الفهرس 
Physiology of the KidneyOnly 14 pages are availabe for public view
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Abstract
The The incidence of acute kidney injury (AKI), previously referred to as acute renal failure, has reached epidemic proportions world-wide, affecting about 7% of hospitalised patients. In the critical care setting, the prevalence of AKI requiring dialysis is about 6%, with a mortality rate exceeding 60% (Parikh and Devarajan, 2008).
A significant increase in morbidity and mortality associated with AKI has been demonstrated in a wide variety of clinical situations, including exposure to radiocontrast dye, cardiopulmonary bypass, mechanical ventilation and sepsis. Once established, the treatment is largely supportive, at an annual cost surpassing $10 billion in the US alone (Parikh and Devarajan; 2008).
The early diagnosis of AKI currently depends on detection of reduced kidney function by the rise in serum creatinine concentration and blood urea nitrogen(BUN), which are delayed and unreliable measures in the acute setting. In general, there are several non-renal factors influencing the serum creatinine concentration such as body weight, muscle mass, race, age, gender, total body volume, drugs, muscle metabolism and protein intake(Parikh and Devarajan; 2008).
In the face of AKI, serum creatinine is an even poorer reflection of kidney function, because the subjects are not in steady state, and serum creatinine therefore lags far behind renal injury. Furthermore, significant chronic kidney disease can exist with minimal or no change in creatinine because of renal reserve and enhanced tubular secretion of creatinine. Ironically, experimental studies have identified interventions that may prevent or treat AKI if instituted early in the disease process, well before the serum creatinine rises (Devarajan; 2008).
A biomarker of AKI that is easily measured, unaffected by other biobiological variables and capable of both early detection and risk stratification would represent a tremendous advance in clinical medicine (Devarajan;2008).
The search for AKI biomarkers is an area of intense contemporary research. Conventional urinary biomarkers such as casts and fractional excretion of sodium are insensitive and non-specific for the early recognition of AKI. Other traditional urinary biomarkers such as filtered high molecular weight proteins and tubular proteins or enzymes have also suffered from lack of specificity (Devarajan; 2008).
Fortunately, the application of innovative technologies such as functional genomics and proteomics to human and animal models of AKI has uncovered several novel genes and gene products that are emerging as biomarker.
The urine may contain sensitive and specific markers of kidney injury that are present due to either impaired tubular reabsorption and catabolism of filtered molecules or release of tubular cell proteins in response to ischemic or nephrotoxic injury. Many potential markers have been studied. Promising injury markers in the urine include Neutrophil gelatinase-associated lipocalin (NGAL), Interleukin 18 (IL-18), Kidney injury molecule 1 (KIM-1), Liver fatty acid binding protein (L-FABP), β2-microglobulin, α1-microglobulin, Retinol Binding Protein,Cystatin-C, Microalbumin, Clusteri, Cysteine-Rich Protein, Osteopontin,Sodium/Hydrogen Exchanger Isoform and Fetuin A (Devarajan; 2008).
New biomarkers of kidney injury hold the promise of substantially improving the diagnostic approach to acute kidney injury. Adequately powered clinical studies of multiple biomarkers are needed to qualify the biomarkers before they can be fully adopted in clinical practice. Once adopted, more sensitive biomarkers of acute kidney injury hold the potential to transform the care of patients with renal disease(Parikh and Devarajan; 2008).