Cerebral Salt Wasting Is a Real Cause of Hyponatremia: COMMENTARY

Palmer, Biff F.; Clegg, Deborah J.

doi:10.34067/kid.0001452022

Cited by 5 publications

(3 citation statements)

References 18 publications

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“…The long-term prognosis of neonatal RSW varies depending on the severity of the initial brain injury, timely intervention, and adherence to proper treatment [15]. Longitudinal studies assessing the neurodevelopmental outcomes of affected neonates are necessary to gain insights into the lasting effects of RSW on the developing brain [16,17].…”

Section: Discussionmentioning

confidence: 99%

Recurrent hyponatremia in neonate: a case of renal salt wasting syndrome

Maryam,

Mazahir,

Khanam

et al. 2024

Egypt Pediatric Association Gaz

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Background Renal salt wasting (RSW) is primarily seen with central nervous disorders and is characterized by hyponatremia, elevated urinary sodium excretion, increased urine output, and hypovolemia. Although there have been reports of RSW in children, it has not been reported in newborns. Case presentation A term (38 weeks 2 days) female weighing 2060 g, born via normal vaginal delivery, to a primi-gravida mother, was admitted to our neonatal intensive care unit. At birth, the baby was non-vigorous, had aspirated meconium, and required bag-and-mask ventilation following which the baby cried. The child was put on CPAP and inotropes for respiratory distress and shock, respectively, along with first-line antibiotics. Over the next few days, the child was weaned off CPAP, inotropes were stopped, and feeds were started. On postnatal day (PND) 8, the baby developed repeated episodes of seizures requiring two-antiepileptics followed by midazolam infusion, had shock requiring inotropes, and also had a tense anterior fontanelle with altered sensorium and tone changes, for which mannitol and 3% saline were given. Antibiotics were upgraded, and neuroimaging (MRI) revealed left basal-ganglia bleed with intraventricular extension and cerebral venous thrombosis. The baby showed gradual clinical improvement with the above measures and was restarted on feeds. However, from PND-19 onwards the baby had repeated episodes of hyponatremia requiring 3% saline infusions, progressive weight loss, and polyuria. Considering RSW, urine sodium was done which was high (110 mmol/L). For polyuria and weight loss, feed volume was increased, whereas, for hyponatremia, table salt was added to the expressed breast milk (1 gm × tds). Subsequently, all the serum sodium values remained within normal limits, and the baby started gaining weight and was discharged on similar advice (PND 38). On further follow-up, table salt was gradually decreased in the feeds and was stopped after 1 month of discharge with normal serum sodium values. Conclusion Management of recurrent hyponatremia in a neonate is challenging. Despite its rarity, RSW in newborns should be considered a differential.

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Section: Discussionmentioning

confidence: 99%

Recurrent hyponatremia in neonate: a case of renal salt wasting syndrome

Maryam,

Mazahir,

Khanam

et al. 2024

Egypt Pediatric Association Gaz

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“…However, the accurate assessment of volume status is clinically unavailable, and achieving a differential diagnosis between CSW and SIAD is difficult. Both conditions present with hyponatremia with a low plasma osmolality, an inappropriately elevated urine osmolality, a urine sodium concentration usually > 40 mmol/L, and a low serum uric acid concentration due to an increased fractional excretion of uric acid [79]. Thus, CSW patients have an unusual combination of hypovolemia and hypouricemia.…”

Section: Csw/rswmentioning

confidence: 99%

Altered Serum Uric Acid Levels in Kidney Disorders

Kim

Jun

2022

Life

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Serum uric acid levels are altered by kidney disorders because the kidneys play a dominant role in uric acid excretion. Here, major kidney disorders which accompany hyperuricemia or hypouricemia, including their pathophysiology, are discussed. Chronic kidney disease (CKD) and hyperuricemia are frequently associated, but recent clinical trials have not supported the pathogenic roles of hyperuricemia in CKD incidence and progression. Diabetes mellitus (DM) is often associated with hyperuricemia, and hyperuricemia may be associated with an increased risk of diabetic kidney disease in patients with type 2 DM. Sodium-glucose cotransporter 2 inhibitors have a uricosuric effect and can relieve hyperuricemia in DM. Autosomal dominant tubulointerstitial kidney disease (ADTKD) is an important hereditary kidney disease, mainly caused by mutations of uromodulin (UMOD) or mucin-1 (MUC-1). Hyperuricemia and gout are the major clinical manifestations of ADTKD-UMOD and ADTKD-MUC1. Renal hypouricemia is caused by URAT1 or GLUT9 loss-of-function mutations and renders patients susceptible to exercise-induced acute kidney injury, probably because of excessive urinary uric acid excretion. Hypouricemia derived from renal uric acid wasting is a component of Fanconi syndrome, which can be hereditary or acquired. During treatment for human immunodeficiency virus, hepatitis B or cytomegalovirus, tenofovir, adefovir, and cidofovir may cause drug-induced renal Fanconi syndrome. In coronavirus disease 2019, hypouricemia due to proximal tubular injury is related to disease severity, including respiratory failure. Finally, serum uric acid and the fractional excretion of uric acid are indicative of plasma volume status; hyperuricemia caused by the enhanced uric acid reabsorption can be induced by volume depletion, and hypouricemia caused by an increased fractional excretion of uric acid is the characteristic finding in syndromes of inappropriate anti-diuresis, cerebral/renal salt wasting, and thiazide-induced hyponatremia. Molecular mechanisms by which uric acid transport is dysregulated in volume or water balance disorders need to be investigated.

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“…The fractional excretions of urate and phosphate after correction of the hyponatremia and measurement of the level of a natriuretic haptoglobin-related protein may clarify the distinction between SIADH and CSW ( 16 , 17 ). However, the proper steps in differentiating between SIADH and CSW are currently disputed ( 17 – 19 ). Further research in this area is required.…”

mentioning

confidence: 99%