488 Serial Measures of the Fractional Excretion of Urea(FEurea), Fractional Excretion of Sodium(FEna) and the Urea/Creatinine Ratio(UCr) for Predicting Changes in Renal Function in Ambulatory Heart Failure Patients

2012 ◽  
Vol 28 (5) ◽  
pp. S279
Author(s):  
M. Saeed ◽  
V. Lim ◽  
A. Malik ◽  
F. Cordova ◽  
P. Tappia ◽  
...  
Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Susan J Cheng ◽  
Olga Laur ◽  
Alexander J Kula ◽  
Chukwuma O Onyebeke ◽  
Steven G Coca ◽  
...  

Background: In the setting of acute decompensated heart failure (ADHF), significant renal dysfunction (RD) is a common both at presentation and during treatment. The fractional excretion of urea (FeUrea) is often recommended to differentiate “pre-renal” from intrinsic RD in patients receiving diuretics. However, the intra-renal physiology regulating urea reabsorption theoretically should be affected by high dose loop diuretics which are commonly utilized in ADHF. Methods: Heart failure patients presenting to the Yale Transition Care Clinic who received treatment with loop diuretics were enrolled (n=64). Urine was collected at baseline and 60-90 minutes following administration of loop diuretics. Possible AKI was defined as a presenting serum creatinine ≥0.3 mg/dl above the lowest outpatient level in the prior 12 months. Results: Overall, 75.9% of the cohort had an estimated glomerular filtration rate < 60 ml/min/1.73m^2 and 66.7% met criteria for possible AKI. As would be expected in a sodium avid HF population, the mean pre-diuretic FeUrea was 31.9 ± 10.2%. This was below the “pre-renal” FeUrea cutoff (<35%) in 62.5% of patients. Following administration of 160 mg (50 to 280) of IV furosemide equivalents, FeUrea increased by an average of 7.3 ±8.5% (p<0.0001). After diuretics, the percentage of patients with a “pre-renal” FeUrea decreased to 37.7% which translated into 42.5% of initially “pre-renal” patients no longer being classified as “pre-renal.” The change in FeUrea was unrelated to the diuretic induced urine output (r=0.19 p=0.14) or the dose of diuretic (r=0.17, p=0.20). There was significant individual variability in the change in FeUrea induced by loop diuretics (Figure) such that a loop diuretic “correction factor” would not be appropriate. Conclusion: Contrary to traditional wisdom, FeUrea does not appear to be a reliable tool to workup changes in renal function in ADHF patients receiving treatment with high dose loop diuretics.


2012 ◽  
Vol 28 (6) ◽  
pp. 728-734 ◽  
Author(s):  
Akiomi Yoshihisa ◽  
Satoshi Suzuki ◽  
Takashi Owada ◽  
Shoji Iwaya ◽  
Hiroyuki Yamauchi ◽  
...  

2008 ◽  
Vol 295 (4) ◽  
pp. F1239-F1247 ◽  
Author(s):  
Alaa E. S. Abdel-Razik ◽  
Richard J. Balment ◽  
Nick Ashton

Urotensin II (UII) has been implicated widely in cardiovascular disease. The mechanism(s) through which it contributes to elevated blood pressure is unknown, but its emerging role as a regulator of mammalian renal function suggests that the kidney might be involved. The aim of this study was to determine the effect of UII on renal function in the spontaneously hypertensive rat (SHR). UII infusion (6 pmol·min−1·100 g body wt−1) in anesthetized SHR and control Wistar-Kyoto (WKY) rats produced marked reductions in glomerular filtration rate (ΔGFR WKY, n = 7, −0.3 ± 0.1 vs. SHR, n = 7, −0.6 ± 0.1 ml·min−1·100 g body wt−1, P = 0.03), urine flow, and sodium excretion rates, which were greater in SHR by comparison with WKY rats. WKY rats also showed an increase in fractional excretion of sodium (ΔFENa; +0.6 ± 0.1%, P = 0.02) in contrast to SHR in which no such change was observed (ΔFENa −0.6 ± 0.2%). Blockade of the UII receptor (UT), and thus endogenous UII activity, with urantide evoked an increase in GFR which was greater in SHR (+0.3 ± 0.1) compared with WKY rats (+0.1 ± 0.1 ml·min−1·100 g body wt−1, P = 0.04) and was accompanied by a diuresis and natriuresis. UII and UT mRNA expression were greater in the renal medulla than the cortex of both strains; however, expression levels were up to threefold higher in SHR tissue. SHR are more sensitive than WKY to UII, which acts primarily to lower GFR thus favoring salt retention in this model of hypertension.


2018 ◽  
Vol 24 (8) ◽  
pp. S26
Author(s):  
Devin Mahoney ◽  
Tariq Ahmad ◽  
Veena Rao ◽  
Meredith Brisco-Bacik ◽  
F. Perry Wilson ◽  
...  

2020 ◽  
Vol 7 (5) ◽  
pp. 2912-2921
Author(s):  
Toshitaka Okabe ◽  
Tadayuki Yakushiji ◽  
Takehiko Kido ◽  
Taro Kimura ◽  
Yu Asukai ◽  
...  

2018 ◽  
Vol 132 (18) ◽  
pp. 2071-2085 ◽  
Author(s):  
Chuan Chuan Ren ◽  
Wen Zhu ◽  
Qing Wei Wang ◽  
Yu Tao Lu ◽  
Yan Wang ◽  
...  

Congenital urinary tract obstruction is one of the most frequent malformations in fetuses or neonates, which usually causes profound impairment of renal function including reductions in both glomerular filtration rate (GFR) and tubular handling of water and solutes. Although obstruction can be released by surgical operation, the child will suffer from diuresis for sometime. It has been reported that erythropoietin (EPO) could prevent the down-regulation of aquaporin-2 (AQP2) and urinary-concentrating defects induced by renal ischemia/reperfusion (I/R) injury. However, whether EPO could promote the recovery of renal function and AQP2 expression after releasing of ureteral obstruction has not been reported yet. The purposes of the present study were to investigate the effects of EPO on renal function and AQP2 expression after release of bilateral ureteral obstruction (BUO-R) in rats. The results showed that EPO could promote interleukin (IL) 10 (IL-10) expression; inhibit tumor necrosis factor-α (TNF-α), IL-6, and inducible nitric oxide synthase (iNOS) expressions; reduce the fractional excretion of sodium (FENa) and plasma creatinine (CREA) and urea; and promote the recovery of water and salt handling and AQP2 expression in BUO-R rats, especially in the high dose of EPO-treated group rats. In conclusion, EPO could promote the recovery of renal function and AQP2 expression in BUO-R rats, which may partially associate with its anti-inflammation effect.


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