View clinical trials related to Acidosis.
Filter by:Background: People s bodies need to break down food into the chemicals. These chemicals are used for energy and growth. Some people cannot process all chemicals very well. Too much of some chemicals can cause diseases. One of these diseases is called propionic acidemia (PA). People with PA can have problems with growth, learning heart, abdomen, and other organs. Researchers want to better understand how these problems happen. Objective: To learn more about propionic acidemia and the genes that might contribute to it. Eligibility: People at least 2 years old with PA who can travel to the clinic Some unaffected family members Design: Participants will have a 3 to 5-day hospital visit every year or every few years. Family members may have just 1 visit. During the family member visit, they may have: Medical history Physical exam Samples of blood and urine Questions about diet and a food diary Doctors and nurses may do additional studies: Samples of saliva, skin and stool Fluid from a gastronomy tube, if participants have one Dental and eye evaluations A kidney test - a small amount of dye will be injected and blood will be collected. Consultations with specialists A test of calories needed at rest. A clear plastic tent is placed over the participant to measure breathing. Stable isotope study. Participants will take a nonradioactive substance then blow into a bag. Photos taken of the face and body with underwear on Ultrasound of the abdomen Heart tests Hand x-ray Brain scan Participants may have other tests if study doctors recommend them. They will get the results of standard medical tests and genetic tests.
The aim of this study is to define the incidence and nature of acidosis after major surgery using Figge's equations to directly measure acidosis. This study will also aim to compare the ability of indirect measures (base deficit, anion gap,corrected anion gap and lactate) to identify the presence of tissue acids in this population. The incidence of postoperative ketoacidosis as a contributor to tissue acidosis will be assessed through the use of point of care urinalysis.
The investigators want to evaluate whether an original action based on the administration of alkali (mainly sodium bicarbonate) is able to significantly modify renal death and to reduce mortality due to cardiovascular events. Methods: This is a proposal of Multicentric, prospective, cohort, randomized, open-label and controlled study. The investigators will Randomize 728 patients with Chronic Kidney Disease(CKD) stage 3b (CKD-3b) and CKD stage 4: 364 of these patients will be included in the study group called Bicarbonate Group (Bic), in which levels of bicarbonate should be kept > 24 mEq/l; the other 364 patients will included in the Usual Treatment Group (no-Bic). Results: The aim of the Research Protocol is to demonstrate if that the optimal correction of uremic acidosis (with administration of sodium bicarbonate or of any other alkalinizing agent, e.g. sodium citrate) reduces renal and cardiovascular mortality. Conclusions. In conclusion the Work Group of the Conservative Therapy for Chronic Renal Insufficiency proposes this cohort, randomized, controlled, prospective, multicentric study to evaluate the effects of correction of acidosis on the progression of the kidney disease considered as renal death in End-Stage Renal Disease (ESRD) patients.
The purpose of this study is to determine whether the plasticity of autologous intravenous application of cord blood stem cells would improve the clinical course of asphyxiated newborns.
Metabolic acidosis is a common complication in incident renal transplant recipients. Protracted acidosis may be associated with osteoporosis, inflammation, negative protein balance and malnutrition, and last but not least may cause renal dysfunction. Preliminary data indicate an increased prevalence of nephrocalcinosis in renal transplant biopsies of incident patients presenting with metabolic acidosis. The present study aims (1)evaluate the prevalence and type of renal tubular acidosis (RTA) in incident renal transplant recipients and to identify clinical correlates and (2) to find associations between RTA, nephrolithiasis and nephrocalcinosis
Methylmalonic acidemia (MMA), one of the most common inborn errors of organic acid metabolism, is heterogeneous in etiology and clinical manifestations. Affected patients with cblA, cblB and mut classes of MMA are medically fragile and can suffer from complications such as metabolic stroke or infarction of the basal ganglia, pancreatitis, end stage renal failure, growth impairment, osteoporosis, and developmental delay. The frequency of these complications and their precipitants remain undefined. Furthermore, current treatment protocol outcomes have continued to demonstrate substantial morbidity and mortality in the patient population. Increasingly, solid organ transplantation (liver, and/or kidney) has been used to treat patients. Disordered transport and intracellular metabolism of vitamin B12 produces a distinct group of disorders that feature methylmalonic acidemia as well as (hyper)homocysteinemia. These conditions are named after the corresponding cellular complementation class (cblC, cblD, cblF, cblJ and cblX) and are also heterogenous, clinically and biochemically. The genetic disorders underlying cblE and cblG feature an isolated impairment of the activity of methionine synthase, a critical enzyme involved in the conversion of homocysteine to methionine and these disorders feature (hyper)homocysteinemia. Lastly, a group of patients can have increased methylmalonic acid and/or homocysteine in the blood or urine caused by variant(s)in recently identified (ACSF3) and unknown genes. In this protocol, we will clinically evaluate patients with methylmalonic acidemia and cobalamin metabolic defects. Routine inpatient admissions will last up to 4-5 days and involve urine collection, blood drawing, ophthalmological examination, radiological procedures, MRI/MRS, skin biopsies in some, and developmental testing. In a subset of patients who have or will receive renal, hepato- or hepato-renal transplants or have an unusual variant or clinical course and have MMA, a lumbar puncture to examine CSF metabolites will be performed. In this small group of patients, CSF metabolite monitoring may be used to adjust therapy. The study objectives will be to further delineate the spectrum of phenotypes and characterize the natural history of these enzymopathies, query for genotype/enzymatic/phenotype correlations, search for new genetic causes of methylmalonic acidemia and/or homocysteinemia, identify new disease biomarkers and define clinical outcome parameters for future clinical trials. The population will consist of participants previously evaluated at NIH, physician referrals, and families directed to the study from clinicaltrials.gov as well as the Organic Acidemia Association, Homocystinuria Network America and other national and international support groups. Most participants will be evaluated only at the NIH Clinical Center. However, if the NIH team decides that a patient under the age of 2 years is a candidate subject for this research protocol, that patient may enroll at the Children s National Medical Center (CNMC) site, pending approval by Dr Chapman, the Principal Investigator of the CNMC location Individuals may also enroll in the tissue collection only part of the study at the UPMC Children s Hospital of Pittsburgh or share medical history and clinical data via telemedicine visits remotely. Outcome measures will largely be descriptive and encompass correlations between clinical, biochemical and molecular parameters.