Active clinical trials for "Diabetes Insipidus"

The investigators aim to retrospectively explore the electronic medical records of all patients who were admitted to the Intensive Care Unit (ICU) of the UZ Brussels in the last 10 years (March 1st 2011- March 1st 2021) and who received prolonged sedation (>24h) with sevoflurane.

Copeptin is accepted as a marker of stress. We want to evaluate the preoperative and early postoperative copeptin leavens in patients undergoing different aortic valve procedures

the purpose of the study is to investigate whether arginine infusion is a new tool to differentiate patients with diabetes insipidus, primary polydipsia and healthy subjects.

OBJECTIVES: I. Determine the relationship between genotype variations and clinical phenotype in patients with congenital nephrogenic diabetes insipidus.

Hyponatremic hypovolemia is a frequent complication of transurethral resection of the prostate gland (TURP). Copeptin has been established as is a surrogate marker of vasopressin and is measured useful for thea clinical assessment of various sodium and water disturbances. The aim of our the study was to assess the utility of serum concentration of copeptin (CPP) and brain natriuretic peptide (NT-proBNP) for the prediction of postoperative alterations of serum sodium concentration. Study population comprised 43 patients with benign prostatic hyperplasia (BPH) undergoing transurethral resection of the prostate gland. In a forward stepwise multiple regression only serum copeptin before the surgery and the duration of TURP significantly explained the variation of sodium concentration for 12 hours from the start of the surgery. Serum NT-proBNP before the surgery did not predict hyponatremia 12 hours after TURP.Conclusion Serum copeptin before TURP surgery but not NT-proBNP may be a clinically useful marker of a decrease of serum sodium after TURP surgery.

The study aim is to measure perioperative copeptin concentration in blood of liver transplant recipients and to assess whether there is a correlation between its level and hemodynamic derangement.

The purpose of this study is to investigate if there is an association between copeptin level in serum and the severity of pancreatitis and if copeptin can be used as a predictor for organ failure and pancreatic necrosis with or without superinfection.

OBJECTIVES: I. Determine whether diverse mutations of the vasopressin-neurophysin II (AVP-NPII) gene cause autosomal dominant familial neurohypophyseal diabetes insipidus by directing the production of an abnormal preprohormone. II. Determine whether the AVP-NPII gene-directed preprohormone accumulates and destroys magnocellular neurons because it cannot be folded and processed efficiently.

This study evaluated the value of using copetin and protein S 100 b to eliminate the diagnosis of stroke in patients presenting with vertigo in emergency departments. All patients benefited from the S 100b protein assay, copeptin and brain MRI.

ST-elevation myocardial infarction (STEMI) has a serious health threaten to population. PCI, which can timely restore the blood flow to the ischemic myocardium, is a well-proved measure in STEMI management. However, the process of the restoration can induce injury. The phenomenon is defined as ischemia/reperfusion (I/R) injury. The studies indicate that I/R injury accounts for up to 50% of the final myocardial infarct size. However, previous attempts to target known mediators of myocardial I/R injury in patients have been disappointing, leading to calls for a reevaluation of factors affecting myocardial I/R injury [1]. Arginine vasopressin (AVP), that response to acute illness, is unstable and cleared rapidly from the circulation. However, copeptin, the C-terminal portion of provasopressin, is released in equimolar amounts to AVP and is easy to determine. So, copeptin can be a surrogate marker for AVP secretion. Recently, copeptin was found to serve as a potential prognostic biomarker in heart failure and acute myocardial infarction (AMI). AMI can activate the AVP axis, which have a causative role in the evolution of heart failure. Increasing copeptin was shown to correlate with myocardial remodeling, mortality and morbidity. In patients with STEMI, myocardial infarct size is a stronger outcome predictor than LV function, and is related to LV remodeling, which often indicates a significant worse prognosis after AMI. As the gold standard for characterisation of cardiac structure and function, cardiac magnetic resonance (CMR) parameters can serve as surrogate end points in clinical trials of STEMI. We hypothesised that plasma copeptin values, tested before and after PCI, are related to myocardial infarct size, myocardial function both and outcomes at baseline and 6 months follow-up as assessed by CMR in patients with STEMI.