View clinical trials related to Acute Renal Failure.
Filter by:Hypothesis: Cystatin C compared with creatinine is a better and earlier marker of contrast-induced nephropathy in high and intermedium risk cardiac catheterization patients. Primary Objective: Establish if Cystatin C is superior detecting contrast-induced nephropathy than creatinine in high and intermedium risk cardiac catheterization patients.
Acute renal failure (ARF) is a rare but serious complication of gastroenteritis and dehydration, the most common reason for pediatric emergency visits. Renal function is determined by the glomerular filtration rate (GFR). Serum creatinine, the current marker of GFR, is insensitive and a late marker of ARF. Unfortunately, "gold standard" methods for measurement of GFR are impractical in the emergency setting. Recently, cystatin C (CysC) was introduced as superior marker for the measurement of GFR, particularly in children. A single random blood sample allows for accurate determination of GFR in the so-called "creatinine-blind" range and independent of the body composition. There is growing evidence that the determination of serum CysC concentration can detect ARF in adults earlier than serum creatinine or urinary fractional sodium excretion. No studies have examined this marker for the early detection of ARF in children at risk. We therefore propose a prospective study that compares CysC with other biomarkers of renal dysfunction for the early detection of ARF in children with dehydration due to gastroenteritis. Patients with minor trauma and a minimal likelihood of ARF will serve as a control. This study may establish CysC as an accurate and cost-effective marker for identifying patients at risk.
We examine the prognosis and etiology of postoperative acute renal failure
The purpose of the study is to combine Urodilatin (ANP analogue), which will increase glomerular filtration rate (GFR), and mannitol, which will increase the rate of urinary flow and solute excretion. We intend to treat twenty consecutive allogeneic bone marrow transplant patients in a phase II study comparing results with historical controls. We hypothesize that the incidence of renal dysfunction, ARF and thus mortality in allogeneic bone marrow transplantation can be significantly reduced by the use of protective agents Urodilatin and mannitol. We feel that this combination is best administered prior to and during the first two weeks of treatment when patients encounter immunosuppressive agents and the onset of early transplantation complications.
To understand how AKI (Acute Kidney Injury) leads to chronic kidney disease so therapies can be found to alter the progression of events thereby significantly impacting the long-term outcomes of children who develop AKI.
Patients within the intensive care unit who have severe infections causing shock and kidney failure have almost a 60% risk of dying despite antibiotic therapy, surgical drainage of the site of infection and intensive care support with fluids, nutrition, mechanical ventilation and continuous artificial kidney support. This persistently high death rate continues to stimulate the development of new approaches to the treatment of septic shock. Much clinical and molecular biology research suggests that these patients die because of an uncontrolled immune system’s response to infection. This response involves the production of several substances (so called “humoral mediators”), which enter the blood stream and affect the patient's organs ability to function and the patient's ability to kill germs. These substances may potentially be removed by new artificial filters similar to those currently used during continuous hemofiltration (the type of artificial kidney support used in intensive care). Recent investigations by ourselves and others, however, have made the following findings: 1. Standard filters currently used in intensive care are ineffective in removing large amounts of these “humoral mediators” because the holes in the filter are too small to allow all of them to pass through 2. The standard filters currently used in intensive care are also ineffective in removing large amounts of these “humoral mediators” because the standard filtration flow through the membrane is less than 100 ml/min 3. When the filtration flow through the membrane is increased to above 100ml/min, patients require a lesser dose of drugs to support their blood pressure which is an indirect sign that the filters are clearing some of the "humoral mediators" 4. Even when the blood flow through standard filters is increased to above 100ml/min, there is still not optimal clearing of "humoral mediators" It is possible, however, that, using a different filter membrane with bigger holes in it, would make it easier to clear the blood of these "humoral mediators". It is thought that this would be noticeable clinically in the amount of drugs required to support blood pressure. A filter that has these bigger holes is now available. It is made of the same material as the standard filters that are currently used in the intensive care unit, only the holes have been made bigger to allow these "humoral mediators" to be removed from the blood. This polyamide filter is made of synthetic semipermeable material. This material is highly compatible with human blood. This modified polyamide filter is made of exactly the same compatible material but the holes in the material are slightly larger through a minor modification of the manufacturing process. This larger hole filter has now been used in preliminary studies in humans and has been found to reduce the blood levels of some "humoral mediators". Laboratory studies conducted by ourselves showed that this new filter can achieve the highest reported clearance of some of the "humoral mediators" with minimal effect on useful proteins in blood such as albumin during hemodialysis. This loss is very small and unlikely to contribute to any detectable clinical changes. We, therefore, now propose to study the effect of using new large hole filters with hemodialysis in patients with severe infections and acute kidney failure. We wish to compare the effect of this new therapy to that of standard filters. The new therapy will be considered to be effective if it lowers the amount of drugs used to support blood pressure and if it lowers the blood levels of some "humoral mediators" more than standard therapy. We will also monitor blood levels of important components of blood such as albumin and electrolytes in each group. This is a pilot study involving only 10 patients who will each receive 4 hours of the standard therapy and 4 hours of the new therapy. Which treatment the patient receives first will be random (like the tossing of a coin). Blood samples will be taken at the start and after 4 hours of each treatment. The waste product of dialysis called spent dialysate will also be collected for the measurement of humoral mediators at the start and after 4 hours of each treatment. The changes in blood pressure and drugs used to support it will be recorded hourly. As patients involved in the study would normally receive hemofiltration because of their kidney failure, all the risks and benefits associated with the procedure would be unchanged. The only risk to patients would come from exposure to a modified membrane and from having two additional spoonfuls of blood taken. If this new membrane were found to have a major effect on the blood level of "humoral mediators" and on the patients’ blood pressure, further studies would then be justified to assess its clinical effects (time in ICU, time in hospital, time on ventilator, duration of organ failure, etc).
The goal of the present study is the comparison of different dialysis strategies in critically ill patients with acute renal failure on the intensive care unit. Patients are treated with either continuous dialysis or hemofiltration. Outcome measures are death, restitution of renal function, days on ICU, hemodynamic stability, dialysis efficiency.
Patients developing kidney failure after open heart surgery experience an abrupt decrease in blood flow to the kidney. The investigators hypothesize that administration of fenoldopam mesylate (a drug that increases blood flow to the kidney) to patients early in the course of their disease could reduce progression to dialysis-dependent acute renal failure. The investigators also hypothesize that restoring blood flow could induce additional injury to the kidney through the release of reactive oxygen species. Therefore, patients in this protocol will be randomized to receive a fenoldopam or the anti-oxidant MESNA. The investigators hypothesize that combination treatment with Fenoldopam and MESNA will decrease the incidence of death or dialysis at 21 days in patients with early post-operative acute renal failure.
In order to optimize anti-cytomegalovirus (CMV) treatment with ganciclovir (GCV), in patients with multi organ failure treated with continuous renal replacement therapy (RRT), more information about ganciclovir pharmacokinetics in this setting is needed. The primary objective is to describe the pharmacokinetics of ganciclovir in critically ill patients with acute renal failure treated with continuous renal replacement therapy, with a special emphasis on the extra-renal clearance and distribution volume. Secondary objectives are to investigate if any co-factors, such as serum creatinine, weight, general hydration status, rest function of the native kidneys, etc. can help to describe the pharmacokinetics of GCV in these patients on continuous RRT as well as the relative influence of filtrations and dialysis on GCV elimination during different modalities of the treatment.
Following heart transplantation many patients develop acute renal failure in the early posttransplant phase and some are in need of renal replacement therapy for shorter or longer time. The cause of this acute renal failure is most probably multi factorial but many reports indicate that cyclosporine has a central role in the pathophysiology and it is generally recommended to lower the cyclosporine load to patients developing acute renal failure in this population. Several in vitro studies on renal cells in culture indicate that the primary metabolites of cyclosporine (AM1, AM9, AM4N) are less toxic to the kidney than cyclosporine itself. However, the secondary metabolite AM19 as well as the cyclic metabolites AM1c and AM1c9 has been associated with decreased renal function and nephrotoxicity renal transplant recipients. The primary objective of this pilot study is to investigate if the concentrations of secondary- and cyclic metabolites of cyclosporine (AM19, AM1c, AM1c9) is related to development of acute renal failure in the early posttransplant phase following heart transplantation. Secondary objectives are to investigate associations between genotypes of P-glycoprotein and CYP3A5 and the metabolic pattern of cyclosporine.