Is there a relationship between hyperchloremia status and the risk of developing acute kidney injury in pediatric patients with diabetic ketoacidosis?

Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes mellitus (T1DM). Prerenal acute kidney injury (AKI) is associated with profound hypovolemia and reduced renal perfusion. Results regarding hyperchloremia-associated AKI in patients with DKA are conflicting; we therefore investigated the potential relationship between hyperchloremia status and the risk of developing AKI. This single-center cohort study included 113 newly diagnosed T1DM patients with DKA admitted to the pediatric intensive care unit. Laboratory parameters, including Na, K, urea, creatinine, and chloride levels, were retrospectively reviewed at the time of presentation and at 12, 24 and 36 h. AKI was defined using the eGFR according to the pediatric RIFLE classification criteria. Twenty-two (19.5%) of the 113 patients were in the AKI group. Two-way repeated-measures ANOVA showed significant (P values ≤ 0.01) time interaction effects within the groups based on the eGFR and the serum chloride, hyperchloremia, and phosphate levels. Serum chloride levels did not differ between the groups during the first 12 h (p > 0.05) but were significantly greater in the AKI group than in the non-AKI group at 24 h and 36 h (p < 0.01). The final DKA resolution time was significantly greater in the AKI group than in the non-AKI group [22.2 (9.5) vs. 17.0 (12.0) h, respectively; p = 0.03]. However, the groups had similar lengths of hospital stay [13.0 (8.0) days vs. 12.0 (4.0) days, respectively; p = 0.17].Conclusions: Hyperchloremia may be iatrogenic rather than causative during treatment. This may worsen renal failure and prolong the recovery and treatment time for DKA patients. What is Known? • Acute kidney injury resulting from severe volume depletion is a common occurrence in diabetic ketoacidosis and typically requires significant volume replacement therapy. • In recent years, hyperchloremia has been associated with increased risks of AKI, morbidity, and mortality in some conditions, such as diabetic ketoacidosis. What is New? • The incidence of hyperchloremia increases over time during the treatment of diabetic ketoacidosis. • Hyperchloremia may be an iatrogenic element rather than a cause of acute kidney injury during the treatment of diabetic ketoacidosis.

Compatibility levels between blood gas analysis and central laboratory hemoglobin and electrolyte tests in pediatric patients: A single-center experience.

INTRODUCTION: We aimed to evaluate the interchangeability of sodium, potassium, hemoglobin, and hematocrit measurement between the blood gas analyzers and laboratory automatic analyzers results. METHODS: This was a retrospective cross-sectional study. The results of 1927 paired samples analyzed simultaneously with the blood gas analyzer and the laboratory automatic analyzer were compared. The Bland-Altman and Cohen's kappa statistic detected the agreement between the two analyses. RESULTS: The limits of agreement (±1.96 standard deviation of the mean difference) were -11.1 to 20.3 for sodium, -1.9 to 0.5 for potassium, -16.1 to 12.9 for hematocrit, and -5.0 to 4.0 for hemoglobin. Agreement between the two analyses was not acceptable within the defined clinically acceptable limits. In addition, none of the kappa values were higher than 0.60, which highlights the lack of agreement between the two analyzers. CONCLUSION: The blood gas analyzers and laboratory automatic analyzers results cannot be used interchangeably.

The comparison of COVID-19 vs seasonal influenza in children.

BACKGROUND: Influenza in children has been well described, whereas there has been a paucity of pediatric data regarding COVID-19. It is crucial for clinicians to differentiate cases of COVID-19 from cases of influenza because of the upcoming influenza season in the new pandemic era. METHODS: This retrospective study included pediatric patients who were diagnosed with laboratory-confirmed COVID-19 between March and September 2020, or seasonal influenza between October 2019 and March 2020. RESULTS: A total of 315 children were included in this study; 151 were diagnosed with influenza and 164 had confirmed COVID-19. The median age of patients with COVID-19 was 10 years (interquartile range [IQR]: 3-15 years), whereas the median age of patients with influenza was 4 years (IQR: 1-6 years) (p = 0.001). In the COVID-19 group, 6.3% of patients had underlying diseases, the most frequent being neurological conditions (3%). In the influenza group, 20.9% of patients had an underlying disease, the most frequent being asthma (14.5%). Fever (odds ratio [OR]: 20.476; 95% confidence interval [CI]: 2.438-171.995; p = 0.005), dyspnea/tachypnea (OR 13.950; 95% CI: 2.607-74.634; p = 0.002), and increased C-reactive protein (CRP) (OR: 7.650; 95% CI: 2.094-27.955; p = 0.002) were main predictors of influenza diagnosis in comparison to COVID-19. Lymphopenia was detected in 43.2% of patients with influenza and 19.9% of patients with COVID-19 (p = 0.001). CONCLUSIONS: The accurate differentiation between "influenza or COVID-19" seems possible by evaluating a combination of factors including cough, fever, vomiting, leucopenia, lymphopenia, pneumonia, in pediatric patients with high CRP as well as age.

The association of vitamin D deficiency with hemogram-derived inflammatory biomarkers in children.

BACKGROUND AND AIMS: One of the extraosseous effects of vitamin D is that it is a potent modulator of inflammatory processes. Many studies have demonstrated the inverse association between vitamin D and inflammation. Therefore, we hypothesize that vitamin D deficiency may affect the inflammatory markers derived from hemogram parameters [neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), lymphocyte to monocyte ratio (LMR), platelet distribution width (PDW), red blood cell distribution width (RDW)] in healthy children. METHODS AND RESULTS: We conducted a retrospective study on healthy children. From 2015 to 2020, 16,321 children with simultaneous vitamin D and hemogram measurements were identified from electronic records. Participants were divided into 2 groups according to whether they had vitamin D deficiency or not. The relationship between vitamin D status and the levels of inflammatory markers was analyzed. All inflammatory markers showed statistically significant differences between vitamin D status (p < 0.001 for all). Vitamin D levels were significantly negatively correlated with NLR (r = -0.285), PLR (r = -0.257), PDW (r = -0.181), and positively correlated with LMR (r = 0.218), and RDW (r = 0.057). In logistic regression analysis, age (OR = 1.15, 95% CI: 1.14-1.16), gender (OR = 1.66, 95% CI: 1.54-1.78), LMR (OR = 0.96, 95% CI: 0.95-0.98), PLR (OR = 1.003, 95% CI: 1.001-1.004), and RDW (OR = 1.10, 95%CI: 1.07-1.13) were found to be independent predictors for vitamin D deficiency. CONCLUSIONS: Statistically significant differences were detected between vitamin D status and inflammatory parameters. However, the difference between the median values of vitamin D groups was very small and the degree of correlation was very weak. Therefore, the clinical significance of the difference should be questioned.

The Potential Role of Cell-Death Mechanisms in the Pathogenesis of Familial Mediterranean Fever Attacks: Granzyme A and Beyond.

BACKGROUND: FMF is the most common autoinflammatory disease. The activation of the pyrin inflammasome is the mainstay of the pathogenesis, which might lead to a specific cell-death mechanism, pyroptosis. Pyroptosis is a programmed inflammatory cell death mediated by gasdermin proteins, featuring cell swelling, membrane rupture, and release of inflammatory contents Aim: In this study we aimed to analyze the cell-death mechanisms in the pathogenesis of FMF attacks. METHODS: Twenty-five FMF patients were included, and PFAPA patients (n = 10) and healthy controls (HC, n = 10) served as controls. We collected plasma samples from FMF and PFAPA patients during the attack and the attack-free period. We measured the soluble plasma levels of sFas, sFasL, granzyme A, granzyme B, perforin, granulysin, IL-2, IL-4, IL-10, IL-6, IL-17A, TNF-α, and IFN-γ by commercial pre-defined cytometric bead array kits. RESULTS: There was no significant difference between groups in terms of sex and age between FMF patients and HCs, but PFAPA patients were younger than other groups due to the nature of the disease. We then analyzed the components of apoptosis and pyroptosis. The levels of sFasL (p = 0.035) and granzyme A (p = 0.038) in FMF patients were significantly increased during the attack period and decreased to levels comparable to HCs during the attack-free period. This increase was not seen in the PFAPA patients, with comparable levels with the HC group both during attack period and attack-free period. During the attack period of FMF patients, granzyme B (p = 0.145) and perforin (p = 0.203) levels were also increased; however, the differences were not statistically significant. The levels of sFasL, granzyme A, granzyme B, and perforin were closely correlated with each other during the attack period of FMF patients. CONCLUSIONS: Our study on death pathways during an FMF attack, suggests an upregulation in both pyroptosis through the granzyme-gasdermin pathway and apoptosis with the increased FasL and perforin levels, which was different from PFAPA patients. These findings might shed light on the reason for the nature of self-limited attacks, but further studies are needed to prove this hypothesis.