The use of B-type natriuretic peptide to assess volume status in patients with end-stage renal disease.

BACKGROUND: Although B-type natriuretic peptide (BNP) levels correlate with volume overload in congestive heart failure, its usefulness in patients with renal dysfunction has been questioned. A simple test to estimate volume overload and assist in the management of dry weight in hemodialysis (HD) patients would be useful. METHODS: Thirty-nine patients--aged 64 +/- 2 years (mean +/- SEM), male-female ratio of 37:2--undergoing HD thrice weekly for at least 30 days were studied. Samples were collected at the start and end of each of 3 consecutive HD sessions. Pre- and postsession weights and blood pressures were recorded. Left ventricular ejection fractions were obtained from echocardiograms performed within 1 year of enrollment. The first session was the dialysis session after a 72-hour interdialytic period, whereas the second and third sessions were after a 48-hour period. Plasma volume changes were measured in a subset of 13 patients. RESULTS: Pre- and postdialysis BNP levels for each of the 3 sessions were 434 and 343 pg/mL, 347 and 231 pg/mL, and 249 and 202 pg/mL, respectively. The values for body weights were 82.6 +/- 3.6 and 78.6 +/- 3.5 kg, 81.5 +/- 3.6 and 78.2 +/- 3.5 kg, and 81.5 +/- 3.46 and 78.3 +/- 3.5 kg, respectively. The values of mean systolic blood pressures were 150 +/- 4 and 134 +/- 3 mm Hg, 142 +/- 4 and 134 +/- 4 mm Hg, and 142 +/- 4 and 131 +/- 4 mm Hg, respectively. The values for mean diastolic blood pressures were 81 +/- 2.5 and 70 +/- 2.4 mm Hg, 74 +/- 2.4 and 72.1 +/- 2.2 mm Hg, and 76 +/- 2.9 and 72 +/- 2.9 mm Hg, respectively. There was no correlation between changes in intradialytic BNP values and other measured parameters. Plasma volume changed minimally during dialysis. CONCLUSIONS: Values of BNP are elevated in patients with end-stage renal disease and decline after each dialysis session. Over the course of a week, BNP levels gradually declined irrespective of changes in weight or blood pressure. The lack of correlation between changes in BNP and changes in measured clinical parameters is partly explained by a lack of a significant change in plasma volume. The highest BNP values were seen in patients with systolic dysfunction.

Dialysis modalities in the intensive care unit.

Acute renal failure in the ICU is a clinically diverse entity. Consequently, the indications for initiation of dialysis therapy are varied. In general, the indications are solute control, volume control, or both. A variety of dialysis modalities are available; however, there is no consensus as to the optimal modality for any particular group of patients. A careful understanding of the particular benefits, limitations, and potential complications of each modality coupled with a thorough assessment of the individual patient's need formulate the basis for dialysis modality selection. In certain circumstances, the more conventional intermittent therapies are sufficient, whereas in other settings, CRRT techniques are advantageous. The impact of modality selection on outcome remains an area of significant controversy. Future studies in which more uniformity within specific subgroups of patients with ARF is sought may shed light on the optimal modality for a particular patient group. Newer therapies aimed at more optimal and more specific blood purification may prove promising in the management of complex critically ill patients with ARF and other comorbid conditions.

Tunicamycin preserves intercellular junctions, cytoarchitecture, and cell-substratum interactions in ATP-depleted epithelial cells.

Pretreatment with the nucleoside antibiotic tunicamycin was found to protect cultured renal epithelial cells in the face of ATP-depletion, in large part by preserving junctional and cellular architecture. Tunicamycin pretreatment of Madin-Darby canine kidney cells not only preserved E-cadherin staining at the plasma membrane, but also inhibited ATP-depletion-mediated E-cadherin degradation. Electron microscopic analysis, together with the preservation of the staining patterns of the tight junction marker ZO-1, the apical/microvillar marker gp135, and basolateral marker Na/K-ATPase suggested that tunicamycin preserved the junctional complex and the polarized epithelial cell phenotype. Tunicamycin pretreatment also prevented reductions in the filamentous actin content of the cells, as well as preserving Golgi architecture. Moreover, a quantitative measure of cell adhesion demonstrated that tunicamycin pretreatment resulted in a fivefold increase in attachment of cells to the substratum (77% versus 16%). Thus, pretreatment with tunicamycin protects polarized epithelial cells from ischemic injury through the preservation of epithelial cell architecture, intercellular junctions, and cell-substratum interactions in the setting of intracellular ATP-depletion.