Acute renal failure requiring dialysis as an atypical presentation of Multisystem Inflammatory Syndrome in Children (MIS-C)

An 18-month -boy presented with fever for 7 days, facial puffi- ness, periorlaital oederna and anuria. He had fever and cough I riefly 3 weeks earlier. All family nieml ers had a similar illness at that time. Examination showed anasarca, pitting oederna and irrital ility. Investigations revealed liaenioglolain 85 g/L. total leu- kocyte count 15.5 x 10’/L (polyrnorplis 44%. 1ym{aliocytes 46 %. rnonocytes 6% and eosinopliils 3% ) and {Platelet count 707 x 10’/L with normal peripheral smear. Biocliernical iivesti- gatioishowed serum sodium 12.9 nirno1/L, {Potassium 6.6 rnniol/ L, blood urea 34.3 nirno1/L and serum creatinine 999. 9 [irno1/L. Blood gas analysis showed pH 7.30, laicarbonate 11.2 mrno1/L and serum lactate 1. 1 rnniol/L (normal: 0.5—1 mrno1/L). His total urine output over the last 24 It was only 5 rnL. As {her I4idney Disease Improving Global Outcomes (ITDIG O) classification, lie was classified as having acute kidney injury (AISI) stage III. His serum C-reactive protein was 54.6 ing/L, n-dimer 3.8 [ig/niL (normal: 0.1—0.5 ), serum filarinogen 275.5 ing/dL (normal: 240—355) and serum interleukin-6 level 17.9 pg/niL (normal 4.4). Aspartame transaminases and alanine transarninase were 3.2.9 U/L (<40 U/L) and 22.0 U/L (<40 U/L). respectively. Lactate deh ydro- genase, serurii ferritin, serum triglycerides, troponin and plasma B-type natriuretic peptide were 2.9.1 .5 U/L (norrnal < 248) 

403.9 rig/niL, 2.50.2 mg/dL (<150 ing/dL), negative and 11 {ag/ rnL (<29.40 pg/niL), respectively. He was initiated on su{aportive t1iera{ay and peritoneal dialysis (PD) using percutaneously inserted peel-away sheath catheter lay Seldinger technique. Urine exarnination showed proteinuria (+2 ), no casts or dysnior{a1iic red lalood cells. Spot urine {Protein/creatinine ratio was 1.4 (normal 0.2). Blood and urine cultures were sterile. Human immunodeficiency virus enzyme-Iin1‹ed imrnunosorlaent assay was non-reactive. Ultrasound of kidney. ureter and laladder (HUB) revealed normal sized kidneys with mildly increased ecliogenicity lailaterally. Dop{aler evaluation of the renal vessels was normal. Coniplernent C 3. C4, antinuclear antilaodies, aiti- cytoplasmic antibodies. serurii all urnin and cholesterol were normal. 

In view of his fever, high inflammatory markers, tlirornbocytosis and the family's febrile respiratory illness 3 weeks {Prior, the clinical possilaility of rnultisysteni inflammatory syn - drome in children (MIS-C) was considered. At the time of {Pre- sentation of this case to hospital, the country was facing the second pandernic wave of C OVID- 19. The patient fulfilled the Royal College of Paediatrics and Cmild Health definition of paedi- atric niultisysteni inflammatory syndrome tem{aoralIy associated with  COVID-19.1  Severe  acute  res{airatory  syndrome coronavirus -2 (SARS-CoV-2) polymerase chain reaction was neg- ative, while SARS -CoV-2 antilaody titres (IgG: 12.56 index; normal 1 index) were elevated, confirming a diagnosis of MIS-C. 

The patient was initiated on oral prednisolone (2 mg/kg/day) and sulacuta neous low-molecular weight heparin ( 1 rug/kg/ da y). Gradually. his urine output improve d to 1 .3 mL/kg/li, and lalood urea ( 5.95 mmol/L) and serum creatinine (6 1.88 [irnol/L) normalised. PD was stopped on day 7 when his kidne y hut ction tests, eIectrolytes and urine exarnination were normal. The patient was discliarged on tapering doses of oral prednisolone (over 6 weeks). 

MIS-C is a post-infectious {Phenomenon usually a{apearing weeks after C OVID- 19 infection. It is difficult to differentiate recent SARS -CoV-2 infection from an infection several months prior leased on just IgG positivity. Studies have shown that aiti- laodies against SARS-CoV-2 may persist for several months after infection tout IgG titres decrease significantly during the first 6 months after ex{aosure.’ " Anderson cr n/. have shown that clil- dreiwith MIS-C have higher levels of IgG antilaodies that ieu- tralise SARS-CoV-2 more effectively compared to children with severe C OVID-19. In our case, the history of a recent conipatit ie illness, with multiple family niemt ers affected at the same time and high daily caseloads suggest recent infection. 

Renal involvement in patients with MIS-C can manifest as pro-teinuria, liaematuria and AISI. AISI has tween reported in quarter to one-third of {Patients with MIS-C. “ McCullocli ct al. have descritaed a 9-year-oId boy with MIS-C requiring PD. In one of the largest series of AISI in MIS-C (57 children with MIS -C ), only 1 required dialysis." AISI may occur due to direct viral tropism to renal parencliyrna, liaeniodynamic com{aromise. cytokine storm and rnultiorgan dysfunction. High levels of ACE2 receptor ex{aression in proximal tulaular e{aitlieIia1 cells may be responsitale for viral tro{aisni and kidney injury. To conclude, AISI requiring renal re{alacement therapy is an unusual presentation of MIS -C. 

References

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