Determinants of Doppler-based renal resistive index in patients with septic shock: impact of hemodynamic parameters, acute kidney injury and predisposing factors

François Beloncle, Natacha Rousseau, Jean-François Hamel, Alexis Donzeau, Anne-Lise Foucher, Marc-Antoine Custaud, Pierre Asfar, René Robert, Nicolas Lerolle, François Beloncle, Natacha Rousseau, Jean-François Hamel, Alexis Donzeau, Anne-Lise Foucher, Marc-Antoine Custaud, Pierre Asfar, René Robert, Nicolas Lerolle

Abstract

Background: Increased renal resistive index (RI) measured by Doppler ultrasonography has been shown to be associated with acute kidney injury (AKI) in septic patients. However, its clinical use is limited by poor sensitivity and specificity which may be explained by its numerous determinants [in particular mean arterial pressure (MAP)]. We measured, in patients with septic shock, RI at different MAP levels over a short period of time on the admission day to ICU (D1) and every 3 days until day 10 (D10) to define the determinants of RI and study specifically the relationship between RI and MAP.

Results: Consecutive patients with septic shock without preexisting chronic renal dysfunction were included in this prospective cohort study in two ICUs. Sixty-five patients were included in the study. Thirty-three (50.8%) and 15 (23.1%) patients had a history of chronic hypertension or diabetes, respectively. At D3, 35 patients presented AKI with AKIN 2 or 3 criteria (severe AKI, AKIN2-3 group) and 30 presented no AKIN or AKIN 1 criteria (AKIN0-1 group). As previously described, RI at D1 was higher in the AKIN2-3 group than in the AKIN0-1 group (0.73 interquartile range [0.67; 0.78] vs. 0.67 [0.59; 0.72], p = 0.001). A linear mixed model for predicting RI from D1 to D10 showed that an increase in pulse pressure, presence of severe AKI and additional day of ICU hospitalization were associated with an increase in RI. An increase in MAP and recovery from severe AKI were associated with a decrease in RI. In the presence of chronic hypertension or diabetes, an increase in MAP resulted in a lower decrease in RI, than in the absence of such factors. Presence of AKI at D3 did not impact the relationship between MAP and RI.

Conclusions: Severe AKI was associated with a reversible increase in RI without significant interaction with the relationship between MAP and RI. Conversely, the presence of chronic hypertension and/or diabetes interacted with this relationship.

Keywords: Acute kidney injury; Clinical study; Critical care; Resistive index; Sepsis; Shock; Vasopressors.

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Renal resistive index (RI) measurements and sequence of RI measurements. A RI measurement corresponded to the mean of five measures performed on five consecutive pulses at one mean arterial pressure (MAP) level. A sequence of RI measurements included from 2 to 5 RI measurements performed in less than 20 min at, at least, 2 MAP levels (aim of at least 15 mmHg apart, between the two levels). When vasopressors were discontinued, the sequence of RI measurements included only one RI measurement at one MAP level
Fig. 2
Fig. 2
Distribution of renal resistive index at day 1 (RI D1) according to AKIN classification at day 3 (AKIN D3). RI D1 corresponds to the mean of RI measured for each patient at different mean arterial pressure levels over a period of 20 min on the ICU admission day. Horizontal lines represent median, first and third quartile values for each group. Overall comparison: p = 0.01

References

    1. Thakar CV, Christianson A, Freyberg R, Almenoff P, Render ML. Incidence and outcomes of acute kidney injury in intensive care units: a Veterans Administration study. Crit Care Med. 2009;37:2552–2558. doi: 10.1097/CCM.0b013e3181a5906f.
    1. Lopes JA, Jorge S, Resina C, Santos C, Pereira A, Neves J, et al. Acute renal failure in patients with sepsis. Crit Care Lond Engl. 2007;11:411. doi: 10.1186/cc5735.
    1. Wan L, Bagshaw SM, Langenberg C, Saotome T, May C, Bellomo R. Pathophysiology of septic acute kidney injury: What do we really know? Crit Care Med. 2008;36:S198–S203. doi: 10.1097/CCM.0b013e318168ccd5.
    1. Aird WC. Vascular bed-specific hemostasis: role of endothelium in sepsis pathogenesis. Crit Care Med. 2001;29:S28-34-35. doi: 10.1097/00003246-200107001-00013.
    1. Piepot HA, Groeneveld ABJ, van Lambalgen AA, Sipkema P. Endotoxin impairs endothelium-dependent vasodilation more in the coronary and renal arteries than in other arteries of the rat. J Surg Res. 2003;110:413–418. doi: 10.1016/S0022-4804(02)00043-4.
    1. Wang Z, Holthoff JH, Seely KA, Pathak E, Spencer HJ, 3rd, Gokden N, et al. Development of oxidative stress in the peritubular capillary microenvironment mediates sepsis-induced renal microcirculatory failure and acute kidney injury. Am J Pathol. 2012;180:505–516. doi: 10.1016/j.ajpath.2011.10.011.
    1. Lerolle N, Guérot E, Faisy C, Bornstain C, Diehl J-L, Fagon J-Y. Renal failure in septic shock: predictive value of Doppler-based renal arterial resistive index. Intensive Care Med. 2006;32:1553–1559. doi: 10.1007/s00134-006-0360-x.
    1. Darmon M, Schortgen F, Vargas F, Liazydi A, Schlemmer B, Brun-Buisson C, et al. Diagnostic accuracy of Doppler renal resistive index for reversibility of acute kidney injury in critically ill patients. Intensive Care Med. 2011;37:68–76. doi: 10.1007/s00134-010-2050-y.
    1. Schnell D, Deruddre S, Harrois A, Pottecher J, Cosson C, Adoui N, et al. Renal resistive index better predicts the occurrence of acute kidney injury than cystatin C. Shock Augusta Ga. 2012;38:592–597. doi: 10.1097/SHK.0b013e318271a39c.
    1. Lerolle N. Please don’t call me RI anymore; I may not be the one you think I am! Crit Care. 2012;16:174. doi: 10.1186/cc11831.
    1. Bude RO, Rubin JM. Relationship between the resistive index and vascular compliance and resistance. Radiology. 1999;211:411–417. doi: 10.1148/radiology.211.2.r99ma48411.
    1. Dewitte A, Coquin J, Meyssignac B, Joannès-Boyau O, Fleureau C, Roze H, et al. Doppler resistive index to reflect regulation of renal vascular tone during sepsis and acute kidney injury. Crit Care. 2012;16:R165. doi: 10.1186/cc11517.
    1. Tublin ME, Tessler FN, Murphy ME. Correlation between renal vascular resistance, pulse pressure, and the resistive index in isolated perfused rabbit kidneys. Radiology. 1999;213:258–264. doi: 10.1148/radiology.213.1.r99oc19258.
    1. Mostbeck GH, Gössinger HD, Mallek R, Siostrzonek P, Schneider B, Tscholakoff D. Effect of heart rate on Doppler measurements of resistive index in renal arteries. Radiology. 1990;175:511–513. doi: 10.1148/radiology.175.2.2183288.
    1. Moussa MD, Scolletta S, Fagnoul D, Pasquier P, Brasseur A, Taccone FS, et al. Effects of fluid administration on renal perfusion in critically ill patients. Crit Care. 2015;19:250. doi: 10.1186/s13054-015-0963-0.
    1. Darmon M, Schortgen F, Leon R, Moutereau S, Mayaux J, Di Marco F, et al. Impact of mild hypoxemia on renal function and renal resistive index during mechanical ventilation. Intensive Care Med. 2009;35:1031–1038. doi: 10.1007/s00134-008-1372-5.
    1. Sharkey RA, Mulloy EM, O’Neill SJ. Acute effects of hypoxaemia, hyperoxaemia and hypercapnia on renal blood flow in normal and renal transplant subjects. Eur Respir J. 1998;12:653–657. doi: 10.1183/09031936.98.12030653.
    1. Deruddre S, Cheisson G, Mazoit J-X, Vicaut E, Benhamou D, Duranteau J. Renal arterial resistance in septic shock: effects of increasing mean arterial pressure with norepinephrine on the renal resistive index assessed with Doppler ultrasonography. Intensive Care Med. 2007;33:1557–1562. doi: 10.1007/s00134-007-0665-4.
    1. Benes J, Chvojka J, Sykora R, Radej J, Krouzecky A, Novak I, et al. Searching for mechanisms that matter in early septic acute kidney injury: an experimental study. Crit Care. 2011;15:R256. doi: 10.1186/cc10517.
    1. van Dokkum RP, Sun CW, Provoost AP, Jacob HJ, Roman RJ. Altered renal hemodynamics and impaired myogenic responses in the fawn-hooded rat. Am J Physiol. 1999;276:R855–R863.
    1. Hayashi K, Epstein M, Loutzenhiser R, Forster H. Impaired myogenic responsiveness of the afferent arteriole in streptozotocin-induced diabetic rats: role of eicosanoid derangements. J Am Soc Nephrol JASN. 1992;2:1578–1586.
    1. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med. 1992;20:864–74.
    1. Pottecher T, Calvat S, Dupont H, Durand-Gasselin J, Gerbeaux P, SFAR/SRLF workgroup Haemodynamic management of severe sepsis: recommendations of the French Intensive Care Societies (SFAR/SRLF) Consensus Conference, 13 October 2005, Paris, France. Crit Care. 2005;10:311.
    1. Mastorakou I, Lindsell DR, Piepoli M, Adamopoulos S, Ledingham JG. Pulsatility and resistance indices in intrarenal arteries of normal adults. Abdom Imaging. 1994;19:369–373. doi: 10.1007/BF00198202.
    1. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al. Acute kidney injury network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11:R31. doi: 10.1186/cc5713.
    1. Vincent JL, Moreno R, Takala J, Willatts S, DeMendonça A, Bruining H, et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive Care Med. 1996;22:707–710. doi: 10.1007/BF01709751.
    1. Le Gall JR, Lemeshow S, Saulnier F. A new Simplified Acute Physiology Score (SAPS II) based on a European/North American multicenter study. JAMA J Am Med Assoc. 1993;270:2957–2963. doi: 10.1001/jama.1993.03510240069035.
    1. Laird NM, Ware JH. Random-effects models for longitudinal data. Biometrics. 1982;38:963–974. doi: 10.2307/2529876.
    1. Baldwin D, Bobes J, Stein DJ, Scharwächter I, Faure M. Paroxetine in social phobia/social anxiety disorder. Randomised, double-blind, placebo-controlled study. Paroxetine Study Group. Br J Psychiatry J Ment Sci. 1999;175:120–126. doi: 10.1192/bjp.175.2.120.
    1. Chen J, Li Y, Wang L, Zhang Z, Lu D, Lu M, et al. Therapeutic benefit of intravenous administration of bone marrow stromal cells after cerebral ischemia in rats. Stroke J Cereb Circ. 2001;32:1005–1011. doi: 10.1161/01.STR.32.4.1005.
    1. Zelen M. The analysis of several 2 × 2 contingency tables. Biometrika. 1971;58:129–137.
    1. Augusto J-F, Teboul J-L, Radermacher P, Asfar P. Interpretation of blood pressure signal: physiological bases, clinical relevance, and objectives during shock states. Intensive Care Med. 2011;37:411–419. doi: 10.1007/s00134-010-2092-1.
    1. Chawla LS, Eggers PW, Star RA, Kimmel PL. Acute kidney injury and chronic kidney disease as interconnected syndromes. N Engl J Med. 2014;371:58–66. doi: 10.1056/NEJMra1214243.
    1. Asfar P, Meziani F, Hamel J-F, Grelon F, Megarbane B, Anguel N, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med. 2014;370:1583–1593. doi: 10.1056/NEJMoa1312173.
    1. Kirkpatrick AW, Colistro R, Laupland KB, Fox DL, Konkin DE, Kock V, et al. Renal arterial resistive index response to intraabdominal hypertension in a porcine model. Crit Care Med. 2007;35:207–213. doi: 10.1097/01.CCM.0000249824.48222.B7.
    1. Cupples WA, Braam B. Assessment of renal autoregulation. Am J Physiol Renal Physiol. 2007;292:F1105–F1123. doi: 10.1152/ajprenal.00194.2006.
    1. Johnson PC. Autoregulation of blood flow. Circ Res. 1986;59:483–495. doi: 10.1161/01.RES.59.5.483.
    1. Gomez H, Ince C, De Backer D, Pickkers P, Payen D, Hotchkiss J, et al. A unified theory of sepsis-induced acute kidney injury: inflammation, microcirculatory dysfunction, bioenergetics, and the tubular cell adaptation to injury. Shock Augusta Ga. 2014;41:3–11. doi: 10.1097/SHK.0000000000000052.

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