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The purpose of this study was to evaluate the relationship between the presence of pneumonia and blood parameters in casesof Coronavirus disease (COVID-19) and to examine their predictive characteristics in terms of pneumonia. We reviewed the filerecords of 151 pediatric patients with a diagnosis of COVID-19 confirmed by the real time-reverse transcription polymerase chainreaction test in nasopharyngeal swabs. The patients were divided into two groups based on direct chest X-ray and computedtomography results in [Group 1 (n:41), with pneumonia findings, and Group 2 (n:110), with no pneumonia findings]. The groups’demographic data, clinical and laboratory findings were compared. Pulmonary involvement was determined in 41 (27.1%) ofthe 151 patients. The [body mass index (BMI) Z-score], red blood cell distribution width (RDW), mean platelet volume (MPV),neutrophil lymphocyte ratio, passive leg raise, and D-dimer levels were significantly higher in patients with pneumonia than thosewithout pneumonia in our study. Based on multivariate logistic regression analysis, BMI Z-score, MPV, and RDW were found tobe independent risk factors of pneumonia in patients. The current study showed higher levels of blood parameters in patients withcoronavirus disease 2019 (COVID -19) presenting with pneumonia than those without pneumonia. We suggest that BMI-Z scoreand MPV value may assist in predicting pulmonary involvement in patients with COVID-19.

Objective Congenital nephrogenic diabetes insipidus (CNDI) is a rare inherited disorder characterized by a renal insensitivity to arginine vasopressin (AVP). In the majority of the cases, CNDI is caused by mutations in the arginine vasopressin receptor 2 (AVPR2) gene. Our objective is to report a novel mutation in the AVPR2 gene causing CNDI in a 6-year-old boy, presenting with growth failure and dull normal cognitive functions. Methods The proband was the third off-spring of non-consanguineous parents and had polyuria (4.3 L/day), polydipsia (5 L/day). The diagnosis of CNDI was established by a water-deprivation test and a desmopressin challenge test. Genetic studies were also carried out in the mother, siblings and affected family members, since excessive fluid intake and diuresis were also reported in these individuals. All exons of the AVPR2 gene for all participants were amplified and sequenced. Bioinformatics analysis for wild-type and mutant AVPR2 were obtained with Swiss-Model and UCSF Chimera 1.10.2. Results A novel, hemizygous, missense mutation was identified at the position 80th in exon 2 (p.H80Y) of AVPR2 in the proband. The proband’s mother, maternal aunt and grandmother were heterozygous and his maternal uncle was hemizygous for this mutation. Bioinformatic analysis indicates this mutation would cause significant conformational changes in protein structure. Conclusion p.H80Y mutation will cause inappropriate folding of the protein compromising water homeostasis via AVPR2 and AVP and leading to diabetes insipidus. We suggest that future functional investigations of the H80Y mutation may provide a basis for understanding the pathophysiology of the NDI in patients with this variant.