Glycemic Control and Critical Illness

Mehta, Ravindra L.

doi:10.1681/asn.2007010109

Cited by 35 publications

(31 citation statements)

References 42 publications

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“…We suggest that the very high incidence of NODAT, particularly early after LTx, is due to a combination of insulin resistance and b-cell dysfunction, caused by 1) immunosuppression with prednisolone and tacrolimus, which are used in particularly high doses in LTRs, as there is a large mass of transplanted alloreactive tissue, and 2) severe acute illness, seen almost universally perioperatively, resulting in a proinflammatory state mediated by counterregulatory hormones and neuroendocrine and cytokine pathways (25,26), Further, the transplanted organ is exposed to the external environment. Chest sepsis requiring intravenous treatment develops in 90% of LTRs in the first 12 months post-Tx (27).…”

Section: Discussionmentioning

confidence: 99%

Prevalence and Predictors of Diabetes After Lung Transplantation: A Prospective, Longitudinal Study

2014

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OBJECTIVETo determine incidence and prevalence of diabetes mellitus (DM) after lung transplantation (LTx), identify risk factors for persistent DM after LTx, and determine its effect on survival. RESEARCH DESIGN AND METHODSThis was a prospective, longitudinal study comparing DM status before and after LTx using oral glucose tolerance tests (OGTTs). DM prevalence and changes in metabolic control over time were determined. Risk factors for persistent DM and survival differences by DM status were assessed. RESULTSBetween August 2010 and December 2012, 156 patients underwent LTx. DM prevalence after 3, 12, and 24 months was 47%, 44%, and 40%, respectively. A further 20%, 11%, and 7% had impaired glucose tolerance and/or impaired fasting glucose. Incidence of new-onset DM after transplant (NODAT) was 32%, 30%, and 24% after 3, 12, and 24 months. Nonfasting insulin levels and second phase insulin release fell 3 months after transplant (Tx) but returned to baseline by 2 years. The only risk factors for NODAT were 1-and 2-h glucose levels on pre-Tx OGTT (OR 1.73 [95% CI 1.19-2.50], P = 0.004, and 1.84 [1.22-2.77], P = 0.004, respectively). Survival was reduced in patients with DM at study end versus those without (estimated mean 979 days [95% CI 888-1,071] vs. 1,140 days [1,070-1,210], P = 0.023). CONCLUSIONSMost patients had dysglycemia during the first year after LTx, and 32% developed NODAT. Hyperglycemia was caused both by b-cell dysfunction and by insulin resistance. Only pre-Tx OGTT glucose levels predicted persistent NODAT. As DM was common and associated with reduced survival, early detection and management of DM in LTx recipients are warranted.Diabetes mellitus (DM) is a common complication of solid organ transplantation and is associated with increased morbidity and mortality (1). It is especially common after lung transplantation (LTx), firstly because LTx recipients (LTR) require highdose immunosuppression with glucocorticoids in combination with calcineurin inhibitors and secondly because a significant minority of patients have cystic fibrosis (CF), which results both in lung damage necessitating LTx and in destruction of insulin-producing b-cells in the pancreas.

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Section: Discussionmentioning

confidence: 99%

Prevalence and Predictors of Diabetes After Lung Transplantation: A Prospective, Longitudinal Study

2014

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“…Mehta [36] showed that the kidney is intimately involved in the development of hyperglycemia in the critically ill patients. Sechi et al [37] demonstrated that abnormal plasma glucose levels were elevated when the GFR was <50 mL/min/1.73 m 2 and overall glucose metabolism parameters were not correlated with microalbuminuria (MA).…”

Section: Discussionmentioning

confidence: 99%

Urinary Extracellular Vesicles: Potential Biomarkers of Renal Function in Diabetic Patients

Kamińska

Platt

Kasprzyk

et al. 2016

Journal of Diabetes Research

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The aim of this study was to check the relationship between the density of urinary EVs, their size distribution, and the progress of early renal damage in type 2 diabetic patients (DMt2). Patients were enrolled to this study, and glycated hemoglobin (HbA1c) below 7% was a threshold for properly controlled diabetic patients (CD) and poorly controlled diabetic patients (UD). Patients were further divided into two groups: diabetic patients without renal failure (NRF) and with renal failure (RF) according to the Glomerular Filtration Rate. Density and diameter of EVs were determined by Tunable Resistive Pulse Sensing. Additionally, EVs were visualized by means of Transmission and Environmental Scanning Electron Microscopy. Nano-liquid chromatography coupled offline with mass spectrometry (MALDI-TOF-MS/MS) was applied for proteomic analysis. RF had reduced density of EVs compared to NRF. The size distribution study showed that CD had larger EVs (mode) than UD (115 versus 109 nm; p < 0.05); nevertheless the mean EVs diameter was smaller in controls than in the CD group (123 versus 134 nm; p < 0.05). It was demonstrated that EVs are abundant in urine. Albumin, uromodulin, and number of unique proteins related to cell stress and secretion were detected in the EVs fraction. Density and size of urinary EVs reflect deteriorated renal function and can be considered as potential renal damage biomarkers.

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“…Despite a lack of influence on hemodynamics, IIT improves the lipid profile in patients with sepsis and MOF, and attenuation of both ischemic and endotoxemic AKI by high density lipoprotein has been demonstrated in experimental models [39-41]. AKI and hyperglycemia are also associated with an increase in expression of inducible nitric oxide synthase (iNOS), endothelial activation of ICAM-1, upregulation of pro-inflammatory cytokines (TNFα, IL-6), release of oxidative stress mediators and infiltration of inflammatory cells, which lead to renal tubular injury [38, 42, 43]. Additionally, APC has anti-inflammatory, antithrombotic and profibrinolytic properties and reduces mortality in severe sepsis [37].…”

Section: Surgical Sepsis and Its Role In Akimentioning

confidence: 99%

Surgical Sepsis and Organ Crosstalk: The Role of the Kidney

White

Chaudhary

Moore

et al. 2011

Journal of Surgical Research

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Acute kidney injury (AKI) is a common complication of hospitalized patients, and clinical outcomes remain poor despite advances in renal replacement therapy. The accepted pathophysiology of AKI in the setting of sepsis has evolved from one of simple decreased renal blood flow to one that involves a more complex interaction of intra-glomerular microcirculatory vasodilation combined with the local release of inflammatory mediators and apoptosis. Evidence from pre-clinical AKI models suggests that crosstalk occurs between kidneys and other organ systems via soluble and cellular inflammatory mediators, and that this involves both the innate and adaptive immune systems. These interactions are reflected by genomic changes and abnormal rates of cellular apoptosis in distant organs including the lungs, heart, gut, liver, and central nervous system. The purpose of this article is to review the influence of AKI, particularly sepsis-associated AKI, on inter-organ crosstalk in the context of systemic inflammation and multiple organ failure (MOF).

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Glycemic Control and Critical Illness

Cited by 35 publications

References 42 publications

Prevalence and Predictors of Diabetes After Lung Transplantation: A Prospective, Longitudinal Study

Prevalence and Predictors of Diabetes After Lung Transplantation: A Prospective, Longitudinal Study

Urinary Extracellular Vesicles: Potential Biomarkers of Renal Function in Diabetic Patients

Surgical Sepsis and Organ Crosstalk: The Role of the Kidney

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