End-Stage Renal Disease: In Vivo Diffusion-Tensor Imaging of Silent White Matter Damage

Background and Purpose: End-stage renal disease (ESRD) results in extensive white matter abnormalities, but the specific damage segment cannot be identified. This study aimed to determine the segmental abnormalities of white matter microstructure in ESRD and its relationship with cognitive and renal function indicators.Methods: Eighteen ESRD patients and 19 healthy controls (HCs) were prospectively recruited. All participants underwent DTI and clinical assessments. Automatic fiber quantification (AFQ) was applied to generate bundle profiles along 16 main white matter tracts. We compared the DTI parameters between groups. Besides, we used partial correlation and multiple linear regression analyses to explore the associations between white matter integrity and cognitive performance as well as renal function indicators.Results: In the global tract level, compared to HCs, ESRD patients had greater MD, AD, and RD values and lower FA value in several fibers (P < 0.05, FDR correction). In the point-wise level, extensive damage existed in specific locations of different fiber tracts, particularly in the left hemisphere (P < 0.05, FDR correction). Among these tracts, the mean AD values of the left cingulum cingulate correlated negatively with MoCA score. Urea and UA level were independent predictors of the AD value of superior component of the left corticospinal. Besides, urea level was the independent predictors of mean MD value of left anterior thalamic radiation (ATR).Conclusion: White matter fiber tract damage in ESRD patients may be characterized by abnormalities in its specific location, especially in the left hemisphere. Aberrational specific located fibers were related to cognitive impairment and renal dysfunction.

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Complement anaphylatoxin C5a contributes to hemodialysis-associated thrombosis

Blood ◽

10.1182/blood-2010-01-264051 ◽

2010 ◽

Vol 116 (4) ◽

pp. 631-639 ◽

Cited By ~ 88

Author(s):

Ioannis Kourtzelis ◽

Maciej M. Markiewski ◽

Michael Doumas ◽

Stavros Rafail ◽

Konstantinos Kambas ◽

...

Keyword(s):

Renal Disease ◽

Complement Activation ◽

End Stage Renal Disease ◽

Granulocyte Colony Stimulating Factor ◽

Colony Stimulating Factor ◽

Anaphylatoxin C5a ◽

Stage Renal Disease ◽

End Stage ◽

Stimulating Factor

Abstract Thrombosis is a common complication of end-stage renal disease, particularly in patients on hemodialysis. Although substantial progress has been made in preventing thrombotic complications in various other groups of patients, the mechanisms of thrombosis during hemodialysis require clarification. In this report, we demonstrate that complement activation triggered by hemodialysis biomaterials, and the subsequent generation of the complement anaphylatoxin C5a, results in the expression of functionally active tissue factor (TF) in peripheral blood neutrophils. Because TF is a key initiator of coagulation in vivo, we postulate that the recurring complement activation that occurs during long-term hemodialysis contributes to thrombosis in dialyzed end-stage renal disease patients. Furthermore, we found that complement contributed to the induction of granulocyte colony-stimulating factor, which has been implicated in the pathogenesis of thrombosis in patients treated with the recombinant form of this molecule. Importantly, the inhibition of complement activation attenuated the TF expression and granulocyte colony-stimulating factor induction in blood passing through a hemodialysis circuit, suggesting that the complement system could become a new therapeutic target for preventing thrombosis in patients with chronic renal failure who are maintained on hemodialysis.

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