New markers for kidney disease.
نویسندگان
چکیده
There is ominous growth in chronic kidney disease among the US population, primarily related to type 2 diabetes (1 ). The current number of patients on dialysis ( 300 000) is growing steadily as the prevalence of endstage kidney disease grows geometrically with a doubling time of 10 years. The epidemic growth in diabetes, the leading cause of chronic kidney disease, portends continuation of this trend (2 ). Most patients with end-stage kidney disease will end up on dialysis because the supply of kidneys for transplants is limited to 13 000 per year. A further warning sign from the National Health and Nutrition Examination survey is that an estimated 8 million Americans have a 50% reduction of their glomerular filtration rate (GFR) (3 ). This group with impaired kidney function is at risk for progression to endstage kidney disease as well as for development of cardiovascular disease. One source of hope for stemming the dire trends in kidney disease is progress in the treatment of impaired kidney function, if it is detected and treated early (1, 2). A recent initiative, termed the National Kidney Disease Education Program, seeks to increase public awareness for preventive therapy. Increased awareness will create new demands on laboratories for early and more sensitive detection of kidney disease and for identification of new laboratory markers, such as one evaluated in this issue of the Journal (4 ). With the recent development of new genomic and proteomic approaches, there is also the potential for identification of many new markers requiring evaluation. The laboratory marker that has long served as the mainstay for detecting impaired kidney function is serum creatinine. Unfortunately, serum creatinine is an insensitive marker of kidney injury. Two factors underlie this insensitivity. The first factor is that the reference interval is relatively wide because it must encompass a large range of creatinine production, which is related to muscle mass. The second factor is that the inverse relationship between GFR and serum creatinine predicts that large reductions in GFR from normal produce only small absolute increases in serum creatinine. Indeed, for small or elderly people with small muscle mass, serum creatinine will remain within the usual reference limits despite substantial kidney damage. Direct measurements of creatinine clearance are not an ideal solution to the shortcomings of serum creatinine because these results often are made inaccurate by tubular creatinine secretion and by errors in specimen collection (5 ). Measurement of creatinine clearance can be useful in patients on a vegetarian diet or with low muscle mass attributable to amputation or severe malnutrition. Measurement of the renal clearance of infused tracers such as inulin, iothalamate, or iohexol can provide accurate measurements of GFR, but they are too costly and cumbersome for routine clinical use. The Kidney Disease Outcome Quality Initiative recently proposed that diagnosis and monitoring of chronic kidney disease should be based on calculated estimates of GFR (5 ). Several formulas have been developed for calculating GFR based on serum creatinine; one of the best-validated examples accounts for influences of age, gender, and race:
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عنوان ژورنال:
- Clinical chemistry
دوره 48 9 شماره
صفحات -
تاریخ انتشار 2002