Hyponatremia is the most common electrolyte abnormality. Its diagnostic and therapeutic approaches are in a state of flux. It is evident that hyponatremic patients are symptomatic with a potential for serious consequences at sodium levels that were once considered trivial. The recommendation to treat virtually all hyponatremics exposes the need to resolve the diagnostic and therapeutic dilemma of deciding whether to water restrict a patient with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or administer salt and water to a renal salt waster. In this review, we briefly discuss the pathophysiology of SIADH and renal salt wasting (RSW), and the difficulty in differentiating SIADH from RSW, and review the origin of the perceived rarity of RSW, as well as the value of determining fractional excretion of urate (FEurate) in differentiating both syndromes, the high prevalence of RSW which highlights the inadequacy of the volume approach to hyponatremia, the importance of changing cerebral salt wasting to RSW, and the proposal to eliminate reset osmostat as a subtype of SIADH, and finally propose a new algorithm to replace the outmoded volume approach by highlighting FEurate. This algorithm eliminates the need to assess the volume status with less reliance on determining urine sodium concentration, plasma renin, aldosterone and atrial/brain natriuretic peptide or the BUN to creatinine ratio.
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http://dx.doi.org/10.3390/jcm3041373 | DOI Listing |
J Clin Med
December 2024
NYU Grossman Long Island School of Medicine, 101 Mineola Blvd., Mineola, NY 11501, USA.
A knowledge gap may exist when attempting to identify the pathogenetic mechanisms resulting in the syndrome of inappropriate antidiuretic hormone (SIADH) or hypotonic hyponatremia. Ectopic secretion of antidiuretic hormone [ADH] is the classic cause of SIADH. But another form of inappropriate secretion of ADH occurs when interleukin 6 is activated.
View Article and Find Full Text PDFGut Microbes
December 2025
Metabolism and Nutrition Research Group, Louvain Drug Research Institute, UCLouvain, Université catholique de Louvain, Brussels, Belgium.
Alterations in bile acid profile and pathways contribute to hepatic inflammation in cancer cachexia, a syndrome worsening the prognosis of cancer patients. As the gut microbiota impinges on host metabolism through bile acids, the current study aimed to explore the functional contribution of gut microbial dysbiosis to bile acid dysmetabolism and associated disorders in cancer cachexia. Using three mouse models of cancer cachexia (the C26, MC38 and HCT116 models), we evidenced a reduction in the hepatic levels of several secondary bile acids, mainly taurodeoxycholic (TDCA).
View Article and Find Full Text PDFIntroduction: Screening for congenital adrenal hyperplasia through the measurement of 17-hydroxyprogesterone on the neonatal blood spot aims to: a) prevent neonatal deaths; b) allow earlier identification and thereby decrease the severity of the initial salt-wasting episode; and c) shorten the time during which a severely virilized genetic female newborn may be assigned the male sex. It is now practiced in the majority of high-income countries, although the positive predictive value of the test is very low in infants born preterm, who seem to be infrequently affected. In almost all low- and middle-income countries, it has not yet been implemented.
View Article and Find Full Text PDFJ Clin Res Pediatr Endocrinol
December 2024
Department of Pediatric Endocrinology, Akdeniz University Hospital, Antalya, Turkey.
Pseudohypoaldosteronism (PHA) is a rare disorder that, if not promptly recognized and treated, can lead to life-threatening hyperkalemia resulting in cardiac arrest and death. Systemic PHA is caused by variants that deactivate the epithelial sodium channel (ENaC) subunits. Management is challenging due to high-dose oral replacement therapy, and patients with systemic PHA require lifelong treatment.
View Article and Find Full Text PDFJ Clin Res Pediatr Endocrinol
January 2025
University of Health Sciences Turkey, Dr. Sami Ulus Child Health and Diseases Training and Research Hospital, Clinic of Pediatric Endocrinology, Ankara, Turkey
Although the most common cause of congenital adrenal hyperplasia (CAH) worldwide is 21-hydroxylase deficiency (21-OHD), which accounts for more than 95% of cases, other rare causes of CAH such as 11-beta-hydroxylase deficiency (11β-OHD), 3-beta-hydroxy steroid dehydrogenase (3β-HSD) deficiency, 17-hydroxylase deficiency and lipoid CAH (LCAH) may also be encountered in clinical practice. 11β-OHD is the most common type of CAH after 21-OHD, and CYP11B1 deficiency in adrenal steroidogenesis causes the inability to produce cortisol and aldosterone and the excessive production of adrenal androgens. Although the clinical and laboratory features are similar to 21-OHD, findings of mineralocorticoid deficiency are not observed.
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