Ultrafiltration control during continuous arteriovenous hemodialysis using paired volumetric dialysate pumps.
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Biomedical subjects
Publications and source records attributed to J T Daugirdas.
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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.
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A 20-year-old man presenting with osteomalacia was found to have the Fanconi syndrome, as evidenced by hypophosphatemia with hyperphosphaturia, glycosuria in the presence of normoglycemia, and generalized aminoaciduria. After removal of a non-ossifying fibroma of the left tibia, the renal tubular abnormalities promptly resolved with subsequent healing of the osteomalacia. A humoral factor released from the tumor may have caused the disorder in proximal renal tubular cell transport.
We have measured total antibody and IgE directed against ethylene oxide-altered human serum albumin (ETO-HSA) in the sera of 24 patients who have experienced anaphylaxis during hemodialysis and of 41 patients who have not had such episodes during hemodialysis. ETO is used to sterilize dialyzers and other medical equipment. The geometric mean level of IgE to ETO-HSA in patients with reactions (0.9 ng ETO-HSA bound to IgE per milliliter of serum) is significantly higher than in nonreacting patients (0.1 ng/ml, p less than 0.0001). Sixteen of 24 patients with reactions had detectable levels of IgE to ETO-HSA, whereas only three of 41 nonreacting patients had detectable levels (p less than 0.0001 chi-square). The geometric mean level of total antibody to ETO-HSA is also significantly higher in patients with reactions (270 ng ETO-HSA bound per milliliter) than in nonreacting patients (31 ng/ml, p less than 0.0001). Fourteen of 24 patients with reactions but only four of 39 nonreacting patients had total antibody binding of ETO-HSA (p less than 0.0001 chi-square). These data extend our previous observations on a small group of 13 patients receiving hemodialysis (seven patients with reactions, and six nonreacting patients) and clearly demonstrate an association between the presence of IgE or total antibody to ETO-HSA and immediate anaphylactic reactions in this group of 65 patients receiving hemodialysis.
End-stage renal failure supervened in two cirrhotic patients with ascites, necessitating maintenance hemodialysis therapy. One patient had a functioning LeVeen peritoneo-jugular shunt (Becton-Dickinson, Rutherford, NJ) in place at the time that hemodialysis was initiated. In the other patient, a LeVeen shunt was inserted 8 months after beginning hemodialysis, after extracorporeal ultrafiltration had failed to resolve his ascites. Both patients achieved control of their ascites and enjoyed relatively long survival. Our results suggest that, in patients with cirrhotic ascites who develop end-stage renal failure, successful long-term management can be obtained using a combination of peritoneo-venous shunting and maintenance hemodialysis.
In a double-blind, crossover trial, 7 chronic hemodialysis patients underwent three 4-week treatment periods. During one period, dialysate contained 135 mEq/l sodium. During another period, dialysate contained 143 mEq/l sodium. During the remaining period, we used "sodium gradient' dialysate, the sodium concentration of which was decreased from 160 to 133 mEq/l during each 4-hour dialysis session. Ultrafiltration was performed at a constant rate to achieve a predetermined post-dialysis weight. Interdialytic weight gain, thirst, blood pressure control, and incidence of side effects were monitored. There was a significant difference in interdialytic weight gain for the 3 treatments (p = 0.005). Interdialytic weight gain using 135 mEq/l sodium dialysate (2.2 +/- 0.9 kg, mean +/- SD) was significantly less than that using either 143 mEq/l sodium dialysate (2.6 +/- 0.8 kg) or sodium gradient dialysate (2.8 +/- 0.7 kg). Self-reported thirst tended to be less severe with 135 mEq/l sodium dialysate than with 143 mEq/l sodium dialysate or with sodium gradient dialysate, but changes in thirst were not statistically significant (p = 0.13). The incidence of intradialytic hypotensive episodes was comparable with the 3 levels of dialysate sodium. The results suggest that the described sodium gradient method does not prevent the increased interdialytic weight gain and thirst seen with other forms of high-sodium dialysis, and probably does not reduce the incidence of side effects.
Fever occurred in a man 6 weeks after renal transplantation. At the time of transplantation, the donor ureter had been anastomosed to a ureteroileal conduit created 6 years previously because of traumatic neurogenic bladder. Initial evaluation failed to reveal the cause of the fever, but ultimately, drainage of the defunctionalized bladder yielded a large amount of pus infected with Klebsiella pneumoniae. Our patient's course suggests that, when fever develops after renal transplantation in patients with previous urinary diversion, pyocystis should be included in the differential diagnosis.
Hemodialysis of chemically sympathectomized dogs using acetate-buffered dialysate was associated with a profound early drop in blood pressure due to a decrease in peripheral vascular resistance. Subsequently, blood pressure and peripheral resistance recovered to near normal levels. An increased pulse rate was also noted. None of these hemodynamic changes occurred when bicarbonate-buffered dialysate was used.
The hemodynamic effects of a decreasing plasma urea level during hemodialysis were studied in acutely uremic, conscious dogs. Each dog was studied twice, during dialytic ultrafiltration against both a urea-free (U-) and a urea-supplemented (U+) dialysate. Plasma osmolality (-13 mosm/kg/H2O +/- 10 SD, p less than 0.01) and urea levels (-43 mg/dl +/- 20, p less than 0.01) decreased when using the (U-) dialysate, but were unchanged with the (U+) dialysate. At the end-point of volume depletion (MAP less than 80 mm Hg) total peripheral resistance index [U (+): 3,376 +/- 743 dyn . s X cm-5 X m2, U(-): 3,091 +/- 537, NS)] and blood volume [U(+): 62.7 +/- 7.4 ml/kg, U(-): 63.7 +/- 7.5, NS)] were comparable whether or not the plasma urea level had been allowed to decrease. The data suggest that an acutely decreasing plasma urea level during dialysis does not impair hemodynamic response to volume depletion in the model described.
To determine the prevalence of blood eosinophilia in patients receiving maintenance peritoneal dialysis, routine peripheral WBC counts of 49 such patients were reviewed. In 29 patients, blood eosinophilia was noted. Elevations in blood eosinophil counts tended to be mild and episodic. They were often associated with concomitant elevation of peritoneal fluid eosinophil counts. Possible predisposing factors included recent peritoneal catheter insertion and antibiotic therapy for peritonitis.
Twenty-one severe reactions to hemodialysis occurred in approximately 260,000 dialysis treatments at three centers within a 10 1/2-year period. Reactions typically appeared within minutes of initiating dialysis, and were characterized by cardiopulmonary, mucocutaneous, and/or gastrointestinal tract symptoms highly suggestive of anaphylaxis. Four respiratory arrests and one death resulted. Analysis of dialyzer use patterns and of each patient's dialyzer exposure history strongly implicated hollow-fiber dialyzers made of cuprammonium cellulose (CC) as a cause of these reactions. No obvious factors could be found to identify predisposed patients. Less than optimal rinsing of the CC hollow-fiber dialyzers prior to use may have been responsible for some, but not all, of these reactions.
A patient had hyperlipidemia associated with apparent hyperphosphatemia. Further tests on his serum and on the lipemic sera from 15 additional patients revealed a method-dependent overestimation of inorganic phosphorus values. The degree of overestimation was found to correlate positively with the serum triglyceride concentration. Unexplained elevation of the serum phosphorus level should alert the physician to the possibility of spurious hyperphosphatemia due to hyperlipidemia.
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