Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu tutaj
© Borgis - New Medicine 1/2016, s. 27-29 | DOI: 10.5604/14270994.1197178
*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.
Glomerular pathophysiology
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

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1


  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3


  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 28 zł
1. Navar LG: Regulation of Renal Hemodynamics. Am J Physiol 1998; 275 (Adv Physiol Educ 20): 221-235. 2. Jessup M, Costanzo MR: The Cardiorenal Syndrome. J Am Coll Cardiol 2009; 53(7): 597-599. 3. O’Connor PM: Renal oxygen delivery: matching delivery to metabolic demand. Clin Exp Pharmacol Physiol 2006; 33(10): 961-967. 4. Ricksten SE, Bragadottir G, Redfors B: Renal oxygenation in clinical acute kidney injury. Critical Care 2013; 17: 221. 5. Bellomo R, Kellum JA, Ronco C: Acute Kidney Injury. Lancet 2012; 380: 756-766 6. Prowle JR, Bellomo R: Sepsis-Associated Acute Kidney Injury: Macrohemodynamic and Microhemodynamic Alterations in the Renal Circulation. Semin Nephrol 2015; 35: 64-74. 7. Langenberg C, Bellomo R, May C et al.: Renal blood flow in sepsis. CritCare 2005; 9: R363-374. 8. Wan L, Bagshaw SM, Langenberg C et al.: Pathophysiology of septic acute kidney injury: What do we really know? Crit Care Med 2008; 36(4): 198-203. 9. Jacob LP, Chazalet JJ, Payen DM et al.: Renal hemodynamic and functional effect of PEEP ventilation in human renal transplantations. Am J Respir Crit Care Med 1995; 152: 103-107. 10. Prowle JR, Molan MP, Hornsey E, Bellomo R: Measurement of renal blood flow by phase-contrast magnetic resonance imaging during septic acute kidney injury: a pilot investigation. Crit Care Med 2012; 40: 1768-1776. 11. Prowle J, Bagshaw SM, Bellomo R: Renal blood flow, fractional excretion of sodium and acute kidney injury: time for a new paradigm? Curr Opin Crit Care 2012; 18: 585-592. 12. Nohria A, Hasselblad V, Stebbins A et al.: Cardiorenal interactions: insights from the ESCAPE trial. J Am Coll Cardiol 2008; 51: 1268-1274. 13. Pham P-TT, Pham P-CT, Rastogi A, Wilkinson AH: Review article: current management of renal dysfunction in the cirrhotic patient. Aliment Pharmacol Ther 2005; 21: 949-961. 14. Leithead JA, Hayes PC, Ferguson JW: Review article: advances in the management of patients with cirrhosis and portal hypertension-related renal dysfunction. Aliment Pharmacol Ther 2014; 39: 699-711. 15. Winton F: The influence of venous pressure on the isolated mammalian kidney. J Physiol 1931; 72: 49-61. 16. Bradley SE, Bradley GP: The Effect Of Increased Intra-Abdominal Pressure On Renal Function In Man. J Clin Invest 1947 Sep; 26(5): 1010-1022. 17. Greenway CV, Lister GE: Capacitance effects and blood reservoire function in the splanchnic vascular bed during non-hypotensive haemorrhage and blood volume expansion in anaesthetized cats. J Physiol 1974; 237: 279-294. 18. Gelman S, Mushlin PS: Catecholamine-induced changes in the splanchnic circulation affecting systemic hemodynamics. Anesthesiology 2004; 100: 434-439. 19. Legrand M, Dupuis C, Simon C et al.: Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: a retrospective observational study. Crit Care 2013; 17: R278. 20. Rajendram R, Prowle JR: Venous congestion: are we adding insult to kidney injury in sepsis? Critical Care 2014; 18: 104-105. 21. Viswanathan G, Gilbert S: The Cardiorenal Syndrome: Making the Connection. International Journal of Nephrology 2011; Article ID 283137, 10 pages. 22. Verbrugge FH, Dupont M, Steels P et al.: Abdominal Contributions to Cardiorenal Dysfunction in Congestive Heart Failure. J Am Coll Cardiol 2013; 62: 485-495. 23. Dalfino L, Tullo L, Donadio I et al.: Intra-abdominal hypertension and acute renal failure in critically ill patients. Intensive Care Med 2008; 34: 707-713. 24. Kirkpatrick AW, Roberts DJ, de Waele J et al.: Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013; 39: 1190-1206. 25. Verbrugge FH, Dupont M, Steels P et al.: Abdominal Contributions to Cardiorenal Dysfunction in Congestive Heart Failure. J Am Coll Cardiol 2013; 62: 485-495. 26. Mullens W, Abrahams Z, Francis GS et al.: Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure. J Am Coll Cardiol 2009; 53: 589-596. 27. Damman K, van Deursen VM, Navis G et al.: Increased Central Venous Pressure Is Associated With Impaired Renal Function and Mortality in a Broad Spectrum of Patients With Cardiovascular Disease. J Am Coll Cardiol 2009; 53: 582-588. 28. van den Akker JP, Egal M, Groeneveld AB: Invasive mechanical ventilation as a risk factor for acute kidney injury in the critically ill: a systematic review and meta-analysis. Crit Care 2013; 17(3): R98.
otrzymano: 2015-11-02
zaakceptowano do druku: 2016-01-04

Adres do korespondencji:
*Csaba Kopitko
Intensive Care Unit Dr. Kenessey Albert Hospital
H-2660 Balassagyarmat
Rakoczi fejedelem ut 125-127, Hungary
tel. +36 30-667-7939, fax: +36 35-505-009
e-mail: kopcsab@freemail.hu

New Medicine 1/2016
Strona internetowa czasopisma New Medicine