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Letters to the Editor

Acute Kidney Injury and COVID-19

Attention to Inflammatory Phenotype

Deep, Akash MD; Bansal, Mehak DNB; Ricci, Zaccaria MD

Author Information
The Pediatric Infectious Disease Journal: October 2020 - Volume 39 - Issue 10 - p e332
doi: 10.1097/INF.0000000000002836
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To the Editors:

Coronavirus disease (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a milder disease in children as compared with adults. COVID-19 can lead to acute kidney injury (AKI) in critically ill patients and is a crucial prognostic marker for disease severity and mortality and, although widely variable in reports, up to 25% of the adult patients with COVID 19 may develop AKI.1 In children, prevalence of AKI in COVID-19 is unknown.

In a recent study, Stewart et al2 have reported a high incidence of renal dysfunction (46%) and AKI (29%) in 52 hospitalized children with COVID-19 that appears much higher than previous pediatric observations coming from China.3 Recently, Europe has reported a pediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2 infection (PIMS-TS) which has similar characteristics to Kawasaki disease or Toxic shock syndrome.4 In Stewart et al’s report, AKI was detected in 38% of critically ill children admitted to pediatric intensive care unit (14/37) and in about half of all PIMS-TS patients (46%) but in only 10% of other children without the hyperinflammatory phenotype. In essence, PIMS-TS in children requiring intensive support is a significant risk factor for AKI.

Multiple reasons can explain the high incidence of AKI in this population: fever leading to high insensible losses, decreased intake of fluids, diarrhea and vomiting leading to dehydration, high inflammatory markers (D-dimers, ferritin, C-reactive protein) and cardiac involvement leading to low cardiac output state. In a recently published PIMS-TS study, inflammation and shock were commonly reported with requirement of inotropic support and fluid resuscitation.5

All these features are well-known risk factors for development of AKI which is evident in Stewart et al’s article. In addition, late presentation to the health care facility due to the fear of COVID-19 pandemic with prolonged renal hypoperfusion can be contributory. In poly-inflammatory condition, the cytokine storm can cause direct damage to the renal parenchyma. AKI is a known complication in 1/3 of Kawasaki disease and, with similar pathophysiology, SARS-CoV-2 antibody positivity could potentially explain the late antibody-mediated immune complex kidney dysfunction.

One important finding of this study was that none of the 52 children with AKI apparently required renal replacement therapy or had persistent AKI. This finding may be related to timely fluid and vasoactive therapy to correct hypotension and renal perfusion but also to local practice and different timing of dialysis start in different centers.6 We would like to emphasize the role of multidisciplinary input of intensive care, infectious disease and rheumatology teams to guide resuscitation, anti-inflammatory and immune-modulatory therapies. This study included only a short-term AKI follow-up (hospital discharge). A multi-center study in this novel cohort of pediatric intensive care unit children with COVID-19 and PIMS-TS is urgently needed to study the prevalence, risk factors and evolution of AKI.

Akash Deep, MD
Pediatric Intensive Care Unit, King’s College Hospital NHS Foundation Trust, London, United Kingdom
Mehak Bansal, DNB
Pediatric Intensive Care Unit, SPS Hospitals, Ludhiana, India
Zaccaria Ricci, MD
Pediatric Cardiac Intensive Care Unit, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy

REFERENCES

1. Richardson S, Hirsch JS, Narasimhan M, et al. Presenting characteristics, comorbidities, and outcomes among 5700 patients hospitalized with COVID-19 in the New York City Area. JAMA. 2020;323:2052–2059.
2. Stewart DJ, Hartley JC, Johnson M, et al. Renal dysfunction in hospitalised children with COVID-19. Lancet Child Adolesc Health. 2020. doi: 10.1016/S2352-4642(20)30178-4. Online ahead of print.
3. Qiu H, Wu J, Hong L, et al. Clinical and epidemiological features of 36 children with coronavirus disease 2019 (COVID-19) in Zhejiang, China: an observational cohort study. Lancet Infect Dis 2020;20:689–696.
4. Riphagen S, Gomez X, Gonzalez-Martinez C, et al. Hyperinflammatory shock in children during COVID-19 pandemic. Lancet. 2020;395:1607–1608.
5. Whittaker E, Bamford A, Kenny J, et al. Clinical characteristics of 58 children with a pediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2. JAMA. 2020. doi: 10.1001/jama.2020.10369. Online ahead of print.
6. Westrope CA, Fleming S, Kapetanstrataki M, et al. Renal replacement therapy in the critically ill child. Pediatr Crit Care Med. 2018;19:210–217.
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