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Suneel M. Udani and Jay L. Koyner

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

Joseph V. Bonventre

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 (1). Examples of biomarkers are proteins; lipids; microRNAs; genomic, metabolomic, or proteomic patterns; imaging determinations; electrical signals; and cells present on a urinalysis. This issue will focus primarily on serum and urine proteins. A partial list of candidate markers for kidney injury is presented in Figure 1 with corresponding sites of injury along the nephron.

Legacy kidney biomarkers include serum creatinine (sCr), blood urea

Deidra C. Crews

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 (1, 2).

Allon Friedman

According to the 2007 National Health Interview survey, fish oil is the most popular dietary supplement used by adult Americans (1). This follows on the heels of decades of well-publicized basic science and clinical research into the biology of long-chain omega-3 fatty acids—the major active ingredient in fish oil—and their influence on a variety of disease processes. Although clinical trials of the use of fish oil in the general population have reported conflicting results, patients with chronic kidney disease (CKD)—in particular end stage renal disease—have several characteristics that may make them an ideal group in which to study

Melanie S. Joy

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 (1). Although the clinician’s time is a limiting factor in conducting nutrient reviews, an even greater problem is the lack of knowledge by clinicians of what nutrients can interact with which drugs and the mechanisms for the interactions. The

Sharon M. Moe

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

Steven Crowley

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

Jens Titze

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 (1). Sodium homeostasis seems to perfectly fit into this model. Sodium is the major cation in the extracellular fluid compartment where it acts to hold water, thereby determining the extracellular volume. Elaborated from this model, three major assumptions dominate

Laura P. Svetkey and Crystal C. Tyson

Renal denervation is an emerging and promising new therapy for resistant hypertension. Although 54 percent of all hypertension is “uncontrolled” (1), not all uncontrolled hypertension is considered resistant. The American Heart Association (AHA) definition of resistant hypertension is BP above goal on at least three antihypertensive medications of different classes, one of which is a diuretic, or BP that requires four or more medications to get to goal. Prevalence in the general hypertensive population is relatively low, but resistant hypertension is commonly seen in nephrology offices.

In evaluating a patient with resistant hypertension, it’s important to consider reversible

Laura P. Svetkey and Crystal C. Tyson

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