Role of cerebrospinal fluid tau protein levels as a biomarker of brain injury in pediatric status epilepticus.

BACKGROUND: Various biomarkers have been studied for predicting etiology and outcome in status epilepticus (SE); cerebrospinal fluid (CSF) total tau (t-tau) protein levels is foremost among them. Only handful of studies are available regarding role of t-tau in childhood SE. METHODOLOGY: This prospective study was conducted in a tertiary care center of Northern India in children 6 months -12 years of age. The Cases were patients with convulsive status epilepticus (CSE) whereas Controls were patients without SE and normal CSF. The t-tau levels were done in CSF of both the groups. The outcome was assessed by GOS-E Peds score. RESULTS: A total of 50 (62% males) cases and 15 (67% males) controls were enrolled in the study. SE was generalized in 78% cases whereas 14% had refractory SE. Most common etiology of CSE was acute symptomatic (52%), followed by prolonged febrile seizure (24%), remote symptomatic group (14%), unknown etiology (8%) and progressive disorder (2%). Case fatality rate was 10%. Poor outcome was seen in 30% cases. Median (IQR) CSF t-tau levels was significantly lower 2.6 × 103 (0.5-9.4 × 103) pg/ml in cases vs 10.6 × 103 (6.0-14.2 × 103) pg/ml in controls (p = 0.004). There was no significant correlation seen between type, duration, etiology and response to antiepileptic drugs of SE with CSF t-tau levels. Also, no significant correlation of poor sensorium, outcome of SE and critical care needs with CSF t-tau levels was noted. CONCLUSION: CSF t-tau is not a useful diagnostic or prognostic biomarker in pediatric SE.

Early diagnosis of kidney injury in a paediatric population: a prospective cohort study (E-DRIP STUDY).

BACKGROUND: Renal Angina Index (RAI) is a bedside tool for risk stratification of patients to predict acute kidney injury (AKI). Kidney biomarkers are better indicators of real-time injury and give us lead time for diagnosing impending AKI. METHODS: We enrolled consecutive children aged 2 months-14 years admitted to a tertiary hospital in northern India over 2 years. RAI was calculated on day 0 (D0) and urinary (u) and plasma (p) neutrophil gelatinase-associated lipocalin (NGAL) were measured within 6 h of admission. Children were followed for the development of severe AKI on day 3 (D3) using Kidney Disease Improving Global Outcomes criteria to define and stage AKI. RESULTS: Of the 253 children enrolled and analysed, 44 (17.4%) developed D3-AKI (stage 1 in 52.2%, stage 2 in 20.5% and stage 3 in 27.3%). Renal angina (RAI ≥ 8) on D0 was present in 66.7% children who developed stage 2/3 D3-AKI vs. 43.5% in children who did not develop D3-AKI /stage 1 AKI (p = 0.065). Area under ROC (AUROC) curve for D0-RAI to predict D3-severe-AKI was 0.66 (95% CI, 0.55-0.77). AUROC curve for uNGAL and pNGAL to predict D3-severe-AKI was 0.62 (95% CI, 0.50-0.74) and 0.48 (95% CI, 0.35-0.61), respectively. The severe AKI group had greater requirement of ventilation and inotropic support with mortality being thrice higher compared to the non-AKI group. CONCLUSION: RAI ≥ 8 and uNGAL had a high negative predictive value but low sensitivity for predicting D3-severe-AKI. pNGAL had a poor predictive value for D3-severe-AKI. A higher resolution version of the Graphical abstract is available as Supplementary information.

Lipoprotein (a) in type 2 diabetes mellitus: Relation to LDL:HDL ratio and glycemic control.

BACKGROUND: Increased lipoprotein (a) [Lp (a)] concentrations are predictive of coronary artery disease (CAD). Type 2 diabetes mellitus also leads to dyslipidemia, like elevated triglyceride levels and low HDL levels, which are known risk factors for CAD. This study was designed to investigate the levels of Lp (a) in type 2 diabetic patients and their association with LDL: HDL ratio and glycemic control. MATERIALS AND METHODS: The study included 60 patients of type 2 diabetes and 50 age and sex matched controls. The Lp(a) levels in the diabetic group were compared with the control group and the relationship between the Lp(a) levels and LDL: HDL ratio was evaluated. Diabetic group was further divided into three subgroups according to levels of glycated hemoglobin. Lp(a) levels and glycated hemoglobin in controlled and uncontrolled diabetes mellitus were also compared to find out any correlation between them. Statistical analysis was done using the students 't' test and Chi square test. RESULTS: Lp(a) levels were found to be significantly increased in the diabetic group as compared to the control group (P< 0.001). LDL: HDL ratio was also increased in the diabetic group as compared to the control group. Lp(a) levels showed no association with LDL: HDL ratio and degree of glycemic control in these patients. CONCLUSIONS: The results of the present study suggest that Lp(a) levels are increased in type 2 diabetic patients. The elevated Lp(a) levels do not reflect the glycemic status and are also independent of increase in LDL:HDL ratio suggesting different metabolic pathways and the genetic connection for LDL and Lp(a).