RESUMO
BACKGROUND: Renal dysfunction is a common complication after heart transplantation (Htx). Glomerular filtration rate (GFR) can be assessed by various estimating equations (eGFR). We evaluated the correlation, agreement, and accuracy between eGFR and mGFR and the ability of eGFR to track changes in mGFR early after Htx. METHODS: A single-center prospective observational study on 55 patients undergoing Htx. Serum creatinine and mGFR (plasma clearance of Cr51-EDTA or iohexol) were measured preoperatively and on the fourth postoperative day. The accuracy of eGFR to predict true mGFR was calculated as the percentage of patients with an eGFR within 30% of mGFR (P30). The agreement between eGFR and mGFR was assessed according to Bland and Altman. A four-quadrant plot was made to evaluate the ability of eGFR to track changes in mGFR. RESULTS: The accuracy of eGFR to assess mGFR was 52%. The bias was 11.2 ± 17.4 mL/min/1.72 m2. The limits of agreement were -23.0 to 45.4 mL/min/1.72 m2 and the error 58%. The concordance rate between eGFR and mGFR was 72%. CONCLUSIONS: eGFR underestimated mGFR and the agreement between eGFR and mGFR was low with an unacceptably large between-group error and low accuracy. Furthermore, the ability of eGFR to assess changes in mGFR, postoperatively, was poor. Thus, the use of estimating equations from serum creatinine will not adequately assess renal function early after major heart surgery. To gain adequate information on renal function early after Htx, GFR needs to be measured, not estimated.
Assuntos
Transplante de Coração , Humanos , Creatinina , Taxa de Filtração Glomerular , Estudos Prospectivos , RimRESUMO
BACKGROUND: Acute kidney injury (AKI) and renal dysfunction after heart transplantation are common and serious complications. Atrial natriuretic peptide (ANP) has been shown to increase glomerular filtration rate (GFR) and exert renoprotective effects when used for the prevention/treatment of AKI in cardiac surgery. We tested the hypothesis that intraoperative and postoperative administration of ANP could prevent a postoperative decrease in renal function early after heart transplantation. METHODS: Seventy patients were randomized to receive either ANP (50 ng/kg/min) (n = 33) or placebo (n = 37) starting after induction of anesthesia and continued for 4 days after heart transplantation or until treatment with dialysis was started. The primary end-point of the present study was measured GFR (mGFR) at day 4, assessed by plasma clearance of a renal filtration marker. Also, the incidence of postoperative AKI and dialysis were assessed. RESULTS: Median (IQR) mGFR at day 4 postoperatively was 60.0 (57.0) and 50.1 (36.3) ml/min/1.72 m2 for the placebo and ANP groups, respectively (p = .705). During ongoing ANP infusion, the need for dialysis was 21.6% and 9.1% for the placebo and ANP groups, respectively (p = .197). The incidences of AKI for the placebo and the ANP groups were 76.5% and 63.6%, respectively (p = .616). The incidences of AKI stage 1 were 32.4% and 21.2% for the placebo and ANP groups, respectively (p = .420) and for AKI stage 2 or 3, 37.8% and 42.4%, respectively (p = .808). CONCLUSION: The study failed to detect that ANP infusion attenuates renal dysfunction or decreases the incidence of AKI after heart transplantation.
Assuntos
Injúria Renal Aguda , Procedimentos Cirúrgicos Cardíacos , Transplante de Coração , Humanos , Fator Natriurético Atrial/uso terapêutico , Fator Natriurético Atrial/farmacologia , Transplante de Coração/efeitos adversos , Injúria Renal Aguda/epidemiologia , Injúria Renal Aguda/etiologia , Injúria Renal Aguda/prevenção & controle , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Taxa de Filtração Glomerular , RimRESUMO
BACKGROUND: Acute kidney injury (AKI) is a common and serious complication after cardiac surgery, and current strategies aimed at treating AKI have proven ineffective. Levosimendan, an inodilatating agent, has been shown to increase renal blood flow and glomerular filtration rate in uncomplicated postoperative patients and in patients with the cardiorenal syndrome. We hypothesized that levosimendan through its specific effects on renal vasculature, a preferential vasodilating effect on preglomerular resistance vessels, could improve renal function in AKI-patients with who did not have clinical indication for inotropic support. METHODS: In this single-center, double-blind, randomized controlled study, adult patients with postoperative AKI within 2 days after cardiac surgery, who were hemodynamically stable with a central venous oxygen saturation (ScvO2) ≥ 60% without inotropic support were eligible for inclusion. After randomization, study drug infusions, levosimendan (n = 16) or placebo (n = 13) were given for 5 h. A bolus infusion of levosimendan (12 µg/kg), were given for 30 min followed by 0.1 µg/kg/min for 5 h. Renal blood flow and glomerular filtration rate were measured using infusion clearance of para-aminohippuric acid and a filtration marker, respectively. As a safety issue, norepinephrine was administered to maintain mean arterial pressure between 70-80 mmHg. Intra-group differences were tested by Mann-Whitney U-tests, and a linear mixed model was used to test time and group interaction. RESULTS: Twenty-nine patients completed the study. At inclusion, the mean serum creatinine was higher in the patients randomized to levosimendan (148 ± 29 vs 127 ± 22 µmol/L, p = 0.030), and the estimated GFR was lower (46 ± 12 vs 57 ± 11 ml/min/1.73 m2, p = 0.025). Levosimendan induced a significantly (p = 0.011) more pronounced increase in renal blood flow (15%) compared placebo (3%) and a more pronounced decrease in renal vascular resistance (- 18% vs. - 4%, respectively, p = 0.043). There was a trend for a minor increase in glomerular filtration rate with levosimendan (4.5%, p = 0.079), which did differ significantly from the placebo group (p = 0.440). The mean norepinephrine dose was increased by 82% in the levosimedan group and decreased by 29% in the placebo group (p = 0.012). CONCLUSIONS: In hemodynamically stable patients with AKI after cardiac surgery, levosimendan increases renal blood flow through renal vasodilatation. Trial registration NCT02531724, prospectly registered on 08/20/2015. https://clinicaltrials.gov/ct2/show/NCT02531724?cond=AKI&cntry=SE&age=1&draw=2&rank=1.
Assuntos
Injúria Renal Aguda/tratamento farmacológico , Circulação Renal/efeitos dos fármacos , Simendana/farmacologia , Injúria Renal Aguda/fisiopatologia , Adulto , Idoso , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Procedimentos Cirúrgicos Cardíacos/métodos , Método Duplo-Cego , Feminino , Taxa de Filtração Glomerular/efeitos dos fármacos , Humanos , Masculino , Pessoa de Meia-Idade , Placebos , Simendana/efeitos adversos , Estatísticas não Paramétricas , Suécia , Vasodilatadores/efeitos adversos , Vasodilatadores/farmacologiaRESUMO
OBJECTIVE: To investigate the correlation between invasively measured renal venous oxygen saturation (SrvO2) and tissue oxygenation (rSO2) measured with near-infrared spectroscopy (NIRS) in adult patients undergoing cardiac surgery. DESIGN: Prospective observational study. SETTING: Single cardiac surgery center at a university hospital. PARTICIPANTS: Thirteen adult patients with skin- to- kidney distance ≤4 cm undergoing open cardiac surgery with cardiopulmonary bypass (CPB). INTERVENTIONS: All patients received renal vein catheters for invasive measurement of SrvO2, and NIRS electrodes for assessment of renal rSO2 were placed over the kidney using ultrasound guidance. Measurements were made before CPB, during CPB at 3 different flow rates (2.4, 2.7, and 3.0 L/min/m2), and after CPB. MEASUREMENTS AND MAIN RESULTS: Repeated- measures correlation analyses and Bland-Altman plots were used to study the correlation and agreement between rSO2 and SrvO2. For all measurement points, renal rSO2 correlated with SrvO2 (rrm = 0.61, p < 0.001), and the mean difference (bias) between rSO2 and SrvO2 was -2.71 ± 7.22 (p = 0.002), with an error of 17.6%. When measurements during CPB and before and after CPB were studied separately, rSO2 and SrvO2 were correlated (rrm = 0.51, p < 0.007 and rrm = 0.73, p < 0.001, respectively). During CPB, renal rSO2 predicted SrvO2 with a bias of -3.41 ± 7.76 (p = 0.009) and an error of 18.8%. Before and after CPB, the mean difference was -1.93 ± 6.60 (p = 0.092), with an error of 16.2%. CONCLUSIONS: Renal rSO2 is correlated to and predicts SrvO2 with a small bias and acceptable agreement. Further studies are needed before renal NIRS can be used as a surrogate marker of renal oxygenation in clinical practice.
Assuntos
Procedimentos Cirúrgicos Cardíacos , Espectroscopia de Luz Próxima ao Infravermelho , Adulto , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Ponte Cardiopulmonar , Humanos , Rim/diagnóstico por imagem , Oximetria , OxigênioRESUMO
OBJECTIVES: Acute kidney injury is a well-known complication after cardiac surgery and cardiopulmonary bypass (CPB). In this experimental animal study, we evaluated the effects of atrial natriuretic peptide (ANP) on renal function, perfusion, oxygenation and tubular injury during CPB. METHODS: Twenty pigs were blindly randomized to continuous infusion of either ANP (50 ng/kg/min) or placebo before, during and after CPB. Renal blood flow as well as cortical and medullary perfusion was measured. Blood was repeatedly sampled from the renal vein. Glomerular filtration rate was measured by infusion clearance of 51Cr-EDTA. RESULTS: Glomerular filtration rate was higher (P < 0.001), whereas renal blood flow or renal oxygen delivery was not affected by ANP during CPB. Renal oxygen consumption did not differ between groups during CPB, whereas renal oxygen extraction was higher in the ANP group (P = 0.03). Urine flow and sodium excretion were higher in the ANP group during CPB. Blood flow in the renal medulla, but not in the cortex, dropped during CPB, an effect that was not seen in the animals that received ANP. CONCLUSIONS: ANP improved renal function during CPB. Despite impaired renal oxygenation, ANP did not cause tubular injury, suggesting a renoprotective effect of ANP during CPB. Also, CPB induced a selectively reduced blood flow in the renal medulla, an effect that was counteracted by ANP.