease in mRNA abundance for the three UTs was observed, bringing their level at five weeks to 1/10th or less of control values. Immunoblotting showed complete disappearance of the 97 and 117 kD bands of UT-A1, and considerable reduction of UT-A2 and UT-B1 in the renal medulla. Similar, but less intense, changes were observed at one-week post-Nx. In addition to the kidney, UT-B1 is also normally expressed in brain and testis. In the brain, its mRNA expression remained normal one-week post-Nx, but decreased to about 30% of normal at five-weeks post-Nx, whereas no change was seen in testis. (1) The decline in urinary concentrating ability seen in CRF is largely due to a major reduction of UTs involved in the process of urea concentration in the urine, while factors enabling the concentration of other solutes are less intensely affected. (2) The marked reduction of brain UT expression in CRF may be responsible for brain edema of dialysis disequilibrium syndrome observed in some patients after fast dialysis.

Prediction of solute kinetics, acid-base status, and blood volume changes during profiled hemodialysis.

A mathematical model of solute kinetics oriented to the simulation of hemodialysis is presented. It includes a three-compartment model of body fluids (plasma, interstitial and intracellular), a two-compartment description of the main solutes (K+, Na+, Cl-, urea, HCO3-, H+), and acid-base equilibrium through two buffer systems (bicarbonate and noncarbonic buffers). Tentative values for the main model parameters can be given a priori, on the basis of body weight and plasma concentration values measured before beginning the session. The model allows computation of the amount of sodium removed during hemodialysis, and may enable the prediction of plasma volume and osmolarity changes induced by a given sodium concentration profile in the dialysate and by a given ultrafiltration profile. Model predictions are compared with clinical data obtained during 11 different profiled hemodialysis sessions, both with all parameters assigned a priori, and after individual estimation of dialysances and mass-transfer coefficients. In most cases, the agreement between the time pattern of model solute concentrations in plasma and clinical data was satisfactory. In two sessions, blood volume changes were directly measured in the patient, and in both cases the agreement with model predictions was acceptable. The present model can be used to improve the dialysis session taking some characteristics of individual patients into account, in order to minimize intradialytic unbalances (such as hypotension or disequilibrium syndrome).

Mathematical Modeling of Solute Kinetics and Body Fluid Changes during Profiled Hemodialysis

A mathematical model of solute kinetics oriented to improve hemodialysis treatment is presented. It includes a two-compartment description of the main solutes (K+, Na+, Cl-, urea, HCO3-, H+, CO2), acid-base equilibrium through two buffer systems (bicarbonate and non-carbonic buffers) and a three-compartment model of body fluids (plasma, interstitial and intracellular). The main model parameters can be individually assigned a priori, on the basis of body weight and plasma concentration values measured before beginning the session. Model predictions are compared with clinical data obtained during 11 different hemodialysis sessions performed on six patients with profiled sodium concentration in the dialysate and profiled ultrafiltration rate. In all cases, the agreement between the time pattern of model solute concentrations in plasma and clinical data turns out fairly good as to urea, sodium, chloride and potassium kinetics. Finally, the time patterns of plasma bicarbonate concentration and pH can be reproduced fairly well with the model, provided CO2 concentration remains constant. Only in two sessions, blood volume was directly measured in the patient, and in both cases the agreement with model predictions was good. In conclusion, the model allows a priori computation of the amount of sodium removed during hemodialysis, and may enable the prediction of plasma volume changes and plasma osmolarity changes induced by a given sodium concentration profile in the dialysate and by a given ultrafiltration profile. Hence, it can be used to improve the dialysis session taking the characteristics of individual patients into account, in order to minimize intradialytic imbalances (such as hypotension or disequilibrium syndrome).

An Algorithm for the Rational Choice of Sodium Profile during Hemodialysis

The incidence of intradialytic disequilibrium syndrome and symptomatic hypotension has increased significantly among dialysis patients over the last ten years. Profiled hemodialysis (PHD) is a new technique, based on the intradialytic modulation of dialysate sodium concentration, which aspires to reduce to previous imbalances. This paper presents a new algorithm for the determination of a rational dialysate sodium profile during PHD. A mathematical model of solute kinetics, monocompartmental for sodium and bicompartmental for urea is used. The algorithm allows the sodium profile to be elaborated a priori before each dialysis session, respecting the individual sodium mass removal and weight gain. A procedure allowing the adjustment of the method to the individual characteristics, on the basis of routine measurements performed before each session is also presented. The method was validated during seven dialysis sessions. Comparison between data measured in vivo and those predicted by the model showed standard deviations corresponding to the range of laboratory measurement errors: 1.50 mEq/L for sodium and 0.87 mmol/L for urea. In vivo implementation of PHD by our algorithm allows one to remove an amount of sodium close to that established a priori on the basis of patient's need.

Hemodialysis increases apparent diffusion coefficient of brain water in nephrectomized rats measured by isotropic diffusion-weighted magnetic resonance imaging.

The nature of brain edema in dialysis disequilibrium syndrome (DDS) was investigated by diffusion-weighted magnetic resonance imaging (DWI). DWI was performed on normal or bilaterally nephrectomized rats before, and immediately after, hemodialysis. Hemodialysis was performed with a custom-made dialyzer (surface area 150 cm2) against a bicarbonate-buffered bath for 90 min with or without 70 mM urea. Hemodialysis with non-urea bath decreased plasma urea by 21 mM, and plasma osmolality by 22 mosmol/kg H2O, and increased brain water content by 8.0% (all < 0.05), while hemodialysis with urea bath did not affect plasma urea, osmolality, or brain water content. Three sets of axial DWI images of the brain were obtained at different gradient weighing factors with an in-plane resolution of 0.39 mm2. The apparent diffusion coefficient (Dapp) of the brain water was not affected by bilateral nephrectomy, or by hemodialysis in normal rats. In nephrectomized rats, brain Dapp was significantly increased after dialysis with non-urea bath (1.15 +/- 0.08 vs 0.89 +/- 0.07 x 10(-9)m2/sec, P < 0.01). No significant changes of brain water Dapp could be observed after dialysis with urea bath. The increased Dapp associated with DDS indicates that brain extracellular water increases and/or intracellular water decreases after hemodialysis. Our results strongly suggest that the brain edema induced by hemodialysis in uremic rats is due to interstitial edema rather than cytotoxic edema. Furthermore, our results support a primary role for the "reverse urea effect" in the pathogenesis of brain edema in DDS.DWI may be a useful diagnostic tool for DDS in patients with end-stage renal disease.

Effect of a new model of hemodialysis potassium removal on the control of ventricular arrhythmias

The primary aim of this multicenter, prospective, randomized cross-over study was to clarify whether a new model of hemodialysis (HD) potassium (K) removal using a decreasing intra-HD dialysate K concentration and a constant plasma-dialysate K gradient (treatment B) is capable of reducing the arrhythmogenic effect of standard HD, which has a constant dialysate K concentration and decreasing plasma-dialysate K gradient (treatment A). The secondary aim was to verify whether this new model is clinically safe. In treatment B, the initial dialysate K concentration had to be 1.5 mEq/liter less than the plasma K concentration, and exponentially decrease to 2.5 mEq/liter at the end of HD. Forty-two chronic HD patients with an increase in premature ventricular complexes (PVC) during dialysis were enrolled from 18 participating centers, and randomly assigned to either sequence 1 (ABA) or sequence 2 (BAB). A pool of 333 of 378 expected ECG Holter recordings were checked for signal quality; 269 (71%) from 36 patients (86%) had a satisfactory signal quality and 108 were selected for analysis (1 per patient per period). There was a difference in the natural logarithm of the increase in PVC/hr and PVC couplets/hr during HD between treatments A and B (1.70 +/- 1.59 vs. 1.09 +/- 1.76 and 0.94 +/- 0.86 vs. 0.64 +/- 1.01, a reduction of 36% and 32%, P = 0.011 and 0.047, respectively) without any carry over effect (P = 0.61 and 0.24, respectively). The fact that this decrease of one third is due to a lower plasma-dialysate K gradient is supported by the observation that it was more evident during the first than the last two hours of HD (a reduction in the natural logarithm of the increase in PVC/hr and PVC couplets/hr of 60% and 60%, P 0.002 and 0.009, vs. 26% and 17%, P = 0.098 and 0.332, respectively): the initial plasma-dialysate K gradient was 2.3 times lower during treatment B than during treatment A, without adversely affecting pre-HD plasma K levels. These results could have a considerably clinical impact not only because of the possibility of physiologically decreasing the arrhythmogenic effect of HD, but also because this effect can be considered a "marker" of the electrophysiological derangement induced by the administration of standard HD three times a week for years ("electric disequilibrium syndrome").

Long-Term Comparative Evaluation of Synthetic and Cellulosic Membranes in Dialysis

A long-term retrospective evaluation (5 years) compares two groups of RDT patients (group 1 on continuous treatment with cellulosic membranes and group 2 with synthetic membranes) regarding survival, general clinical morbidity, and beta 2M-related morbidity. The results showed no significant long-term differences between the groups either for survival or general morbidity despite some differences in biocompatibility. The higher intradialytic removal of beta 2M by synthetic membranes did not lead to a reduction in either pre-dialysis beta 2M values or beta 2M related morbidity. The higher cost of synthetic over cellulosic membranes and the disappointing of many clinical expectations suggest that the use of such membranes, in association with alternative techniques, should take place only according to certain "elective" indications such as old age, diabetes, vascular instability or intradialytic disequilibrium syndrome.

Continuous venovenous hemodialysis

Hemodialysis and peritoneal dialysis are the main renal replacement therapies for patients with acute renal failure. These patients are often unable to tolerate drastic fluid shifts and other complications of conventional dialysis. Continuous hemodialysis, however, provides protection from the hemodynamic consequences and osmotic stressors of conventional dialysis and is rapidly becoming the treatment of choice for critically ill patients. We present a case in which a patient with a spontaneous cerebellar hemorrhage developed acute renal failure. Surgical evacuation was not an option. Clinical management included the use of continuous venovenous hemodialysis, which is described in the setting of a patient with a posterior fossa mass. The risks of anticoagulation, hemodynamic instability, and development of dialysis disequilibrium syndrome are discussed.

Auditory brainstem potentials in uraemia.

Evoked response audiometry was carried out to assess the viability of the auditory pathway in haemodialysed patients. The latency of the waves III and V and I-V interpeak latencies were significantly longer in the renal patients compared to the control group. The I-V interpeak latency was longer in 8 of our 13 patients than the upper limit (4.38 ms) in our laboratory. The possible cause for the central auditory dysfunction may be multifactorial, including the effect of metastatic calcifications, repeated occurrence of disequilibrium syndrome, or some small, molecular, toxic, metabolic substance. The significance of the different factors may vary among different haemodialysis centres.

Dialysis disequilibrium syndrome (DDS) in the rat: Role of the “reverse urea effect”

DDS is characterized by neurologic deterioration and cerebral edema which occurs after hemodialysis. To investigate the pathogenesis of DDDS, we studied the effects of rapid hemodialysis on plasma and brain electrolytes, urea, and osmolality in the rat. Forty-two hours after bilateral nephrectomy, nine uremic rats were hemodialyzed for 90 minutes against dialysate without urea (model of DDS), yielding a decrease in plasma urea from 72 +/- 2 mM to 34 +/- 2 mM (P less than 0.01) and an 8% (29 mOsm/kg) decrease in plasma osmolality. This group was compared to three control groups: 11 uremic animals dialyzed against a bath with urea added so that no fall in plasma urea occurred, and 15 uremic and 12 nonuremic animals that were not dialyzed. In animals dialyzed without urea, compared to uremic non-dialyzed animals, there was a 6% increase in brain water (3.89 +/- 0.04 liter/kg dry wt vs. 3.67 +/- 0.03, P less than 0.01) and an increase in the brain to plasma (urea) ratio (1.30 +/- 0.06 vs. 0.79 +/- 0.05, P less than 0.01). Comparison of these parameters in animals dialyzed without urea versus other control groups yielded similar results. In animals dialyzed without urea, the 53% decrease in plasma urea was associated with only a 13% decrease in brain urea content. Brain content of sodium and potassium was not significantly different among groups. Retention of brain urea despite the large decrease in plasma urea was able to account for the increased brain water observed in animals dialyzed without urea.(ABSTRACT TRUNCATED AT 250 WORDS)

Neurosurgical Management of Dialyzed Patients

Cerebrovascular disease is a lethal complication for patients with renal failure because of the hemostatic disturbance and equivocality about management of the central nervous system. Appropriate management of the renal failure in neurosurgical patients was considered on the basis of experience. Hemodialysis (HD), which is the most common dialysis method, has a serious disadvantage: the elevation of intracranial pressure during dialysis due to the "disequilibrium syndrome." It is important to stabilize the serum osmolarity during dialysis in order to prevent the disequilibrium syndrome. From this point of view, continuous ambulatory peritoneal dialysis (CAPD) has great advantages; serum osmolarity is not rapidly changed and no anticoagulants are required during dialysis. CAPD is recommended as the first method of choice in neurosurgical management of renal failure patients. However, if a patient has to be maintained with HD because of a history of laparotomy or peritonitis, it is essential to keep the serum osmolarity as stable as possible using the extracorporeal ultrafiltration method, hypernatremic HD, bicarbonate HD, and intravenous administration of glycerol.

Hemodialisis crónica en niños

The clinical features of eight patients, four females, aged 4 to 15 years under chronic hemodialysis for terminal renal failure (creatinine clearance 10 ml.min.1,73 m2 or less) are reported. Initial diseases were Alport syndrome, systemic lupus erythematosus, chronic glomerulonephritis (n = 2), bilateral polycystic kidney, prune belly syndrome and reflux nephropathy (n = 2). Distal vascular approach by means of arteriovenous fistulas was preferred for these patients and the kinetic urea model was used to evaluate the performance of the procedure. Patients required nine to twelve hours of hemodialysis per week for optimal results. Mean weight decreases of 1 to 3 kg and reductions in blood urea nitrogen and serum potassium of 40 mg.dl and 2,5 mEq.1, respectively, were observed. The main complications of hemodialysis were the disequilibrium syndrome, infections at the site of insertion of the arteriovenous fistulae and congestive heart failure. Three patients were submitted to renal transplantation with live donors homografts: one died and the other two remain alive but under chronic hemodialysis. Five children are attending school regularly, and two of them are waiting a kidney donor for transplantation. Despite encouraging results chronic hemodialysis in children constitutes only primary supportive therapy prior to renal transplantation.