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R Bellomo

Publications and source records attributed to R Bellomo.

At least 163 records · Page 9Linked to original sources
PubMed1998

Continuous renal replacement therapy: evolution in technology and current nomenclature.

The evolution of technology and biomaterials has permitted a parallel development of renal replacement therapies in the acute, critically ill patient. From the original description of continuous arteriovenous hemofiltration (CAVH), new techniques such as continuous venous venous hemofiltration (CVVH), hemodiafiltration (HDF) and high flux dialysis (HFD) have been developed and clinically utilized. A parallel improvement in efficiency has been achieved with daily clearances of urea as high as 50 liters or more. The use of special highly permeable dialyzers has also permitted increases in the clearances of larger solutes, thus leading to significant removals of chemical substances involved the acute inflammation and sepsis. In this field, recent observations have suggested the use of hemofiltration with high volumes of fluid exchange. The hardware and software of the newer continuous renal replacement therapy (CRRT) systems are certainly the key points in achieving these results and in safely performing such challenging techniques.

Acute Kidney Injury↗
PubMed1998

Quo vadis CRRT?

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Acute Kidney Injury↗
PubMed1998

Continuous renal replacement therapy: continuous blood purification in the intensive care unit.

Severe acute renal failure (SARF) occurs when renal dysfunction is such that haemodialysis or haemofiltration becomes necessary to maintain homeostasis. SARF is increasingly seen in association with multiorgan failure and has become a predominantly Intensive Care Unit disorder. Because of this change in epidemiology, the treatment of SARF has evolved from being exclusively nephrologist and intermittent haemodialysis-based to being mostly intensivist and continuous haemofiltration-based, particularly in European countries with a strong ICU tradition and in Australia. Continuous renal replacement therapy (CRRT) has several advantages in critically ill patients, including greater flexibility, excellent haemodynamic tolerance, outstanding fluid balance control, excellent control of uraemia, prevention of cerebral oedema, ability to provide full and aggressive nutrition, and a possible anti-inflammatory effect. The blood purification effect of CRRT may, in fact, go beyond the simple control of uraemia. Several animal studies have now shown that CRRT attenuates the haemodynamic consequences of bacteraemia or endotoxaemia. Such studies have also shown that increasing the intensity of fluid exchange may offer further beneficial effects in the setting of sepsis. In the light of these findings, CRRT is moving into the area of adjuvant treatment of sepsis, and pilot randomized controlled trials are being conducted to test the hypothesis that CRRT, either in standard or high fluid exchange volumes, attenuates the inflammatory effects of sepsis in humans. In the future, the use of CRRT may extend beyond its initial scope into the area of adjuvant management of sepsis and continuous blood purification may become part of a complex multifaceted approach to multiorgan dysfunction.

Acute Kidney Injury↗
PubMed1998

Cytokine-induced expression of killer inhibitory receptors in human T lymphocytes.

Killer inhibitory receptors (KIRs) represent a new family of HLA-class I-specific receptors. KIRs are involved in the function of Natural Killer cells and allow these cells to discriminate between normal cells and cells with impaired expression of HLA-class I molecules. KIRs are also expressed by a subset of cytolytic T lymphocytes in which they may exert an inhibitory effect on TCR-mediated function. Here we review recent data indicating that cytokines such as IL-15, may induce the de novo expression of CD94/NKG2A (a KIR which operationally detects the expression of various HLA-class I alleles). The expression of CD94/NKG2A has been documented not only in CD34+ precursors undergoing maturation towards NK cells, but also in mature T cells which respond in vitro to superantigens or allogeneic cells.

Animals↗
PubMed1997

Interleukin-15-induced maturation of human natural killer cells from early thymic precursors: selective expression of CD94/NKG2-A as the only HLA class I-specific inhibitory receptor.

Immature postnatal thymocytes were shown to contain precursors which, under suitable culture conditions, give rise to phenotypically and functionally mature natural killer (NK) cells. Here, we analyzed the effect of different cytokines for their ability to induce the expression of HLA class I-specific inhibitory receptor(s) during the process of NK cell development from immature thymocytes. From thymocyte cell suspensions depleted of CD2+, CD3+, CD4+, CD8+, CD56+, and CD16+ cells, we further removed cells expressing HLA class I-specific inhibitory receptors including CD94/NKG2-A, p58.1, and p58.2 by immunomagnetic bead separation. The resulting cells did not contain any of the above NK receptors as determined by immunofluorescence and flow cytometric analysis, as well as by reverse transcriptase polymerase chain reaction (RT-PCR) amplification using appropriate sets of primers. Although different cytokines have been used, including interleukin (IL)-7, stem cell factor (SCF), IL-2, and IL-15, only IL-2 or IL-15 induced cell proliferation when used alone. Moreover, maturation towards CD3- CD56+ cells displaying cytolytic activity against the HLA class I- targets K562 or 221 was detectable in cultures containing IL-15 used alone or in combination with IL-7 or SCF. On the other hand, these CD3- CD56+ cell populations did not lyse HLA class I+ target cells, including autologous PHA blasts. Analysis of the expression of the various HLA class I-specific inhibitory NK receptors revealed the presence of high proportions of CD94/ NKG2-A+ cells, while the NK receptors belonging to the Ig superfamily were undetectable both by immunofluorescence and by RT-PCR analysis. The expression of CD94/NKG2-A appeared to be responsible for the inability of cells to lyse HLA class I+ target cells. Thus, addition of anti-CD94 monoclonal antibodies of IgM isotype resulted in lysis of autologous target cells. The use of 221 cells transfected with different HLA class I alleles as target cells confirmed the broad class I specificity of CD94/NKG2-A receptor. Our experiments indicate that IL-15 provides an appropriate stimulus to the expression of CD94/NKG2-A, but not of other class I-specific NK receptors in the process of maturation of NK cells from thymocyte precursors.

Alleles↗
PubMed1997

Out of hospital outcome and quality of life in survivors of combined acute multiple organ and renal failure treated with continuous venovenous hemofiltration/hemodiafiltration.

OBJECTIVE: To study the out-of-hospital quality of life and long-term survival of critically ill patients with combined multiple organ failure and acute renal failure treated with continuous renal replacement therapy (CRRT). DESIGN: Study based on responses to postal questionnaire and clinical information obtained during treatment in the intensive care unit (ICU). SETTING: ICUs of two tertiary institutions. PATIENTS: 85 survivors from a pool of 250 patients with combined acute multiple organ and renal failure who were treated with CRRT. METHOD AND RESULTS: Anonymous postal questionnaire based on an activity index, mental function index, and a simplified version of the Nottingham Health Profile. Of the 250 patients, 85 (34%) survived to be discharged from hospital: 57 males (67%) and 28 females (33%), mean age 56.9 years (range 13.4-81). Mean duration of ICU stay was 10.9 days (range 2-52), mean admission Acute Physiology and Chronic Health Evaluation II score was 24.2 (range 15-41), and mean duration of CRRT was 6.2 days (range 1-34). Mean follow-up time was 2.5 years (range 0.1-5.3). Thirty-three of the 85 patients (38.8%) did not reply to the questionnaire; 35 patients (41.7%) were alive at the time of response and 17 (20%) were deceased. Of the 35 responders, 68.5% were satisfied with their present state of health, despite 60.6% stating that their mobility had been affected, with 41.9% being unable to walk more than 200 metres. Most (94.5%) survivors, however, felt that their treatment had been worthwhile, and 91.2% said that they would undergo the same treatment again if necessary. The approximate cost for each year of survival was U.S. $ 50000. CONCLUSIONS: In the majority of patients who survived to be discharged from hospital after combined acute multiple organ and renal failure, the overall state of health and quality of life seemed acceptable. Most patients felt that their treatment was worthwhile and that they would undergo the same treatment again if necessary. Our findings suggest that the cost and effort associated with CRRT and ICU care in these patients are high but broadly comparable to those associated with the care of other serious illnesses. They are also seen as worthwhile by survivors, who consider their life to be of acceptable quality.

APACHE↗
PubMed1997

New CRRT systems: impact on dose delivery.

The evolution of technology and biomaterials has permitted a parallel development of renal replacement therapies in the acute, critically ill patient. From the original description of continuous arteriovenous hemofiltration, new techniques such as continuous venovenous hemofiltration, hemodiafiltration, and high flux dialysis have been developed and clinically used. A parallel improvement in efficiency has been achieved with urea daily clearances as high as 50 L or more. The use of special highly permeable dialyzers has also permitted an increase in the clearances of larger solutes, thus leading to significant removals of chemical substances involved in acute inflammation and sepsis. In this field, recent observations have suggested using hemofiltration with high volumes of fluid exchange. The hardware and software of the newer CRRT systems are key in achieving these results and in safely performing such challenging techniques.

Hemofiltration↗
PubMed1997

Renal replacement therapy in the ICU: the Australian experience.

The structure of health care drives medical practice in a powerful way, shaping choices of therapy and approaches, and influencing scientific evidence. The Australian experience with continuous renal replacement therapy (CRRT) confirms the importance of structure. A public health system like that of Australia's contains the following variables: well-developed intensive care tradition and expertise, a dominant "closed" intensive care unit (ICU) model, well-developed training of intensive care nurses with established one-to-one nurse-patient ratios, salaried medical practitioners, overworked general dialysis units with inadequate nursing resources, and lack of fee-for-service incentive for nephrologists to see ICU patients with acute renal failure. The likely outcome of such a system is for CRRT to be run by intensive care staff. As shown by a recent regional survey, this approach, although somewhat unique, is dominant and appears to work well with excellent clinical results and constant clinical research output.

Australia↗
PubMed1997

Who should manage CRRT in the ICU? The intensivist's viewpoint.

The arrival of continuous renal replacement therapy (CRRT) has given the intensivist and the intensive care nurse the opportunity to treat acute renal failure (ARF) independently by giving them the necessary technology and taking CRRT away from absolute nephrological control. This structural shift has created a controversy between those countries where control of CRRT has completely shifted to the intensivist and those countries where nephrological input is still dominant. The argument in favor of intensivist-driven CRRT rests upon several observations, including the fact that therapy is continuous, as is the presence of the intensivist in the intensive care unit (ICU). Critically ill patients require rapid changes in treatment that are best directed by physicians who are at the bedside all the time. CRRT must be seen within the totality of patient care, and the intensivist can see the larger picture more accurately. Intensivists are successfully performing more and more procedures that were previously seen as part of other specialties and, last but not least, "closed" models of ICU care appear to work best. Australian intensivists have taken up CRRT from the start and now control it. Patient outcomes under such a system, as reported here, are above average, and confirm the effectiveness of such an approach.

Acute Kidney Injury↗
PubMed1997

Splanchnic buffering of metabolic acid during early endotoxemia.

PURPOSE: We sought to determine the sites of metabolic acid production and clearance during acute endotoxemia. MATERIALS AND METHODS: In 10 pentobarbital-anesthetized dogs, flow was measured (ultrasonic probes) for the protal vein, hepatic artery, and renal artery. Catheters were inserted into the hepatic vein, pulmonary artery, renal vein and portal vein. Measurements of blood gases and strong ions were obtained from each site during control conditions and after 30 minutes of intravenous infusion of 1 mg/kg of Escherichia coli endotoxin. The total metabolic acid flux across each organ was calculated using the standard base excess formula and the effective strong ion difference method. PaCO2 was maintained by controlled ventilation. RESULTS: Mean arterial pH decreased from 7.34 to 7.22 with acute endotoxemia. Although transvisceral pH gradients revealed net acid release, the source of this was purely respiratory (carbon dioxide). During early endotoxemia, the gut significantly increased metabolic acid uptake (36.60 +/- 6.60 mmol/h, P < .05). CONCLUSIONS: We conclude that during early endotoxemia in the dog, the gut is a major site of metabolic acid removal.

Acid-Base Equilibrium↗
PubMed1997

HLA-class I-specific inhibitory receptors in human cytolytic T lymphocytes: molecular characterization, distribution in lymphoid tissues and co-expression by individual T cells.

A subset of cytolytic T lymphocytes has been shown to express receptors of the NK type (NKR) which can inhibit T cell cytotoxicity induced via the TCR-CD3 pathway. In this study, by the analysis of full length cDNA amplified from representative T cell clones, we show that NKR belonging either to the lg superfamily, including p58.1, p58.2, p70 and p140, or to the C-type lectin superfamily (CD94/NKG2A), display sequences which are identical to those of the corresponding NKR expressed by CD3-NK cells. Moreover, a fragment of cDNA encoding the NKG2A protein was consistently amplified from all CD94+ T cell clones analyzed. Since different NKR types can be expressed by T cells, we analyzed whether individual T cells could co-express more than one NKR. Analysis of either resting or activated (and cultured) T cell populations revealed that two or more NKR can be co-expressed by single T cells. Moreover, by the analysis of T cell clones, we show that co-expressed receptors are functional and can inhibit independently the TCR-induced cytolytic function. Finally, we investigated whether NKR+ T lymphocytes were also present in lymphoid tissues. No such cells were found in thymus or cord blood, thus further supporting the notion that they represent memory T cells. On the other hand, they were present in all the peripheral tissues analyzed including spleen, lymph nodes and tonsils.

Animals↗
PubMed1997

Release of lactate by the lung in acute lung injury.

UNLABELLED: The pathogenesis of hyperlactatemia during sepsis is poorly understood. We have previously described an increase in lactate concentration across the lung in the dog during early endotoxemia. Accordingly, we sought to determine if the lung releases lactate in humans and what relation this has with lung injury. METHODS: We measured lactate concentrations across the lung and lung injury scores (LIS) in two groups of patients. Group 1 consisted of nine patients with acute lung injury (LIS > or = 2.0) and elevated lactate concentrations (> 2.0 mmol/L). Group 2 contained 12 patients with no acute lung injury (LIS scores < or = 1.5), with or without increased lactate concentrations. Simultaneous measurements of plasma lactate and blood gases were obtained from indwelling arterial and pulmonary artery catheters. Measurements of cardiac output were also obtained. Lactate measurements were done using a lactate analyzer (YSI; Yellow Springs, Ohio). RESULTS: For each patient with acute lung injury and hyperlactatemia, an arterial-venous lactate gradient existed demonstrating release of lactate by the lung. This gradient persisted after correction for changes in hemoconcentration across the lung. The lactate gradient across the lung was 0.4 +/- 0.2 mmol/L for group 1 vs 0.05 +/- 0.1 mmol/L for group 2 (p = 0.001). This corresponded to a mean pulmonary lactate flux of 231.3 +/- 211.3 vs 5.0 +/- 37.2 mmol/h (p = 0.001). The lactate flux and the arterial-venous lactate difference correlated with LIS both for the entire sample and for the subgroup with hyperlactatemia (r = 0.69, p < 0.01). Pulmonary lactate flux was not related to arterial lactate levels (r = 0.25). CONCLUSION: In patients with acute lung injury and hyperlactatemia, the lung is a major source of lactate and lactate flux correlates with LIS. This lactate flux could explain some of the hyperlactatemia seen in sepsis.

Adult↗