Author
HARDIN, S - BAYLOR COLL OF MEDICINE | |
Ellis, Kenneth | |
WILSON, DON - BAYLOR COLL OF MEDICINE |
Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only Publication Acceptance Date: 6/20/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Bartter's Syndrome (BS) is characterized by renal tubular dysfunction with resultant severe hypokalemia. These patients exhibit poor linear growth, but clinicians have been reluctant to treat with growth hormone secondary to insulin resistance (IR) which could be worsened by growth hormone (hGH). The goal of this study was to determine insulin sensitivity in BS, utilizing the hyperinsulinemic euglycemic clamp model, and to determine th relationship between IR and hypokalemia. We studied a male BS (12 yrs, 33 kg, Tanner II, Z score-2). Serum potassium (K+) averaged 3.9 meq/L over the previous 4 months. All medications were held for 18 hours prior to the study. The patient underwent two hyperinsulinemic euglycemic clamps (40 mU/m2/min); clamp #1 K+ = 2.5meq/L & clamp #2 K+ = 4.1meq/L. K+ was maintained at the initial level during each clamp. Total body potassium, 40K, was measured prior to the second clamp in BS. Growth hormone levels were measured at the initiation of each clamp. Results were compared to an age, weight, Z score and Tanner stage matched volunteer (C). Insulin sensitivity is reported as one-half maximal glucose disposal rate (GDR, mg/kg/min) measured at steady state after 2.5 hrs. GDR for the normal volunteer was 8.8 mg/kg/min. GDR for the BS patient was: clamp #1, hypokalemia, 4.0 mg/kg/min; clamp #2, normokalemia, 8.5 mg/kg/min. The peripheral insulin levels achieved during all clamp studies were similar (70mU/ml +/-4). 40K was normal prior to clamp #2 in BS. hGH levels were undetectable in the BS patient and did not change with normalization of K+ (BS#1<1.0,BS#2<1.0,C=1.8 ng/ml). |