Active clinical trials for "Acute Kidney Injury"

Background: Acute kidney injury (AKI) often occurs after thoracoscopic lobectomy in high risk patients. Insufficient intraoperative infusion is risk factor of AKI. Goal-directed fluid therapy (GDFT) is individualized fluid infusion strategy, the infusion rate and type is adjusted according to the individual's fluid response. GDFT during operation can reduce the incidence of AKI after major surgery. Enhanced recovery after surgery (ERAS) integrates a range of perioperative interventions to decrease postoperative complications after surgery. In ERAS protocol of lobectomy, restrictive fluid therapy during operation is recommended. In this study, the investigators will compare the effects of GDFT and restrictive fluid therapy during operation combined with ERAS protocol on the incidence of AKI after thoracoscopic lobectomy in high risk patients. Methods/design: This is prospective single-center single-blind randomized controlled trial. 276 patients scheduled to undergo thoracoscopic lobectomy under general anesthesia combined with paravertebral block are randomly divided into GDFT group and restrictive fluid therapy group at a 1:1 ratio. The primary outcome is the incidence of AKI after operation. The secondary outcomes are (1) the incidence of renal replacement therapy, (2) length of intensive care unit (ICU) stay after operation, (3) length of hospital stay after operation , (4) incidence of other complications including: infection, acute lung injury (ALI), pneumonia, arrhythmia, heart failure, myocardial injury after noncardiac surgery (MINS), cardiac infarction. Discussion: This is the first study to compare GDFT and restrictive fluid therapy during operation combined with ERAS protocol on the incidence of AKI after thoracoscopic lobectomy in high risk patients. The investigators expected that the two methods have the same effect on the incidence of AKI, but restrictive fluid therapy is simpler to applied than GDFT.

In recent years there has been a significant increase in the number of participants in high intensity and duration sports events. This type of physical exercise has been reported to lead to an apparently transitory deterioration in kidney function. The injury mechanisms involved in this process have not been fully studied, but several have been proposed as potential causes, such as tissue ischemia, disruption of the permeability of the glomerular basement membrane, damage to the ultra-structure of skeletal muscle, structural involvement of the renal parenchyma, exercise-associated hyperthermia or insufficient hydration during exercise. Urinary biomarkers, which are a more precise tool than serum creatinine when it comes to detecting subclinical kidney damage, may be key to elucidate the characteristics of exercise-related kidney injury. The aim of this study is to carry out an integrative analysis of the development of exercise-associated subclinical acute kidney injury.

The aim of this study is to detect early renal dysfunction that may occur during the surgical procedure in geriatric patients who will undergo laparotomy surgery. In elderly patients undergoing surgery, accurate estimation of organ function is often not possible. Accurate measurement of kidney function is vital to the routine care of patients. Determining kidney function status can predict the progression of kidney disease and prevent toxic drug levels in the body.The biochemical marker creatinine, found in serum and urine, is widely used in the estimation of GFR. Although glomerular filtration rate decreases with aging, creatinine also decreases in the elderly due to muscle loss. Even moderately elevated blood creatinine may be indicative of severe kidney failure. Creatinine clearance (CrCl) is the volume of blood plasma cleared of creatinine per unit time. It is a fast and cost-effective method for measuring kidney function. Creatine is a breakdown product of creatine phosphate found in skeletal muscle. Its production in the body depends on muscle mass. The CrCl ratio approximates the GFR calculation as it freely filters the glomerular creatine. High serum creatinine levels and decreased CrCl ratio are usually indicators of abnormal kidney function.One of the markers of acute kidney injury is to look at plasma NGAL values. Plasma NGAL (neutrophil gelatinase associated lipocalin) increases in response to damaged kidney status and can predict acute kidney injury as an early marker. Data on investigating plasma NGAL values as a predictive biomarker of acute kidney injury in patients undergoing non-cardiovascular surgery are very limited NGAL is produced from the epithelium of kidneys, lungs, colon, liver, adipose tissue, and inflammatory cells. NGAL is elevated in serum and urine after acute tubular injury, making it possible to diagnose kidney damage within 2 hours of injury. However, the increase of other traditional markers such as creatinine may be delayed for up to 48 hours after acute kidney injury.To determine the roles of primary outcome serum creatinine, creatinine clearance rates and plasma NGAL levels in the diagnosis of acute renal failure

Acute kidney injury (AKI) is a common problem encountered in the intensive care unit (ICU), estimated to occur in up to 60% of all critically ill patients, depending on the definition. Recent large randomized clinical trials in critical care nephrology have focused on the optimal timing of initiation of acute kidney replacement therapy (KRT). However, less is known about the ideal circumstances in which KRT may be successfully discontinued. The novel serum-biomarker proenkephalin A 119-159 (penkid) has been found to be strongly negatively correlated with measured GFR. Whether penkid may have a role in initiation and discontinuation of KRT remains unknown.

Acute renal failure (ARF) is a serious and common complication in hospitalized patients, occurring in more than 25% of intensive care unit (ICU) patients. Hypomagnesemia is a common disorder, occurring in approximately 12% of hospitalized patients, with an incidence of 60% in ICU patients. The majority of those patients have are asymptomatic hypomagnesemia, and patients with mild hypomagnesemia do not need treatment, only the correction of the underlying cause. Hypomagnesemia potentiates postischemic renal failure in rats, and is associated, in humans, with acute renal failure. To date, there is no study that demonstrated a benefit of maintain normal levels of magnesium in the incidence of ARF in critically ill patients. Thus, we suggest that a treatment aimed to maintain normal magnesium levels during ICU stay can decrease the incidence of ARF. We will perform a randomized clinical trial that will include all patients admitted to an ICU that, develop hypomagnesemia. It will be excluded from the study: patients younger than 18 years, participants from other studies, pregnant women, patients with creatinine greater than or equal to 3.5 mg / dl or on dialysis, patients who used intravenous contrast for radiological studies, patients weighing less than 40kg, suffering from advanced malignant disease, with severe hypomagnesemia (serum magnesium less than or equal to 1.1 mg / dl), with a diagnosis of Torsades de Pointes or symptomatic hypomagnesemia prior to randomization. Patients included in the study will be randomized to one of the following groups: placebo (saline solution 0.9%) or 50% Magnesium Sulfate. Patients will receive an administration of 48 mEq Magnesium diluted in 250 ml saline 0.9% for 24 hours in an infusion rate of 10.4 ml / hr. Therapy will be continued for 3 days, and repeated during ICU stay to maintain magnesium levels in the normal range. Placebo group will receive exactly the same infusion only with saline administration. The therapy will be discontinued if the patient has hypermagnesemia or signs of magnesium intoxication. The main outcome measurement will be the occurrence of ARF during ICU stay.

The purpose of this research study is to compare the effectiveness of intravenous isotonic sodium bicarbonate with intravenous isotonic sodium chloride and oral N-acetylcysteine (NAC) with oral placebo for the prevention of serious adverse outcomes following angiographic procedures in high-risk patients.

The purpose of this study is to learn about the impact of ischemic preconditioning in reducing contrast induced kidney damage in people with pre-existing kidney problems who are undergoing cardiac catheterization procedures.

The investigators have a new technique of looking at urine to see whether it contains protein fragments that are released by damaged kidneys. These fragments seem to be more accurate than the current blood tests that the investigators use to diagnose renal failure. This technique needs to be validated with a group of patients that have a relatively high incidence of renal failure, cardiopulmonary bypass. The investigators hypothesise that using novel markers of renal dysfunction will identify patients who go on to develop renal failure earlier, and in a higher number than the standard blood tests. The investigators aim to collect urine from patients before going onto bypass, and then at Day 1 and Day 2 after bypass. This urine will be analysed for protein fragments, as well as other new markers of renal dysfunction. The investigators will also take blood at baseline and for the first two days in Cardiac Intensive Care, and compare the accuracy of the new tests with the 'gold standard' that is creatinine.

Randomized prospective trial of patients with diuretic unresponsive acute kidney injury where patients will receive standard supportive therapy with diuretics versus intra-renal delivery of the vasodilator fenoldopam mesylate. Patients with rising creatinine who fail to respond to bolus diuretics will be treated with a prolonged course of diuretics or undergo placement of a catheter within the renal arteries that allows for infusion of fenoldopam mesylate. The rational is that early delivery of a high dose vasodilator may reverse the decline of renal function in patients with severe acute kidney injury.

The purpose of this study is to evaluate the efficacy of acetylcysteine compared to placebo for the contrast-induced nephropathy prevention, between 48 and 96 hours after procedures that use contrast. Contrast-induced nephropathy is defined as an increase of 25% in serum creatinine before the procedure.