Left Ventricular End-Diastolic Pressure and B-Type Natriuretic Peptide Levels Guidance of Low-Dose Furosemide Treatment to Prevent Contrast-Induced Nephropathy in Patients with Percutaneous Coronary Intervention: A Randomized Controlled Trial

Objective. We aimed to explore the preventive effect of low-dose furosemide administration guided by left ventricular end-diastolic pressure (LVEDP) and B-type natriuretic peptide (BNP) based on adequate hydration on contrast-induced nephropathy (CIN) in patients with percutaneous coronary intervention (PCI). Methods. This parallel randomized clinical trial was conducted at a tertiary hospital in China. A total of 1053 consecutive patients (71.98% men) who underwent PCI at our hospital were enrolled. Pre-PCI plasma BNP levels were recorded. Patients enrolled received a continuous intravenous infusion of normal saline starting 4 h before PCI until 24 h after surgery. LVEDP was measured immediately after surgery. Patients in the control group received intravenous furosemide injection (20 mg). Patients in the experimental group received furosemide if they showed LVEDP ≥15 mmHg, a post-PCI BNP level ≥100 pg/mL, and/or a post-PCI BNP value > 150% of the pre-PCI value. The primary and secondary outcome measures were serum creatinine levels, glomerular filtration rate, and creatinine clearance rate measured before and after PCI. CIN incidence was compared between the two groups. Logistic regression analysis was used to study the risk factors for CIN. Results. CIN incidence was significantly higher in the control group than in the experimental group ( P < 0.05 ). Logistic regression analysis showed that elevated LVEDP and BNP levels were risk factors. As LVEDP increased, the CIN incidence also increased (odds ratio (OR) 1.038, 95% confidence interval (CI) 1.006–1.070). The OR of BNP was 1.001 (95% CI 1.000–1.002). Conclusions. Low-dose furosemide administration guided by LVEDP or BNP is superior to direct low-dose administration on the basis of adequate hydration during PCI. This trial is registered with ChiCTR-IOR-14005250

The retrospective study of perioperative application of dexamethasone and furosemide for postoperative anti-inflammation in patients undergoing percutaneous nephrolithotomy

Objectives To investigate whether the perioperatively combined application of dexamethasone and furosemide could alleviate the inflammation in patients undergoing percutaneous nephrolithotomy (PCNL). Patients and methods 147 patients undergoing PCNL between November 2018 and October 2019 were enrolled in the study. 77 patients accepted a single dose of dexamethasone and furosemide administration (EXP group, n = 77), and 70 patients did not (CON group, n = 70). Demographic and perioperative data, inflammatory markers including interleukin-6 (IL-6) and procalcitonin (PCT), and clinical outcomes were compared between the two groups. Results Compared with the CON group, the incidence rate of urosepsis of the EXP group were significantly lower (11.69% vs. 24.29%, p = 0.046). 3 patients developed severe urosepsis in the EXP group, while 5 patients developed severe urosepsis in the CON group. Compared with those in the CON group, the patients with postoperative urosepsis in the EXP group showed lower serum levels of IL-6 at postoperative hour two (p = 0.045) and at postoperative day one (p = 0.031) and lower serum levels of PCT at postoperative day one (p = 0.015). There was a better clinical outcome of a shorter postoperative hospital stay (p = 0.015) in patients with postoperative urosepsis in the EXP group than in those in the CON group. Conclusion The perioperatively combined application of dexamethasone and furosemide was beneficial for alleviating postoperative inflammatory reaction and caused a better clinical outcome of a shorter postoperative hospital stay.

Prognosis of acute kidney injury during acute heart failure: the role of diuretics

Background Acute kidney injury (AKI) frequently occurs after diuretic treatment initiation during acute heart failure (AHF). Treatment-induced hemoconcentration seems associated with improved prognosis. Transient AKI, with or without hemoconcentration, is of unsettled prognosis. Purpose We aimed to determine the independent prognostic values of transient AKI, persistent AKI and hemoconcentration in the context of hospitalized AHF. Methods Data were obtained from our institution's Clinical Data Warehouse. Patients that visited our unit at least once were screened. All hospitalizations in our institution were examined (&gt;30 hospitals). Inclusion criteria were: ≥1 hospitalization with ≥1 recorded furosemide administration and ≥1 AHF ICD-10 code. Only the first hospitalization fulfilling these criteria was considered. AKI during 1–13 days following first furosemide administration was defined based on Kidney Disease Improving Global Outcome guidelines. Hemoconcentration was defined as an increase in serum proteins ≥5 g/l during the same period. We performed multivariate logistic regression to determine which characteristics were predictive of AKI. We used Cox regression of 100-days all-cause mortality using several confounders to determine the prognostic values of transient AKI (lasting &lt;14 days), persistent AKI (lasting ≥14 days) and hemoconcentration. To account for immortality bias, AKI and hemoconcentration were treated as time-dependent covariates. Results We included 579 patients in the study. Median follow-up was 114 days. AKI following furosemide initiation occurred in 234 patients (40.4%). Patients that experienced AKI more frequently suffered from chronic kidney disease (43.6% vs. 33%, p=0.01) or presented with right ventricular dilatation (12% vs. 6.7%, p=0.04). Independent predictors of AKI were arterial hypertension (adjusted OR: 1.86 [1.08–3.22]), elevated serum creatinine at baseline (adjusted OR: 1.07 [1.01–1.14] per 10 μmol/l increase) and initial intravenous furosemide (adjusted OR: 2.42 [1.39–4.29]). Death during follow-up occurred in 35% of patients in the AKI group compared to 21% in the non-AKI group (p&lt;0.001). In Cox regression, persistent AKI was independently associated with increased mortality in a period of 100 days following furosemide initiation (adjusted HR: 2.31 [1.07–4.99]). Transient AKI was not significantly associated with mortality (adjusted HR: 0.64 [0.34–1.19]). Hemoconcentration was independently associated with decreased mortality (adjusted HR: 0.46 [0.27–0.79]). Conclusion In the context of hospitalized AHF, AKI that developed 1–13 days after furosemide initiation and that lasted ≥14 days was independently associated with decreased 100 days survival. Hemoconcentration, using a clinically relevant definition, was independently associated with improved survival. These findings show that serum creatinine and proteins, routinely used and with limited cost, accurately stratify mortality risk during AHF. Kaplan-Meier curves Funding Acknowledgement Type of funding source: None

TO019PROGNOSTIC VALUE OF ACUTE KIDNEY INJURY AND HEMOCONCENTRATION DURING ACUTE HEART FAILURE

Background and Aims Acute kidney injury (AKI) occurring after diuretic treatment initiation for acute heart failure (AHF) is a common phenomenon, with an incidence estimated between 20 and 50% of AHF hospitalizations. Previous studies found that persistent AKI is associated with poor prognosis. Treatment-induced hemoconcentration is associated with improved prognosis, but several definitions previously used are not suited for clinical practice. Transient AKI, with or without hemoconcentration, is of unsettled prognosis. We aim to determine the independent prognostic value of transient AKI, persistent AKI and hemoconcentration in the context of AHF hospitalization, using practical definitions. Method Data were obtained from the Greater Paris University Hospitals (GPUH) Clinical Data Warehouse. Patients hospitalized for AHF in various GPUH units were included. AHF hospitalization was defined as hospitalization with at least one AHF ICD-10 code and at least one recorded furosemide administration. Bumetanide is rarely used in GPUH hospitals hence it was not considered. AKI in a period of 14 days following first furosemide administration was defined based on KDIGO guidelines. Hemoconcentration was defined as an increase in serum proteins ≥ 5 g/l during the same period. Multivariate logistic regression was performed to determine which characteristics were predictive of AKI. Cox regression of 100 days all-cause mortality using multiple confounders was performed to determine the prognostic value of transient AKI (&lt; 14 days), persistent AKI (≥ 14 days) and hemoconcentration. Patients with AKI upon hospital entry were excluded from regression analyses. AKI and hemoconcentration were treated as time-dependent covariates to adjust for immortality bias. Results Five hundred seventy nine patients were included. Among them, 529 had no AKI upon hospital entry and 513 had at least one recorded serum proteins and creatinine value following furosemide initiation. Median follow-up was 114 days. AKI in a period of 14 days following furosemide initiation occurred in 234 patients (40.4%). At baseline, patients in the AKI group more frequently suffered from chronic kidney disease or presented with clinical and echocardiographic signs of right heart failure. Independent predictors of AKI were arterial hypertension upon furosemide initiation (adjusted OR 1.86 [1.08 – 3.22]), elevated serum creatinine upon furosemide initiation (adjusted OR 1.07 [1.01 – 1.14] per 10 µmol/l increase) and initial intravenous administration of furosemide (adjusted OR 2.42 [1.39 – 4.29]). Death during follow-up occurred in 35% of patients in the AKI group compared to 21% in the non-AKI group (p &lt; 0.001). In multivariate analysis, persistent AKI was independently associated with increased mortality in a period of 100 days following furosemide initiation (adjusted HR 2.31 [1.07 – 4.99]). Transient AKI was not significantly associated with mortality (adjusted HR 0.64 [0.34 – 1.19]). Hemoconcentration was independently associated with decreased mortality (adjusted HR 0.46 [0.27 – 0.79]). Conclusion After furosemide initiation during hospitalization for AHF, persistent AKI (≥ 14 days) was independently associated with increased 100 days mortality. Hemoconcentration, using a definition suited for clinical practice (≥ 5 g/l increase in serum proteins), was independently associated with decreased 100 days mortality. No significant association was found between mortality and transient AKI (&lt; 14 days). Those findings show that laboratory tests at a limited cost – serum proteins and creatinine – are helpful to evaluate treatment response and mortality risk during AHF. Prospective randomized controlled trials are needed to establish diuretic strategies based on both AKI and hemoconcentration.

Effect of Furosemide on Urinary Oxygenation in Patients with Septic Shock

Background: Renal medullary hypoxia precedes the development of acute kidney injury in experimental sepsis and can now be assessed by continuous measurement of urinary oxygen tension (PuO2). Objectives: We aimed to test if PuO2 measurements in patients with septic shock would be similar to those shown in experimental sepsis and would detect changes induced by the administration of furosemide. Method: Pilot prospective observational cohort study in a tertiary intensive care unit (ICU). Seven adult patients with septic shock admitted to ICU had PuO2 measurements recorded minutely. There were 29 episodes of intravenous furosemide (20 mg n = 19; 40 mg n = 10). Results: The median pre-furosemide PuO2 was low at 21.2 mm Hg (interquartile range [IQR] 17.73–24.86) and increased to 26 mm Hg (IQR 20.27–29.95) at 20 min (p < 0.01), to 27.5 mm Hg (IQR 24.06–33.18) at 40 min (p < 0.01) and to 28.5 mm Hg (IQR 22.65–31.03) at 60 min (p < 0.01). The increase in PuO2 was greater in episodes with a diuretic response >2 mL/kg/h than during episodes without such a response (p < 0.01). Conclusions: PuO2 measurements in patients are reflective of the low values reported in experimental models of sepsis. PuO2 values increased following furosemide administration with a response independently associated with greater diuresis.