Skip to main content

Main menu

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • JASN Podcasts
    • Article Collections
    • Archives
    • Kidney Week Abstracts
    • Saved Searches
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Editorial Team
  • Editorial Fellowship
    • Editorial Fellowship Team
    • Editorial Fellowship Application Process
  • More
    • About JASN
    • Advertising
    • Alerts
    • Feedback
    • Impact Factor
    • Reprints
    • Subscriptions
  • ASN Kidney News
  • Other
    • ASN Publications
    • CJASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology

User menu

  • Subscribe
  • My alerts
  • Log in
  • My Cart

Search

  • Advanced search
American Society of Nephrology
  • Other
    • ASN Publications
    • CJASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology
  • Subscribe
  • My alerts
  • Log in
  • My Cart
Advertisement
American Society of Nephrology

Advanced Search

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • JASN Podcasts
    • Article Collections
    • Archives
    • Kidney Week Abstracts
    • Saved Searches
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Editorial Team
  • Editorial Fellowship
    • Editorial Fellowship Team
    • Editorial Fellowship Application Process
  • More
    • About JASN
    • Advertising
    • Alerts
    • Feedback
    • Impact Factor
    • Reprints
    • Subscriptions
  • ASN Kidney News
  • Follow JASN on Twitter
  • Visit ASN on Facebook
  • Follow JASN on RSS
  • Community Forum
UP FRONT MATTERSClinical Commentary
You have accessRestricted Access

Glycemic Control and Critical Illness: Is the Kidney Involved?

Ravindra L. Mehta
JASN October 2007, 18 (10) 2623-2627; DOI: https://doi.org/10.1681/ASN.2007010109
Ravindra L. Mehta
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data Supps
  • Info & Metrics
  • View PDF
Loading

Abstract

The pathophysiology, consequences, and management of hyperglycemia during critical illness is an important clinical issue. Uncontrolled hyperglycemia in this setting is associated with a variety of adverse events, including mortality. The kidneys have a major role in glucose and insulin metabolism, and emerging evidence suggests that they both are actively involved in the development, maintenance, and resolution of hyperglycemia. The development of acute kidney injury is also a risk in this setting. This article discusses potential approaches for efficient and effective management of hyperglycemia.

Effective management of hyperglycemia in critically ill patients has been a major topic of discussion since a landmark study demonstrated a significant reduction in mortality and morbidity in surgical patients who were treated with an intensive regimen to control blood glucose.1 Subsequent studies have highlighted the importance of hyperglycemia for adverse outcomes in various populations and proposed algorithms for glycemic control.2–4 However, achieving glycemic control is not easy, and additional questions have emerged.5,6 These include identifying potential mechanisms for the deleterious effects of hyperglycemia and the protective role of insulin in glycemic control.7,8 The risk for hypoglycemia has also prompted concerns that one must identify patients who are most likely to benefit from insulin therapy.9 Emerging evidence raises intriguing questions on the role of the kidney in this process and provides an opportunity to learn from these observations.

A key feature of hyperglycemia in critical illness is the development of insulin resistance coupled with alterations in glucose production and cellular glucose transport. Hepatic glucose production is increased through gluconeogenesis and glycogenolysis despite high levels of serum insulin that ordinarily suppress these pathways. Glucose utilization by cells normally occurs through facilitated uptake via glucose transporters (GLUT), which are widely distributed in tissues, including the kidney. Insulin-independent GLUT-1–mediated transport occurs in most tissues and accounts for basal glucose uptake, whereas expression and binding through GLUT-4 in skeletal muscle are regulated by insulin.8,10

Normally, hyperglycemia leads cells to internalize GLUT proteins to protect themselves from glucose overloading. However, in critical illness, membrane expression of GLUT-1, GLUT-2, and GLUT-3 proteins is upregulated and allows glucose to enter cells more in proportion to extracellular glucose levels. This contributes to glucose overload in several tissues, including brain neurons, hepatocytes, endothelial cells, and renal tubules. These events are associated with various cytokines (TNF-α and IL-6), hormones (cortisol, catecholamines, and growth hormone), and other molecules (vascular endothelial growth factor and TGF) that are also upregulated in multiorgan failure.11 Several additional pathways are also invoked, including cytokine-induced nitric oxide production, oxidative stress and hyperlipidemia. In this complicated series of events, what role does the kidney play?

A large multicenter study of patients with acute kidney injury (AKI) found that insulin resistance is common and the degree of hyperglycemia correlated with mortality.12 Mean insulin concentrations and mean homeostasis model of insulin resistance levels were significantly higher and IGF binding protein-3 concentrations were significantly lower among nonsurvivors compared with survivors.13 Additional data from the same cohort point to a much higher prevalence of elevated pro- and counterinflammatory cytokines, cellular paralysis of cytokine production, and increased markers of oxidative stress that all correlate with increased mortality.14–16 Although the development of AKI is associated with severe metabolic derangements, we have no clear evidence for a causal relationship.

The kidney also plays an important role in glucose homeostasis.17 Renal tubular handling of glucose is mediated by the facilitative GLUT proteins and the Na+/glucose co-transporter (SGLT) family.18 In humans, renal glucose production contributes approximately 25% to systemic glucose production, whereas renal glucose uptake accounts for 20% of systemic glucose removal.17 Because glucose homeostasis in the kidney is regulated by insulin, loss of kidney metabolic function could account for a component of insulin resistance as a result of loss of a major target organ for insulin action. Uremia is also associated with decreased hepatic and peripheral glucose uptake and a reduction in peripheral tissue glucose transporters.19,20 Hypertriglyceridemia, hyperglycemia, and hyperinsulinemia were seen in an animal model of cisplatin nephrotoxicity, and biochemical studies demonstrated the accumulation of nonesterified fatty acids, and triglycerides in serum, urine, and kidney tissue despite increased levels of plasma insulin.21 A reduced plasma glucose level, impaired renal tissue perfusion and GFR, and increased fractional glucose excretion were associated with decreased expression of SGLT2, SGLT3, and GLUT2 in an LPS model of sepsis, and similar findings were observed after application of TNF-α, IL-1β, IL-6, or IFN-γ.22

Insulin is also metabolized by the kidney, and reduced renal function prolongs the half-life of insulin and can contribute to hypoglycemic events.17 One of the major risk factors for development of hypoglycemia in the intensive care unit (ICU) was the presence of preexisting renal dysfunction and the need for renal replacement therapy.1,3,9 Multiple lines of evidence in human and animal studies point to the importance of the kidney in glucose homeostasis and as a potent contributor to insulin resistance, suggesting that it is an active participant in these metabolic derangements during critical illness.

In the absence of diabetes, mild to moderate elevations of glucose have not been associated with alterations in kidney function. Data from the glycemic control studies (Table 1), however, suggest otherwise and support the need for reappraisal. The Leuven study demonstrated that maintaining blood glucose levels <110 mg/dl reduced the onset of new renal failure from 12.3 to 9% (P = 0.04) and need for dialysis by 41%.1 Whereas the lowered blood glucose level was related to reduced mortality and other complications, the insulin dosage was an independent determinant for prevention of AKI.23 Two large intervention studies in medical and surgical ICU patients confirmed a similar association and found that the development of newly acquired AKI decreased by 7524 and 45%, respectively.3 In a large observational study, patients who did and did not have diabetes and required glycemic control had more infections, anemia, and AKI (11 and 7 versus 4%; P < 0.001) compared with control subjects.2 Additional observational studies from different populations suggest a linkage of hyperglycemia and the metabolic syndrome on the development of AKI.25–27 Most of these studies used a doubling of creatinine or a creatinine level >2.5 mg/dl as a criterion for AKI; however, a more sensitive criterion (0.5 mg/dl creatinine change) would likely increase the incidence of AKI. Whether these associations are simply a consequence of the deranged metabolic milieu that accompanies critical illness or there is a direct effect of hyperglycemia and insulin resistance on the kidney still needs more evaluation.

View this table:
  • View inline
  • View popup
Table 1.

Evidence for hyperglycemia in critical illness as a risk factor for acute kidney injurya

The mechanisms for the insulin resistance seen in chronic metabolic syndrome may mediate renal injury through several different pathways (Figure 1).28 Are these mechanisms operative in AKI, and, if so, what is the time course to develop renal injury? Findings from a wide variety of models of AKI, including ischemia/reperfusion, cisplatin, endotoxemia, glomerulonephritis, and ureteral obstruction, provide support for a direct contribution of hyperglycemia and insulin resistance to renal injury.21,29,30 Accumulation of nonesterified fatty acids seems to be a major factor contributing to mitochondrial dysfunction, influencing cellular recovery in renal tubular cells.29,31 These events operate through a variety of molecular and signaling pathways.8,28,29

Figure 1.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 1.

Mechanisms by which insulin resistance can contribute to renal injury. Adapted from Sarafadis et al.,28 with permission from S. Karger AG, Basel, Switzerland.

On the basis of these AKI models, it seems that the same pathways may influence critically ill patients,8 although experimental events as described here seem accelerated in contrast to the longer duration required for chronic insulin resistance to produce AKI (Figure 2). A likely scenario is that stress-related hyperglycemia induces compensatory responses in the kidney with resulting glycosuria. However, if the primary illness is not controlled, then the consequences of hyperglycemia and insulin resistance (hypertriglyceridemia, oxidative stress, and decreased nitric oxide) might directly mediate AKI.32 There also seems to be some time dependence to these events, because the maximum benefit of glycemic control was seen in patients who had hyperglycemia for >3 d and in whom glucose levels were kept at <110 mg/dl. This would fit well with the notion that critical illness evolves over time and there may be recruitment of various deteriorating organs as additional pathways are brought to bear. The kidney may have a dual role in conditioning the response to initial injury through preexisting or concurrent alterations in renal function and may also be a target of the altered metabolic pathways.

Figure 2.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 2.

Pathophysiology of accelerated effects of hyperglycemia in critical illness. Adapted from Van den Berghe et al.,8 with permission from the American Society for Clinical Investigation.

What are the lessons learned? Although several pieces of the puzzle linking hyperglycemia and kidney function are still missing, there is enough evidence now to suggest that the kidneys are active in the process and a target for new injury. On the basis of these conclusions, hyperglycemia should be considered a major risk factor for AKI in the ICU and should prompt specific measures to be instituted as follows:

First, clinicians should seek out a history of hyperglycemia as part of the evaluation of critically ill patients who are at risk or develop AKI and institute preventive and therapeutic measures. A variety of therapies may contribute directly or indirectly to the onset of hyperglycemia and should be avoided (Table 2). For instance, it is not uncommon to use 5% dextrose solutions to replace free water, and some centers still use dextrose-containing solutions in peritoneal dialysis or in the infusate for continuous renal replacement therapy. Dialysate solutions for intermittent hemodialysis also contain variable amounts of glucose and contribute to the dextrose load.32–34

View this table:
  • View inline
  • View popup
Table 2.

Modifiable factors contributing to hyper- and hypoglycemia in critically ill patients with renal dysfunctiona

Second, when hyperglycemia exists, early intervention to achieve and maintain glycemic control should be initiated. Several different regimens have been described; however, none specifically considers altered renal function, particularly with respect to the target range for blood glucose.35,36 Given the higher likelihood of hypoglycemia with reduced GFR, it maybe prudent to select a conservative target glucose of 100 to 149 mg/dl rather than an aggressive target of 80 to 109 mg/dl.37 Dynamic scales should be used to adjust insulin delivery rates on the basis of 1- to 4-h glucose monitoring. Insulin regimens should be combined with simultaneous enteral feeding to minimize hypoglycemia.36,38 Renal function should be monitored daily and a urinalysis performed for glycosuria, proteinuria, cells, and casts.

Third, altered renal function should be recognized as a risk factor for insulin resistance and its downstream effects. An estimated or measured GFR should be a part of the initial evaluation of ICU patients. Patients with decreased GFR should be considered a special subset for risk for glycemic control and hypoglycemia. In addition, the effect of reduced GFR on enhancing risk for drug-induced hyperglycemia and, to a lesser extent, hypoglycemia, particularly with antibiotics such as gatifloxacin, should be recognized.39,40 Similar adjustments may be required when calcineurin inhibitors and steroids are used in delayed graft function after renal transplants.41 When dialysis is instituted, further adjustments in insulin dosing and more frequent glucose monitoring may be required. One study evaluating risk factors for hypoglycemia found a strong relationship with bicarbonate but not lactate-based continuous renal replacement therapy.9 Although it is unclear why this would occur, fluctuations in insulin clearance may contribute to hypoglycemia if adjustments in insulin dosage are not made when dialysis is stopped.

Fourth, future studies should focus on assessing hyperglycemia or the metabolic syndrome as risks for AKI to ascertain the mechanisms and pathways contributing to renal injury. Patients with diabetes may have a different threshold for hyperglycemic injury, although the relationship to preexisting renal disease is unclear.2 The influence of a reduced GFR and dialysis on glucose and insulin levels needs to be explored further. Two large studies evaluating strategies for glycemic control are under way and could offer information in this regard.6

Current evidence suggests that the kidney is intimately involved in the development and resolution of hyperglycemia in the critically ill patient. It is time we recognized the interdependence of various organs and the expanded role of the kidney in modulating the response to catastrophic illness.

Disclosures

None.

Footnotes

  • Published online ahead of print. Publication date available at www.jasn.org.

  • © 2007 American Society of Nephrology

References

  1. ↵
    van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R: Intensive insulin therapy in the critically ill patients. N Engl J Med 345 : 1359 –1367, 2001
    OpenUrlCrossRefPubMed
  2. ↵
    Rady MY, Johnson DJ, Patel BM, Larson JS, Helmers RA: Influence of individual characteristics on outcome of glycemic control in intensive care unit patients with or without diabetes mellitus. Mayo Clin Proc 80 : 1558 –1567, 2005
    OpenUrlCrossRefPubMed
  3. ↵
    Van den Berghe G, Wilmer A, Hermans G, Meersseman W, Wouters PJ, Milants I, Van Wijngaerden E, Bobbaers H, Bouillon R: Intensive insulin therapy in the medical ICU. N Engl J Med 354 : 449 –461, 2006
    OpenUrlCrossRefPubMed
  4. ↵
    Krinsley JS: Intensive glucose control in the ICU: An expert interview with James S. Krinsley, MD by Antonios Liolios. Med Gen Med 6 : 33 , 2004
    OpenUrl
  5. ↵
    Finney SJ, Zekveld C, Elia A, Evans TW: Glucose control and mortality in critically ill patients. JAMA 290 : 2041 –2047, 2003
    OpenUrlCrossRefPubMed
  6. ↵
    Bellomo R, Egi M: Glycemic control in the intensive care unit: Why we should wait for NICE-SUGAR. Mayo Clin Proc 80 : 1546 –1568, 2005
    OpenUrlCrossRefPubMed
  7. ↵
    Turina M, Christ-Crain M, Polk HC Jr: Diabetes and hyperglycemia: Strict glycemic control. Crit Care Med 34[Suppl] : S291 –S300, 2006
    OpenUrlCrossRefPubMed
  8. ↵
    Van den Berghe G: How does blood glucose control with insulin save lives in intensive care? J Clin Invest 114 : 1187 –1195, 2004
    OpenUrlCrossRefPubMed
  9. ↵
    Vriesendorp TM, van Santen S, DeVries JH, de Jonge E, Rosendaal FR, Schultz MJ, Hoekstra JB: Predisposing factors for hypoglycemia in the intensive care unit. Crit Care Med 34 : 96 –101, 2006
    OpenUrlCrossRefPubMed
  10. ↵
    Andreelli F, Jacquier D, Troy S: Molecular aspects of insulin therapy in critically ill patients. Curr Opin Clin Nutr Metab Care 9 : 124 –130, 2006
    OpenUrlCrossRefPubMed
  11. ↵
    Vanhorebeek I, Langouche L, Van den Berghe G: Glycemic and nonglycemic effects of insulin: How do they contribute to a better outcome of critical illness? Curr Opin Crit Care 11 : 304 –311, 2005
    OpenUrlCrossRefPubMed
  12. ↵
    Mehta RL, Pascual MT, Soroko S, Savage BR, Himmelfarb J, Ikizler TA, Paganini EP, Chertow GM: Spectrum of acute renal failure in the intensive care unit: The PICARD experience. Kidney Int 66 : 1613 –1621, 2004
    OpenUrlCrossRefPubMed
  13. ↵
    Basi S, Pupim LB, Simmons EM, Sezer MT, Shyr Y, Freedman S, Chertow GM, Mehta RL, Paganini E, Himmelfarb J, Ikizler TA: Insulin resistance in critically ill patients with acute renal failure. Am J Physiol Renal Physiol 289 : F259 –F264, 2005
    OpenUrlCrossRefPubMed
  14. ↵
    Simmons EM, Himmelfarb J, Sezer MT, Chertow GM, Mehta RL, Paganini EP, Soroko S, Freedman S, Becker K, Spratt D, Shyr Y, Ikizler TA: Plasma cytokine levels predict mortality in patients with acute renal failure. Kidney Int 65 : 1357 –1365, 2004
    OpenUrlCrossRefPubMed
  15. Himmelfarb J, Le P, Klenzak J, Freedman S, McMenamin ME, Ikizler TA: Impaired monocyte cytokine production in critically ill patients with acute renal failure. Kidney Int 66 : 2354 –2360, 2004
    OpenUrlCrossRefPubMed
  16. Himmelfarb J, McMonagle E, Freedman S, Klenzak J, McMenamin E, Le P, Pupim LB, Ikizler TA, The PG: Oxidative stress is increased in critically ill patients with acute renal failure. J Am Soc Nephrol 15 : 2449 –2456, 2004
    OpenUrlAbstract/FREE Full Text
  17. ↵
    Meyer C, Dostou JM, Gerich JE: Role of the human kidney in glucose counterregulation. Diabetes 48 : 943 –948, 1999
    OpenUrlAbstract
  18. ↵
    Asano T, Ogihara T, Katagiri H, Sakoda H, Ono H, Fujishiro M, Anai M, Kurihara H, Uchijima Y: Glucose transporter and Na+/glucose cotransporter as molecular targets of anti-diabetic drugs. Curr Med Chem 11 : 2717 –2724, 2004
    OpenUrlPubMed
  19. ↵
    Friedman JE, Dohm GL, Elton CW, Rovira A, Chen JJ, Leggett-Frazier N, Atkinson SM Jr, Thomas FT, Long SD, Caro JF: Muscle insulin resistance in uremic humans: Glucose transport, glucose transporters, and insulin receptors. Am J Physiol 261 : E87 –E94, 1991
    OpenUrlPubMed
  20. ↵
    Jacobs DB, Hayes GR, Truglia JA, Lockwood DH: Alterations of glucose transporter systems in insulin-resistant uremic rats. Am J Physiol 257 : E193 –E197, 1989
    OpenUrlPubMed
  21. ↵
    Portilla D, Li S, Nagothu KK, Megyesi J, Kaissling B, Schnackenberg L, Safirstein RL, Beger RD: Metabolomic study of cisplatin-induced nephrotoxicity. Kidney Int 69 : 2194 –2204, 2006
    OpenUrlCrossRefPubMed
  22. ↵
    Schmidt C, Hocherl K, Bucher M: Regulation of renal glucose transporters during severe inflammation. Am J Physiol Renal Physiol 292 : F804 –F811, 2007
    OpenUrlCrossRefPubMed
  23. ↵
    Van den Berghe G, Wouters PJ, Bouillon R, Weekers F, Verwaest C, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P: Outcome benefit of intensive insulin therapy in the critically ill: Insulin dose versus glycemic control. Crit Care Med 31 : 359 –366, 2003
    OpenUrlCrossRefPubMed
  24. ↵
    Krinsley JS: Effect of an intensive glucose management protocol on the mortality of critically ill adult patients. Mayo Clin Proc 79 : 992 –1000, 2004
    OpenUrlCrossRefPubMed
  25. ↵
    Clavijo LC, Pinto TL, Kuchulakanti PK, Torguson R, Chu WW, Satler LF, Kent KM, Suddath WO, Pichard AD, Waksman R: Metabolic syndrome in patients with acute myocardial infarction is associated with increased infarct size and in-hospital complications. Cardiovasc Revasc Med 7 : 7 –11, 2006
    OpenUrlCrossRefPubMed
  26. Holm C, Horbrand F, Mayr M, von Donnersmarck GH, Muhlbauer W: Acute hyperglycaemia following thermal injury: Friend or foe? Resuscitation 60 : 71 –77, 2004
    OpenUrlCrossRefPubMed
  27. ↵
    Cheung NW, Napier B, Zaccaria C, Fletcher JP: Hyperglycemia is associated with adverse outcomes in patients receiving total parenteral nutrition. Diabetes Care 28 : 2367 –2371, 2005
    OpenUrlAbstract/FREE Full Text
  28. ↵
    Sarafidis PA, Ruilope LM: Insulin resistance, hyperinsulinemia, and renal injury: Mechanisms and implications. Am J Nephrol 26 : 232 –244, 2006
    OpenUrlCrossRefPubMed
  29. ↵
    Feldkamp T, Kribben A, Roeser NF, Senter RA, Weinberg JM: Accumulation of nonesterified fatty acids causes the sustained energetic deficit in kidney proximal tubules after hypoxia-reoxygenation. Am J Physiol Renal Physiol 290 : F465 –F477, 2006
    OpenUrlCrossRefPubMed
  30. ↵
    Zager RA, Johnson AC, Hanson SY: Renal tubular triglyceride accumulation following endotoxic, toxic, and ischemic injury. Kidney Int 67 : 111 –121, 2005
    OpenUrlCrossRefPubMed
  31. ↵
    Weinberg JM: Lipotoxicity. Kidney Int 70 : 1560 –1566, 2006
    OpenUrlCrossRefPubMed
  32. ↵
    Frankenfield DC, Reynolds HN: Nutritional effect of continuous hemodiafiltration. Nutrition 11 : 388 –393, 1995
    OpenUrlPubMed
  33. Wooley JA, Btaiche IF, Good KL: Metabolic and nutritional aspects of acute renal failure in critically ill patients requiring continuous renal replacement therapy. Nutr Clin Pract 20 : 176 –191, 2005
    OpenUrlCrossRefPubMed
  34. ↵
    Monson P, Mehta R: Nutritional considerations in continuous replacement therapy. Semin Dial 9 : 152 –160, 1996
    OpenUrlCrossRef
  35. ↵
    Lonergan T, Compte AL, Willacy M, Chase JG, Shaw GM, Hann CE, Lotz T, Lin J, Wong XW: A pilot study of the SPRINT protocol for tight glycemic control in critically ill patients. Diabetes Technol Ther 8 : 449 –462, 2006
    OpenUrlCrossRefPubMed
  36. ↵
    Meijering S, Corstjens AM, Tulleken JE, Meertens JH, Zijlstra JG, Ligtenberg JJ: Towards a feasible algorithm for tight glycaemic control in critically ill patients: A systematic review of the literature. Crit Care 10 : R19 , 2006
    OpenUrlCrossRefPubMed
  37. ↵
    Lioubov S, Braithwaite S: Practical aspects of intensive insulinization in the intensive care unit. Curr Opin Clin Nutr Metab Care 10 : 197 –205, 2007
    OpenUrlCrossRefPubMed
  38. ↵
    Lonergan T, Le Compte A, Willacy M, Chase JG, Shaw GM, Wong XW, Lotz T, Lin J, Hann CE: A simple insulin-nutrition protocol for tight glycemic control in critical illness: Development and protocol comparison. Diabetes Technol Ther 8 : 191 –206, 2006
    OpenUrlCrossRefPubMed
  39. ↵
    Beste LA, Mersfelder TL: Hyperglycemia and gatifloxacin: A case report and summary of current literature. Am J Geriatr Pharmacother 3 : 262 –265, 2005
    OpenUrlCrossRefPubMed
  40. ↵
    Mohr JF, McKinnon PS, Peymann PJ, Kenton I, Septimus E, Okhuysen PC: A retrospective, comparative evaluation of dysglycemias in hospitalized patients receiving gatifloxacin, levofloxacin, ciprofloxacin, or ceftriaxone. Pharmacotherapy 25 : 1303 –1309, 2005
    OpenUrlCrossRefPubMed
  41. ↵
    Penfornis A, Kury-Paulin S: Immunosuppressive drug-induced diabetes. Diabetes Metab 32 : 539 –546, 2006
    OpenUrlCrossRefPubMed
PreviousNext
Back to top

In this issue

Journal of the American Society of Nephrology: 18 (10)
Journal of the American Society of Nephrology
Vol. 18, Issue 10
October 2007
  • Table of Contents
  • Table of Contents (PDF)
  • Index by author
View Selected Citations (0)
Print
Download PDF
Sign up for Alerts
Email Article
Thank you for your help in sharing the high-quality science in JASN.
Enter multiple addresses on separate lines or separate them with commas.
Glycemic Control and Critical Illness: Is the Kidney Involved?
(Your Name) has sent you a message from American Society of Nephrology
(Your Name) thought you would like to see the American Society of Nephrology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Glycemic Control and Critical Illness: Is the Kidney Involved?
Ravindra L. Mehta
JASN Oct 2007, 18 (10) 2623-2627; DOI: 10.1681/ASN.2007010109

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Request Permissions
Share
Glycemic Control and Critical Illness: Is the Kidney Involved?
Ravindra L. Mehta
JASN Oct 2007, 18 (10) 2623-2627; DOI: 10.1681/ASN.2007010109
del.icio.us logo Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Jump to section

  • Article
    • Abstract
    • Disclosures
    • Footnotes
    • References
  • Figures & Data Supps
  • Info & Metrics
  • View PDF

More in this TOC Section

UP FRONT MATTERS

  • Collaboration between Dialysis Providers
  • Unfulfilled Expectations Open New Horizons: What Have We Learned about Volume-Regulated Anion Channels in the Kidney?
  • Polycystin-2 in the Endoplasmic Reticulum: Bending Ideas about the Role of the Cilium
Show more UP FRONT MATTERS

Clinical Commentary

  • Trends in Discharge Claims for Acute Myocardial Infarction among Patients on Dialysis
  • Reassessing Medical Risk in Living Kidney Donors
  • Commentary on the 2014 BP Guidelines from the Panel Appointed to the Eighth Joint National Committee (JNC 8)
Show more Clinical Commentary

Cited By...

  • Approach to the Metabolic Implications of Peritoneal Dialysis in Acute Kidney Injury
  • Prevalence and Predictors of Diabetes After Lung Transplantation: A Prospective, Longitudinal Study
  • Google Scholar

Similar Articles

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Articles

  • Current Issue
  • Early Access
  • Subject Collections
  • Article Archive
  • ASN Annual Meeting Abstracts

Information for Authors

  • Submit a Manuscript
  • Author Resources
  • Editorial Fellowship Program
  • ASN Journal Policies
  • Reuse/Reprint Policy

About

  • JASN
  • ASN
  • ASN Journals
  • ASN Kidney News

Journal Information

  • About JASN
  • JASN Email Alerts
  • JASN Key Impact Information
  • JASN Podcasts
  • JASN RSS Feeds
  • Editorial Board

More Information

  • Advertise
  • ASN Podcasts
  • ASN Publications
  • Become an ASN Member
  • Feedback
  • Follow on Twitter
  • Password/Email Address Changes
  • Subscribe to ASN Journals
  • Wolters Kluwer Partnership

© 2022 American Society of Nephrology

Print ISSN - 1046-6673 Online ISSN - 1533-3450

Powered by HighWire