Recurrent hypoglycemia leads to HAAF, with blunted counterregulatory hormone responses to subsequent hypoglycemic episodes. A recent report suggested inter-individual differences in susceptibility to HAAF (JCEM 102:3571, 2017). Since adrenergic receptor blockade prevents HAAF (Diabetes 60:602, 2011), we investigated to what extent the rises in plasma epinephrine (EPI) associated with hypoglycemia predict the development of HAAF. Healthy non-diabetic subjects (n=18, age 43±2years, BMI 25±1 kg/m2) underwent two 2-hour hypoglycemic clamp studies (nadir 54mg/dl; 0-2h and 4-6 h) on Day 1 followed by a third 2-hour hypoglycemic clamp on Day 2. Twelve subjects (67%) developed HAAF by the third episode, as defined by at least 20% reductions in peak EPI levels (peak EPI 1st vs. 3rd episode: HAAF subjects 1072±156 vs. 530±87pg/ml, p<0.001). Importantly, peak EPI levels during the 1st hypoglycemic episode were ∼83% higher in the subjects who developed HAAF compared to those who did not (p=0.02). To specifically define the role of EPI in the pathogenesis of HAAF, we challenged an additional seven non-diabetic subjects (age 32±4 years, BMI 25±1 kg/m2) with two 2-hour infusions of EPI (0.03 μg/kg/min;0-2h and 4-6 h) on Day 1 followed by 200-minute stepped hypoglycemic clamps (90, 80, 70 and 60 mg/dl, each for 50 minutes) on Day 2. Compared to saline, EPI infusion on Day 1 induced 40% and 28% reductions in epinephrine response to hypoglycemia at the 70 and 60 mg/dl glucose steps on Day 2, respectively (all p<0.05). There were parallel reductions in hypoglycemic symptoms (all p<0.05). Furthermore, the rate of glucose infusion was higher at all steps after EPI infusion (all p<0.05), consistent with a trend towards lower endogenous glucose production (6,6-D2-glucose). Thus, rises in EPI similar to those seen with hypoglycemia reproduce key features of HAAF in non-diabetic subjects. Marked inter-individual variability in EPI levels in response to hypoglycemia may explain why some people are more prone to develop HAAF. Disclosure E. Lontchi Yimagou: None. S. Aleksic: None. L. Upadhyay: None. S. Sharma: None. M. Carey: None. A. Goyal: None. J. You: None. R. Hulkower: None. S. Murthi: None. W.G. Mitchell: None. H. Shamoon: None. M. Hawkins: Other Relationship; Self; Novo Nordisk Inc. Funding American Diabetes Association (1-18-PMF-024 to E.L.Y.); National Institutes of Health (R01DK079974)

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Introduction: Chronic kidney disease (CKD) is common cause of renal failure. It involves a progressive loss in the structure and function of the kidneys over the course of months, with or without decreased glomerular filtration rate (GFR). CKD can be diagnosed by its pathological abnormalities, changes in the levels of renal function markers in the blood or urine, or by imaging investigations (E.g. USG etc). Objectives: The purpose of our study is 1) To correlate renal echogenicity with serum creatinine in order to determine the significance of renal echogenicity for identifying the progression of chronic kidney disease (CKD) and for the sonographic grading of CKD, 2) To study association of blood pressure, renal cortical cysts and renal size with grade of chronic renal disease. Methods: This hospital based cross sectional study was carried out at National Kidney Centre, Banasthali Kathmandu. Two hundred patients above 20 years, diagnosed with CKD according to the guidelines of the National Kidney Foundation and referred for USG, were included in the study. Patients with kidney transplant, on dialysis, with liver disease and renal tumors were excluded. Ultrasound of kidneys was performed by senior consultant radiologist who was blind to the patients’ serum creatinine levels. The relationship between grade of CKD with serum creatinine, kidney size, blood pressure and cortical cysts were assessed. Statistical analysis was performed by Kruskal wallis test using SPSS version 17. P values less than 0.05 were considered statistically significant. Results: Mean serum creatinine was 1.7 mg/dl for Grade 1 (range: 1.1- 4.7 mg/dl, STD 0.44), 2.38 mg/dl for Grade 2 (range: 1.8-3.9 mg/dl STD 0.40), 4.18 mg/dl for Grade 3 (range: 2.6-6.0 mg/dl, STD 0.88), and 5.65 mg/dl for Grade 4 (range: 3.1-12 mg/dl, STD 2.0. Conclusion: Renal echogenicity and its grading correlates better with serum creatinine in CKD than other sonographic parameters. Hence, renal echogenicity is a better parameter than serum creatinine for estimating renal function in CKD, and has the added advantage of irreversibility.

Sturge–Weber syndrome is a rare congenital neurocutaneous disorder characterized by dermatological, ophthalmological, and neurological manifestations. It occurs due to abnormal persistence of embryonic vascular plexus. Here, we describe a case of four years seven months female with seizures, developmental delay, intellectual disability, and bilateral port-wine stain diagnosed as type I (classical) Sturge–Weber syndrome. The ophthalmological evaluation was unremarkable. Electroencephalogram showed abnormalities suggestive of a structural lesion in the right cerebral hemisphere. CT scan of the head revealed volume loss of right brain parenchyma with linear, cortical, as well as subcortical calcifications more evident in the right hemisphere. The child should be followed up regularly until adulthood for ophthalmological evaluation, recurrence of seizures, and other manifestations of this disorder.