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      Relationship between Natriuretic Peptides and Residual Diuresis during Continuous Hemodiafiltration

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          Background: The reasons for the decrease or increase of urine output following the start of continuous venovenous hemodiafiltration (CVVHDF) have not yet been explained sufficiently. The renoprotective properties of natriuretic peptides were described. Methods: The levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were measured in 23 mechanically ventilated patients before and during the first 48 h of CVVHDF. Samples were drawn both from the ports proximal and distal to the filter. The results were compared between the group where daily diuresis (Vu) remained low or decreased and the group where diuresis increased to the level of 1.5 ml·kg<sup>–1</sup>·h<sup>–1</sup> or higher after 48 h of treatment. Left ventricular dysfunction (LVD) was defined as LV ejection fraction below 40%. A control group consisted of 10 patients exposed to abdominal surgery. Results: The average AVdiff (%) of ANP and BNP on filter were insignificant. Patients with increasing diuresis (n = 12) had significantly lower levels of both ANP (p < 0.001) and BNP (p < 0.005) than the patients with decreasing diuresis (n = 11). Significant correlations were revealed for ANP and Vu (p < 0.01) and for BNP and Vu (p < 0.05). The levels of both peptides were grossly elevated in comparison to controls and were predictive of survival. The differences between cardiac and non-cardiac patients were significant both for ANP and for BNP. Conclusions: The elimination of ANP and BNP by the CVVHDF is negligible. The levels of natriuretic peptides are inversely related to Vu and predict survival. ANP and BNP levels correlate with left ventricular function even during acute renal failure and CVVHDF.

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          Most cited references 8

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          Natriuretic peptides.

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            Epidemiology, management, and outcome of severe acute renal failure of critical illness in Australia.

            To study the epidemiology, style of management, and outcome of intensive care patients with acute renal failure requiring replacement therapy in Australia. Prospective epidemiologic study. Australian adult intensive care units providing acute renal replacement therapy. Adult intensive care patients with acute renal failure treated with renal replacement therapy. Demographic and clinical data collection for 3 months. A standardized data collection form for each case of severe acute renal failure was used to collect demographic, biochemical, clinical, and outcome data. Severe acute renal failure affected 299 patients (approximately eight cases per 100,000 adults per year). Among these patients, 99 (33.1%) had impaired baseline renal function, 238 (79.6%) needed mechanical ventilation, and 232 (77.6%) needed continuous vasoactive drug administration. Critical care physicians controlled patient care and renal replacement therapy in 289 cases (96.7%). Critical care nurses performed such therapy alone in 288 (96.3%) cases. Continuous renal replacement therapy was used in 292 (97.7%) patients. There was no nephrological input in 173 (57.8%) cases. Predicted mortality rates were 52.1% by Simplified Acute Physiology Score II, 49.5% by Acute Physiology and Chronic Health Evaluation II score, and 51.9% by an acute renal failure-specific score. Actual mortality rate was 46.8%. Only 25 (15.7%) patients were dialysis-dependent at hospital discharge. Of these patients, 20 (80%) had premorbid chronic impairment of renal function. In Australia, critical care physicians and nurses manage severe acute renal failure with limited consultative nephrological input. Renal replacement therapy is continuous and outcomes are satisfactory. Our findings support the view that this approach to management of severe acute renal failure is safe.
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              Role of diuretics in the preservation of residual renal function in patients on continuous ambulatory peritoneal dialysis.

              Patients on continuous ambulatory peritoneal dialysis (CAPD) are dependent on residual renal function for solute and water clearances, and this declines with time on dialysis. Loop diuretics have been postulated to slow this decline. Sixty-one patients new to dialysis were randomly assigned to either furosemide 250 mg every day or no furosemide at the time of CAPD training and were followed prospectively. Urine volume (UV), urea clearance (C(Urea)), and creatinine clearance on cimetidine (C(Cr)) were measured at randomization at six months and at one year. Patients underwent a standard four-hour peritoneum equilibrium test, and total body water was measured by bioelectrical impedance. Results were expressed on an intention-to-treat basis. UV, C(Cr), and C(Urea) were similar at randomization (1020 +/- 104 vs. 1040 +/- 130 mL/24 hours, 4.95 +/- 0.51 vs. 4.07 +/- 0.40 mL/min/1.73 m2, 0.91 +/- 0.09 vs. 0.84 +/- 0.08, diuretic vs. control). UV in the diuretic-treated group increased, whereas in the control group, it declined (+176 vs. -200 mL/24 hours at 6 months and +48.8 vs. -305 mL/24 hours at 1 year, P < 0.05). C(Cr) and C(Urea) declined at a constant rate and were unaffected by diuretic administration (0.12 +/- 0.05 vs. 0.071 +/- 0.04 mL/min/1.73 m2/month, 0.020 +/- 0.01 vs. 0.019 +/- 0.01 per month). Urinary sodium excretion increased in the diuretic group and declined in the control group (+0.72 +/- 0.85 vs. -2.56 +/- 1.31 mmol/24 hours/month, P = 0.04). Body weight rose in both groups (4.3 vs. 3.0 kg), but the percentage of total body weight rose in the control group and remained constant in the diuretic group (52 +/- 2.4 vs. 64 +/- 6.6%, P = 0.10). Long-term furosemide produces a significant increase in UV over 12 months when on CAPD and may result in clinically significant improvement in fluid balance. However, furosemide has no effect on preserving residual renal function.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                03 November 2003
                : 21
                : 6
                : 401-408
                aDepartment of Anaesthesia and Intensive Care, University Hospital Královské Vinohrady, Prague, bDepartment of Clinical Biochemistry and Hematology, District Hospital, Kladno, cDepartment of Kinanthropology, Charles University, Prague, and d2nd Department of Medicine, University Hospital Královské Vinohrady, Prague, CzechRepublic
                73443 Blood Purif 2003;21:401–408
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, References: 26, Pages: 8
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/73443
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