Kidney international
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Kidney international · Dec 2010
CommentKlotho in acute kidney injury: biomarker, therapy, or a bit of both?
Acute kidney injury (AKI) diagnosis is based on an increase in serum creatinine or a decrease in urine output. To be effective, treatment of AKI should be started very early after the insult and well before the rise of serum creatinine. Thus, sensitive biologic markers of renal tubular injury in AKI are strongly needed. Hu et al. suggest that Klotho could be a novel biomarker and therapeutic target of ischemia-induced AKI.
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Kidney international · Nov 2010
The duration of postoperative acute kidney injury is an additional parameter predicting long-term survival in diabetic veterans.
Acute kidney injury (AKI) is primarily defined and staged according to the magnitude of the rise in serum creatinine. Here we sought to determine if the duration of AKI adds additional prognostic information above that from the magnitude of injury alone. We prospectively studied 35,302 diabetic patients from 123 Veterans Affairs Medical Centers undergoing their first noncardiac surgery. ⋯ However, within each of the duration categories, the stage was not associated with mortality. When considered separately in multivariate analyses, both a higher stage and duration were independently associated with increased risk of long-term mortality. Hence, the duration of AKI adds additional information to predict long-term mortality.
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Kidney international · Oct 2010
Acute kidney injury following coronary angiography is associated with a long-term decline in kidney function.
To determine whether acute kidney injury results in later long-term decline in kidney function we measured changes in kidney function over a 3-year period in adults undergoing coronary angiography who had serum creatinine measurements as part of their clinical care. Acute kidney injury was categorized by the magnitude of increase in serum creatinine (mild (50-99% or >or=0.3 mg/dl) and moderate or severe (>or=100%)) within 7 days of coronary angiography. ⋯ Among those with an estimated glomerular filtration rate after angiography less than 90 ml/min per 1.73 m(2), the subsequent adjusted mean rate of decline in estimated glomerular filtration rate during long-term follow-up (all normalized to 1.73 m(2) per year) was 0.2 ml/min in patients without acute kidney injury, 0.8 ml/min following mild injury, and 2.8 ml/min following moderate to severe acute kidney injury. Thus, acute kidney injury following coronary angiography is associated with a sustained loss and a larger rate of future decline in kidney function.
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Kidney international · Sep 2010
CommentUrinary kidney injury biomarkers and urine creatinine normalization: a false premise or not?
Substantial research has focused on the discovery of urinary biomarkers to detect acute kidney injury (AKI) before a rise in serum creatinine. As in chronic kidney diseases, the concentrations of urinary AKI biomarkers have been normalized to urine creatinine concentration to account for creatinine clearance and urine flow. Waikar et al. challenge the assumption that normalization to creatinine clearance in a chronic disease state can be extrapolated to an acute state, in which creatinine clearance is, by definition, changing acutely.
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Kidney international · Aug 2010
Comparative StudyUrinary CD80 is elevated in minimal change disease but not in focal segmental glomerulosclerosis.
Controversy exists as to whether minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) represent different diseases or are manifestations within the same disease spectrum. Urinary excretion of CD80 (also known as B7.1) is elevated in patients with MCD and hence we tested whether urinary CD80 excretion might distinguish between patients with MCD from those with FSGS. Urinary CD80 was measured in 17 patients with biopsy-proven MCD and 22 with proven FSGS using a commercially available enzyme-linked immunosorbent assay and its molecular size determined by western blot analysis. ⋯ No CD80 was found in glomeruli of two patients with FSGS and another MCD patient in remission. Thus, our study supports the hypothesis that MCD and FSGS represent two different diseases rather than a continuum of one disease. Urinary CD80 excretion may be a useful marker to differentiate between MCD and FSGS.