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Haemostatic activation and proteinuria as factors in the progression of chronic renal failure
M P Gordge1, B R Leaker, P B Rylance
1Department of Renal Medicine, University College and Middlesex School of Medicine, University College London, UK.
Insights
Patients with chronic renal failure (CRF) and diabetic nephropathy show heightened haemostatic activation. Proteinuria, serum thromboxane B2 (TxB2), and von Willebrand factor antigen (vWFAg) are key factors in disease progression.
Area of Science:
- Nephrology
- Hematology
- Clinical Biochemistry
Background:
- Chronic renal failure (CRF) and diabetic nephropathy are associated with complex pathophysiological changes.
- Haemostatic system activation is implicated in various chronic diseases, but its role in progressive renal failure requires further elucidation.
Purpose of the Study:
- To investigate haemostatic activation in patients with non-diabetic CRF and diabetic nephropathy.
- To determine the relationship between specific haemostatic markers and the rate of renal function decline in these patient groups.
Main Methods:
- Comparison of haemostatic markers (D dimer, vWFAg, CRP, platelet aggregation, platelet factor 4, serum TxB2) between patients and healthy controls.
- Multiple regression analysis to identify independent predictors of renal failure progression.
Main Results:
- Both patient groups exhibited significantly elevated D dimer, vWFAg, and CRP, along with increased spontaneous platelet aggregation compared to controls.
- Proteinuria was independently associated with the rate of progression in both non-diabetic CRF and diabetic nephropathy.
- Serum TxB2 independently predicted progression in non-diabetic CRF, while vWFAg independently predicted progression in diabetic nephropathy.
Conclusions:
- Haemostatic activation is present in progressive non-diabetic and diabetic renal failure.
- Proteinuria, serum TxB2, and vWFAg are significant determinants of renal failure progression and may hold prognostic value.
Abstract:
Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
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