scholarly journals Daily Urinary Sodium Excretion Monitoring in Critical Care Setting: A Simple Method for an Early Detection of Acute Kidney Injury

2021 ◽  
Vol 0 (0) ◽  
pp. 0
Author(s):  
CarlosG Musso ◽  
Diana Silva ◽  
Fernanda Propato ◽  
Yeny Molina ◽  
María de losÁngeles Velez-Verbel ◽  
...  
Author(s):  
Lulu Kong ◽  
Di Fan ◽  
Lin Zhou ◽  
Shaohua Wei

Acute kidney injury (AKI) is a severe clinical disease with extremely high morbidity and mortality. It is challenging to find a simple method for early detection of AKI and monitoring...


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Ulla Toft ◽  
Charlotte Cerquira ◽  
Torben Jørgensen

Background: Tanaka et al (J Hum Hypert 2002; 16: 97-103) developed a simple method to estimate populational 24-h urinary sodium excretion using a casual urine specimen. However, this method was developed and validated in a Japanese population and thus this method might not be valid in populations that differ markedly from this population. Hypothesis: We assessed the hypothesis that the 24 hour urinary sodium excretion can be estimated from a casual spot urine using the Tanaka prediction method in a Danish general population. Methods: Overall 473 Danish individuals provided both a 24h urine collection and a spot urine sample. Data were collected in the Danthyr study (248 women aged 25-30 years and 60-65 years) and the Inter99 study (102 men and 113 women aged 30-60 years), respectively. Only participants with complete 24h urine collection (validated by the PABA method) were included. We compared the estimated daily sodium excretion through 24h urine (the gold standard) with the predicted 24 h sodium excretion from a causal urine specimen, using the Tanaka prediction method. Results: The predicted median 24 h sodium excretion (median [5 and 95 percentile]) was 8.6 gram [3.7;17.5] compared with a median measured 24 h sodium excretion of 8.9 [5.4; 13:1]. The mean (sd) residual (measured minus predicted 24 h sodium excretion) was 0.08 (3.7). The correlation (Spearman) between predicted and measured 24 h sodium excretion was 0.39 and the R 2 was 0.17. The proportion of individuals classified in the same or adjacent quintiles was 67%. Gross misclassification was found for 3% of the individuals. However, a Bland-Altman plot indicated a tendency of underestimation the sodium excretion for individuals with a high level of sodium excretion (>14 g per day). Conclusion: The Tanaka prediction model gives a reasonable estimate of sodium intake in a Danish population using casual spot urines. However, the validation study showed a tendency of underestimation of the sodium intake for individuals with a high sodium excretion (>14 g per day).


2008 ◽  
Vol 294 (6) ◽  
pp. F1473-F1480 ◽  
Author(s):  
Weidong Wang ◽  
Chunling Li ◽  
Sandra N. Summer ◽  
Sandor Falk ◽  
Wei Wang ◽  
...  

The effect of endotoxemia (lipopolysaccharide, 2.5 mg/kg ip) was investigated in aquaporin (AQP) 1 knockout (KO) compared with wild-type (WT) mice. At baseline, KO mice exhibited higher water intake (WI) and urine output (UO). After endotoxemia, WI and UO remained higher in the KO than WT mice, and urine osmolality was lower. The higher serum osmolality in AQP1-KO mice during endotoxemia was associated with higher AQP2 (133 ± 8 vs. 100 ± 3%, P < 0.01), AQP3 (140 ± 8 vs. 100 ± 4%, P < 0.001) and Na+-K+-2Cl− cotransporter type 2 (NKCC2; 152 ± 14 vs. 100 ± 15%, P < 0.05) expression than that in WT mice. These responses during endotoxemia in the AQP1-KO mice compared with WT were associated with lower glomerular filtration rate (GFR) (69 ± 8 vs. 96 ± 8 ml/min, P < 0.05) and renal blood flow (0.77 ± 0.1 vs. 1.01 ± 0.1 ml/min, P < 0.01). Urinary sodium excretion and fractional sodium excretion were higher in KO compared with WT mice in endotoxemia and were accompanied by more severe tubular injury. With water repletion and comparable serum osmolalities, GFR was still lower in KO (57 ± 13 vs. 120 ± 6 ml/min, P < 0.01) compared with WT during endotoxemia. The abundance of AQP2 and AQP3 protein in KO mice was not different from WT mice; however, NKCC2, Na+/H+ exchanger type 3, and fractional sodium excretion remained higher in KO compared with WT. Thus the polyuria in AQP1-KO mice does not protect against endotoxemia-induced acute kidney injury but rather absence of AQP1 predisposed to enhanced endotoximic renal injury.


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