Peripheral vascular disease (PVD) is prevalent among dialysis patients, and many dialysis patients undergo PVD-related procedures. We aimed to examine the risk factors for and prognosis after such procedures in the dialysis setting.
In a national prospective cohort study of 1041 incident dialysis patients, we examined the factors that are associated with PVD procedures (lower extremity amputations and bypasses) after the start of dialysis. Adjusted risk for PVD procedures of various factors was estimated using multivariable Cox proportional hazards models. Incidence rates of subsequent cardiovascular events, infectious hospitalizations, PVD- and cardiovascular disease-related mortality, and all-cause mortality were compared for those with and without a PVD procedure.
Overall, 217 (21%) patients underwent a PVD procedure after the start of dialysis. For those without diabetes, only PVD history (relative hazard [RH] 2.9; 95% confidence interval [CI] 1.3 to 6.6) and increased fibrinogen (RH 1.2; 95% CI 1.0 to 1.5) predicted PVD procedures. For those with diabetes, increased serum phosphate (RH 1.2; 95% CI 1.1 to 1.4), along with decreased albumin, increased C-reactive protein and fibrinogen, and lower SBP, was associated with risk for PVD procedures. Of those who had a procedure compared with those who did not, 68 versus 30% experienced a subsequent cardiovascular event, 85 versus 66% an infectious hospitalization, 11 versus 2% a PVD-related death, and 81 versus 59% all-cause death (mean follow-up 3.0 yr).
Prognosis after PVD procedures is poor, and providers should be aware that risk factors for PVD procedures may differ by diabetes status.
"In recent years, hyperphosphatemia has emerged as a risk factor for vascular calcification and cardiovascular mortality (Plantinga et al., 2009; Ellamz and Chico, 2012) Phosphate overload and eventual hyperphosphatemia are features of chronic kidney disease (Emilio et al., 2012). Furthermore, dietary phosphate load influences outcomes in chronic kidney disease (Noori et al., 2010; Parker et al., 2009). "
[Show abstract][Hide abstract] ABSTRACT: Hyperphosphatemia is associated with severe decline of renal function in chronic kidney disease and elevates cardiovascular mortality. Type II sodium dependent phosphate transporter 2A (Npt2A) plays a major role in renal phosphate reabsorption and could be explored as a target for anti-hyperphosphatemia therapy. Human Npt2A transporter activity was examined upon transfection into CHO, MDCK, HEK293, Flp-In-CHO and Flp-In-HEK293 cells. Only kidney-derived cells expressed functional Npt2A. HEK293 and Flp-In-HEK293 cell lines stably transfected with hNpt2A could be selected, but these cells were inactive in phosphate transport. This suggests that high-level, constitutive Npt2A expression has deleterious effects on the cell. By using the conditional promoter in the Flp-In-Trex vector, functional expression of Npt2A was achieved by doxycycline induction in HEK293 cells. The EGFP tagged and non-tagged, inducible stable hNpt2A-HEK293 cell lines afforded development of a robust phosphate uptake assay mediated by hNpt2A, which can be used to screen hNpt2A inhibitors and inducers of hNpt2A expression. Using this assay, the small molecule LC-1 was identified as a potent inhibitor of hNpt2A, suggesting that it's feasible to develop potent specific hNpt2A inhibitors to control phosphate overloading for hyperphosphatemia therapy.
European journal of pharmacology 09/2013; 721(1-3). DOI:10.1016/j.ejphar.2013.09.005 · 2.53 Impact Factor
"who may not be readily identified as having CKD by their physicians. In recent years, hyperphosphatemia has emerged as a risk factor for vascular calcification and cardiovascular mortality  . Hyperphosphatemia is also associated with left ventricular hypertrophy (LVH)  and progression of CKD . "
[Show abstract][Hide abstract] ABSTRACT: The kidneys excrete excess dietary phosphate, and patients with chronic kidney disease may suffer from phosphate overload and hyperphosphatemia. In chronic kidney disease, hyperphosphatemia has emerged as a risk factor for vascular calcification, cardiovascular mortality, left ventricular hypertrophy, and progression of chronic kidney disease. Serum phosphate at the upper limits of normal has also been associated with adverse outcomes in patients with relatively preserved kidney function. Of note, hyperphosphatemia is not a sensitive indicator of phosphate overload. In this regard, increased circulating fibroblast growth factor-23, a phosphatonin that is released in response to phosphate overload, is independently associated with adverse outcomes in patients with and without chronic kidney disease. Direct effects of extracellular phosphate on vascular calcification or cardiovascular cell biology; adverse consequences of adaptive mechanisms activated to limit phosphate overload, such as left ventricular hypertrophy induced by fibroblast growth factor-23; or epidemiological associations of additional cardiovascular risk factors with chronic kidney disease may underlie these observations. We now review the pathophysiology of phosphate, its relationship with cardiovascular outcomes, the potential consequences for patient care related to dietary phosphate and phosphate binders, and the clinical relevance for patients without overt chronic kidney disease.
Cardiovascular pathology: the official journal of the Society for Cardiovascular Pathology 03/2012; 21(5):372-81. DOI:10.1016/j.carpath.2012.02.008 · 2.00 Impact Factor
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