In our case, the onset of fever, followed by cracked lips, generalized rash, swollen hands and feet, and extensive peeling in the erythematous perineal area occurs in the acute phase of KD, which typically lasts 10–14 days.

Diffuse erythema in the genital area that peels during the acute phase is seen in up to half of patients. The average platelet count and absence of coronary artery dilatation initially indicate the acute clinical phase.

The subacute phase began when the fever was resolved, the skin was desquamated in the hands and feet, and the increase in platelets over time required repeated echocardiography, which showed the characteristic condition at this stage: coronary artery dilatation [1, 20, 22].

Since KD is a systemic vasculitis, there can be several organs involved. Coronary lesions are the most severe and common complications in KD, which occur in 25% of untreated children [5,6,7, 22]. During the COVID-19 pandemic, the suspicion of a multisystemic inflammatory syndrome in children (MIS-C) is logical after a history of fever lasting more than 24 hours in individuals aged < 21 years, with evidence of inflammation (elevated levels of erythrocyte sedimentation rate, C-reactive protein, ferritin, and D-dimer); severe illness requiring hospitalization with multiple systems involving more than two systems, including echocardiogram findings; AKI; and dermatologic findings (rash, dry lips with crack), with fulfillment of partial criteria for atypical KD.

MIS-C criteria must include positive results for current or recent SARS-CoV-2 infection detected on polymerase chain reaction, serology, or antigen testing or COVID-19 exposure within 4 weeks prior, which were all negative in the present case. Furthermore, normal fibrinogen, procalcitonin, and LDH do not support the diagnosis [19].

As for renal involvement in KD, sterile pyuria is the most common urinary presentation, followed by various other manifestations, such as proteinuria and hematuria [1, 8,9,10,11]. It is unsurprising that the patient, in this case, had sterile pyuria and microscopic hematuria (Table 3).

AKI is rarely associated with KD. Interestingly, Chuang et al. investigated the clinical features and data of 336 Taiwanese patients with KD, including their serum creatinine (SCr) levels, and reported that 28% of them developed AKI. They linked the risk to two factors: the young age, which applies to our case, and the high alanine transaminase level, which does not apply to our case, as she had normal levels [12].

Mousa et al. [2] were the first to report cases of KD in Saudi Arabia, with three cases were saudi nationals.

From the capital, that is, the central region, Ghazal et al. [3] studied 29 patients with KD at Sulaimania Children’s Hospital in Riyadh for 8 years. Muzaffer et al. reviewed 13 medical records/referral letters of patients diagnosed with KD at King Faisal Specialist Hospital and Research Center, Riyadh (1997–2001). None of them reported having AKI [7].

Alsaggaf et al. analyzed 56 children diagnosed with atypical KD for over 12 years [17]. Khalid Alharbi studied 51 patients suspected of having KD [5], and Lardhi also studied 35 patients [6], none of whom had AKI. These studies took place in the western and eastern parts of the Kingdom.

In addition, a retrospective study was conducted in the southwest of the Kingdom (Albaha), which included 40 children with KD, none of whom reported having AKI [21].

On the contrary, AKI is not uncommon in the Kingdom. In a recent multicenter prospective cohort study by the Kingdom of Saudi Arabia (KSA) conducted using the KDIGO definition, 37.4% of critically ill children had AKI. Although sepsis, infections, and postcardiac surgery were the most common causes, KD was not reported as an etiology [10].

AKI is usually divided into three broad groups depending on the cause: prerenal AKI, described by reduced kidney perfusion in cases with no parenchymal injury; renal parenchymal injuries causing renal AKI; and postrenal AKI caused by obstruction of the urinary tract [10].

Both prerenal and renal AKI have been reported in patients with KD. Tubular interstitial nephritis, hemolytic uremic syndrome, immune-complex mediated nephropathy, and KD shock syndrome have been described as causes of renal AKI. Meanwhile, acute congestive heart failure and fluid loss have been described as causes of prerenal AKI [8, 10, 14, 15].

AKI in our patient may have been due to prerenal AKI, which is secondary to dehydration, as there was evidence of poor intake for several days before presentation, which explains the cracked lips and poor appetite. The kidney biopsy was not performed when the patient’s kidneys opened, and the renal function normalized with the beginning of AKI management.

Treatment of KD patients with prerenal AKI involves the appropriate restoration of normal circulating blood volume, and it must be adjusted to the severity of AKI through fluid restriction, diuretic use, and renal replacement therapy, in addition to the specific therapy for KD [10]. This describes the response of the intravenous bolus and Lasix, intravenous immunoglobulin, and aspirin [22]. Fortunately, the recovery was achieved without dialysis.

Kari [23] showed that AKI is associated with increased mortality after discharge, and oliguria is a predictor that increases mortality [10].

Regular follow-up appointments were given to the patient, and the parents were informed of its importance.

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