Beneficial Effects of Short-term Vasopressin Infusion during Severe Septic Shock

Patel, B. M.; Chittock, Dean R.; Russell, James A.; Walley, Keith R.

doi:10.1097/00000542-200203000-00011

Cited by 513 publications

(337 citation statements)

References 39 publications

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“…These results are consistent with previous small studies showing that vasopressin compared to norepinephrine increased urine output and creatinine clearance [9][10][11][12].…”

Section: Comparison Of Vasopressin V Norepinephrinesupporting

confidence: 93%

“…In addition to its potent vasoconstrictor effects, vasopressin may also have specific beneficial effects on renal function secondary to its binding to a family of vasopressin receptors [8]. In several small studies of vasodilatory shock, vasopressin increased glomerular filtration rate, urine output and creatinine clearance [9][10][11][12]. However, to date no large studies have assessed the effect of vasopressin, as compared with norepinephrine, on the outcome of acute kidney injury.…”

Section: Introductionmentioning

confidence: 99%

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The effects of vasopressin on acute kidney injury in septic shock

et al. 2009

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Kidney injury was present in 464 patients (59.6%) at study entry. In patients in the RIFLE "Risk" category (n=106) vasopressin as compared with norepinephrine was associated with a trend to a lower rate of progression to renal "Failure" or "Loss" categories (20.8% v 39.6% respectively, p=0.03), and a lower rate of use of renal replacement therapy (17.0% v 37.7%, p=0.02). Mortality rates in the "Risk" category patients treated with vasopressin compared to norepinephrine were 30.8% v 54.7%, p=0.01, but this did not reach significance in a multiple logistic regression analysis (OR=0.33, 99%CI 0.10-1.09, p=0.02). The interaction of treatment group and RIFLE category was significant in predicting mortality. Conclusions:Vasopressin may reduce progression to renal failure and mortality in patients at risk of kidney injury who have septic shock.

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“…These results are consistent with previous small studies showing that vasopressin compared to norepinephrine increased urine output and creatinine clearance [9][10][11][12].…”

Section: Comparison Of Vasopressin V Norepinephrinesupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

The effects of vasopressin on acute kidney injury in septic shock

et al. 2009

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“…Vaso pressin has, therefore, been suggested as an additional or an alternative therapy in catecholaminedependent vasodilatory shock [49]. It has also been reported that vasopressin increases creatinine clearance, a surrogate variable of GFR, in these patients [50]. A more detailed analysis on the eff ects of low-dose vasopressin on renal oxygenation is lacking.…”

Section: Low-dose Vasopressin and Renal Oxygenationmentioning

confidence: 99%

Renal Oxygenation in Clinical Acute Kidney Injury

Ricksten¹,

Bragadottir²,

Redfors³

2013

Annual Update in Intensive Care and Emergency Medicine 2013

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Renal oxygenation is defi ned as the relationship between renal oxygen delivery (DO 2 ) and renal oxygen consumption (VO 2 ) and it can easily be shown that the inverse of this relationship is equivalent to renal extraction of O 2 (O 2 Ex). An increase in renal O 2 Ex means that renal DO 2 has decreased in relation to renal VO 2 , i. e., renal oxygenation is impaired, and vice versa. When compared to other major organs, renal VO 2 is relatively high, second only to the heart. In sedated, mechanically ventilated patients, renal VO 2 is two-thirds (10 ml/min) that of myocardial oxygen consumption (15 ml/min) (Table 1) [1,2]. Renal blo od fl ow, w hich accounts for approximately 20 % of cardiac output, is three times higher than myocardial blood fl ow in this group of patients. Renal O 2 Ex in the non-failing kidney is therefore low, 10 %, compared with, e.g., the heart, in which O 2 E X is 55 % (Table 1). Determin a nts of renal oxygenationIt is well known from experimental studies that tubular sodium reabsorption is the major determinant of renal VO 2 [3] and tha t under normal physiological conditions, approximately 80 % is used to drive active tubular transport of particularly sodium, but also glucose, amino acids and other solutes. Tubular transport processes are highly load-dependent and it has been shown in experimental studies [4] and in p atients [2,[5][6][7] that the re i s a close linear correlation between glomerular fi ltration rate (GFR), renal sodium reabsorption and renal VO 2 (Fig. 1). Th e fi l tered load of sodium is, thus, an important determi nant of renal VO 2 and maneuvers that decrease GFR and the tubular sodium load act to decrease tubular sodium reabsorption and renal VO 2 , and vice versa [8]. It has b een shown that renal O 2 Ex remains stable over a wide range of renal blood fl ows, which means that changes in renal DO 2 , caused by changes in renal blood fl ow, are directly off set by changes in renal VO 2 [9], i. e., r enal VO 2 is fl ow-dependent. Th us, unlike other organs where increases in blood fl ow will improve oxygenation, increased renal blood fl ow augments GFR and the fi ltered load of sodium, which will increase renal VO 2 . Due to this fl ow-dependency of renal VO 2 , renal oxygenation will re main constant, as long as renal blood fl ow and GFR change in parallel. Regional intrarenal oxygenation and medullary hypoxiaTh e relatively high renal blood fl ow is directed preferentially to the cortex to optimize the fi ltration process and solute reabsorption. In contrast, blood fl ow in the outer medulla is less than 50 % of the cortical blood fl ow to preserve osmotic gradients and to enhance urinary concentration [10]. Th e combi nation of low me dullary perfusion, high oxygen consumption of the medullary thick ascending limbs (mTAL) and the countercurrent exchange of oxygen within the vasa recta, results in a poorly oxygenated outer medulla [11]. Oxygen av ailability is, therefore, low in the outer medulla, which has an oxygen tissue partial pressure (PO 2 ) of 10-20 mm Hg ...

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“…Arginine vasopressin administration in 16 patients with septic shock and hyporesponsiveness to catecholamines increased BP, systemic vascular resistance, and urine output (15). A randomized trial in 24 patients with septic shock demonstrated that a 4-h infusion of arginine vasopressin improved urine output and creatinine clearance with similar effects on BP and cardiac output, as compared with norepinephrine (16).…”

Section: Vasopressorsmentioning

confidence: 99%