PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 16612412

Beta2-microglobulin, a uremic toxin with a double meaning.

B Canaud·M Morena·J P Cristol·D Krieter
View original source ↗Export metadata ↓

Abstract

beta(2)M is a strong and independent indicator of hemodialysis patient outcomes and an excellent surrogate for middle molecules, and deserves to be routinely monitored and incorporated into dialysis adequacy targets. beta(2)M has a double meaning, reflecting both dialysis efficacy in terms of solute mass transfer and patient bioactivity. The work of Ward et al. in this issue warrants a study to test the hypothesis that long daily hemodiafiltration treatment would be the optimal renal replacement modality to improve dialysis patient outcomes.

Explore related subjects

Body Fluid CompartmentsHemodiafiltrationHemodialysis SolutionsHumansKineticsModels, BiologicalUremiabeta 2-MicroglobulinCommentJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B Canaud, M Morena, J P Cristol, D Krieter. 2006. Beta2-microglobulin, a uremic toxin with a double meaning.. https://doi.org/10.1038/sj.ki.5000389

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Bradykinin shifts endothelial fluid passage from para- to transcellular routes.

The signalling peptide bradykinin (BK) is implicated in inflammation and angiogenesis. It promotes fluid transport from blood vessels to interstitial space, and thus facilitates oedema formation. To clarify whether paracellular or transcellular pathways mediate this effect, we investigated the BK-stimulated fluid transport across endothelial monolayers in vitro by comparison of electrical and fluorescence methods. Electrical cell impedance sensing monitored a biphasic response of cell layers to BK with high time resolution: a short decrease (18%, 1 min) was followed by a more sustained increase in paracellular resistance (30%, 10 min). The two phases can be assigned to second messengers of the BK-signalling pathway: Ca(2+) for the decrease and cyclic adenosine monophosphate for the rise of resistance, respectively. Despite tightening of the intercellular clefts, BK increased the fluid permeability by 39%, indicating transcellular fluid transport. Additionally, BK stimulated both in- and outwardly directed membrane trafficking as assessed by vesicular fluid uptake (by 49%) and secretion of von Willebrandt factor (by 85%). In conclusion, the combination of electrical and fluorescence data suggests that BK induces a shift from para- to transcellular fluid transport across endothelium.

Body Fluid Compartments↗
PubMed2006

Hypovolemia and dehydration in the oncology patient.

Dehydration is commonly but often inappropriately diagnosed in cancer patients. Dehydration is the loss of water from the intracellular compartment due to hypernatremia. Dehydration can occur among patients who are hypervolemic, euvolemic, or hypovolemic. Cancer patients are more often hypovolemic, reflecting depletion of water from the extracellular space due to excessive loss, such as from vomiting and diarrhea, or inadequate intake of fluids. Hypovolemia can be hypernatremic, eunatremic, or hyponatremic. The appropriate state of the patient should be determined prior to attempts at correcting the problem. A hyponatremic patient would rehydrate more quickly with a solution higher in sodium, whereas this solution could be dangerous for a hypernatremic patient. Rapid or inappropriate treatment of hypernatremia can lead to death. Subjective findings, physical findings, and laboratory values will help direct the appropriate resuscitation methods. This paper reviews the physiologic control of extracellular volume and electrolytes, diagnosis of sodium and water balance problems, and the management of these concerns.

Body Fluid Compartments↗