A new clinical multivariable model that predicts postoperative acute kidney injury: impact of endogenous ouabain

Simonini, Marco; Lanzani, Chiara; Bignami, Elena; Casamassima, Nunzia; Frati, Elena; Meroni, Roberta; Messaggio, Elisabetta; Alfieri, Ottavio; Hamlyn, John M.; Body, Simon C.; Collard, Charles D.; Muehlschlegel, Jochen D.; Shernan, Stanton K.; Fox, Amanda A.; Zangrillo, Alberto; Manunta, Paolo

doi:10.1093/ndt/gfu200

Cited by 33 publications

(32 citation statements)

References 38 publications

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“…2,[48][49][50][51] Although there are measures to treat pre-and postrenal AKI, intrinsic AKI caused by drugs (antibiotics or contrast agents), inflammation, hypoxia-reperfusion injury (e.g., due to prerenal injury), or any other noxa is not treatable till today. Most approaches are indeed limited to strategies that prevent the underlying cause or are focused on protecting the kidneys from additional insults.…”

Section: Discussionmentioning

confidence: 99%

Minor Postoperative Increases of Creatinine Are Associated With Higher Mortality and Longer Hospital Length of Stay in Surgical Patients

Kork

Balzer

Spies

et al. 2016

Survey of Anesthesiology

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Section: Discussionmentioning

confidence: 99%

Minor Postoperative Increases of Creatinine Are Associated With Higher Mortality and Longer Hospital Length of Stay in Surgical Patients

Kork

Balzer

Spies

et al. 2016

Survey of Anesthesiology

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show abstract

“…2,48–51 Although there are measures to treat pre- and postrenal AKI, intrinsic AKI caused by drugs (antibiotics or contrast agents), inflammation, hypoxia–reperfusion injury ( e.g. , due to prerenal injury), or any other noxa is not treatable till today.…”

Section: Discussionmentioning

confidence: 99%

Minor Postoperative Increases of Creatinine Are Associated with Higher Mortality and Longer Hospital Length of Stay in Surgical Patients

et al. 2015

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Background Surgical patients frequently experience postoperative increases in creatinine levels. The authors hypothesized that even small increases in postoperative creatinine levels are associated with adverse outcomes. Methods The authors examined the association of postoperative changes from preoperative baseline creatinine with all-cause in-hospital mortality and hospital length of stay (HLOS) in a retrospective analysis of surgical patients at a single tertiary care center between January 2006 and June 2012. Results The data of 39,369 surgical patients (noncardiac surgery n = 37,345; cardiac surgery n = 2,024) were analyzed. Acute kidney injury (AKI)—by definition of the Kidney Disease: Improving Global Outcome group—was associated with a five-fold higher mortality (odds ratio [OR], 4.8; 95% CI, 4.1 to 5.7; P < 0.001) and a longer HLOS of 5 days (P < 0.001) after adjusting for age, sex, comorbidities, congestive heart failure, preoperative hemoglobin, preoperative creatinine, exposure to radiocontrast agent, type of surgery, and surgical AKI risk factors. Importantly, even minor creatinine increases (Δcreatinine 25 to 49% above baseline but < 0.3 mg/dl) not meeting AKI criteria were associated with a two-fold increased risk of death (OR, 1.7; 95% CI, 1.3 to 2.4; P < 0.001) and 2 days longer HLOS (P < 0.001). This was more pronounced in noncardiac surgery patients. Patients with minor creatinine increases had a five-fold risk of death (OR, 5.4; 95% CI, 1.5 to 20.3; P < 0.05) and a 3-day longer HLOS (P < 0.01) when undergoing noncardiac surgery. Conclusions Even minor postoperative increases in creatinine levels are associated with adverse outcomes. These results emphasize the importance to find effective therapeutic approaches to prevent or treat even mild forms of postoperative kidney dysfunction to improve surgical outcomes.

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“…Most recently, we demonstrated the power of two clinical risk score models to predict AKI. Strikingly, the predictive power of both models was further and significantly improved by the addition of preoperative plasma EO levels 99 . Thus, preoperative EO appears to be a marker for preexisting renal injury and, as shown by the experimental studies, can be a direct cause of kidney damage.…”

Section: Implications For Therapymentioning

confidence: 98%

Endogenous Cardiotonic Steroids in Kidney Failure: A Review and an Hypothesis

Hamlyn

Manunta

2015

Advances in Chronic Kidney Disease

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In response to progressive nephron loss, volume and humoral signals in the circulation have increasing relevance. These signals, including plasma sodium, angiotensin II and those related to volume status, activate a slow neuromodulatory pathway within the central nervous system (CNS). The slow CNS pathway includes specific receptors for angiotensin II, mineralocorticoids, and endogenous ouabain (EO). Stimulation of the pathway leads to elevated sympathetic nervous system activity (SNA) and increased circulating EO. The sustained elevation of circulating EO (or ouabain) stimulates central and peripheral mechanisms that amplify the impact of SNA on vascular tone. These include: changes in synaptic plasticity in the brain and sympathetic ganglia that increase preganglionic tone and amplify ganglionic transmission, amplification of the impact of SNA on arterial tone in the vascular wall, and the reprogramming of calcium signaling proteins in arterial myocytes. These increase SNA, raise basal and evoked arterial tone, and elevate blood pressure (BP). In the setting of chronic kidney disease, we suggest that sustained elevation of the slow CNS pathway, plasma EO and the cardiotonic steroid marinobufagenin (MBG), comprise a feed-forward system that raises BP and accelerates kidney and cardiac damage. Block of the slow CNS pathway and/or circulating EO and MBG may reduce BP and slow the progression to end stage renal disease.

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A new clinical multivariable model that predicts postoperative acute kidney injury: impact of endogenous ouabain

Cited by 33 publications

References 38 publications

Minor Postoperative Increases of Creatinine Are Associated With Higher Mortality and Longer Hospital Length of Stay in Surgical Patients

Minor Postoperative Increases of Creatinine Are Associated With Higher Mortality and Longer Hospital Length of Stay in Surgical Patients

Minor Postoperative Increases of Creatinine Are Associated with Higher Mortality and Longer Hospital Length of Stay in Surgical Patients

Endogenous Cardiotonic Steroids in Kidney Failure: A Review and an Hypothesis

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