Does intensive insulin therapy really reduce the incidence of acute renal injury in critically ill patients? An analysis using the rifle criteria

Purpose: This study examined the effect of permissive underfeeding compared to target feeding and intensive insulin therapy (IIT) compared to conventional insulin therapy (CIT) on the inflammatory mediators monocyte chemoattractant protein 1 (MCP-1), soluble intercellular adhesion molecule 1 (sICAM-1), and tissue factor (TF) in critically ill patients. Methodology: This was a substudy of a 2 × 2 factorial design randomized controlled trial in which intensive care unit (ICU) patients were randomized into permissive underfeeding compared to target feeding groups and into IIT compared to CIT groups (ISRCTN96294863). In this substudy, we included 91 patients with almost equal numbers across randomization groups. Blood samples were collected at baseline and at days 3, 5, and 7 of an ICU stay. Linear mixed models were used to assess the differences in MCP-1, sICAM-1, and TF across randomization groups over time. Results: Baseline characteristics were balanced across randomization groups. Daily caloric intake was significantly higher in the target feeding than in the permissive underfeeding groups (P-value < 0.01), and the daily insulin dose was significantly higher in the IIT than in the CIT groups (P-value < 0.01). MCP-1, sICAM-1, and TF did not show any significant difference between the randomization groups, while there was a time effect for MCP-1. Baseline sequential organ failure assessment (SOFA) score and platelets had a significant effect on sICAM-1 (P-value < 0.01). For TF, there was a significant association with age (P-value < 0.01). Conclusions: Although it has been previously demonstrated that insulin inhibits MCP-1, sICAM-1 in critically ill patients, and TF in non-critically ill patients, our study demonstrated that IIT in critically ill patients did not affect these inflammatory mediators. Similarly, caloric intake had a negligible effect on the inflammatory mediators studied.

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A carbohydrate-restrictive strategy is safer and as efficient as intensive insulin therapy in critically ill patients

Journal of Critical Care ◽

10.1016/j.jcrc.2008.10.011 ◽

2010 ◽

Vol 25 (1) ◽

pp. 84-89 ◽

Cited By ~ 19

Author(s):

José Raimundo A. de Azevedo ◽

Leonardo Oliveira de Araujo ◽

Widlani Sousa da Silva ◽

Renato Palácio de Azevedo

Keyword(s):

Insulin Therapy ◽

Critically Ill ◽

Intensive Insulin Therapy ◽

Critically Ill Patients

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A Literature Review of Intensive Insulin Therapy and Mortality in Critically Ill Patients

Clinical Nurse Specialist ◽

10.1097/nur.0b013e3181cf55af ◽

2010 ◽

Vol 24 (2) ◽

pp. 80-86 ◽

Cited By ~ 10

Author(s):

LIFEN CHEN

Keyword(s):

Literature Review ◽

Insulin Therapy ◽

Critically Ill ◽

Intensive Insulin Therapy ◽

Critically Ill Patients

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Does intensive insulin therapy protect renal function in critically ill patients?

Nature Clinical Practice Nephrology ◽

10.1038/ncpneph0855 ◽

2008 ◽

Vol 4 (8) ◽

pp. 412-413 ◽

Cited By ~ 3

Author(s):

Rinaldo Bellomo

Keyword(s):

Renal Function ◽

Insulin Therapy ◽

Critically Ill ◽

Intensive Insulin Therapy ◽

Critically Ill Patients

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Intensive Insulin Therapy in Critically Ill Patients

New England Journal of Medicine ◽

10.1056/nejmoa011300 ◽

2001 ◽

Vol 345 (19) ◽

pp. 1359-1367 ◽

Cited By ~ 6580

Author(s):

Greet Van den Berghe ◽

Pieter Wouters ◽

Frank Weekers ◽

Charles Verwaest ◽

Frans Bruyninckx ◽

...

Keyword(s):

Insulin Therapy ◽

Critically Ill ◽

Intensive Insulin Therapy ◽

Critically Ill Patients

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Thiamine Levels During Intensive Insulin Therapy in Critically Ill Patients

Journal of Intensive Care Medicine ◽

10.1177/0885066616659429 ◽

2016 ◽

Vol 32 (9) ◽

pp. 559-564 ◽

Cited By ~ 5

Author(s):

Wouter van Snippenburg ◽

Mariet G. J. Reijnders ◽

Jose G. M. Hofhuis ◽

Rien de Vos ◽

Stephan Kamphuis ◽

...

Keyword(s):

Insulin Therapy ◽

Critically Ill ◽

Intensive Insulin Therapy ◽

Critically Ill Patients ◽

Thiamine Deficiency ◽

Gastrointestinal Disease ◽

Glucose Levels ◽

Gastrointestinal Pathology ◽

Observational Prospective Cohort Study ◽

Thiamine Level

Introduction: Thiamine is an essential cofactor in carbohydrate metabolism, and deficiency can therefore cause various organ dysfunctions. Little is known about the prevalence and possible worsening of thiamine deficiency in critically ill patients. In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores. Materials and Methods: An observational prospective cohort study was carried out in a medical–surgical ICU in a general teaching hospital in Apeldoorn, the Netherlands. All adults who were treated during that time with intensive insulin therapy were included. Deficiency was defined as a thiamine level <100 nmol/L. No thiamine supplementation was administered except for normal amounts present in standard enteral feeding. Results: A total of 58 patients were available for analysis. Median thiamine level at admission was 111 nmol/L. Deficiency was present in 39.7% of patients and was significantly associated with the presence of gastrointestinal pathology and with recent surgery. Thiamine levels increased a median of 14 nmol/L in 48 hours. Only 3.4% of patients showed a predefined relevant decline in thiamine levels. Conclusion: Intensive insulin therapy does not appear to cause or worsen thiamine deficiency. However, based on the high prevalence of deficiency at admission, it might be warranted to supplement thiamine in all patients admitted to the ICU, especially when there is an underlying gastrointestinal disease or recent surgery.

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