Pulsatile Hematuria From Procurement Core Needle Biopsy: A Case Report.

Core needle biopsies are still widely performed to evaluate the pathologic suitability of a kidney allograft. Here, we report a case of pulsatile hematuria from a procurement core needle biopsy where the patient had to be taken emergently to interventional radiology for coil embolization immediately after organ reperfusion.

Liver graft failure and hyperbilirubinemia in liver transplantation recipients after Clostridium difficile infection.

INTRODUCTION: Liver transplant recipients are at high risk for Clostridium difficile infection. We have recently encountered multiple cases of CDI in our liver transplant recipients and for some of them it led to severe hyperbilirubinemia, liver failure, and even death. Our goals are to report our experience and analyze the factors that contributed to unfavorable outcomes. MATERIAL AND METHODS: All liver transplant recipients diagnosed with CDI between December 1, 2007, and January 30, 2009, were included and retrospectively reviewed. RESULTS: Twenty-four patients were identified, 14 men and 10 women. Fourteen patients experienced hyperbilirubinemia after the infection and 7 progressed to liver failure. Pre-CDI biopsy-proven liver abnormality, use of extended-criteria donors (ECDs) and a donor risk index (DRI) greater than 1.9 were associated with a higher risk of graft failure (P<.05). Hepatitis C, inpatient versus outpatient diagnosis, and a donor age greater than 50 years were not associated with a higher risk of graft failure. Use of ECDs and timing of the infection at more than 1 month but less than 1.5 years posttransplant were also associated with higher chances of sustained hyperbilirubinemia (P<.05). CONCLUSION: CDI in liver transplant patients can be very serious and may lead to sustained hyperbilirubinemia or graft failure. Marginal grafts are more susceptible to decompensate after such an infection than standard criteria grafts; moreover, already abnormal grafts do not tolerate this infection well and decompensate to complete failure in 85% of the cases.

Open abdomen management with human acellular dermal matrix in liver transplant recipients.

BACKGROUND: Abdominal wall closure after liver transplantation is not always feasible and may result in increased intra-abdominal pressure along with associated complications. Various temporary closure techniques as well as open wound management have been used to address this complex problem. The aim of this series was to describe an approach to definitive wound closure of the open abdomen in liver transplant patients. METHODS: We performed a retrospective review of all liver transplant patients at our institution from September 2005 to November 2007. The management of the open abdomen in 10 liver transplant patients was reviewed, and a novel approach described to manage these defects. RESULTS: Ten patients with open wounds were closed during the study period using human acellular dermal matrix (HADM). There were 7 men and 3 women of median age 55 years. Average size of HADM was 235 cm(2). The median follow-up is 10 months with no incidence of evisceration or hernia. In 1 patient, the graft failed along the lateral side due to infection; it dislodged during vacuum-assisted closure dressing change in another patient at 5 months after closure. Fascial closure was not possible due to organ edema (n = 3), a large liver (n = 4) or wound infection with dehiscence (n = 3). CONCLUSIONS: HADM can be used for primary wound closure in both clean and contaminated wounds as an alternative to an open abdomen post-liver transplantation.

Response of glucose disposal to hyperinsulinaemia in human hypothyroidism and hyperthyroidism.

We have examined insulin action on glucose metabolism in six hypothyroid patients before and after regular thyroid hormone treatment, and in six healthy volunteers before and after transient induction of moderate hyperthyroidism. Insulin was infused under euglycaemic and eukalaemic clamps. An appropriate amino acid infusion was used to blunt insulin-induced decreases in amino acid levels. Glucose kinetics were assessed using a primed continuous infusion of [6,6-(2)H(2)]glucose. The results showed that basal plasma insulin and glucose levels (i.e. before infusion) were similar in each case. Despite similar insulin infusion rates, the plateau value of insulin was lower after thyroid treatment in both hypothyroid patients and healthy volunteers. The rate of exogenous glucose needed to maintain plasma glucose at a steady-state level was increased by thyroid hormone in hypothyroid patients (P <0.05), but not in healthy volunteers. Thyroid treatment resulted in a significant increase in basal glucose disposal in both groups (P <0.05). Insulin, in conjunction with glucose and amino acids, significantly stimulated glucose disposal (P <0.05) under all conditions. The incremental increase in glucose disposal after infusion tended to be higher following thyroid hormone treatment, but this was not statistically significant. However, the ratio of the incremental increase in glucose disposal to the increase in plasma insulin was significantly improved after thyroid hormone treatment in hypothyroid patients (P <0.05). It was also increased in healthy volunteers, but not significantly. We conclude that thyroid hormones improve the ability of insulin to stimulate glucose disposal related to insulinaemia. This phenomenon may be highly sensitive, because it was only apparent at low thyroid hormone levels.

Response of leucine metabolism to hyperinsulinemia in hypothyroid patients before and after thyroxine replacement.

We have investigated the effect of hypothyroidism and insulin on protein metabolism in humans. Six hypothyroid patients were studied in a postabsorptive state before and after 5 months of regular treatment for hypothyroidism (153 +/- 17 microg/day of L-T4). The effect of insulin was assessed under hyperinsulinemic euglycemic and eukalemic conditions. Insulin was infused for 140 min at 0.0063 +/- 0.0002 nmol/kg x min. An amino acid infusion was used to blunt insulin-induced hypoaminoacidemia. Whole body protein turnover was measured using L-[1-13C] leucine. When compared to L-T4-induced subclinical thyrotoxic state, hypothyroidism induced a significant decrease (P < 0.05) in leucine endogenous appearance rate (a reflection of proteolysis; 0.89 +/- 0.09 vs. 1.33 +/- 0.05 micromol/kg x min), oxidation (0.19 +/- 0.02 vs. 0.25 +/- 0.03 micromol/kg x min), and nonoxidative disposal (a reflection of protein synthesis; 0.87 +/- 0.11 vs. 1.30 +/- 0.05 micromol/ kg x min). Insulin lowered proteolysis during both the subclinical thyrotoxic and hypothyroid states. Hypothyroidism impaired the antiproteolytic effects of insulin. Thyroid hormones are, therefore, essential for the normal antiproteolytic action of insulin.

Insulin action on skeletal muscle protein metabolism during catabolic states.

Insulin plays a major role in the regulation of skeletal muscle protein turnover but its mechanism of action is not fully understood, especially in vivo during catabolic states. These aspects are presently reviewed. Insulin inhibits the ATP-ubiquitin proteasome proteolytic pathway which is presumably the predominant pathway involved in the breakdown of muscle protein. Evidence of the ability of insulin to stimulate muscle protein synthesis in vivo was also presented. Many catabolic states in rats, e.g. streptozotocin diabetes, glucocorticoid excess or sepsis-induced cytokines, resulted in a decrease in insulin action on protein synthesis or degradation. The effect of catabolic factors would therefore be facilitated. In contrast, the antiproteolytic action of insulin was improved during hyperthyroidism in man and early lactation in goats. Excessive muscle protein breakdown should therefore be prevented. In other words, the anabolic hormone insulin partly controlled the 'catabolic drive'. Advances in the understanding of insulin signalling pathways and targets should provide information on the interactions between insulin action, muscle protein turnover and catabolic factors.

Threonine and methionine are limiting amino acids for protein synthesis in patients with AIDS.

This study was conducted to identify the most rate-limiting amino acids for whole-body protein synthesis in acquired immunodeficiency syndrome (AIDS) patients. We postulated that an essential amino acid that would be rate limiting in AIDS should have a low basal plasma concentration and should remain at a low level during amino acid infusion. Seven male AIDS patients (median age 37 y, CD4 cell count: 76 mm-3) without any clinically active opportunistic infection during the month before the experiment were infused intravenously with a complete amino acid-glucose mixture for 2.5 h. Eight healthy volunteers were used as controls. Before the infusion, the concentrations of most free essential amino acids (methionine, threonine, histidine, isoleucine, leucine and tryptophan) were significantly lower (P < 0.05) in AIDS patients than in controls. Most plasma free essential amino acids increased significantly during infusion. However, the absolute increase above basal levels for threonine, valine, lysine, (P < 0.05) and methionine (P < 0.073) was smaller in AIDS patients than in control subjects. Thus, threonine and possibly methionine may be rate limiting for whole-body protein synthesis in AIDS patients, suggesting that there are selective amino acid requirements in patients with AIDS.

Fructose and sucrose feeding during pregnancy and lactation in rats changes maternal and pup fuel metabolism.

We examined the effects of feeding a fructose, sucrose or reference diet during gestation and lactation on blood substrate levels and insulin sensitivity in rat adipose tissue. Female rats were fed either 50% fructose or 50% sucrose purified diets or a nonpurified diet ad libitum during gestation and lactation. Fasting blood samples were taken on d 10 of gestation and one oral glucose tolerance test was conducted on d 19 of gestation, with a second test performed on the day of weaning. All dams were killed 2 d after weaning. During gestation, fructose feeding induced hyperglycemia and hypertriglyceridemia in early pregnancy (d 10) relative to sucrose-fed rats, and hypotriglyceridemia in late pregnancy (d 19) as compared with the group fed the reference diet. Compared with the reference group, sucrose feeding also caused hypotriglyceridemia during late pregnancy. Pups delivered to fructose-fed dams were hyperglycemic at birth. In comparison with the reference group, fructose-fed dams were hypoglycemic, whereas sucrose-fed dams were hypertriglyceridemic at weaning. There was no difference in each of the two oral glucose tolerance test responses between the three groups after adjusting for the baseline difference in glucose levels. However, lipid synthesis in isolated fat cells in response to insulin stimulation was significantly lower in fructose-fed and sucrose-fed rats relative to the reference group.