Renal Parenchymal Oxygenation and Hypoxia Adaptation in Acute Kidney Injury

Rosenberger, Christian; Rosen, Seymour; Heyman, Samuel N.

doi:10.1111/j.1440-1681.2006.04472.x

Cited by 108 publications

(97 citation statements)

References 83 publications

(136 reference statements)

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“…In the same study, implanting cells expressing functional eNOS also improved renal function, suggesting a pivotal role for the dysfunction of both endothelial cells and eNOS in postischemic renal injury. Incomplete restoration of endothelium-dependent vasodilation, however, suggests that other pathways could be involved in this dysfunction, such as prostaglandins or endotheliumderived hyperpolarizing factor (EDHF) (66,67). Furthermore, during I/R, a lack of tetrahydrobiopterin (BH4)-an essential cofactor of NOS-has also been implicated in endothelial dysfunction after I/R injury (56).…”

Section: Microvascular Dysfunction and The Balance Between Vasoconstrmentioning

confidence: 99%

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Legrand

Mik

Johannes³

et al. 2008

Mol Med

237

169

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Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.

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Section: Microvascular Dysfunction and The Balance Between Vasoconstrmentioning

confidence: 99%

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Legrand

Mik

Johannes³

et al. 2008

Mol Med

237

169

View full text Add to dashboard Cite

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“…Renal oxygenation is very heterogeneous, with PO 2 falling to levels as low as 25 mmHg in the outer medulla under normal physiologic conditions and to even lower values in the papilla [3,4,19]. Changes in renal parenchymal microcirculation and oxygenation have been thoroughly investigated in acute and chronic renal disorders [19,20].…”

Section: Hif Expression Under Hypoxic Stress and Tissue Injurymentioning

confidence: 99%

Hypoxia-inducible Factors and the Prevention of Acute Organ Injury

Heyman¹,

Rosen²,

Rosenberger³

2011

Annual Update in Intensive Care and Emergency Medicine 2011

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“…Postoperative AKI in this group of patients is c onsidered a consequence of impaired renal DO 2 , in turn caused by intra-operative hypotension and hemodilution-induced anemia [32], as well as perioperative low cardiac output [29] . It has provocatively been stated that "acute ren al failure is acute renal success" [33,34], as a reduction in GFR in AKI should lead to a reduction in the renal reabsorptive workload, thus preserving medullary oxygenatio n wi th a reduced risk of further aggravation of ischemia. In patients with AKI, there are few data on renal VO 2 , renal blood fl ow, GFR and renal oxygenation and current views on renal oxygenation are presumptive and largely based on experimental studies.…”

Section: Renal Oxygenation In Clinical Ischemic Acute Kidney Injurymentioning

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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Renal Parenchymal Oxygenation and Hypoxia Adaptation in Acute Kidney Injury

Cited by 108 publications

References 83 publications

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Hypoxia-inducible Factors and the Prevention of Acute Organ Injury

Renal Oxygenation in Clinical Acute Kidney Injury

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