We describe a method to produce bicarbonate-based dialysates containing similar to 100 mg/dl ethanol by introducing the alcohol into one of the dialysate concentrate solutions geared for the production of bicarbonate-based dialysates.

The Aksys PHD system is designed for short quotidian dialysis employing a 52‐liter batch of ultrapure dialysate and up to 30 in situ hot water reuses of the entire extracorporeal circuit including a 40‐liter physical cleaning before each dialysis. Methods: We studied the effect of the 52‐liter tank during 108 long 5–8 hour dialysis 3.5–6 times/week in 5 patients and one 50‐liter patient simulator for 4 weeks. Phosphate (PO4), beta‐2 microglobulin (b‐2), urea (BUN), and creatinine (creat) were measured pre‐, during, and post‐dialysis 86 times and in total dialysate 74 times during long dialysis. Tank saturation, Kt/V, and monthly chemistries were also measured. Results: Patient weight 76 ± 2 kg, QB 234 ± 23 ml/min, QD 498 ± 13 ml/min. Dialysate was recirculated 4.8 times during 8 hours. Analyte Short Long dialysis p Pre‐BUN 70 ± 18 49 ± 15 <0.0001 Pre‐creat 12 ± 3 10 ± 2 <0.0002 Pre‐PO4 5.2 ± 1.5 4.1 ± 1.1 <0.003 Pre‐b‐2 34.0 ± 5.3 27.8 ± 4.5 <0.0001 All patients on 8 hrs × 5 dialyses/week stopped phosphate binders within 3 weeks. eKt/V(urea) rose to 0.5 in one hour and then slowly to 0.8 at 8 hours. Weekly stdKt/V: Dialyses/week/Hrs: 2 5 8 5 2.2 2.7 3.0 6 2.7 3.4 3.6 7 3.1 3.8 4.4 At 8 hrs the tank was 99 ± 8% saturated with BUN, 86 ± 12% with creat, 77 ± 18% with PO4, and only 12 ± 5% with b‐2. Total removal per dialysis increased 2 gm BUN, 0.4 gm creat, 0.4 gm PO4, and 40 mg b‐2. The decline per reuse in conductivity clearance was only 0.7 ± 1.2% during short and 1.4 ± 1.4% during long dialysis (p = 0.11). There was no change in monthly chemistries or hematologies. Discussion: The data show that the Aksys PHD is very effective for long 8‐hour dialysis. The data for PO4 and b‐2 are the same as reported for conventional dialysis machines using 5 times as much dialysate, and the weekly stdKt/V if the PHD is used every night is twice the standard defined by K/DOQI. The exceptional cleanliness and biocompatibility by way of the one‐per‐month reuse should be a great advantage to patients. The full automatization saves the patient one hour every night and 30 minutes every morning. The PHD also economizes on filters and dialysate and is good for the environment.

As the frequency of hemodialysis sessions has always been a concern, it is not astonishing that interest in quotidian (daily) hemodialysis appears to be growing worldwide. The main reasons for more frequent dialysis are to maximize well-being and minimize both intra- and interdialytic symptoms, as well as to improve the treatment of patients with severe underlying medical problems, particularly cardiovascular disease. Moreover, studies also indicate overall potential cost savings as compared with current conventional hemodialysis. There are two options available, namely short daily and long nightly treatments. The main difference centers on the ability of the nightly regimen to remove greater amounts of phosphate and beta-2-microglobulin. Even so, there is no doubt that both treatments are highly preferable to conventional three times weekly dialysis. Further issues which are discussed include the requirements necessary to run dialysis programs, vascular access requirements, and the management of complications and risks such as calcium and phosphorus control. This is the first publication devoted solely to daily hemodialysis therapies: Concentrating on clinical and technical issues, it is an important contribution to the practical development of daily hemodialysis and is highly recommended to nephrologists, nurses, managers of renal programs and others involved in renal care.

revolutionized the management of patients with kidney disease (1-3). It was already considered to be a safe procedure by the mid 1960s, carrying a nephrectomy risk of 1:1,616 (0.06%) and a mortality risk of 1:2,000 to 5,000 (0.02%-0.05%) (4-7), but many improvements were added later, including radiological assistance, the biopsy gun system, and safer needles (8-20). Yet there remain situations in which percutaneous biopsy may not be safe, such as when the patient cannot cooperate, when there is bleeding diathesis, solitary kidney, horseshoe kidney, severe hypertension, or endstage renal disease (4, 21). An alternative approach, transjugular renal biopsy, merits consideration in some of these situations. It was derived as an offshoot of transjugular liver biopsy, especially after renal tissue was obtained unintentionally during some of these procedures (22). This led French investigators to use this approach to access the kidney, and between 1990 and 1996 they reported that transjugular biopsy could be done safely to diagnose renal disease (22-24). Since the early 1990s the equipment used for transjugular biopsies has been improved, the modified Colapinto needles (Mal transjugular renal biopsy set, William Cook Europe, Bjaerskov, Denmark) being replaced by the Quick Core (Cook, Inc, Bloomington, IN) biopsy system (25). The procedure consists of accessing a jugular vein (preferentially the right) under sonogram guidance with a needle, passing a guide wire through the needle, which is then removed (26). A nine French vascular sheath is now inserted through the guide wire, and this is followed by inserting a 5-F multipurpose curved catheter (26). The curved catheter is maneuvered into the outermost posterior portion of the right renal vein (26), the original guide wire is removed, and a 0.089-cm diameter, 145-cm long Amplatz Super Stiff wire (Boston Scientific, Watertown, MA) is inserted instead (26). At this point the 5-F multipurpose curved catheter is removed and a 7-F guiding cannulae introduced over the Super Stiff wire (26). Finally, after removing the Super Stiff wire, a 60-cm, 18-G biopsy needle with a 2-cm throw length is used to obtain kidney tissue (26). Some 30-50 ml of contrast material may need to be injected during the procedure (26). In the most recent reports on transjugular biopsy the authors have obtained adequate tissue (26, 27). This was the case in 95.8% and 97% of biopsies in the last two studies, the average number of glomeruli procured being 14.4 and 19.4 (26, 27). Transjugular renal biopsy has been performed in different series of 29, 200, and 400 patients without deaths or loss of kidney (23, 26, 27). Cluzel et al reported only four major complications in 400 biopsies–neck hematoma in one (requiring a blood transfusion), and large perirenal hematomas in three (requiring a blood transfusion in one and embolectomy in two) (27). Perirenal hematomas, reported in 3 23% of biopsies, are the result of penetration of the renal capsule, as one needs to move well into the kidney tissue to obtain glomeruli (23, 26). Puncture of the renal pelvis or its tributaries may also occur, because the collecting system is situated between the venous system and the cortex of the kidney (a complication that may be delineated by a post-biopsy venous contrast injection showing extravasation of contrast into the collecting system). Another potential complication, contrast-induced nephropathy, has not been a problem, probably because the amount of dye injected is small (22, 26). Comparing percutaneous and transjugular renal biopsies, the adequacy of tissue obtained has been similar in the most recent studies (26, 27). Not a single kidney was lost in more than 600 reported cases of transjugular renal biopsy, but then the same can be said about percutaneous biopsies. In fact, Cluzel et al found the incidence of major complications to be similar with the two methods (27). Yet one might surmise that the transjugular route would be safer than the percutaneous technique, because although capsular or collecting system penetration is possible, most bleeding would occur into the patient's own venous system, the site of entry into the kidney. Bleeding, moreover, has been unusual, despite Editorial The International Journal of Artificial Organs / Vol. 24 / no. 9, 2001/ pp. 595-597

A maintenance hemodialysis patient developed metabolic alkalosis in the absence of vomiting or nasogastric suction. The cause of the metabolic alkalosis was ingestion of an exogenous alkali in the form of Bromoseltzer. The metabolic alkalosis improved with hemodialysis using a low-bicarbonate bath.

Urea and creatinine levels in spent hemodialysates showed only small declines in spite of incubation at 37 degrees C for 36 hours, in the determination of dialysate-side solute removal, it would seem prudent to keep spent dialysate cold during collection to retard bacterial breakdown of these waste products.

Foscarnet is an antiviral agent widely used in the treatment of cytomegalovirus (CMV) infection. We describe a cardiac transplant patient, who while being maintained with hemodialysis because of tobramycin-induced acute renal failure, was given Foscarnet for disseminated CMV infection. Using dialysate-side clearance methodology, we found the dialyzer clearance of Foscarnet to be in the order of 89 ml/min. (Int J Artif Organs 2000; 23: 165–7)

Obstruction of the lumen by fibrin deposits is a complication of long-term, indwelling intraperitoneal catheters. Such obstruction can cause poor flow, with resultant inadequate dialysis. Urokinase, a thrombolytic agent, has been infused into clotted peritoneal dialysis catheters to achieve fibrinolysis and thus maintain patency. 1 Strippoli P Pilolli D Mingrone G Dimaggio A Coviello F Orbello G Querques M Scatizzi A A hemostasis study in CAPD patients during fibrinolytic intraperitoneal therapy with urokinase (UK). Adv Perit Dial. 1989; 5: 97-99 PubMed Google Scholar With the recent unavailability of urokinase in the United States, declotting of these catheters has become more difficult. Indeed, the removal of catheters in which the fibrin plugs potentially could have been dissolved by thrombolytic agents is not uncommon.

Intensive high-flux hemodiafiltration is often used in the management of vancomycin toxicity. We describe two patients who developed hypophosphatemia as a consequence of this form of therapy. The first patient was treated with an intravenous phosphorus infusion. For the second patient, hypophosphatemia was corrected, during hemodiafiltration, with the use of a phosphorus-enriched dialysate. The latter dialysate was prepared by adding sodium phosphate salts to the "base concentrate" of a dual-concentrate, bicarbonate-based dialysate delivery system. This simple method was more efficient than intravenous therapy in ameliorating the hypophosphatemia secondary to aggressive hemodiafiltration treatment.

The finding of an abnormally high number of eosinophils in the peritoneum is a curious phenomenon, the cause and importance of which are not fully understood. Classically, peritoneal fluid eosinophilia has been noted in a restricted number of diseases, most notably, helminthic infections and allergic diseases. However, peritoneal fluid eosinophilia is a rather common event that occurs irregularly and intermittently during the course of peritoneal dialysis in the absence of known clinical entities. Except for its role in occasionally enticing the unwary clinician to make an incorrect diagnosis of bacterial peritonitis due to its cloudy effluent, no significant functional properties have traditionally been attributed to peritoneal fluid eosinophilia.The phenomenon of eosinophils in the peritoneal fluid of chronic peritoneal dialysis patients was first reported in 1967 by Lee and Schoen [1]in a 39-year-old female on maintenance intermittent peritoneal dialysis for 3 months. Clinical characteristics were the presence of diffuse abdominal cramps, cloudy yellow dialysate effluent, 56% eosinophils, peripheral blood eosinophil count of 15%, culture negative, and the absence of malignancy, polyserositis, vasculitis, or parasitic disease.Eosinophilic infiltration of the peritoneal cavity has been termed 'eosinophilic peritonitis' [2]. It is a syndrome characterized by abdominal pain and peritoneal and peripheral eosinophilia associated with complete recovery. Eosinophilic infiltration of the peritoneal fluid of patients undergoing chronic maintenance peritoneal dialysis has been termed 'sterile peritonitis' to emphasize its noninfectious etiology [3]; however, the term 'peritoneal fluid eosinophilia' is preferred to distinguish it as a clinical entity with diagnostic considerations separate from those of known infectious etiological processes [1].The peritoneal fluid nonerythrocyte cell count is normally <300/mm3, of which less than 10% are eosinophils. Consequently, the absolute eosinophil count is normally <30/mm3 [4]. Most investigators believe that the normal eosinophil count in peritoneal fluid in patients on peritoneal dialysis is in the 68 ± 18 range [4, 5]. Peritoneal fluid eosinophilia is defined by the presence of >100 eosinophils/mm3 of peritoneal effluent [5]or as an eosinophil count >10% of the total nonerythrocyte count [5, 6].The incidence of peritoneal fluid eosinophilia is highly variable, ranging from 16 to 60% [4, 5, 7]. The majority of the patients develop peritoneal fluid eosinophila within the first 3 months of the initiation of dialysis, but this phenomenon has been reported as early as 1 day and as late as 6 months after dialysis. It is very rare later in peritoneal dialysis.The entity of peritoneal fluid eosinophilia has a characteristic presentation which allows for its distinction from more common bacterial peritonitis [8]. The classic presentation is a cloudy peritoneal fluid, present on an intermittent basis, and may not be seen with every bag exchange (table 1). Abdominal pain, nausea, vomiting, or rebound tenderness are usually absent and have no correlation with the number of peritoneal fluid eosinophils [4]. The peritoneal fluid white cell count is >100/mm3, usually in the range from 170 to 1,900/mm3, but rarely in the thousand range. The differential cell count is characteristic in that there are <60% polymorphonuclear neutrophils and >10% eosinophils. Cultures for microorganisms do not yield any growth and tests for endotoxins are negative [3, 7, 8]. There is no history to suggest a global hypereosinophilic syndrome, allergic disease, parasitic infestation, polyserositis, immunodeficiency syndrome, tuberculosis, malignancy, or connective tissue disease. The peritoneal eosinophilia may last from a few days to several months and usually resolves without peritoneal sequelae [8].Concomitant peripheral blood eosinophilia may be present in over 50% of cases, but tends to be mild. Patients with a higher peritoneal fluid eosinophil count appear to have a higher incidence of peripheral blood eosinophilia elevation [9]. The peak peritoneal fluid eosinophil count does not correlate with that in the peripheral blood nor with the prevailing IgE concentration [5, 9]. Peripheral blood eosinophil levels were not found to be elevated, but serum IgE concentration was much higher in patients who subsequently developed peritoneal fluid eosinophilia [5].Peritoneal fluid eosinophilia has to be differentiated from bacterial peritonitis, where signs and symptoms of abdominal pain, nausea, vomiting, fever, and allergic symptomatology dominate the clinical findings. The peritoneal fluid white blood cell count is in the thousand range, with polymorphonuclear cell percentage >75%. Eosinophils are absent. Peritoneal fluid cultures are usually positive for infectious agents. All patients with a cloudy effluent should have a differential white cell count in the peritoneal dialysis effluent, and antibiotics should be withheld pending culture if a high eosinophil count is found [3].Peritoneal fluid eosinophilia is not usually a cause for concern, and treatment is not warranted, unless the fluid is so markedly turbid as to threaten the patency of the catheter. Occasionally, peritoneal fluid eosinophilia can linger for months, and a short course of intraperitoneally administered hydrocortisone [10], by producing reversible sequestration of eosinophils in the reticuloendothelial system [11], may result in resolution. Histamine is reported to be a chemotactic for eosinophils, and a combination of prednisone and diphenhydramine [12], by previously mentioned steroid effect and suppressing histamine release [13], may be used in the treatment of peritoneal fluid eosinophilia. Treatment with ketotifen [14]and glycyrrhizin [15]has also resulted in successful resolution. Overzealous treatment of this self-limiting condition with steroids may invite opportunistic infections of the peritoneal cavity.The natural history of peritoneal fluid eosinophilia appears to be self-limiting, although the process can persist for a long time. Patients with peritoneal fluid eosinophilia do not have a significantly different number of peritonitis episodes from that of patients without [5]. The presence of eosinophils and other inflammatory cells can result in increased fibrin formation in the peritoneal effluent, leading to an increased risk of catheter obstruction, though none has been reported as yet. Short-term peritoneal fluid eosinophilia has not been shown to cause permanent adverse effects upon the peritoneal membrane function, as judged by urea and creatinine clearances, dialysate protein content, and ultrafiltration capacity of the membrane [8]; however, long-term effects of peritoneal fluid eosinophilia on peritoneal membrane function are not known.The role and mechanism for peritoneal fluid eosinophilia are uncertain. Eosinophils are cells that originate from myeloid stem cells, develop in the bone marrow, and spend most of their lives within tissues rather than in the blood or bone marrow. They are terminally differentiated cells incapable of cell division; their granule contents are responsible for many stimulatory and inhibitory effects on inflammation. The function of eosinophils in pathological states is better understood than their role in normal homeostasis. They play a distinct role in the pathogenesis of allergic and other inflammatory diseases by virtue of their multiple functional capabilities and interactions with lymphocytes and endothelials cells. Their presence in the peritoneal cavity and other tissue sites is probably related to their host defense capabilities. Eosinophils can stimulate lymphocyte responses by acting as antigen-processing and antigen-presenting cells, have autocrine and paracrine functions, and abrogate some aspects of hypersensitivity reactions [16].Examination of the character of eosinophils in peritoneal fluid eosinophilia reveals that, as eosinophilic peritonitis resolves, there is a concomitant drop in the percentage of hypodense eosinophils recovered from peritoneal dialysate as well as a drop in fluid major basic protein levels. Blood eosinophil differential percentages were low, but the percentage of hypodense eosinophils in the blood tended to be relatively increased. Leukotriene C4 levels remained relatively constant as did white blood cell counts. Flow-cytometric analysis of lymphocytes and granulocytes from peritoneal dialysis fluid and blood revealed high levels of CD23-positive lymphocytes [17]. This observation is in accordance with the well-established observations that metabolism and behavior of eosinophils vary under different circumstances and that the pathologic states associated with eosinophilia are associated with alterations in eosinophil function [18]. Activated eosinophils are markedly different in density from normal eosinophils, having already released their dense granule contents. Surface receptor expression is enhanced when cells are activated. Since the release of granule contents and reactive oxygen species does not occur in normal tissues when eosinophils are not activated, it is probable that eosinophils are more important in inactivating inflammatory mediators under normal than under pathological conditions in which they are increased in number and altered in function.Since peritoneal fluid eosinophilia occurs after catheter insertion and initiation of peritoneal dialysis [19], it has been suggested to be a hypersensitivity reaction to some constituent of the peritoneal dialysis system [3, 7]. Mechanical trauma during insertion of catheter, hypersensitivity reaction to ethylene oxide and other sterilants used in the preparation of dialysate bags [20, 21], plasticizers, additives, impurities, decomposition products and reaction products, still unidentified compounds released from polyvinyl chloride bags and iodine solution used for continuous ambulatory peritoneal dialysis with possible exposure of the peritoneal membrane to iodine, and mechanical irritant action of large volumes of fluid on the peritoneum have all been implicated in the induction of peritoneal fluid eosinophilia [22]. Saline lavage alone has been shown to be a sufficient stimulus for peritoneal eosinophil production in animal models [23]. Introduction of air into the peritoneum during the process of dialysis bag exchange results in peritoneal fluid eosinophilia. Resolution of peritoneal fluid pleocytosis correlates temporarily with absorption of subdiaphragmatic air [24]. Allergic reaction to intraperitoneally administered heparin [25]and antibiotics for the treatment of bacterial peritonitis [22]could be associated with the development of peritoneal fluid eosinophilia. Uremia per se [26], viral infection [27], Paecilomyces variotti infection [28], and Aspergillus niger infection [29]can cause peritoneal fluid eosinophilia. Peritoneal fluid eosinophilia may occur in response to particulate fungal cell antigens being washed into the peritoneal cavity during dialysis. In non-dialysis patients the etiology is varied and can be an expression of a subserous form of eosinophilic gastroenteritis [30]or an unusual manifestation of spontaneous bacterial peritonitis [31](table 2).Fibrin formed during the process of peritoneal dialysis may cause peritoneal fluid eosinophilia. A variety of materials, many of them proteolytic enzymes, and even inert materials, activate the coagulation mechanism to produce fibrin. It has been demonstrated that fibrin or proteolytic enzymes that promote fibrin formation are chemotactic for eosinophils and that eosinophils contain profibrinolysin in their granules [32].Eosinophilic response occurs as a result of reactions associated with the interaction of antigens and antibodies. Investigation of peritoneal eosinophil counts during intermittent peritoneal dialysis over a 1-year period revealed a wide range in the mean eosinophil percentage per patient during the first 6 months of dialysis (0–84%) that narrowed to 0–9% after 6 months. The peritoneal eosinophil proportion fell from 18 ± 2% during the first 2 months of dialysis to 3 ± 0.4% 6 months after dialysis. The absolute number of eosinophils per cubic millimeter fell from 586 ± 126 to 61 ± 18. The majority of the high initial eosinophil counts resolved after 2 months [7]. These observations are in accordance with the known function of eosinophils. Eosinophils are involved early in immune response, accumulating within hours of antigen presentation [33]. Excess antigen or antibody production inhibits these effects [34]. It is possible that increased antigen and antibody load, produced as the inflammation progresses during chronic peritoneal dialysis [35, 36], resulted in the inhibition of eosinophilic response noted in the study. It is also possible that the preferential accumulation of eosinophils in certain inflammatory states in the peritoneum may be due to the different expression of different leukocyte subgroups and the differential regulation of endothelial cell ligand expression [37, 38](table 3).Peritoneal fluid eosinophilia cannot be explained by hypersensitivity reaction alone. Recent work on so-called 'adhesion molecules' has brought about a different perspective to this issue. A chronic inflammatory state persists in the peritoneum of dialysis patients due to mechanical and chemical irritation [35, 36]. The specific accumulation of eosinophils in the peritoneal fluid may be due to the release of chemoattractants in inflammatory tissue sites [37]. Cytokines released at sites of inflammation, the peritoneum, may cause eosinophil activation. The cytokines interleukin 5, granulocyte-macrophage colony-stimulating factor, and interleukin 3 are produced by the mononuclear cells, including T cells and monocytes, and promote eosinophilopoesis and prolong eosinophil survival. Interleukin 5 seems to be specific for eosinophils [37]. Chemoattractants are not specific for eosinophils, as they are also active in neutrophil recruitment, and hence, the predominant infiltration of eosinophils in the peritoneal fluid cannot be explained solely by their release. The absence of a single agent that functions solely as the predominant chemoattractant mechanism responsible for eosinophil influx into various tissue sites is in accordance with the growing understanding that the final preferential mobilization of eosinophils into tissue sites involves a complex and cumulative interplay of many molecules and pathways [38, 39].Peritoneal fluid eosinophilia occurs intermittently and irregularly, and not all peritoneal dialysis patients, though exposed to repeated chemical and mechanical stimuli, respond with peritoneal fluid eosinophilia. The preferential accumulation of eosinophils in certain inflammatory states may be explained by the observations that the different leukocyte subgroups can express different surface adhesion molecules and that there is a differential regulation of endothelial cell ligand expression [38, 39].Peritoneal fluid eosinophilia has to be differentiated from other diagnostic considerations such as bacterial peritonitis and unusual presentations of spontaneous bacterial peritonitis. Chronic fungal catheter infection should be excluded in cases of late onset, persistent peritoneal eosinophilia on continuous ambulatory peritoneal dialysis [28], and removal of the external Tenckhoff catheter may be required for cure in some cases [40].Chronic hypersensitivity reactions and conditions of local eosinophilia such as pulmonary eosinophilic syndromes have been associated with various degrees of tissue damage, and though the relevance of eosinophilia in the pathophysiology of renal disease has not been established, it has been implicated in chronic sclerotic change and damage to the glomerular capillary wall [41]. Recent findings suggest that eosinophils may be involved in vascular injury in renal allograft rejection and necrotizing renal vasculitides and may also have a role in the interstitial lesions in renal graft rejection [42, 43]. These recent developments about the effects of eosinophils may prompt us to reconsider their role in other renal-related diseases, including peritoneal fluid eosinophilia.

A 64-year-old woman presented with coma and shock due to severe ethanol intoxication. Her initial, markedly elevated blood alcohol level of 136.5 mM fell only by 16% after a 4-hour period of conservative treatment consisting of mechanical respiration and the administration of intravenous fluids, vasopressors and inotropics. Subsequent hemodialysis rapidly reduced her blood ethanol concentrations to less threatening levels, with prompt restoration of her consciousness. Hemodialysis may be life-saving and should be considered in patients with severe ethanol intoxication.

A patient with end-stage renal disease developed severe hyperchloremic acidosis (venous serum total CO 2 level of 10 mmol/L) after treatment with 16 L of isotonic saline. Analysis of this case and published literature indicates that dilutional acidosis may result when very large volumes of isotonic saline are administered intravenously, especially in patients with impaired or absent renal function.

We describe a patient who suffered from renal failure-associated pericarditis and underwent daily 3.5-hour hemodialysis treatments for 17 days. The initially elevated serum phosphorus level gradually fell to below normal on days 11 and 12 as a result of the intensive dialytic therapy. Phosphorus was added to the "base concentrate" of a dual-concentrate, bicarbonate-based dialysate delivery system on days 13 to 17. Because of this phosphorus-enrichment, we were able to maintain the patient's serum phosphorus levels within normal limits in spite of continued daily dialysis treatments.

In 22 hemodialysis patients, during a dialysis session, the solute removal index (SRI) for urea obtained from the use of a partial spent dialysate collection method was compared with that derived from the use of a total spent dialysate collection technique. The partial spent dialysate collection method was used to harvest a small representative sample of the total spent dialysate. The volumes of spent dialysate collected by the partial and the total spent dialysate collection methods were 1.7 +/- 0.4 L and 129.6 +/- 15.3 L, respectively. The total amount of urea nitrogen removed by dialysis as estimated by the partial spent dialysate collection method was similar to that determined by the total spent dialysate collection approach. As a result, the SRI value for urea obtained by the partial spent dialysate collection method (namely, 63% +/- 8%) correlated very well (r = 0.95, P < 0.001) with that derived by the total spent dialysate collection technique (namely, 62% +/- 8%). Our data suggest that it is feasible to use a simple partial spent dialysate collection method to obtain SRI results in patients treated with hemodialysis.

Hypophosphatemia developed in a normophosphatemic patient after 9 h of hemodialysis therapy (using a phosphate-free dialysate) administered for the treatment of ethylene glycol poisoning. The hypophosphatemia was promptly improved with additional hemodialysis treatment using a phosphorus-enriched dialysate.

A phosphorus-enriched dialysate was used to intensively hemodialyze two non-uremic and non-hyperphosphatemic patients poisoned with ethylene glycol. As a consequence of the use of such a dialysate, we were able to prevent a fall in plasma inorganic phosphorus levels in these patients in spite of the intensive dialytic therapy.

Yung, C. Y.; Patel, J. A.; Chow, M. T.; Patel, J. S.; Zhou, F. Q.; Ing, T. S. Author Information