Clinicians view kidney disease as a continuum where kidney failure results from a combination of patient susceptibility factors (diabetes, hypertension, or low nephron mass) combined with episodes of kidney injury (acute kidney injury [AKI]). Clinicians use traditional biomarkers such as serum creatinine, urine output, and albumin as indices of kidney function to diagnose, prognosticate, implement therapy, and monitor progression. These traditional biomarkers are far from ideal. Serum creatinine is a surrogate for kidney function, not injury, and often only signals the injury after several days. Creatinine is also a poor surrogate for renal reserve in assessing patients for chronic kidney
The burden of renal disease is continuing to increase not only in the U.S. population but worldwide, as comorbidity factors such as obesity and diabetes become more prevalent (1). This year, the CDC estimates that more than 10 percent of adults in the United States, approximately 20 million people, may have chronic kidney disease (CKD) in varying degrees of severity, with many people being unaware that they either have CKD or are at increased risk of developing it (2).
The prevalence of CKD, now and in the future, truly represents a public health challenge. The area
Cirrhosis is a major contributor to the burden of disease in society, and much of the morbidity and mortality associated with cirrhosis is due to the complications of portal hypertension. Acute kidney injury (AKI) is a frequent complication in patients with cirrhosis, occurring in up to 20 percent of hospitalized patients (1). Despite the high rate of AKI in this patient population, there is often a delay in early diagnosis of AKI. Furthermore, there are clinical challenges in correctly diagnosing the etiology of AKI, which in turn can alter specific therapy. This article will focus on the current
There has been considerable interest in studying novel biomarkers in chronic kidney disease (CKD) beyond the conventional clinical indices, such as serum creatinine, blood urea nitrogen, and urine protein or urine albumin. The motivation for this is similar to what has been outlined in other articles in this issue of ASN Kidney News. For example, novel biomarkers may improve our ability to better risk classify patients and guide clinical actions (e.g., closer follow-up and more intense treatment for patients at higher risk of progression of CKD), to identify high-risk patients for enrollment into clinical trials (as enriched enrollment
Contrast-induced acute kidney injury (CI-AKI) is a common condition that is associated with serious, adverse short- and long-term outcomes. Despite substantial advancements in our understanding of CI-AKI, the capacity to effectively risk-stratify patients, diagnose incipient renal injury before elevations in serum creatinine (SCr) manifest, and identify patients at highest risk for adverse downstream events is limited. Blood and urine biomarkers of kidney injury hold promise as a means by which the risk-stratification, diagnosis, and prediction of prognosis of CI-AKI could be significantly enhanced, and the judicious implementation of cost-effective preventive care and treatment to mitigate adverse outcomes substantially improved.
The search for biomarkers in body fluids is evolving into a broader quest for molecular phenotyping of tissue and disease reclassification. The original biomarker concept was too limited, failing to recognize that the interpretation of the molecular changes in body fluids requires a molecular understanding of the diseased tissue.
A molecular biomarker in nephrology implies a molecule that can be measured in body fluids as an indicator of a pathologic state in kidney tissue, perhaps avoiding biopsies by providing similar information. This demands that the biomarker is superior to current laboratory assessments such as creatinine
Renal insufficiency is prevalent and clinically relevant in the setting of congestive heart failure. When admitted for acute decompensation, on average 1 out of 5 patients has a rise in serum creatinine, 1 out of 10 requires some form of dialysis, and 1 out of 20 requires long-term renal replacement therapies (1). These startling observations highlight the fact that adequate renal function plays a pivotal role in the clinical stability of heart failure. Hence, the term “cardio-renal syndrome” (CRS) has been coined to describe the extreme of cardio-renal dysregulation whereby therapy to relieve congestive symptoms of heart failure
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 (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
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).