In a non-diabetic Japanese population, the combination of macroalbuminuria and increased urine beta 2-microglobulin predicts a decline of renal function: the Takahata study

Several studies have shown that patients who have been dialyzed with high-flux biocompatible membranes have a lower plasma level of beta 2-microglobulin and a lower incidence of amyloid disease compared with patients who have been dialyzed with low-flux bioincompatible membranes. However, because high-flux membranes are associated with significant dialytic removal of beta 2-microglobulin, the specific role of membrane biocompatibility in influencing the rate of increase of beta 2-microglobulin has not been previously determined. This study investigated the effect of biocompatibility on the rate of increase of plasma levels of beta 2-microglobulin in 159 new hemodialysis patients from 13 dialysis centers (ten centers affiliated with Dallas Nephrology Associates and three with Vanderbilt University Medical Center) by using two low-flux membranes with widely different biocompatibilities. These patients were prospectively randomized to be dialyzed with either a low-flux biocompatible membrane or a low-flux bioincompatible membrane. Plasma beta 2-microglobulin levels were measured at 0, 3, 6, 9, 12, and 18 months. Sixty-six patients completed the 18-month study. Plasma beta 2-microglobulin increased in all patients; however, the increase was not significantly different from baseline at any time point in the group that used the biocompatible membrane. In this group, beta 2-microglobulin increased from (mean +/- SD) 27.8 +/- 14.8 mg/L to 34.0 +/- 10.0 mg/L at 18 months (P = not significant), and the mean increase at 18 months was 2.6 +/- 14.7 mg/L. In contrast, the increase in plasma beta 2-microglobulin level in the bioincompatible membrane group became significant in Month 6 when the levels had increased from a baseline of 24.8 +/- 9.6 mg/L to 29.5 +/- 12.2 mg/L (P < 0.001); these increases continued to be significant until Month 18, when serum beta 2-microglobulin reached 36.8 +/- 13.9 mg/L with an average increase of 11.8 +/- 11.2 mg/L (P < 0.0001). The higher rate of plasma B2-microglobulin increase in the group that had been dialyzed with the bioincompatible membrane was also evident when only patients who had completed the study were analyzed. There were no significant differences in the actual level of beta 2-microglobulin or in residual renal function between the two groups during the 18 months of the study. It was concluded that over a period of 18 months, the use of biocompatible membranes, even in the low-flux configuration, is associated with a significantly slower increase in plasma beta 2-microglobulin, independent of the influence of residual renal function.

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DIAGNOSTIC SIGNIFICANCE OF BETA 2-MICROGLOBULIN IN THE ASSESSMENT OF NEONATAL RENAL FUNCTION

Pediatric Research ◽

10.1203/00006450-198404001-01587 ◽

1984 ◽

Vol 18 ◽

pp. 357A-357A

Author(s):

Farahnak K Assadi ◽

Eunice G John ◽

Dharmapuri Vidyasagar ◽

Parvin Justice ◽

Linda Fornell

Keyword(s):

Renal Function ◽

Diagnostic Significance ◽

Beta 2 ◽

Beta 2 Microglobulin

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Beta-2 microglobulin (B2M) is an independent prognostic factor for clinical outcomes in patients with CLL treated with frontline fludarabine, cyclophosphamide, and rituximab (FCR) regardless of age, creatinine clearance (CrCl)

Journal of Clinical Oncology ◽

10.1200/jco.2007.25.18_suppl.7034 ◽

2007 ◽

Vol 25 (18_suppl) ◽

pp. 7034-7034 ◽

Cited By ~ 1

Author(s):

A. M. Tsimberidou ◽

C. Tam ◽

W. Wierda ◽

S. O' Brien ◽

S. Lerner ◽

...

Keyword(s):

Renal Function ◽

Prognostic Factor ◽

Clinical Outcomes ◽

The Other ◽

Adverse Prognostic Factor ◽

Younger Age ◽

Beta 2 ◽

Beta 2 Microglobulin ◽

Independent Adverse Prognostic Factor

7034 Introduction: High β2M levels are a risk factor in CLL. PCR therapy has been reported to be better tolerated than FCR in older or with decrease renal function pts (Shanafelt, Blood 108:15a). We assessed the association between age, CrCl, PS, β2M and outcomes in pts treated with FCR. Methods: From 7/99 to 1/04, 300 pts received rituximab 375 mg/m2 D1; fludarabine 25 mg/m2/d D2–3; and cyclophosphamide 250 mg/m2/d D2–3. Serum β2M levels were measured by radioimmunoassay. CrCl was calculated (Cockcroft-Gault equation). Results: The median age was 57 yrs (≥70, 14%). Age ≥70 was associated with fewer FCR courses (p<.0001); lower rates of CR (p=.001), overall response (OR; p=.04), survival (OS; p<.0001), and FFS (p=.008); and higher rates of G3–4 thrombopenia (p<.0001) or anemia (p=.002) compared with age<70. The median CrCl was 90 mL/min (CrCl <70, 27%). Pts with CrCl <70 had higher rates of G3–4 thrombopenia (p=.006) or anemia (p=.01) than others. There were no differences between the 2 groups in the other outcomes. PS was 0 in 40%, 1 in 57%, and 2 in 3% of pts. Better PS was associated with higher rates of CR (p=.007) and FFS (p=.02) but did not affect OR or OS. The median β2M level was 3.7 mg/L (β2M ≥ 4, 43%). The rates of CR, survival, and FFS were lower in pts with β2M ≥ 4 compared with others (p<.0001 each). High β2M levels were associated with older age, lower CrCl levels, poorer PS (p<.0001 each), higher rates of G3–4 neutropenia (p=.005), thrombocytopenia (p=.01), and infections (p=.03), and fewer FCR courses (p=.004). The median follow-up was 5 yrs. The rates of CR, 3-yr OS and 3-yr FFS were 72%, 87% and 76%, respectively. Independent factors predicting response were lower β2M (p=.0004) and lower WBC counts (p=.02). Independent factors predicting longer OS were younger age (p=.001), lower β2M (p=.003) and lower WBC (p=.03). Independent factors predicting longer FFS were lower β2M levels (p=.0006), and lower WBC counts (p=.005). Conclusion: Age ≥70 yrs and poor PS, but not CrCl level were associated with poor clinical outcomes. High β2M levels are an independent adverse prognostic factor for CR, OS, and FFS in the context of other prognostic factors. No significant financial relationships to disclose.

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Evidence for Dependance of Beta Thromboglobulin Levels on Renal Function

10.1055/s-0039-1687050 ◽

1979 ◽

Author(s):

D. Deppermann ◽

K. Andrassy ◽

H. Seelig ◽

E. Ritz ◽

D. Post

Keyword(s):

Renal Failure ◽

Renal Function ◽

Serum Concentration ◽

Normal Renal Function ◽

Impaired Renal Function ◽

Sensitive Indicator ◽

Tubular Proteinuria ◽

Normal Range ◽

Beta 2 ◽

Beta 2 Microglobulin

Beta-Thromboglobulin (TG) is a thrombocytic protein which is released into the circulation upon lysis of thrombocytes. Its serum concentration is thought to be a sensitive indicator of thrombocyte consumption. Although a relation of TG platelet consumption could be observed by us in patients with normal renal function, no such relation was found in pat. with renal failure (RF). Therefore we examined whether TG, similar to beta-2-microglobulin (BMG), behaves like a tubular protein. - Patients and methods - 90 pat. with RF were examined. None of the pat. had diseases with known platelet consumption or medication which interferes with platelets. TG and BMG were measured by RIA. - Results - There was a highly significant correlation between TG, serum creat. (r=0,78) and Ccr (r=0,73) and BMG. The normal range (x ±SD) of TG was 33,9± 9,7 ng/ml and values consistantly about 50 ng/ml were observed at Ccr < 50 ml/l,73 m2. TG was found in tubular proteinuria. - Conclusion - TG is a tubular protein the concentration of which rises in patients with renal failure. This finding invalidates the use of TG for detection of thrombosis in patients with impaired renal function.

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Renal Elimination of Beta-2-Microglobulin and Myoglobin in Patients with Normal and Impaired Renal Function

Nephron ◽

10.1159/000186000 ◽

1990 ◽

Vol 55 (4) ◽

pp. 361-367 ◽

Cited By ~ 5

Author(s):

J. Floege ◽

M.F. Wilks ◽

M. Soose ◽

J. Kotzerke ◽

S. Shaldon ◽

...

Keyword(s):

Renal Function ◽

Impaired Renal Function ◽

Renal Elimination ◽

Beta 2 ◽

Beta 2 Microglobulin

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No evidence of renal toxicity from amalgam fillings

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.271.4.r941 ◽

1996 ◽

Vol 271 (4) ◽

pp. R941-R945 ◽

Cited By ~ 2

Author(s):

G. Sandborgh-Englund ◽

A. T. Nygren ◽

J. Ekstrand ◽

C. G. Elinder

Keyword(s):

Renal Function ◽

Renal Toxicity ◽

Dental Amalgam ◽

Before And After ◽

Tooth Surfaces ◽

51Cr Edta ◽

Beta 2 ◽

Beta 2 Microglobulin ◽

Amalgam Removal ◽

Amalgam Fillings

Dental amalgam continuously releases mercury. Studies of sheep [Boyd et al., Am. J. Physiol. 261 (Regulatory Integrative Comp. Physiol. 30): R1010-R1014, 1991] showed decreased renal function after placement of amalgam fillings. In this study, renal function was investigated in 10 healthy volunteers before and after amalgam removal. The subjects had an average of 18 tooth surfaces filled with amalgam, which was removed during one dental session. One week before and sixty days after removal, the glomerular filtration rate (GFR) was determined by 51Cr-EDTA clearance technique. Blood and urine samples were collected for analysis of mercury, creatinine, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and albumin 1 wk before and 1, 2, and 60 days after amalgam removal. The plasma mercury concentration increased significantly 1 day after removal. Sixty days later, significantly lower mercury levels were found in blood, plasma, and urine. The GFR values were similar before and after mercury exposure (mean 94 and 94 ml/min per 1.73 m2, respectively). No detectable effects occurred on excretion of NAG, beta 2-microglobulin, or albumin. It is concluded that no signs of renal toxicity could be found in conjunction with mercury released from amalgam fillings.

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