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Vascular access is the Achilles’ heel of hemodialysis. Current vascular access approaches for hemodialysis include arteriovenous (AV) fistula, AV graft, and central venous catheter. Strengths and weaknesses of each access type are described. New technology and procedures in introducing an access, monitoring access function, and salvaging a non-functioning access are also described.

Severe methanol poisoning requires treatment with prolonged and intensive hemodialytic therapy. Such treatment can engender either the de novo development of hypophosphatemia or the worsening of pre-existing hypophosphatemia. Phosphorus-enriched hemodialysis therapy can prevent the occurrence of this complication. We report three patients with severe methanol poisoning who were treated with phosphorus-enriched hemodialysis. Prevention or treatment of hypophosphatemia was successfully achieved with this dialytic technique.

Urea and creatinine levels in spent hemodialysates showed only small declines in spite of incubation at 37° 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.

In 6 hemodialysis patients, enriching the "base concentrate" of a bicarbonate-containing dialysate-generating system with phosphorus succeeded in raising plasma phosphorus levels.

The buffering capacity of the residual peritoneal dialysate fluid from each of 5 patients undergoing continuous ambulatory peritoneal dialysis was assessed by titrating with fresh, conventional, acidic, and lactate-containing peritoneal dialysis solutions. It was found that residual fluids had considerable buffering capacity.

Acidic (pH 5.2) incubation mixtures containing pyruvate-based or lactate-based peritoneal dialysis solutions (PDSN's) induced comparable degrees of intracellular acidosis in neutrophils. However, addition of an acidic (pH 5.2), pyruvate-based PDSN to a pH-7.4, neutrophil/phosphate-buffered saline mixture brought about higher extracellular and intracellular (neutrophil) pH values when compared to the introduction of an equally acidic, lactate-based PDSN. This poor ability of acidic (pH 5.0-5.5), pyruvate-based PDSN's to resist alkalinizing influences is the cause for the above higher pH values. The higher intracellular pH levels so obtained may be a reason behind why acidic, pyruvate-based PDSN's appear to be more biocompatible than their equally acidic, lactate-based counterparts.

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.

Neutrophil superoxide formation was similar when cells were incubated in self-made, non-autoclaved, pH 7.4, lactate-based peritoneal dialysis solutions or in their self-made, non-autoclaved, pH 7.4, bicarbonate-based counterparts. On the other hand, commercially available, autoclaved, pH 7.4, lactate-based peritoneal dialysis solutions resulted in inhibition of superoxide production when compared to their self-made, non-autoclaved, pH 7.4, lactate-based or bicarbonate-based counterparts. The cause for this inhibition of superoxide generation is at present unknown.

The effects of euhydric, lactate-based peritoneal dialysis solutions and those of their euhydric, bicarbonate-based counterparts, on neutrophil intracellular pH are comparable. This similarity in effects on intracellular acidity may have bearings on the influences of these solutions on cellular functions in general.

Continuous ambulatory peritoneal dialysis was successfully carried out in 6 end-stage renal failure patients using self-made, ultrafiltration-sterilized dialysis solutions. A Y-set was used to deliver the above solutions to sterile plastic bags.

Exposure of human neutrophils to conventional, acidic, lactate-based peritoneal dialysis solutions for 5 minutes results in a depression of superoxide generation. In spite of restoration of extracellular pH to 7.4, these stunned cells failed to recover their ability to generate the anion after a period of an hour.

By replacing the liquid acetic acid present in the “acid concentrate” of a bicarbonate-based dialysis solution-generating system with an equimolar amount of solid L-lactic acid and by using the dry forms of the remaining constituents, we were able to create a dry “acid concentrate” just prior to use, and successfully employed this “acid concentrate” to produce a bicarbonate-based solution to hemodialyze patients.

An exposure of human neutrophils to an acidic (pH 5.2), lactate-based incubation mixture containing a conventional, acidic, lactate-based peritoneal dialysis solution (PDS) resulted in the development of a prompt and substantial intracellular acidosis. A comparable exposure to a euhydric, bicarbonate-based incubation mixture containing a euhydric, bicarbonate-based PDS did not bring about similar changes in intracellular pH. The absence of an intracellular acidosis in the instance of the euhydric, bicarbonate-based PDS may be the reason why this solution is more biocompatible than its acidic, lactate-based counterpart.

Exposure of human neutrophils to a conventional, acidic, lactate-containing peritoneal dialysis solution (PDS) resulted in the development of a prompt and substantial intracellular acidosis. It is possible that this intracellular acidosis contributes to cellular dysfunction.

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)

A patient with end-stage renal disease developed severe hyperchloremic acidosis (venous serum total CO2 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.

Various modalities of high-intensity hemodialysis are gathering increasing popularity. Some of the advantages of these new dialysis regimens are presented. Time and the increasing use of these novel approaches will ultimately determine their role in the overall management of patients with end-stage renal disease.

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.

The absence of osmotic diuresis modifies the effects of hyperglycemia on body fluids in patients with advanced renal failure. To determine the relationship between clinical manifestations and abnormalities in tonicity and extracellular volume in such patients, we analyzed 43 episodes of severe dialysis-associated hyperglycemia (serum glucose exceeding 600 mg/dL) treated only with insulin. The main manifestations were dyspnea in 22 cases (pulmonary edema in 19), nausea and vomiting in 15, coma in 13 and seizures in 3, while 5 patients had no symptoms. Treatment with insulin resulted in a decrease in serum glucose value from 913 ± 197 mg/dL to 170 ± 78 mg/dL, an increase in serum sodium level from 125 ± 5 to 136 ± 5 mmol/L, and a fall in calculated serum tonicity value from 300 ± 13 to 282 ± 11 mmol/kg (all at p < 0.001). The ratio of the change in serum sodium level over change in serum glucose concentration was –1.50 ± 0.22 mmol/L per 100 mg/dL. The percent increase in extracellular volume secondary to hyperglycemia developing from the prior euglycemic state and calculated from changes in serum sodium and chloride concentrations, was 10.9% ± 4.6% (1.5% ± 0.6% per 100 mg/dL increase in serum glucose level). All clinical manifestations dissipated after correction of hyperglycemia in 42 patients. One woman developed during treatment a fatal myocardial infarction. Dialysis patients with severe hyperglycemia may develop symptoms as a result of hypertonicity and extracellular expansion. Insulin alone may be sufficient treatment for these symptoms. The changes in serum tonicity and electrolytes during treatment are consistent with theoretical predictions.

Each of seven hypophosphatemic hemodialysis patients was dialyzed with a phosphorus-enriched, bicarbonate-buffered dialysate. The latter was prepared by the introduction of sodium phosphate salts to the “acid concentrate” of a bicarbonate-buffered dialysate delivery system. The patients tolerated the procedure well and their hypophosphatemia improved.

Peritoneal dialysis was performed on 7 end-stage renal failure patients using an I-lactate-containing solution sterilized by ultrafiltration through polyamide filters. The patients tolerated the procedure well while their metabolic acidosis and azotemia improved.

We performed acute peritoneal dialysis on eight end-stage renal disease patients using a bicarbonate-containing solution sterilized by ultrafiltration through polyamide filters. The patients tolerated the procedure well; their azotemia and metabolic acidosis improved.

Metastatic calcification has been reported in several disease entities, including chronic renal failure. Various imaging modalities have been shown to be useful in the detection of metastatic soft tissue calcification. Radionuclide imaging may detect metastatic soft tissue calcification more readily than routine diagnostic modalities and be a valuable noninvasive method to establish an early diagnosis in high-risk patients. The authors report a patient with extensive soft tissue metastatic calcification who had a myriad of clinical symptoms. The extensive calcification was detected with a radionuclide imaging.

A normophosphatemic patient suffering from lithium intoxication was hemodialyzed with a phosphorus-enriched, bicarbonate-based dialysis solution. A post-dialysis fall in plasma phosphorus level was prevented.

The best approach to treatment of pericarditis accompanied by substantial pericardial effusion in end-stage renal disease (ESRD) patients is unknown. In a review of our experience, we found that ESRD patients with moderate-to-large or large (circa 250 mL or larger) pericardial effusions usually failed to improve with intensive dialysis and ultimately required surgical drainage of the effusion. Multivariate analysis revealed that effusion size was by far the most important factor predicting need for surgery. Since early pericardial drainage obviates the risk of sudden tamponade, we recommend that surgery without prior intensive dialysis therapy be considered in such patients.

Peritoneal sclerosis occurred in two patients treated by continuous ambulatory peritoneal dialysis (CAPD) using only lactate-buffered dialysate. Both patients had recurrent peritonitis and the second patient had multiple, minor abdominal operations. Patients receiving lactate-buffered CAPD are not immune from peritoneal sclerosis. Recurrent peritonitis and repeated abdominal surgery might be important causative factors.

We evaluated the feasibility of using L-lactate as a base for hemodialysis. In one study, acid-base changes using 40 mM L- or DL-lactate were compared. In a second study, acid-base status using various amounts of L-lactate exclusively was studied. The third study compared symptoms and acid-base changes during 9 weeks of high-efficiency dialysis when using L-lactate, acetate, or bicarbonate as base. In the first study, plasma bicarbonate changes were equivalent with 40 mM L-lactate and 40 mM DL-lactate, but overall correction of acidosis appeared to be suboptimal. In the second study, when compared to a bicarbonate control period, correction of acidosis was reduced when using 40 mM L-lactate + 4 mM acetate solution, but increased when using a 46 mM L-lactate + 4 mM acetate solution. In the third study, correction of acidosis was comparable when using 42 mM L-lactate + 4 mM acetate, 39 mM acetate, or 35 mM HCO3 + 4 mM acetate. Whereas 46% ± 12 (SEM) treatments “failed” because of symptoms when using acetate, the percentages of “failed” treatments were only 7%±4.2 with L-lactate (p The results suggest that L-lactate is a suitable dialysis solution base that is capable of correcting chronic uremic acidosis. During high-efficiency dialysis, the incidence of intradialytic symptoms with L-lactate is comparable to that with bicarbonate and less than that with acetate.

Hemodynamic response to volume depletion by isolated ultrafiltration was compared in uremic (U) and nonuremic (N) conscious dogs. Fluid was removed at a constant rate until mean arterial pressure (MAP) decreased to less than 80 mmHg. Initial MAP was higher in the uremic dogs [132 +/- 8.6 (SD) mmHg] than in nonuremic controls (106 +/- 12, P less than 0.001). Initial cardiac index [U 4.97 +/- 0.831 X min-1 X m-2, N 4.44 +/- 0.62] and total peripheral vascular resistance index [(TPRI) U 2,160 +/- 353 dyn X s X cm-5 X m-2, N 1,976 +/- 420] were slightly, but not significantly, higher in uremic animals. Initial central venous pressure, wedge pressure, and plasma norepinephrine level were greater in the uremic dogs. At the end point of volume depletion, both uremic and nonuremic animals had achieved similar levels of TPRI, despite greatly attenuated or absent increases in plasma renin activity in the uremic group. At end point, blood volumes and plasma norepinephrine levels were comparable. The increase in pulse rate was higher in the uremic animals (59 +/- 37 pulses/min) compared with controls (25 +/- 52, P less than 0.05). In an additional group of uremic dogs, cardiovascular responses to hemorrhage and isolated ultrafiltration were compared and found to be similar, after allowance for blood viscosity changes had been made. The data suggest that in acutely uremic conscious dogs, despite reduced renin-angiotensin responses, hemodynamic adaptation to rapid volume depletion is not impaired.

Splanchnic erythrocyte content decreases during hemodialysis: A new compensatory mechanism for hypovolemia. Splanchnic and splenic erythrocyte volumes decrease during postural changes and exercise to help maintain central blood volume and cardiac output. The contribution of this compensatory mechanism to hemodynamic stability during dialysis has not been studied, however. In 8 ESRD patients, age 51.0 ± 4.5 years old, we measured changes in the splanchnic/splenic erythrocyte volume during dialysis by tagging the patients' erythrocytes with technetium and following abdominal radioactivity over time. Splanchnic radioactivity decreased to 90.2 ± 3.8% (mean ± SEM) of the baseline value after 2hr of accelerated fluid removal (3.7 ±0.4 liters) during dialysis (DUF), while it remained relatively unchanged after two hours of dialysis without fluid removal (DD) [106.5 ± 2.3%, P (DUF vs. DD) =; 0.03]. Splenic radioactivity decreased to 89.2 ± 5.0% of the initial value during DUF versus 103 ± 3.8% during DD, but the decrease was noted only during the last 30 minutes of DUF and did not attain statistical significance. Autonomic nervous system integrity was measured by the spontaneous variation of the R-R interval during deep respiration (E/I ratio) and by the Valsalva ratio. The mean E/I and Valsalva ratios in the eight patients were 1.13 ± 0.03 (± SEM) and 1.42 ± 0.1 respectively, suggesting reasonably adequate autonomic nervous system functioning. The results suggest that contraction of the splanchnic, and possibly the splenic, vascular beds occurs during fluid removal associated with hemodialysis. The resultant addition of erythrocytes to the circulation may help maintain central blood volume and cardiac output.

Antibody responses to influenza vaccination in patients with chronic renal failure. A bivalent type A inactivated influenza virus vaccine containing both sets of H3N2 and HSW1N1 antigens was given to patients with chronic renal failure and to control subjects. The patients were divided into an azotemic group in whom dialysis was not yet required and a hemodialyzed group. Hemagglutination-inhibition (HI) antibody responses were measured at time intervals of 1, 3, and 4 weeks after vaccination. We found that the mean postvaccination HI titers against both sets of antigens in the patients as a group did not differ significantly from those found in the control subjects as a group. The proportion of responders showing a fourfold or greater increase in post-vaccination antibody responses over prevaccination antibody values for either set of antigens was similar in both groups of patients and the group of control subjects. In general, an inverse correlation was found between prevaccination antibody levels and postvaccination antibody responses in both patients and control subjects. The only exception to this trend was the response of two of the azotemic patients to the H3N2 antigens who failed to respond despite low prevaccination antibody levels. These were the patients with the highest serum creatinine values.

Thrombocytopenia associated with the presence of a heparin-dependent platelet aggregating factor developed in two patients after hemodialysis with heparin. It resolved in one patient after heparin was stopped; but persisted in the other during a two-week heparin-free period and intermittently thereafter. We suggest that when heparin causes thrombocytopenia in dialysis patients the heparin should be stopped whenever possible, but this may not be necessary in all patients.

Peritoneal dialysis using a chloride-rich dialysate succeeded in correcting systemic metabolic alkalosis in a patient with renal failure. The present approach may have a place in the therapy of metabolic alkalosis.

In vitro binding of amantadine to plasma protein was assessed by ultrafiltration of plasma samples (from a blood bank) to which amantadine hydrochloride had been added. Approximately two-thirds of the amantadine was found to be protein-bound. The degree of protein binding was constant over a plasma amantadine concentration range of 100-2,000 ng/ml.

Hemofiltration using the postdilution technique and a modified saline solution as the replacement fluid succeeded in treating the metabolic alkalosis of two patients with renal failure.