ライフサイエンスコーパス: prerenal

1 Our results suggest that the classical "prerenal acute kidney injury" and "acute tubular necrosi

2 higher in intrinsic AKI (1955 ng/mL) than in prerenal AKI (P < 0.001).

3 torenal syndrome (HRS), a functional type of prerenal AKI exclusive of cirrhosis that does not respon

4 trenal causes of AKI and aid in diagnosis of prerenal AKI through volume assessment.

5 sis are prerenal azotemia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal s

6 Thirty-five patients (21.6%) had prerenal AKI, 64 (39.5%) HRS-AKI, 27 (16.7%) acute tubul

7 ) in the differentiation of intrinsic versus prerenal AKI.

8 ng biomarker for the differentiation between prerenal and intrinsic acute kidney injury (AKI) in the

9 omising biomarker for the differentiation of prerenal and intrinsic acute renal allograft failure.

10 The clinical differentiation of prerenal and intrinsic graft failure was performed eithe

11 The causes of AKI were prerenal azotemia (68.6 %), acute tubular necrosis (25.7

12 0), hepatorenal syndrome (HRS) (n = 18), and prerenal azotemia (PRA) (n = 22).

13 common etiologies of AKI in this setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), a

14 d interchangeably with AKI) in cirrhosis are prerenal azotemia (volume-responsive prerenal AKI), acut

15 the role of arterial underfilling in causing prerenal azotemia in the presence of an increase in tota

16 stinguish acute injury from normal function, prerenal azotemia, and chronic kidney disease and predic

17 kidney injury from chronic kidney disease or prerenal azotemia.

18 restriction, resulting in susceptibility to prerenal azotemia.

19 eed to be developed to systematically manage prerenal conditions and specific infections.

20 f acute renal failure in children, including prerenal disease, intrinsic renal failure, which include

21 samples from mice with intrarenal (maleate), prerenal (endotoxemia), or postrenal (ureteral obstructi

22 healthy controls (54.8 ng/mL, P = 0.70) and prerenal graft failure (53.8 ng/mL, P = 0.62).

23 ses of intrinsic acute allograft failure, 27 prerenal graft failures, 118 patients with stable graft

24 The present finding that odorants comprising prerenal odortypes are already present in blood, albeit

25 However, pure prerenal physiology is unusual in hospitalized patients,

26 and classification of these abnormalities as prerenal will undoubtedly lead to incorrect management d