Spinal cord injury and vitamin D metabolism.
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Biomedical subjects
Publications and source records attributed to T S Ing.
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Although the hypotensive effects of food ingestion during hemodialysis have been documented, the hemodynamic mechanism is unclear. It could be decreased cardiac output due to splanchnic sequestration or decreased vascular resistance due to splanchnic vasorelaxation. Also, the effects of caffeine, which block postprandial hypotension in the elderly, have not been studied in a dialysis setting. Central hemodynamics were monitored by thoracic electric bioimpedance in 10 dialysis patients who ingested a test meal 1 h into dialysis. All ultrafiltration was done during the initial 2 h. Bicarbonate dialysate was used. Each patient was studied three times in a double-blind (with respect to placebo/caffeine) cross-over trial: placebo/no meal, placebo/meal, and caffeine/meal. Blood pressure decreased sooner and to a great extent in the treatments in which food ingestion accompanied ultrafiltration (e.g., at 30 min after food ingestion, percent change in mean arterial pressure was -12.4 +/- 1.8 versus -2.4 +/- 3.5 mm Hg when food was not ingested; P < 0.05). The hemodynamic mechanism of food-associated hypotension was found to be a fall in systemic vascular resistance (SVRI). Caffeine pretreatment (200 mg), which resulted in intradialytic plasma caffeine levels of about 4 micrograms/mL at time of food ingestion, had no effect on food-associated reductions in blood pressure or SVRI. The results suggest that food ingestion during dialysis causes hypotension primarily because of decreased SVRI. The effects of food ingestion on mean arterial pressure and SVRI are not attenuated by the ingestion of 200 mg of caffeine 1 h before dialysis.
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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.
Skin necrosis similar to that induced by warfarin was seen in a patient who had never received the drug but who was vitamin K-deficient due to malnutrition and prolonged treatment with broad-spectrum antibiotics. He also had end-stage renal failure and was receiving prophylactic subcutaneous heparin therapy because of immobilization. His plasma protein C antigen level and, disproportionately, his plasma protein C functional activity were decreased. Both protein C values improved after vitamin K therapy, discontinuation of heparin, and initiation of hemodialysis. We surmise that skin necrosis occurred as a result of protein C deficiency caused by vitamin K depletion. Production of abnormal (descarboxy) protein C/protein S due to vitamin K deficiency and increased protein C inhibitory activity associated with renal failure and/or heparin administration may have contributed to the clinical picture. This rare but serious complication of a relatively common disorder, viz., vitamin K deficiency, reinforces the importance of vitamin K supplementation in malnourished patients who receive long-term antibiotic maintenance therapy.
Penile calcification was detected in 6 of 32 patients (19%) with end-stage renal disease (ESRD) using soft tissue x-ray techniques. Having been maintained on hemodialysis for a minimum of one year, all the affected patients showed clinical evidence of secondary hyperparathyroidism and calcification in the blood vessels of some other tissues. All had erectile impotence, while in 1 patient gangrene of the penis developed. Penile calcification is probably more common in ESRD patients than realized and should be looked for as a possible cause of impotence in male patients treated with maintenance hemodialysis.
Several extracorporeal techniques have been used to remove N-acetylprocainamide (NAPA), the major metabolite of procainamide, in patients intoxicated with this substance. We report a patient with life-threatening NAPA intoxication who was rapidly and successfully treated with combined high-efficiency hemodialysis and charcoal hemoperfusion. The hemodialyzer and hemoperfusion cartridge were placed in series such that the patient's blood was dialyzed before reaching the cartridge. Overall clearance of NAPA was 153 mL/min, with clearance due to hemodialysis averaging 102 mL/min and that due to hemoperfusion averaging 88 mL/min. Thus, addition of the hemoperfusion cartridge into the extracorporeal circuit resulted in a 50% increase in clearance over that obtainable by high-efficiency hemodialysis alone. In comparison to other modalities, this technique is more effective than either hemodialysis or charcoal hemoperfusion alone and can achieve a more rapid reduction of serum NAPA levels than that observed with slow continuous hemofiltration or hemodiafiltration.
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.
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.
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.
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.
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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.
Involvement of the placenta by glycosphingolipid deposits in Fabry's disease has not been previously reported. We describe the presence of such deposits in the maternal half of a placenta obtained from a heterozygous carrier of the disease.
Hemodynamic changes were measured during high-efficiency hemodialysis (HEHD) using three dialysis solutions: L-lactate (46 mM), bicarbonate (35 mM + 4 mM acetate), and acetate (39 mM). Cardiac output was determined by changes in thoracic electrical bioimpedance. Although there appeared to be subtle differences in hemodynamic response to L-lactate versus bicarbonate, the blood pressure, cardiac output, and total peripheral resistance were affected less with either of these solutions than with acetate. In particular, neither L-lactate nor bicarbonate HEHD were associated with a change in cardiac output, whereas with acetate HEHD a marked (22%) increase in cardiac output was seen concurrently with a moderate fall in blood pressure and TPR. Both acetate and L-lactate HEHD were associated with hypoxemia, whereas with bicarbonate HEHD the PO2 did not change. With L-lactate HEHD, correction of pH and plasma HCO3 concentrations was delayed but these values were not significantly different from those obtained with bicarbonate HEHD by one hour after dialysis. Potassium removal was comparable with the three dialysis solutions. Phosphorus removal with L-lactate tended to be slightly less than with bicarbonate, but not less than with acetate. Our results suggest that L-lactate (46 mM) dialysis solution may be a suitable alternative to acetate for HEHD, being associated with a hemodynamic profile that is similar to that of bicarbonate and better than that of acetate. Our results further suggest that the hypoxemia associated with the use of acetate dialysis solution is not intrinsic to acetate, but is due either to a low dialysis solution PCO2 level or to accelerated consumption of oxygen during substrate metabolism.