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Over the past decade there has been an explosion of research investigating biomarkers of acute kidney injury (AKI). The research was borne out of the desire to replace serum creatinine, and in part urine output, as for a variety of reasons both serve as suboptimal tools in the diagnosis of acute renal tubular injury. The biomarker movement has been assisted by internationally accepted, standardized, consensus definitions of AKI. Whereas decades ago AKI definitions varied from study to study, the implementation and validation of the RIFLE (Risk, Injury, Failure, Loss and End Stage) and AKI Network criteria paved the way for
A biomarker is defined as a characteristic that can be objectively measured and evaluated as an indicator of normal biologic or pathogenic processes of pharmacological responses to a therapeutic intervention (
Legacy kidney biomarkers include serum creatinine (sCr), blood urea
Individuals at high risk for the development of chronic kidney disease (CKD), or who already have the disease, are frequently encouraged by their health care providers to follow a “healthful” diet. Such a diet may be particularly difficult to follow if the recommended foods cannot be easily acquired—a situation that individuals living in poverty often face.
Poverty affects over 46 million (15 percent) Americans and has a disproportionate impact on racial and ethnic minorities (e.g., 35 percent of African Americans live in poverty), who also bear the greatest burden of advanced and progressive CKD (
According to the 2007 National Health Interview survey, fish oil is the most popular dietary supplement used by adult Americans (
Clinicians are trained to review prescription drugs with patients during their clinic visits and hospital admissions. However, less emphasis is placed on appropriate review and documentation of foods and nutrients that are known or suspected to interact with medications. This scenario places kidney disease patients at significant risk, given the 10 to 12 different medications that are typically prescribed (
Phosphorus levels are elevated in patients with chronic kidney disease due to decreased urinary excretion. Higher levels of blood phosphorus are associated with increased mortality in patients on dialysis, patients with kidney disease not yet on dialysis, and in the general population. In animal studies, adding phosphorus to the diet causes calcification of arteries and progression of kidney disease.
In the petri dish in the lab, adding phosphorus to artery vascular smooth muscle cells results in a change of the cell to become a bone-like cell and to calcify. This and other data support the hypothesis that phosphorus is a
Although cardiologists and nephrologists have debated for years about the relative contributions of the vasculature and the kidney to the pathogenesis of hypertension, new data have emerged that may recast essential hypertension as an autoimmune disease. These studies do not discount the importance of vascular tone and regulation of intravascular volume in the determination of blood pressure. Rather, these novel experiments illustrate that immune cells and inflammatory mediators can influence blood pressure precisely by impacting vascular function and renal sodium handling. Moreover, these recent findings have stimulated renewed interest in earlier, pioneering studies that first hinted at a role for
Body sodium content is most intimately coupled with extracellular water content. The idea is that body fluids inside and outside the cells readily equilibrate, resulting in constant electrolyte concentrations in extra- and intracellular fluids. This concept of constancy of internal environment composition is perhaps one of the hallmarks of medical physiology established by Claude Bernard in the 19th century (
Renal denervation is an emerging and promising new therapy for resistant hypertension. Although 54 percent of all hypertension is “uncontrolled” (
In evaluating a patient with resistant hypertension, it’s important to consider reversible
Most people with chronic kidney disease (CKD) have high blood pressure. Treatment of hypertension in patients with CKD is considered critical to prevent CKD progression and related cardiovascular events. However, questions remain about the appropriate BP goal. Most evidence indicates there is no benefit of treating to a goal any lower than 140/90 mm Hg, but there is some suggestion that such a goal may be appropriate for patients with albuminuria. Given recent evidence that a lower goal in patients with diabetes (without CKD) actually increases risk, and the subsequent change in American Diabetes Association guidelines from 130/80 mm Hg
