FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2002010280> ?p ?o ?g. }

• W2002010280 endingPage "476" @default.
• W2002010280 startingPage "474" @default.
• W2002010280 abstract "Only a few clinical methods are available for the intraoperative assessment of a transplanted kidney. Conventional management includes direct observation of the graft's color, turgor, and size, as well as monitoring of the immediate onset of urine production. All of these variables are insensitive and nonspecific. Duplex sonography is an established monitoring procedure for posttransplant follow-up [1-3], but there are only a few studies that have used ultrasonography for renal blood flow determination during kidney transplantation [4]. Furthermore, renal scintigraphy is used to analyze renal blood flow after transplantation [5]. To estimate the changes in regional oxygen supply during living donor kidney transplantation, we measured local tissue PO2 in the superficial cortex of the kidney before nephrectomy in the living donor and immediately after revascularization in the recipient. We compared the results with routinely determined markers of the primary renal function. Methods After approval by the local ethics committee and informed consent were obtained, we studied 18 patients (9 living related kidney donors and 9 organ recipients). General anesthesia was used in both the donor group and the recipient group. Anesthesia was induced using fentanyl (1-2 [micro sign]g/kg) and thiopental (5 mg/kg). To facilitate endotracheal intubation, succinylcholine (1 mg/kg) was given. Anesthesia was maintained with nitrous oxide in oxygen and isoflurane. Atracurium was used to provide neuromuscular blockade. Ventilation was adjusted to maintain normoxia (SpO2 >or=to95%) and normocapnia (PETCO2 35-45 mm Hg) throughout the investigation period. No preoperative volume expansion was performed. To maintain intravascular volume, lactated Ringer's solution or saline 0.9% and albumin were administered. Dopamine (3 [micro sign]g [center dot] kg-1 [center dot] min-1) was started after the induction of anesthesia in both groups. Kidney recipients received 1 g of methylprednisolone. To promote diuresis in the grafted kidney, mannitol 37.5 g and furosemide 80 mg were given just before the release of the vascular clamps. Heart rate (HR) and mean arterial pressure (MAP), measured with an oscillometry device, were recorded. The SpO2 value determined by pulse oximetry, the inspiratory oxygen content (FIO2), and the PETCO2 value were measured throughout the operation. Central venous blood samples were drawn for blood gas analysis. The tissue oxygen pressure was measured by using a multiwire tissue surface PO2 electrode and temperature probe (LICOX; GMS, Kiel-Mielkendorf, Germany). This polarographic Clark-type probe is assembled with eight PO2-sensitive platinum microelectrodes, each 15 [micro sign]m in diameter. The microelectrode array (3 mm in diameter) is arranged in the center of the tissue contact area. The polarographic silver anode is positioned at its circumference. To avoid tissue damage, the light-weight probe (2.3 g) was placed without pressure on the renal cortex. After reaching steady state, the average of the eight local tissue values was automatically sampled every 5 s for 1 min. In the living donors, cardiorespiratory variables and renocortical tissue PO2 values were measured before cross-clamping of the renal vessels. In the recipients, these data were obtained after revascularization and construction of the urinary drainage were completed. Furthermore, in one case, we measured renocortical tissue PO2 in the renal graft during cold-preservation with University of Wisconsin solution. To assess the primary function of the grafted kidney, the daily urine output, serum creatinine, and creatinine clearance were recorded on the first and third postoperative days. Data are expressed as mean +/- SD. The biometric, cardiorespiratory, and volume therapy data were compared by using Student's t-test. To determine differences in renocortical tissue PO2, a paired Student's t-test was used. P values <0.05 were considered significant. Results Kidney recipients had a significantly lower body weights compared with the donors (Table 1). The two groups did not differ with regard to FIO2, SpO (2), PVO2, and PVCO2. The kidney recipients had higher MAPs. In addition, pH, base excess, and hematocrit were lower in this group. The kidney donors received significantly more crystalloids than the organ recipients (Table 1). There were no differences between the groups with regard to the renocortical tissue PO2 (72 +/- 20 mm Hg in the donor group versus 75 +/- 16 mm Hg in the recipient group). The changes in renocortical tissue PO2 of an individual graft before nephrectomy (79 mm Hg), during cold ischemia (1 mm Hg), and after the vascular and urinary tract anastomosis (80 mm Hg) are shown in Figure 1. The mean cold ischemia time was 107 +/- 55 min. The postoperative courses of the daily urine output, serum creatinine, and creatinine clearance are presented in Table 2.Table 1: Demographic Profile, Cardiorespiratory Data, and Cumulative Volume TherapyFigure 1: Changes in renocortical tissue PO2 (trace 1) and tissue temperature (trace 2) in a single kidney graft. Between the measurements, the tissue surface probe is placed in a holder for storage in humid air (PO2 = 150 mm Hg) and for stable temperature (21[degree sign]C).Table 2: Postoperative Renal FunctionDiscussion The main goal of our investigation was to evaluate the blood supply of the transplanted kidney immediately after revascularization by measuring renocortical tissue PO2. Assessing organ tissue PO2 by polarography with Clark-type electrodes is an established procedure [6,7]. It has been used under experimental conditions in a variety of organs, including the human kidney [8-11]. Local tissue PO2 in the transplanted human kidney has been evaluated by others, as well [12,13]. No data are available in the literature for patients undergoing living related donor kidney transplantation. The lower pH, base excess, and hematocrit, as well as the higher MAP, in the kidney recipients may result from the underlying renal disease. No patient required additional vasoactive therapy during the study period. The organ recipients required less volume therapy during surgery to preserve an adequate perfusion pressure. The main results of this study demonstrate that during living donor kidney transplantation, renocortical tissue PO2 measurement can be used to determine the regional oxygen supply in the grafted organ. Tissue PO2 is determined by the balance between local oxygen delivery and oxygen consumption by the tissue. There was no difference in renocortical tissue PO2 in the grafted kidney compared with in situ measurements in the living donor. This indicates an immediate recovery from ischemia with no major alteration in renal macro- and microcirculation after transplantation. Ischemic insults to the kidney are associated with a marked decrease in blood flow to the outer renal cortex and a concomitant increase in flow to the juxtamedullary glomeruli [14]. In contrast to data obtained from measurements of renal cortical blood flow, the determination of total renal flow rates did not provide a reliable predictive index of organ function after transplantation [15]. Using a canine model, Kram et al. [11] demonstrated that renocortical tissue PO2 is a sensitive measurement of renal surface perfusion. The baseline (mean +/- SEM) value for renocortical tissue PO2 reported by this group was 77 +/- 4 mm Hg during ventilation with a constant FIO2 of 0.21. Wilms [9] investigated changes in renocortical tissue PO2 during autologous kidney transplantation in a canine model and found a slight decrease in renocortical tissue PO2 immediately after revascularization to 86% of the values obtained before nephrectomy, which emphasizes that systemic hypotension during revascularization is followed by a strong decrease in renocortical oxygen supply. The effects of the cold ischemia time on renocortical tissue PO2 in cadaver kidney recipients were evaluated by Schott and Prom [13], who reported a pronounced benefit of intraarterial diltiazem administration for kidneys exposed to longer cold ischemia times and initially indifferent postischemic baseline histograms. Furthermore, these authors demonstrated that a good postischemic histogram correlates well with prompt initial renal function. In the present study, the early postoperative course was uneventful in all patients. Specifically, there was no primary graft dysfunction, as indicated by an adequate diuresis and a continuous decrease in serum creatinine. Furthermore, no patient required dialysis after transplantation. The occurrence of delayed primary graft function is associated with a 20%-25% decrease in long-term survival of the graft [16] and an increase of 3%-10% in early mortality of the recipient [17]. Therefore, an immediate diagnosis of changes in the graft's microcirculation by assessing renocortical tissue PO2 yields additional information for the patient's management. Further studies, however, are required to determine critically low renocortical tissue PO2 values." @default.
• W2002010280 created "2016-06-24" @default.
• W2002010280 creator A5022077604 @default.
• W2002010280 creator A5036218939 @default.
• W2002010280 creator A5040007127 @default.
• W2002010280 creator A5045096607 @default.
• W2002010280 creator A5056245846 @default.
• W2002010280 creator A5060756025 @default.
• W2002010280 creator A5087116192 @default.
• W2002010280 date "1998-08-01" @default.
• W2002010280 modified "2023-09-23" @default.
• W2002010280 title "Renocortical Tissue Oxygen Pressure Measurements in Patients Undergoing Living Donor Kidney Transplantation" @default.
• W2002010280 cites W1987525080 @default.
• W2002010280 cites W2000121566 @default.
• W2002010280 cites W2002372572 @default.
• W2002010280 cites W2003500637 @default.
• W2002010280 cites W2004643468 @default.
• W2002010280 cites W2067385943 @default.
• W2002010280 cites W2316674859 @default.
• W2002010280 doi "https://doi.org/10.1097/00000539-199808000-00045" @default.
• W2002010280 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9706953" @default.
• W2002010280 hasPublicationYear "1998" @default.
• W2002010280 type Work @default.
• W2002010280 sameAs 2002010280 @default.
• W2002010280 citedByCount "13" @default.
• W2002010280 countsByYear W20020102802015 @default.
• W2002010280 countsByYear W20020102802016 @default.
• W2002010280 countsByYear W20020102802018 @default.
• W2002010280 countsByYear W20020102802019 @default.
• W2002010280 countsByYear W20020102802020 @default.
• W2002010280 countsByYear W20020102802021 @default.
• W2002010280 countsByYear W20020102802022 @default.
• W2002010280 crossrefType "journal-article" @default.
• W2002010280 hasAuthorship W2002010280A5022077604 @default.
• W2002010280 hasAuthorship W2002010280A5036218939 @default.
• W2002010280 hasAuthorship W2002010280A5040007127 @default.
• W2002010280 hasAuthorship W2002010280A5045096607 @default.
• W2002010280 hasAuthorship W2002010280A5056245846 @default.
• W2002010280 hasAuthorship W2002010280A5060756025 @default.
• W2002010280 hasAuthorship W2002010280A5087116192 @default.
• W2002010280 hasBestOaLocation W20020102801 @default.
• W2002010280 hasConcept C126322002 @default.
• W2002010280 hasConcept C141071460 @default.
• W2002010280 hasConcept C177713679 @default.
• W2002010280 hasConcept C178790620 @default.
• W2002010280 hasConcept C185592680 @default.
• W2002010280 hasConcept C2780091579 @default.
• W2002010280 hasConcept C2780303639 @default.
• W2002010280 hasConcept C2911091166 @default.
• W2002010280 hasConcept C2992704956 @default.
• W2002010280 hasConcept C540031477 @default.
• W2002010280 hasConcept C71924100 @default.
• W2002010280 hasConceptScore W2002010280C126322002 @default.
• W2002010280 hasConceptScore W2002010280C141071460 @default.
• W2002010280 hasConceptScore W2002010280C177713679 @default.
• W2002010280 hasConceptScore W2002010280C178790620 @default.
• W2002010280 hasConceptScore W2002010280C185592680 @default.
• W2002010280 hasConceptScore W2002010280C2780091579 @default.
• W2002010280 hasConceptScore W2002010280C2780303639 @default.
• W2002010280 hasConceptScore W2002010280C2911091166 @default.
• W2002010280 hasConceptScore W2002010280C2992704956 @default.
• W2002010280 hasConceptScore W2002010280C540031477 @default.
• W2002010280 hasConceptScore W2002010280C71924100 @default.
• W2002010280 hasIssue "2" @default.
• W2002010280 hasLocation W20020102801 @default.
• W2002010280 hasLocation W20020102802 @default.
• W2002010280 hasLocation W20020102803 @default.
• W2002010280 hasOpenAccess W2002010280 @default.
• W2002010280 hasPrimaryLocation W20020102801 @default.
• W2002010280 hasRelatedWork W1990329229 @default.
• W2002010280 hasRelatedWork W2043010282 @default.
• W2002010280 hasRelatedWork W2088078594 @default.
• W2002010280 hasRelatedWork W2090748462 @default.
• W2002010280 hasRelatedWork W2114046963 @default.
• W2002010280 hasRelatedWork W2372524402 @default.
• W2002010280 hasRelatedWork W2378019284 @default.
• W2002010280 hasRelatedWork W2382568077 @default.
• W2002010280 hasRelatedWork W2407111357 @default.
• W2002010280 hasRelatedWork W3030709858 @default.
• W2002010280 hasVolume "87" @default.
• W2002010280 isParatext "false" @default.
• W2002010280 isRetracted "false" @default.
• W2002010280 magId "2002010280" @default.
• W2002010280 workType "article" @default.