Objectives
To test the hypothesis that, without diagnostic changes in serum creatinine, increased NGAL levels identify patients with subclinical acute kidney injury (AKI) and, therefore, worse prognosis.
Background
Neutrophil gelatinase-associated lipocalin (NGAL) detects subclinical AKI hours to days before increases in serum creatinine indicate manifest loss of renal function.
Methods
We analyzed pooled data from 2,322 patients with cardiorenal syndrome type 1 from ten prospective observational studies of NGAL. We used the terms NGAL(−) or NGAL(+) according to study-specific NGAL cut-off for optimal AKI prediction and the terms sCREA(−) or sCREA(+) to consensus diagnostic increases in serum creatinine defining AKI. A-priori-defined outcomes included need for renal replacement therapy (primary endpoint), hospital mortality, their combination and duration of stay in intensive care and in-hospital.
Results
Of study patients, 1,296 (55.8%) were NGAL(−)/sCREA(−), 445 (19.2%) NGAL(+)/sCREA(−), 107 (4.6%) NGAL(−)/sCREA(+) and 474 (20.4%) NGAL(+)/sCREA(+). According to the four study groups, there was a stepwise increase in subsequent renal replacement therapy initiation, (NGAL(−)/sCREA(−): 0.0015% vs. NGAL(+)/sCREA(−): 2.5% [odds ratio 16.4, 95% CI 3.6–76.9, P<0.001], NGAL(−)/sCREA(+): 7.5% and NGAL(−)/sCREA(−): 8.0%, respectively), hospital mortality (4.8%, 12.4%, 8.4%, 14.7%, respectively) and their combination (four-group comparisons: all P<0.001). There was a similar and consistent progressive increase in median number of intensive care and in-hospital days with increasing biomarker positivity: NGAL(−)/sCREA(−): 4.2 and 8.8 days; NGAL(+)/sCREA(−): 7.1 and 17.0 days; NGAL(−)/sCREA(+): 6.5 and 17.8 days; NGAL(+)/sCREA(+): 9.0 and 21.9 days; four-group comparisons: P=0.003 and P=0.040, respectively. Urine and plasma NGAL indicated a similar outcome pattern.
Conclusions
In the absence of diagnostic increases in serum creatinine, NGAL detects patients with subclinical AKI who have an increased risk of adverse outcomes. The concept and definition of AKI may need re-assessment.
Nonmeckelian jejunoileal diverticula (JID) are rare, but potentially clinically significant lesions. Despite recent advances in modern diagnostic modalities, diagnosis of JID may be problematic. Upper gastrointestinal contrast series with small bowel follow-through examination and mainly enteroclysis are the 2 main diagnostic methods. In selected cases (mainly complicated JID), the physician could use other diagnostic methods, such as ultrasound, computed tomography, endoscopy, intraoperative endoscopy, laparoscopy, radiotagged erythrocyte bleeding scans, and selective mesenteric arteriography. JID may be clinically silent or symptomatic causing chronic pain or malabsorption or other acute complications, such as hemorrhage, inflammation, perforation, etc. Laparotomy remains the gold standard for definite diagnosis of asymptomatic and complicated diverticula. Treatment should be individualized. Surgery could be indicated, mainly in symptomatic diverticula. The extent of resection may be a problem, especially in patients with extensive disease involving large parts of the bowel. In these cases, clinical judgment is required from the part of surgeon to avoid short bowel syndrome.
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