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Renal Blood Flow, Glomerular Filtration Rate, and Renal Oxygenation in Early Clinical Septic Shock

Artikel i vetenskaplig tidskrift
Författare Jenny Skytte Larsson
Vitus Krumbholz
Anders Enskog
Gudrun Bragadottir
Bengt Redfors
Sven-Erik Ricksten
Publicerad i Critical Care Medicine
Volym 46
Nummer/häfte 6
Sidor E560-E566
ISSN 0090-3493
Publiceringsår 2018
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för anestesiologi och intensivvård
Sidor E560-E566
Språk en
Länkar dx.doi.org/10.1097/ccm.000000000000...
Ämnesord glomerular filtration rate, kidney failure, acute, oxygen consumption, sepsis, renal blood flow, acute kidney injury, sympathetic-nerve activity, cardiac surgery, patients, critically-ill patients, intensive-care units, nitric-oxide, cardiopulmonary bypass, severe sepsis, failure, norepinephrine, General & Internal Medicine
Ämneskategorier Intensivvård, Invärtesmedicin

Sammanfattning

Objective: Data on renal hemodynamics, function, and oxygenation in early clinical septic shock are lacking. We therefore measured renal blood flow, glomerular filtration rate, renal oxygen consumption, and oxygenation in patients with early septic shock. Patients: Patients with norepinephrine-dependent early septic shock (n = 8) were studied within 24 hours after arrival in the ICU and compared with postcardiac surgery patients without acute kidney injury (comparator group, n = 58). Measurements and Main Results: Data on systemic hemodynamics and renal variables were obtained during two 30-minute periods. Renal blood flow was measured by the infusion clearance of para-aminohippuric acid, corrected for renal extraction of para-aminohippuric acid. Renal filtration fraction was measured by renal extraction of chromium-51 labeled EDTA. Renal oxygenation was estimated from renal oxygen extraction. Renal oxygen delivery (-24%; p = 0.037) and the renal blood flow-to-cardiac index ratio (-21%; p = 0.018) were lower, renal vascular resistance was higher (26%; p = 0.027), whereas renal blood flow tended to be lower (-19%; p = 0.068) in the septic group. Glomerular filtration rate (-32%; p = 0.006) and renal sodium reabsorption (-29%; p = 0.014) were both lower in the septic group. Neither renal filtration fraction nor renal oxygen consumption differed significantly between groups. Renal oxygen extraction was significantly higher in the septic group (28%; p = 0.022). In the septic group, markers of tubular injury were elevated. Conclusions: In early clinical septic shock, renal function was lower, which was accompanied by renal vasoconstriction, a lower renal oxygen delivery, impaired renal oxygenation, and tubular sodium reabsorption at a high oxygen cost compared with controls.

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