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Classic adipsic vasopressin deficiency features hypotonic polyuria and absent thirst despite hypernatremia. We report a 21-year-old patient with prior resected pilocytic astrocytoma who presented dehydration and hypernatremia of 158 mEq/L (158 mmol/L) (reference range, 135-145 mEq/L [SI: 135-145 mmol/L]). He denied thirst and had no polyuria or polydipsia. Plasma and urinary osmolalities were 317 mOsm/Kg (317 mmol/Kg) (reference range, 282-295 mOsm/Kg [282-295 mmol/Kg]) and 878 mOsm/Kg (878 mmol/Kg) (reference range, 200-1200 mOsm/Kg [200-1200 mmol/Kg]), respectively. After prescribed oral water intake, serum sodium normalized and urinary volume remained normal. To assess osmoregulation, plasma copeptin and thirst visual scale were assessed during 3% saline infusion. Despite increases in serum sodium, the patient reported no change in thirst, confirming adipsia. Copeptin value was 3.2 pmol/L at the end of the saline infusion (reference range, 3.7-43.3 pmol/L) and 4.1 pmol/L during hypovolemic hypernatremia, both low-normal values considering hypernatremia, suggesting impaired osmolality-driven vasopressin secretion. This case illustrates a partial defect in osmoregulatory vasopressin release with maintained renal response and highlights the diagnostic utility of osmotic-stimulated copeptin measurement for functional characterization of vasopressin dynamics in rare adipsic disorders.

Aim: Vital signs, blood parameters, and some blood biomarkers in patients with gastrointestinal (GI) bleeding vary depending on the severity of the bleeding. The aim of this study is to investigate the association of vital signs and copeptin levels with transfusion requirements, and patient prognosis, including hospitalization duration and 30-day mortality. Materials and Methods: Prospective, cross-sectional, observational study, conducted in the emergency department (ED) of a tertiary care university hospital, between June 2021 and May 2022. Admission serum copeptin levels and vital parameters of patients with a diagnosis of GI bleeding were noted and evaluated in terms of outcome measures. Results: The study included 118 patients, 75 (63.6%) of whom were male. The median age was 72 years (interquartile range: 58-83). A total of 18 (15%) patients died within 30 days. Serum copeptin levels did not differ between deceased patients and survivors. Logistic regression analysis showed that a shock index above 0.70 and patients aged 75 years and older together [p=0.017, odds ratio (OR)=6.824; 95% confidence interval (CI): (1.419-32.811)] lead to an increase in 30-day mortality. Lower systolic blood pressure at the admission to the ED was associated with increased 30-day mortality [p=0.003, OR=0.952; 95% CI: (0.922-0.983)]. Conclusion: Although serum copeptin levels failed to predict 30-day mortality in patients admitted to the ED due to GI bleeding, our models demonstrated that age over 75 years, lower systolic blood pressure, and the shock index, were superior predictors of mortality.

The present study provides a detailed review of cardiovascular biomarkers critical for the diagnosis, prognosis, and pathophysiology of cardiovascular diseases, the leading cause of global morbidity and mortality. These biomarkers aid in detecting disease onset, progression, and therapeutic responses, providing insights into molecular mechanisms. Enzyme markers like AST, CK-MB, LDH, CA-III, and HBDH are pivotal for detecting myocardial injury during acute events. Protein markers such as CRP, H-FABP, and MPO shed light on inflammation and oxidative stress. Cardiac Troponins, the gold standard for myocardial infarction diagnosis, exhibit high specificity and sensitivity, while IMA and GPBB indicate ischemia and early myocardial damage. Peptide markers, including BNP and NT-proBNP, are crucial for heart failure diagnosis and management, reflecting ventricular stress and remodeling. Novel peptides like MR-proANP and MR-proADM aid in assessing disease severity. Lipid markers such as lipoprotein-associated phospholipase A2 and oxylipins provide insights into lipid metabolism and atherosclerosis. Inflammatory and stress-related biomarkers, including TNFα, IL-6, GDF-15, and Pentraxin 3, illuminate chronic inflammation in CVDs. Hormonal markers like copeptin and endothelin-1 highlight neurohormonal activation, while emerging markers such as ST2, galectin-3, PAPP-A, and TMAO elucidate fibrosis, remodeling, and metabolic dysregulation. The inclusion of microRNAs and long non-coding RNAs represents a breakthrough in biomarker research, offering sensitive tools for early detection, risk stratification, and therapeutic targeting. This review emphasizes the diagnostic and prognostic utility of these biomarkers, advancing cardiovascular care through personalized medicine.

Arginine Vasopressin (AVP) and copeptin derive from the same precursor molecule. Due to the equimolar secretion, copeptin responds as rapidly as AVP to osmotic, hemodynamic and unspecific stress-related stimuli and both peptides show a very strong correlation. The physiological functions of AVP are homeostasis of fluid balance, vascular tonus and regulation of the endocrine stress response. In contrast, the exact function of copeptin remains unknown. Since copeptin, in contrast to AVP, can easily be measured with a sandwich immunoassay, its main function so far that it indirectly indicates the amount of AVP in the circulation. Copeptin has emerged as a useful measure in different diseases. On one hand, through its characteristics as a marker of stress, it provides a unique measure of the individual stress burden. As such, it is a prognostic marker in different acute diseases such as ischemic stroke or myocardial infarction. On the other side, it has emerged as a promising marker in the diagnosis of AVP-dependent fluid disorders. Copeptin reliably differentiates various entities of the polyuria polydipsia syndrome; baseline levels >20 pmol/L without prior fluid deprivation identify patients with nephrogenic diabetes insipidus, whereas levels measured upon osmotic stimulation with hypertonic saline or upon non-osmotic stimulation with arginine differentiate primary polydipsia from central diabetes insipidus. In patients with hyponatremia, low levels of copeptin together with low urine osmolality identify patients with primary polydipsia, but copeptin levels overlap in all other causes of hyponatremia, limiting its diagnostic use in hyponatremia. Copeptin has also been put forward as predictive marker for autosomal dominant polycystic kidney disease and for diabetes mellitus, but more studies are needed to confirm these findings.

Purpose An increasing body of evidence suggests that excreting a generous volume of diluted urine is associated with short- and long-term beneficial health effects, especially for kidney and metabolic function. However, water intake and hydration remain under-investigated and optimal hydration is poorly and inconsistently defined. This review tests the hypothesis that optimal chronic water intake positively impacts various aspects of health and proposes an evidence-based definition of optimal hydration. Methods Search strategy included PubMed and Google Scholar using relevant keywords for each health outcome, complemented by manual search of article reference lists and the expertise of relevant practitioners for each area studied. Results The available literature suggest the effects of increased water intake on health may be direct, due to increased urine flow or urine dilution, or indirect, mediated by a reduction in osmotically -stimulated vasopressin (AVP). Urine flow affects the formation of kidney stones and recurrence of urinary tract infection, while increased circulating AVP is implicated in metabolic disease, chronic kidney disease, and autosomal dominant polycystic kidney disease. Conclusion In order to ensure optimal hydration, it is proposed that optimal total water intake should approach 2.5 to 3.5 L day −1 to allow for the daily excretion of 2 to 3 L of dilute (< 500 mOsm kg −1 ) urine. Simple urinary markers of hydration such as urine color or void frequency may be used to monitor and adjust intake.

Arginine vasopressin deficiency (AVP-D) is one of the main entities of the polyuria-polydipsia syndrome. Its correct diagnosis and differentiation from the other two causes - AVP resistance and primary polydipsia – is crucial as this determines the further management of these patients.Over the last years, several new diagnostic tests using copeptin, the stable surrogate marker of AVP, have been introduced. Among them, hypertonic saline stimulated copeptin was confirmed to reliably and safely improve the diagnostic accuracy to diagnose AVP-D. Due to its simplicity, arginine stimulated copeptin was put forward as alternative test procedure. Glucagon-stimulated copeptin also showed promising results, while the oral growth hormone secretagogue Macimorelin failed to provide a sufficient stimulus. Interestingly, an approach using machine learning techniques also showed promising results concerning diagnostic accuracy.Once AVP-D is diagnosed, further workup is needed to evaluate its etiology. This will partly define the further treatment and management. In general, treatment of AVP-D focuses on desmopressin substitution, with oral formulations currently showing the best tolerance and safety profile. However, in addition to desmopressin substitution, recent data also showed that psychopathological factors play an important role in managing AVP-D patients.

IntroductionOpioid system activity was found disturbed in several reward circuit areas in restrictive anorexia nervosa (AN) patients but also at the pituitary level. The role of this specific abnormality in AN physiopathology remains unknown.OObjectivesWe aimed to evaluate the relationship of upper mentioned AN abnormality with its classical pituitary features and eating behavior traits.MethodsPET [11C] diprenorphin binding potential (BPND) were processed for each pituitary part in three groups of young women: 12 AN, 11 recovered AN patients (ANrec), and 12 Controls. Anterior pituitary hormones and neurohypophysis (NH) 12 points circadian profile including copeptin and oxytocin, psychological scores were evaluated in these subjects as well as in 13 bulimic (BN) patients.Results[11C] diprenorphin pituitary binding was found to be fully localized in NH. Only AN patients’ NH present lower [11C] diprenorphin BPND than Controls, interpreted as a higher opioid tone. Both AN and ANrec show lower copeptin/24h than in Controls but no difference in oxytocin. BN showed increased copeptin and low oxytocin. In AN patients copeptin inversely correlate with Restrained Eating while oxytocin correlate with the External Eating score. NH [11C] diprenorphin BPND correlated with leptin but not with copeptin or oxytocin.ConclusionsNeurohypopysis opioid tone in anorexia nervosa seem not to impact the vasopressin or oxytocin release but still may interfere in gonadal axis regulation. Copeptin, a good indicator of hydration state, may be a good tool to detect hidden restrictive or purging behaviors. Specific correlates with AN psychologic features still suggest a physiopathological involvement.DisclosureNo significant relationships.

Background The identification of new biomarkers in autosomal-dominant polycystic kidney disease (ADPKD) is crucial to improve and simplify prognostic assessment as a basis for patient selection for targeted therapies. Post hoc analyses of the TEMPO 3:4 study indicated that copeptin could be one of those biomarkers. Methods Copeptin was tested in serum samples from patients of the AD(H)PKD study. Serum copeptin levels were measured using a time-resolved amplified cryptate emission (TRACE)-based assay. In total, we collected 711 values from 389 patients without tolvaptan treatment and a total of 243 values (of which 64 were pre-tolvaptan) from 94 patients on tolvaptan. These were associated with rapid progression and disease-causing gene variants and their predictive capacity tested and compared with the Mayo Classification. Results As expected, copeptin levels showed a significant negative correlation with estimated glomerular filtration rate (eGFR). Measurements on tolvaptan showed significantly higher copeptin levels (9.871 pmol/L vs 23.90 pmol/L at 90/30 mg; P < .0001) in all chronic kidney disease stages. Linear regression models (n = 133) show that copeptin is an independent predictor of eGFR slope. A clinical model (including eGFR, age, gender, copeptin) was nearly as good (R2 = 0.1196) as our optimal model (including height-adjusted total kidney volume, eGFR, copeptin, R2 = 0.1256). Adding copeptin to the Mayo model improved future eGFR estimation. Conclusion Copeptin levels are associated with kidney function and independently explained future eGFR slopes. As expected, treatment with tolvaptan strongly increases copeptin levels. Lay Summary Autosomal-dominant polycystic kidney disease (ADPKD) is a genetic condition that can cause kidney damage. Researchers have been looking for new ways to predict how the disease will progress, so that patients can be offered the best treatment options. Copeptin is a substance that has been identified as a possible new marker for ADPKD. In this study, researchers measured copeptin levels in the blood of tolvaptan-naive ADPKD patients and ADPKD patients taking tolvaptan, a medication that can slow the progression of the disease. They found that copeptin levels were linked to kidney function and could help predict how the disease would progress in the future. The study also showed that tolvaptan increased copeptin levels. This research could help doctors make better treatment decisions for ADPKD patients.

Diagnosis in stroke patients is based mainly on clinical and radiological findings; therefore, there is a need for serological markers that can orient the clinician. Copeptin is a new blood marker for diagnosis and prognosis in several neurological conditions, such as ischemic stroke, hemorrhagic stroke, aneurysmal subarachnoid hemorrhage, and multiple sclerosis. The aim of our study was to highlight the diagnostic value of copeptin in differentiating between stroke subtypes and stroke mimics. We performed a literature review by searching the PubMed and Scopus databases for papers with the following keywords: “stroke AND copeptin AND differential”. The PRISMA criteria were used. We identified 29 papers that met the criteria. We analyzed only original research articles, excluding reviews and only including those in English. Some studies did not find any significant differences between cerebral infarction, intracerebral hemorrhage, and subarachnoid hemorrhage, but one study demonstrated significant correlations. All studies agreed that copeptin levels can help in differentiating stroke patients from stroke-free patients. Copeptin levels were correlated with prognostic scales For stroke mimics, copeptin levels were extremely broad and for vestibular disorders; it was shown that a normal level of copeptin excludes stroke. Copeptin is a new blood marker that can help clinicians in the acute neurological field. It may help in diagnosing stroke, in differentiating between stroke subtypes and stroke mimics, and in evaluating the prognosis of these patients, but further studies are needed.