Paecilomyces peritonitis: case report and review of the literature.

While filamentous fungi are a rare cause of peritonitis in peritoneal dialysis patients, there is increasing recognition of Paecilomyces species as pathogens in such patients. We herein report a case of fungal peritonitis secondary to the filamentous Paecilomyces variotii species. The patient had a long and ultimately fatal course of illness despite catheter removal, discontinuation of peritoneal dialysis, recurrent intraabdominal abscess drainage, and prolonged courses of antifungal therapy. Our experience with this case and a review of the literature suggests that infection with this fungus can cause substantial morbidity and is probably best treated with prompt catheter removal, aggressive antifungal therapy and vigilant observation for complications.

Adjunctive antibiotic/anticoagulant lock therapy in the treatment of bacteremia associated with the use of a subcutaneously implanted hemodialysis access device.

To improve vascular access for hemodialysis, a new device (Dialock Hemodialysis Access System, Biolink Corporation, Middleboro, MA) has been developed. Implanted subcutaneously, the device is accessed by percutaneous puncture. Attached to the device are two catheters that are implanted into the superior vena cava or right atrium. Clinical results thus far have been promising. However, use of this device is not free from infectious complications. In the present pilot study, 25 maintenance hemodialysis patients were implanted with 26 Dialock devices. The incidence of bacteremia was 2.9/1,000 catheter days. In 14 episodes of bacteremia in 8 patients the infection was successfully treated with a combination of systemic antibiotic treatment and adjunctive antibiotic/anticoagulant lock therapy. The lock therapy entailed the instillation of both an antibiotic and an anticoagulant into the device. We believe that the antibiotic/anticoagulant lock technique is an effective, adjunctive therapeutic modality in the treatment of infections related to the use of indwelling vascular access devices.

Initial results of a new access device for hemodialysis technical note.

BACKGROUND: A new subcutaneous device (DIALOCKtrade mark) provides vascular access to patients who currently require hemodialysis (HD). The device consists of a port-like valve, implanted subcutaneously below the clavicle, which provides a linear flow passage to two catheters placed in the right atrium via the internal or external jugular vein. The valve is accessed percutaneously with needle-cannulas that functionally convert the device to twin catheters for connecting the patient to the HD lines. METHODS: The device was implanted in 10 outpatients under local anesthesia. Patients used the device during dialysis 3 times/week, and data were collected on blood flow, pressures, adverse events and patient and nurse satisfaction. RESULTS: The device was used for HD almost immediately (median 3 days after implantation) and functioned successfully for more than nine months (mean +/- SD 7.3 +/- 1.5) in all but one patient who died of unrelated causes after one month; there were >800 dialysis sessions total. Blood flows over 300 ml/min were consistently achieved (average 326 +/- 40) with venous and arterial pressures of 200 +/- 44 and -246 +/- 29 mm Hg, respectively. After 66 patient-months, condition of the needle puncture sites remained satisfactory. Five systemic infections occurred in four patients, producing 2.3 bacteremic episodes per 1000 patient-days. All resolved without the need for device removal. There were no infections at the puncture sites. Two patients required fibrin sheath stripping of their catheters, one whose heparin lock was not changed for 23 days (for reasons unrelated to the device). Patient and nurse acceptance was excellent. CONCLUSION: The device represents a positive improvement in the area of HD access.

New access device for hemodialysis.

A new subcutaneous device (Dialock; Biolink Corp., Middleboro, MA) provides vascular access to patients who currently require hemodialysis (HD). The device consists of a port-like valve, implanted subcutaneously below the clavicle, which provides a linear flow passage to two catheters placed in the right atrium via the jugular vein. The valve is accessed percutaneously with needle-cannulas that functionally convert the device to twin catheters for connecting the patient to the HD lines. Interdialytic patency is maintained using a standard heparin lock. The device has been implanted in 10 outpatients under local anesthesia, with almost immediate use for HD (median, 3 days) and has functioned successfully for more than 6 months (mean +/- SD, 4.0 +/- 1.7; > 400 dialysis sessions). Blood flows over 300 ml/min were consistently achieved (average, 320 +/- 50) with venous and arterial pressures of 197 +/- 42 mmHg and -241 +/- 31 mmHg, respectively. After 40 patient-months, condition of the needle puncture sites remains satisfactory. Four systemic infections have occurred in three patients; all have resolved without the need for device removal. There have been no infections at the puncture sites. One patient whose heparin lock was not changed for 23 days (for reasons unrelated to the device) required fibrin sheath stripping of his catheters. Patient and nurse acceptance has been excellent. The device may offer substantial improvement over conventional devices for HD access.

Use of a phosphorus-enriched hemodialysate to prevent hypophosphatemia in a patient with renal failure-related pericarditis.

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.

Metastatic soft tissue calcification in chronic renal failure detected by radionuclide imaging.

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.

Hypomagnesemia in continuous ambulatory peritoneal dialysis patients dialyzed with a low-magnesium peritoneal dialysis solution.

OBJECTIVE: Previous studies have shown a decrease in serum magnesium (Mg) concentration when continuous ambulatory peritoneal dialysis (CAPD) patients previously maintained on a 1.0-1.2 mEq/L Mg peritoneal dialysis solution (PDS) were dialyzed with a 0.5 mEq/L Mg PDS. However, the prevalence of hypomagnesemia in CAPD patients dialyzed with low-Mg PDS is unknown. DESIGN: A retrospective study to determine the prevalence of hypomagnesemia and the factors associated with its occurrence in CAPD patients dialyzed using a 0.5 mEq/L Mg PDS. SETTING: A CAPD unit in a large Veterans Affairs Hospital. PATIENTS: All our CAPD patients (33) enrolled over a 52-month period. RESULTS: All patients had serum magnesium levels higher than 1.25 mEq/L prior to use of low-Mg PDS. Hypomagnesemia (serum Mg < 1.25 mEq/L) developed in 21/33 patients (64%) when a 0.5 mEq/L Mg PDS was employed. Hypomagnesemia developed a mean of 8.2 months after beginning treatments. The duration of dialysis and the number of episodes of peritonitis did not differ between patients with and those without hypomagnesemia. Serum albumin levels were significantly lower in patients with hypomagnesemia (2.5 +/- 0.12 g/dL vs 3.2 +/- 0.12, p < 0.01). Magnesium supplements were given to 13 patients; following this therapy, serum magnesium values became normal. CONCLUSIONS: CAPD patients dialyzed with a 0.5 mEq/L Mg PDS may develop a considerable fall in serum magnesium level and may require magnesium supplements in order to restore normal serum values.

Continuous ambulatory peritoneal dialysis using self-made, ultrafiltration-sterilized, L-lactate-based dialysis solution.

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.

Employing L-lactic acid powder in the preparation of a dry "acid concentrate" for use in a bicarbonate-based dialysis solution-generating system: experience in hemodialysis patients.

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.

Increasing plasma phosphorus values by enriching with phosphorus the "acid concentrate" of a bicarbonate-buffered dialysate delivery system.

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 using conventional, lactate--containing solution sterilized by ultrafiltration.

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.

Neutrophilic intracellular acidosis induced by conventional, lactate-containing peritoneal dialysis solutions.

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.

Penile calcification in maintenance hemodialysis patients.

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.

Protein kinase C modulates the release of [3H]5-hydroxytryptamine in the spinal cord of the rat: the role of L-type voltage-dependent calcium channels.

The present studies examined the relationship between protein kinase C (PKC) and L-type voltage-dependent calcium channels in modulating the release of neurotransmitter from K(+)-depolarized rat spinal cord synaptosomes. Activators of PKC, such as phorbol 12-myristate 13-acetate (PMA), mezerein and oleoyl acetylglycerol produced a concentration-dependent potentiation of K(+)-induced release of [3H]5-hydroxytryptamine ([3H]5-HT). Enhanced release was dependent on the concentration of both Ca2+ and K+ in the superfusion medium. Calcium-independent release of [3H]5-HT or release induced by the Ca2+ ionophore were unaffected by PKC activators. Calcium-dependent release of [3H]5-HT, evoked by K+, was enhanced under similar conditions by the L-type Ca2+ channel agonists Bay K 8644 and (+)-SDZ 202-791. Nimodipine, an L-type Ca2+ channel antagonist, while having no independent effect on K(+)-induced release of [3H]5-HT, abolished the potentiative effects of Bay K 8644 and PMA. Similarly, the PKC inhibitors, polymyxin B and staurosporine, blocked effects of both PMA and Bay K 8644 on K(+)-stimulated release of [3H]5-HT. Neither PMA nor Bay K 8644 altered the uptake of [3H]5-HT. These results suggest that PKC-dependent mechanisms utilize calcium influx, via the L-type calcium channel, to modulate release of neurotransmitter and indicate a possible functional link between PKC and L-type voltage-dependent calcium channels in the spinal cord.

Raising plasma phosphorus levels by phosphorus-enriched, bicarbonate-containing dialysate in hemodialysis patients.

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

Fluoxetine-induced inhibition of synaptosomal [3H]5-HT release: possible Ca(2+)-channel inhibition.

Fluoxetine, a selective 5-HT uptake inhibitor, inhibited 15 mM K(+)-induced [3H]5-HT release from rat spinal cord and cortical synaptosomes at concentrations greater than 0.5 uM. This effect reflected a property shared by another selective 5-HT uptake inhibitor paroxetine but not by less selective uptake inhibitors such as amitriptyline, desipramine, imipramine or nortriptyline. Inhibition of release by fluoxetine was inversely related to both the concentration of K+ used to depolarize the synaptosomes and the concentration of external Ca2+. Experiments aimed at determining a mechanism of action revealed that fluoxetine did not inhibit voltage-independent release of [3H]5-HT release induced by the Ca(2+)-ionophore A 23187 or Ca(2+)-independent release induced by fenfluramine. Moreover the 5-HT autoreceptor antagonist methiothepin did not reverse the inhibitory actions of fluoxetine on K(+)-induced release. Further studies examined the effects of fluoxetine on voltage-dependent Ca2+ channels and Ca2+ entry. Whereas fluoxetine and paroxetine inhibited binding of [3H]nitrendipine to the dihydropyridine-sensitive L-type Ca2+ channel, the less selective uptake inhibitors did not alter binding. The dihydropyridine antagonist nimodipine partially blocked fluoxetine-induced inhibition of release. Moreover enhanced K(+)-stimulated release due to the dihydropyridine agonist Bay K 8644 was reversed by fluoxetine. Fluoxetine also inhibited the K(+)-induced increase in intracellular free Ca2+ in fura-2 loaded synaptosomes. These data are consistent with the suggestion that fluoxetine inhibits K(+)-induced [3H]5-HT release by antagonizing voltage-dependent Ca2+ entry into nerve terminals.

Peritoneal dialysis using bicarbonate-containing solution sterilized by ultrafiltration.

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.

Modulation of [3H]serotonin release by dihydropyridines in spinal cord synaptosomes.

The release of [3H]monoamines from preloaded synaptosomes from spinal cord is K(+)-dependent and can be modulated by L-type Ca2+ channel agonists such as the 1,4-dihydropyridine (1,4-DHP), Bay K 8644. Whereas the basal release of [3H]monoamines was not altered by Bay K 8644, K(+)-stimulated release of [3H]norepinephrine was enhanced 35% and [3H]serotonin 50%. Modulation of release by Bay K 8644 was dependent on the K+ concentration in the medium, being present only at submaximal depolarization with 15 mM K+. Enhanced release in the presence of Bay K 8644 was concentration-dependent and Ca2(+)-dependent. Ca2(+)-independent release induced by fenfluramine was not enhanced by Bay K 8644. Both nimodipine and nitrendipine, 1,4-DHP antagonists, produced a concentration-dependent block of the Bay K 8644-induced monoamine release and had no independent effect on basal or K(+)-stimulated release. omega-Conotoxin GVIA (omega-CgTx) produced a concentration dependent decrease of K(+)-stimulated serotonin release, which antagonized the stimulatory effect of low concentrations of Bay K 8644. However, omega-CgTx did not alter the enhancement of K(+)-stimulated release at higher concentrations of Bay K 8644. The data from the present work establish the conditions for modulation of K(+)-evoked monoamine release in spinal cord by 1,4-DHP agonists and suggest a role for the L-type voltage dependent Ca2+ channel in this process.