| 1. |
- Uhlin, Fredrik, et al.
(författare)
-
Estimation of delivered dialysis dose by on-line monitoring of the ultraviolet absorbance in the spent dialysate
- 2003
-
Ingår i: American Journal of Kidney Diseases. - 0272-6386 .- 1523-6838. ; 41:5, s. 1026-1036
-
Tidskriftsartikel (refereegranskat)abstract
- Background:Several methods are available to determine Kt/V, from predialysis and postdialysis blood samples to using on-line dialysate urea monitors or to ionic dialysance using a conductivity method. The aim of this study is to compare Kt/V calculated from the slope of the logarithmic on-line ultraviolet (UV) absorbance measurements, blood urea Kt/V, dialysate urea Kt/V, and Kt/V from the Urea Monitor 1000 (UM; Baxter Healthcare Corp, Deerfield, IL).Methods:Thirteen uremic patients on chronic thrice-weekly hemodialysis therapy were included in the study. The method uses absorption of UV radiation by means of a spectrophotometric set-up. Measurements were performed on-line with the spectrophotometer connected to the fluid outlet of the dialysis machine; all spent dialysate passed through a specially designed cuvette for optical single-wavelength measurements. UV absorbance measurements were compared with those calculated using blood urea and dialysate urea, and, in a subset of treatments, the UM.Results:Equilibrated Kt/V (eKt/V) obtained with UV absorbance (eKt/Va) was 1.19 ± 0.23; blood urea (eKt/Vb), 1.30 ± 0.20, and dialysate urea (eKt/Vd), 1.26 ± 0.21, and Kt/V in a subset measured by the UM (UM Kt/V) was 1.24 ± 0.18. The difference between eKt/Vb and eKt/Va was 0.10 ± 0.11, showing a variation similar to the difference between eKt/Vb and eKt/Vd (0.03 ± 0.10) and in a subset between eKt/Vb and UM Kt/V (−0.02 ± 0.11).Conclusion:The study suggests that urea Kt/V can be estimated by on-line measurement of UV absorption in the spent dialysate.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
- Hellstrom, L, et al.
(författare)
-
Cadmium exposure and end-stage renal disease
- 2001
-
Ingår i: American journal of kidney diseases : the official journal of the National Kidney Foundation. - : Elsevier BV. - 1523-6838. ; 38:5, s. 1001-1008
-
Tidskriftsartikel (refereegranskat)
|
|
| 5. |
- Hellström, L, et al.
(författare)
-
Cadmium exposure and end-stage renal disease
- 2001
-
Ingår i: American Journal of Kidney Diseases. - 0272-6386 .- 1523-6838. ; 38:5, s. 1001-1008
-
Tidskriftsartikel (refereegranskat)abstract
- Environmental exposure to cadmium may cause kidney damage and tubular proteinuria. We investigated the relationship between low-level cadmium exposure and end-stage renal disease (ESRD), indicated by renal replacement therapy (RRT), in a Swedish population environmentally or occupationally exposed to cadmium. Based on records of all persons in the population previously or presently employed in cadmium-battery production or residing in cadmium-polluted areas near the battery plants, we defined exposure as high (occupational), moderate (domicile < 2 km from a plant), low (domicile 2 to 10 km from a plant), or no exposure (domicile > 10 km from a plant). Comprehensive data were available for all individuals undergoing RRT since 1978. The annual incidence of RRT increased from 41 per million in the age group 20 to 29 years to 243 per million in the age group 70 to 79 years and was greater in a priori-defined populations with cadmium exposure. Adjusting for age and sex gave an increased Mantel-Haenszel rate ratio (MH-RR) of 1.8 (95% confidence interval [CI], 1.3 to 2.3) for RRT in the cadmium-exposed population compared with the unexposed group, the MH-RR was even higher for women (MH-RR, 2.3, 95% CI, 1.5 to 3.5). Directly age-standardized rate ratios for RRT and cadmium exposure increased from 1.4 (95% CI, 0.8 to 2.0) in the low-exposure group to 1.9 (95% CI, 1.3 to 2.5) and 2.3 (95% CI, 0.6 to 6.0) in the moderate- and high-exposure groups, respectively. We conclude that exposure to occupational or relatively low environmental levels of cadmium appears to be a determinant for the development of ESRD. ⌐ 2001 by the National Kidney Foundation, Inc.
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
- Plaisier, E, et al.
(författare)
-
Anti-glomerular basement membrane nephritis and bullous pemphigoid caused by distinct anti-alpha 3(IV)NC1 and anti-BP180 antibodies in a patient with Crohn's disease
- 2002
-
Ingår i: American Journal of Kidney Diseases. - : Elsevier BV. - 1523-6838 .- 0272-6386. ; 40:3, s. 649-654
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Anti-glomerular basement membrane (GBM) nephritis is a rare disease induced by antibodies directed against alpha3(IV)NC1, the Goodpasture antigen. We report a patient with Crohn's disease who developed anti-GBM nephritis and the skin blistering disorder bullous pemphigoid, owing to distinct autoantibodies. Methods: Frozen sections of skin and kidney biopsies were incubated with antisera specific for human IgG, IgA, IgM, fibrin, and C3. Reactivity of the patient's serum with GBM antigens was studied by Western blot using bovine solubilized type IV collagen and by enzyme-linked immunosorbent assays using alpha1(IV), alpha3(IV), and alpha5(IV)NC1 recombinant proteins. Reactivity studies against skin antigens were done by Western blot using human keratinocyte and dermal extracts and three recombinant forms of the bullous pemphigoid antigen180 (BP180, also called BPAG2 or type XVII collagen). The patient's serum was affinity fractionated on a (IV)NC1 column, and the bound and unbound fractions were analyzed for their reactivity against GBM and skin antigens. Results: The patient had deposits of IgG along the GBM and the epidermal basement membrane zone. Circulating IgG antibodies against alpha3(IV)NC1 were detected. The patient's autoantibodies immunoblotted the intracellular domain but not the extracellular domain of BP180. Reactivity of the patient's IgG with BP180 was found only in the unbound fraction of the serum. Conclusion: The simultaneous development of a rare renal and skin autoimmune disorder, resulting from non-cross-reactive autoantibodies, suggests that a common triggering event could be responsible for the autoimmune injury. (C) 2002 by the National Kidney Foundation, Inc.
|
|
| 9. |
|
|
| 10. |
|
|
