John Ferretti

Insulin regulation of renal glucose metabolism in humans

Eighteen healthy subjects had arterialized hand and renal veins catheterized after an overnight fast. Systemic and renal glucose and glycerol kinetics were measured with [6,6-2H2]glucose and [2-13C]glycerol before and after 180-min peripheral infusions of insulin at 0.125 (LO) or 0.25 (HI) mU. kg-1. min-1 with variable [6, 6-2H2]dextrose or saline (control). Renal plasma flow was determined by plasma p-aminohippurate clearance. Arterial insulin increased from 37 +/- 8 to 53 +/- 5 (LO) and to 102 +/- 10 pM (HI, P < 0.01) but not in control (35 +/- 8 pM). Arterial glucose did not change and averaged 5.2 +/- 0.1 (control), 4.7 +/- 0.2 (LO), and 5.1 +/- 0. 2 (HI) micromol/ml; renal vein glucose decreased from 4.8 +/- 0.2 to 4.5 +/- 0.2 micromol/ml (LO) and from 5.3 +/- 0.2 to 4.9 +/- 0.1 micromol/ml (HI) with insulin but not saline infusion (5.3 +/- 0.1 micromol/ml). Endogenous glucose production decreased from 9.9 +/- 0. 7 to 6.9 +/- 0.5 (LO) and to 5.7 +/- 0.5 (HI) micromol. kg-1. min-1; renal glucose production decreased from 2.5 +/- 0.6 to 1.5 +/- 0.5 (LO) and to 1.2 +/- 0.6 (HI) micromol. kg-1. min-1, whereas renal glucose utilization increased from 1.5 +/- 0.6 to 2.6 +/- 0.7 (LO) and to 2.9 +/- 0.7 (HI) micromol. kg-1. min-1 after insulin infusion (all P < 0.05 vs. baseline). Neither endogenous glucose production (10.0 +/- 0.4), renal glucose production (1.1 +/- 0.4), nor renal glucose utilization (0.8 +/- 0.4) changed in the control group. During insulin infusion, systemic gluconeogenesis from glycerol decreased from 0.67 +/- 0.05 to 0.18 +/- 0.02 (LO) and from 0.60 +/- 0.04 to 0.20 +/- 0.02 (HI) micromol. kg-1. min-1 (P < 0.01), and renal gluconeogenesis from glycerol decreased from 0.10 +/- 0.02 to 0.02 +/- 0.02 (LO) and from 0.15 +/- 0.03 to 0.09 +/- 0.03 (HI) micromol. kg-1. min-1 (P < 0.05). In contrast, during saline infusion, systemic (0.66 +/- 0.03 vs. 0.82 +/- 0.05 micromol. kg-1. min-1) and renal gluconeogenesis from glycerol (0.11 +/- 0.02 vs. 0. 41 +/- 0.04 micromol. kg-1. min-1) increased (P < 0.05 vs. baseline). We conclude that glucose production and utilization by the kidney are important insulin-responsive components of glucose metabolism in humans.Eighteen healthy subjects had arterialized hand and renal veins catheterized after an overnight fast. Systemic and renal glucose and glycerol kinetics were measured with [6,6-2H2]glucose and [2-13C]glycerol before and after 180-min peripheral infusions of insulin at 0.125 (LO) or 0.25 (HI) mU ⋅ kg-1 ⋅ min-1with variable [6,6-2H2]dextrose or saline (control). Renal plasma flow was determined by plasma p-aminohippurate clearance. Arterial insulin increased from 37 ± 8 to 53 ± 5 (LO) and to 102 ± 10 pM (HI, P < 0.01) but not in control (35 ± 8 pM). Arterial glucose did not change and averaged 5.2 ± 0.1 (control), 4.7 ± 0.2 (LO), and 5.1 ± 0.2 (HI) μmol/ml; renal vein glucose decreased from 4.8 ± 0.2 to 4.5 ± 0.2 μmol/ml (LO) and from 5.3 ± 0.2 to 4.9 ± 0.1 μmol/ml (HI) with insulin but not saline infusion (5.3 ± 0.1 μmol/ml). Endogenous glucose production decreased from 9.9 ± 0.7 to 6.9 ± 0.5 (LO) and to 5.7 ± 0.5 (HI) μmol ⋅ kg-1 ⋅ min-1; renal glucose production decreased from 2.5 ± 0.6 to 1.5 ± 0.5 (LO) and to 1.2 ± 0.6 (HI) μmol ⋅ kg-1 ⋅ min-1, whereas renal glucose utilization increased from 1.5 ± 0.6 to 2.6 ± 0.7 (LO) and to 2.9 ± 0.7 (HI) μmol ⋅ kg-1 ⋅ min-1after insulin infusion (all P < 0.05 vs. baseline). Neither endogenous glucose production (10.0 ± 0.4), renal glucose production (1.1 ± 0.4), nor renal glucose utilization (0.8 ± 0.4) changed in the control group. During insulin infusion, systemic gluconeogenesis from glycerol decreased from 0.67 ± 0.05 to 0.18 ± 0.02 (LO) and from 0.60 ± 0.04 to 0.20 ± 0.02 (HI) μmol ⋅ kg-1 ⋅ min-1( P < 0.01), and renal gluconeogenesis from glycerol decreased from 0.10 ± 0.02 to 0.02 ± 0.02 (LO) and from 0.15 ± 0.03 to 0.09 ± 0.03 (HI) μmol ⋅ kg-1 ⋅ min-1( P < 0.05). In contrast, during saline infusion, systemic (0.66 ± 0.03 vs. 0.82 ± 0.05 μmol ⋅ kg-1 ⋅ min-1) and renal gluconeogenesis from glycerol (0.11 ± 0.02 vs. 0.41 ± 0.04 μmol ⋅ kg-1 ⋅ min-1) increased ( P < 0.05 vs. baseline). We conclude that glucose production and utilization by the kidney are important insulin-responsive components of glucose metabolism in humans.

Regulation of splanchnic and renal substrate supply by insulin in humans.

To determine the effects of peripheral insulin infusion on total, hepatic, and renal glucose production and on the percent contribution to glucose production of gluconeogenesis versus glycogenolysis, 10 healthy subjects had arterialized hand and hepatic vein catheterization after an overnight fast and the results were compared with data from 12 age- and weight-matched subjects with renal vein catheterization during a 180-minute infusion of either insulin (0.25 mU/kg x min) with dextrose, or saline. Endogenous, hepatic, and renal glucose production was measured with [6,6(-2)H2]glucose, regional lactate, alanine, and glycerol balance by arteriovenous difference; hepatic blood flow by indocyanine green clearance; and renal blood flow by p-aminohippurate clearance, before and every 30 minutes during each infusion period. Insulin increased from about 42 to 98 pmol/L and blood glucose remained constant in all studies (3.8 +/- 0.2 v4.4 +/- 0.1 micromol/ml, hepatic vrenal vein). In response to insulin infusion, endogenous, hepatic, and renal glucose production decreased immediately (30 minutes) and reached a lower plateau value (10.8 +/- 0.8 v6.4 +/- 0.7, 10.4 +/- 1.1 v7.8 +/- 1.0, and 2.8 +/- 0.6 v 1.5 +/- 0.6 micromol/kg x min, respectively) between 120 and 180 minutes (all P < .05). Net renal uptake of lactate (2.4 +/- 0.4 v0.9 +/- 0.6) decreased earlier (30 minutes) and returned to baseline between 120 and 180 minutes (2.4 +/- 0.5 micromol/kg x min), whereas net splanchnic uptake of lactate (5.7 +/- 0.7 v 0.7 +/- 0.6) and alanine (1.8 +/- 0.1 v 1.0 +/- 0.5 micromol/kg x min) decreased later (120 to 180 minutes). Net renal (0.3 +/- 0.1 v 0.1 +/- 0.1) and splanchnic (0.7 +/- 0.3 v 0.4 +/- 0.2 micromol/kg x min) glycerol uptake decreased 90 to 180 minutes after insulin and increased (P < .05) with saline infusion (0.4 +/- 0.1 v0.6 +/- 0.3 and 1.0 +/- 0.5 v1.8 +/- 0.4 micromol/kg x min, respectively). These data indicate that the rapid suppression of endogenous glucose production by insulin reflects primarily a decrease in hepatic glucose release, most likely due to inhibition of net glycogenolysis, combined with suppression of renal gluconeogenesis. Inhibition of hepatic gluconeogenesis presumably occurs later during hyperinsulinemia. We conclude that peripheral insulin, in addition to its inhibition of glycogen degradation, regulates endogenous glucose production, in part, by modifying the splanchnic and renal substrate supply.

Endovascular Covered Stenting for Visceral Artery Pseudoaneurysm Rupture: Report of 2 Cases and a Summary of the Disease Process and Treatment Options

We present 2 cases of hemorrhage from a visceral artery pseudoaneurysm, managed successfully with endovascular covered stent placement. The first case was a 59-year-old man, 3 months after a laparoscopic distal pancreatectomy for adenoma, presenting with diffuse abdominal pain. The patient was evaluated with a computed tomography scan revealing a splenic artery pseudoaneurysm (PA) bleeding into a pancreatic pseudocyst. He was emergently taken to the angiography suite where a covered stent was deployed at the level of splenic artery PA. The second case was a 52-year-old woman with recurrent left retroperitoneal mass 5 years after distal pancreatectomy and splenectomy for a nonfunctional neuroendocrine tumor. She underwent resection of the mass in the left upper quadrant. Postoperative course was complicated by hematoma, abscess formation, reexploration, and repair of the duodenotomy and the portal vein. Subsequently, she was noted to have intermittent gastrointestinal hemorrhage, which prompted an angiogram revealing a hepatic artery PA that was repaired with a covered balloon-expandable stent. A completion angiogram was obtained in each case demonstrating exclusion of the PA. Our experience with these 2 cases supports the notion that endovascular covered stenting is a safe and effective therapy for exclusion of visceral artery aneurysm.

Prospective determination of candidates for thrombolysis in patients with acute proximal deep vein thrombosis.

PURPOSE To prospectively determine the distribution, extent, and age of venous thrombosis in patients presenting with acute signs and symptoms of venous thromboembolism and identify candidates for thrombolysis. MATERIALS AND METHODS Five hundred seventy-six consecutive patients (281 male, 295 female; mean age 58) referred for lower extremity deep vein thrombosis (DVT) assessment between November 2007 and April 2008 were included in the study. Documented cases of DVT were categorized by age (acute, chronic, and acute on chronic), anatomic location, and extent. Patients with iliofemoral and femoropopliteal DVT were evaluated for thrombolysis using standard criteria. RESULTS DVT was found in 19% of patients (112/576). Of these, 31 patients (27.7%, 31/112) had isolated calf DVT, 61 patients (54.5%, 61/112) had proximal vein thrombosis extending into the femoropopliteal venous segments, and 20 patients (17.9%, 20/112) presented with iliofemoral DVT. Using standard criteria, 12 patients were selected as potential candidates for pharmacomechanical thrombolysis (PhMT). This equated to an incidence of 2% (12/576) in the population studied, 11% of patients (12/112) with DVT, 26.1% of patients (12/46) presenting with acute proximal DVT, and 20% of patients (4/20) with iliofemoral DVT. CONCLUSION The incidence of potential candidates for thrombolysis is low. These data should be considered when recruiting centers to participate in ongoing clinical trials assessing the efficacy of these techniques.

Endovascular repair of an arteriovenous fistula from a ruptured hypogastric artery aneurysm--a case report.

A spontaneous ilioiliac arteriovenous fistula secondary to rupture of a hypogastric artery aneurysm is an unusual occurrence. A case of an endovascular repair of this challenging problem is reported.

Inferior vena cava filter migration with severe deformity of filter.

6. Hartung O, Grisoli D, Boufi M, et al. Endovascular stenting in the treatment of pelvic vein congestion caused by nutcracker syndrome: lessons learned from the first five cases. J Vasc Surg 2005; 42:275–280. 7. Basile A, Tsetis D, Calcara G, et al. Percutaneous nitinol stent implantation in the treatment of nutcracker syndrome in young adults, J Vasc Interv Radiol 2007; 18:1042–1046. 8. Kim SJ, Kim CW, Kim S, et al. Long-term follow-up after endovascular stent placement for treatment of nutcracker syndrome, J Vasc Interv Radiol 2005; 16:428–431.

Evolution of Type II Endoleaks Based on Different Ultrasound-Identified Patterns

Objective: The objective of this study was to delineate the specific types of waveforms that exist in type II endoleaks (T2ELs) and their effect on aneurysm sac size. Methods: Patients who underwent an endovascular aneurysm repair and were diagnosed with a T2EL were included in the study. The flow velocity characteristics of the T2ELs were evaluated in detail with duplex ultrasound. Four different flow patterns were identified: high resistance, low flow; low resistance, low flow; low resistance, high flow; and to‐fro flow. The type and number of vessels involved, time at detection, evolution, and need for treatment were recorded. The aneurysm sac diameter was monitored with duplex ultrasound. A computed tomography scan was always performed at baseline within 1 month of the procedure and repeated only when symptoms developed or there were changes in the ultrasound examination findings, such as sac enlargement. Results: Of 382 patients who underwent endovascular aneurysm repair in our institution, 56 (14.65%) were found to have a T2EL. There were 52 male and four female patients with a mean age of 74 years (61–86 years). The T2EL was diagnosed within the first month in 32 patients; 9 patients were diagnosed at 3 months, 5 patients at 6 months, 3 patients at 9 months, and 7 patients at 1 year or later. There were 43 patients who had a T2EL involving one vessel; two vessels were involved in 11 patients and three vessels were involved in two patients. During follow‐up, several changes were observed for the different types of T2EL. High‐resistance, low‐flow endoleak was detected in 14 patients; of those, 13 were occluded and 1 converted to high flow. Low‐resistance, low‐flow endoleak was detected in seven patients; of those, 5 were occluded, 1 remained stable, and 1 converted to high flow with sac enlargement requiring treatment. Low‐resistance, high‐flow endoleak was found in 13 patients; of those, 8 were occluded, 3 remained stable, and 2 had sac enlargement requiring treatment; 1 patient presented with rupture. Finally, to‐fro flow was identified in the majority of the patients (22); of those, 14 occluded, 3 remained stable, and 5 had sac enlargement requiring treatment; 2 patients presented with rupture. No deaths due to T2EL were encountered. Conclusions: Most of the T2ELs resulted in spontaneous occlusion and were not associated with sac enlargement. A low‐resistance, high‐flow or to‐fro flow T2EL has higher chances of sac enlargement, rupture, and requiring reintervention.

Abstract from the 2017 Society for Clinical Vascular Surgery Annual MeetingEvolution of Type II Endoleaks Based on Different Ultrasound-Identified Patterns

Christian-Alexander Behrendt, MD, Sebastian Debus, MD, PhD, Yskert von Kodolitsch, MD, Devin Zarkowsky, MD, Richard J. Powell, MD, Melanie Pepin, MS, CGC, Peter Byers, MD, Peter LawrenceMD. UniversityofWashington,Seattle,WA; DivisionofVascular Surgery, University of California Los Angeles, Los Angeles, CA; Section of Vascular Surgery, University of Michigan, Ann Arbor, MI; Department of Cardiovascular and Thoracic Sciences, University of Messina, Messina, Italy; Division of Human Genetics, Cincinnati Children’s Hospital Medical Center, Cinncinnati, OH; The Heart Institute and Division of Human Genetics at Cincinnati Children’s, Cinncinnati, OH; Beth Israel Deaconess Medical Center, Boston, MA; Mayo Clinic Division of Vascular Surgery, Rochester, MN; University of California, Davis Medical Center, Sacramento, CA; Department of Cardiothoracic and Vascular Surgery, McGovern Medical School, University of Texas Health Science Center at Houston (UTHealth), Houston, TX; Department of Vascular Medicine, University Heart Center Hamburg, Hamburg, Germany; Department of Cardiology, University Heart Center,Hamburg,Germany; DivisionofVascularSurgery,DartmouthHitchcock Medical Center, Lebanon, NH; Medical Genetics, Department of Pathology, Seattle, WA; Medical Genetics, Department of Pathology, University of Washington, Seattle, WA

Renal Artery Pseudoaneurysm in Kawasaki Disease.

Whereas coronary aneurysms are commonly associated with Kawasaki disease, involvement of the renal vasculature is exceedingly rare. Genitourinary involvement in patients with Kawasaki disease is typically limited to sterile pyuria and proteinuria. In this case, a 13-year-old girl who presented with right flank pain and microhematuria was found to have an intraparenchymal hemorrhagic mass on computerized tomography scan. Renal arteriography confirmed the diagnosis of pseudoaneurysm in a lower pole segmental artery branch and complete occlusion was achieved with endovascular embolization.

Stone Disease Imaging: There Is More to X-Rays Than What We See!

Urolithiasis is the condition where kidney stones are formed anywhere along the course of the urinary tract. Diagnostic imaging is used in patients with symptoms suggestive of renal stones to confirm that Urolithiasis is the source of the patient’s pain and to identify the location, size and possible complications of the kidney stones. It will also dictate the most appropriate treatment to follow [1].