*Csaba Kopitko1, Laszlo Medve1, Tibor Gondos2
Pathophysiology of renal blood supply
1Department of Anaesthesiology and Intensive Care Medicine, Dr. Kenessey Albert Hospital, Balassagyarmat, Hungary
Head of Hospital: Gèza Szabó, MD, General Director
2Department of Clinical Studies, Faculty of Health Sciences, Semmelweis University, Budapest, Hungary
Head of Faculty: Prof. Zoltán Zsolt Nagy, MD, PhD
Acute kidney injury has an increasing incidence and high mortality rate with enormous financial and healthcare implications. The pathophysiology differs in various clinical situations (e.g. sepsis, cardiac arrest or other low flow states, cardiorenal and hepatorenal syndromes etc.), but the impaired blood supply plays an important role in destroying renal function. Unfortunately, despite of the multiple technical possibilities, monitoring of renal blood flow is unavailable in clinical practice, because of the high personal and environmental demand of the measurements. One should always remind himself of the fact, that the net filtration pressure in glomeruli is about 10 mmHg in physiological circumstances. Kidneys are in the vessel-rich group of organs with brain, heart and liver, therefore receive a very high amount of cardiac output (about 20%) with relatively low oxygen extraction rate (10%). Equally, the decreased arterial flow, the intrarenal imbalance and the venous side anomalies can cause renal failure. We would like to show a holistic picture from the pathophysiology of renal circulation.
The occurrence of acute kidney injury (AKI) dramatically increases the mortality rate in intensive care unit either in septic or postoperative patients. This fact has not been changed with the development of renal replacement techniques, therefore the prevention of AKI is very important. The understanding the physiology of renal blood supply in normal and in pathological circumstances is essential for doing the best clinical practice. Although the change of glomerular arterial resistances has been investigated in most studies, increasing amount of evidences supports the role of venous factors. The aim of our work was to review the clinically relevant data.
Physiology of the renal circulation
Renal blood flow (RBF) takes normally approximately 20% of cardiac output, which is 10-50 times greater than other organs regarding their weight (1, 2). The glomerular effective filtration pressure depends on the mean capillary pressure (normally 45 mmHg), opposing the intracapsular/interstitial pressure (10 mmHg) and the mean colloid osmotic pressure (25 mmHg). Therefore physiologically the net filtration pressure gradient is about 10 mmHg. Any change in the colloid and hydrostatic pressures changes the number of filtrating glomeruli or the surface area serving as functional reserve capacity. A major determinant of the glomerular filtration rate (GFR) is the glomerular pressure depending on the balance between afferent and efferent arteriolar resistance. Regulation of RBF comes from factors (1) that are both extrarenal (sympathic nerves, circulating agents, e.g. renin-angiotensin II-aldosteron system, nor/epinephrine thromboxane, 20-hydroxyeicosatetraenoic acid, prostacyclin) and intrarenal (preglomerular arterial myogenic response, tubuloglomerular feedback, nitric oxide, endothelium-derived hyperpolarizing factor). The unimpaired autoregulatory mechanism keeps the GFR constant in a wide range of mean arterial pressures (MAP).
Renal oxygen consumption is 10 ml/min/100 g but the extraction ratio from the oxygen supply is quite low (10% in the kidneys vs. 55% in the heart). The reason for this is that RBF comprises a relatively high proportion of cardiac output (3, 4). The highest oxygen-dependent intrarenal process is the tubular reabsorption of sodium. Increasing RBF normally raises the GFR and tubular sodium load, so that renal oxygen extraction remains the same over a wide range of RBF. The partial pressure of oxygen in the kidneys is different. It is 10-20 mmHg in the outer medulla compared to 50 mmHg in the cortex, due to the regional distribution of blood supply.
The kidney in SIRS/sepsis
The sepsis-associated AKI (SA-AKI) seems to be inflammatory and ischaemic in origin. In experimental sepsis with hyperkinetic circulation the GFR decreased and AKI occurred even though the RBF was undiminished (5, 6). In human studies the RBF increased in sepsis, and the only significant predictor of this was cardiac output (7, 8). In other studies it was reported that the proportion of RBF decreased from the normal 20% to 7% of cardiac output (8). The renal autoregulation is impaired either in sepsis or in AKI, respectively (9-11). The consequence of this impairment is vasodilatation (partially) caused by nitric oxide resulting cardiac output dependency of RBF. Interestingly, inhibiting the nitric oxide synthase did not influence the kidney injury in sheep (6, 11). Vasodilatation favors the efferent arteriolae, and together with the myogenic increase in the afferent arteriolar resistance leads to the deterioration of glomerular ultrafiltration.
Furthermore, in sepsis the intrarenal microcirculation distribution is altered exposing the medulla to ischaemic risk and tubular dysfunction, as measured by Doppler flowmetry (6). In different septic animal models the occurrence of capillary leakage precedes the changes in RBF, indicating the role of local inflammatory processes. Despite decreasing RBF, tissue oxygen tension is maintained, mitochondrial respiration is undisturbed and renal adenosine triphosphat levels are sustained – however renal function fails. In ischaemic animal models, unclamping resolves the RBF, but later on it once more decreases in spite of physiological macrocirculation implicating intrarenal factors. Many other nonvascular processes seem to be taking place in SA-AKI, e.g. tubuloglomerular feedback activation, tubular obstruction and tubular back-leakage. The predictor of sustained AKI is elevated tubular and intracapsular pressure.
Cardiorenal and hepatorenal syndromes
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