Jogender Kumar.
Newborn Unit, Nehru Hospital, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
ADDRESS FOR CORRESPONDENCE
Dr. Jogender Kumar; Senior Resident, Newborn Unit, Third Floor, Nehru Hospital, Post Graduate Institute of Medical Education and Research, Chandigarh, India.160012.
Email: jogendrayadv@gmail.com | To the Editor
In the present journal, a case report of Congenital Hypothyroidism Leading to Acute Kidney Injury with Hypernatremic Dehydration was published. (1) We read it with great interest. There are certain things which need clarification. First and foremost is it is not congenital hypothyroidism, which is directly implicated in the pathogenesis of Acute Kidney Injury (AKI) and dehydration. The author stated that the baby was having poor feeding and that is the cause of dehydration and AKI. Any child with lethargy and poor feeding can have dehydration so to state hypothyroidism as a cause of hypernatremia will not be true. Second; author mentioned that the baby had muffled heart sounds, but didn’t mention whether there was pericardial effusion or not; which is a well-known entity in hypothyroidism. (2) Third; author mentioned that child was initially rehydrated with two boluses 60cc/kg of 0.9% normal saline; what is the rationale for that. According to guidelines of fluid resuscitation in newborns boluses of 10 ml/kg saline upto 60 ml/kg should be given unless perfusion improves or hepatomegaly develops. (3) Fourth; author mentioned that ultrasound abdomen revealed bilateral medullary nephrocalcinosis (secondary to dehydration); probably it was increased in the attenuation of the renal medulla secondary to dehydration, which is commonly known as “dense renal medulla” sign which is well described in the literature. (4,5) Dense renal medulla is defined as the increased attention of the medulla as compared to the renal cortex. It is seen in conditions which increase urine osmolality like dehydration, hypernatremia and high-protein diet. Medullary nephrocalcinosis is one of the differential diagnosis. The disappearance of this hyperdensity following adequate hydration clinches the diagnosis. So; whether we repeated ultrasonography in this baby or not? | | | | Compliance with Ethical Standards | | Funding None | | | | Conflict of Interest None | | |
- Inamdar RP, Bellad MR, Herekar RV. Congenital Hypothyroidism Leading to Acute Kidney Injury with Hypernatremic Dehydration. Pediatr Oncall J 2016; 2.
- Zaki SA, Dolas A. Refractory cardiogenic shock in an infant with congenital hypothyroidism. Indian J Crit Care Med. 2012; 16(3):151-153. [CrossRef] [PMC free article]
- Wynn JL, Wong HR. Pathophysiology and Treatment of Septic Shock in Neonates. Clinics in perinatology. 2010; 37(2):439-479. [CrossRef] [PMC free article]
- Sureka B, Bansal K, Arora A. Dense renal medulla sign. Indian J Nephrol. 2016; 26(3):223-224. [CrossRef] [PMC free article]
- Tublin ME, Tessler FN, McCauley TR, Kesack TC. Effect of hydration status on renal medulla attenuation on unenhanced CT scans. Am J Roent.1 997 168:1, 257-259.
DOI: https://doi.org/10.7199/ped.oncall.2017.22
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| Cite this article as: | | Kumar J. Comment on Congenital Hypothyroidism Leading to Acute Kidney Injury with Hypernatremic Dehydration: A Letter to Editor. Pediatr Oncall J. 2017;14: 45. doi: 10.7199/ped.oncall.2017.22 |
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