Abdominal Pressure and Fluid Status After Kidney Transplantation

We read with great interest the article by Dupont et al.1Dupont V. Bonnet-Lebrun A.S. Boileve A. et al.A pilot study on the association between early fluid status indicators after kidney transplantation and graft function recovery.Kidney Int Rep. 2022; 7: 1416-1419Abstract Full Text Full Text PDF Scopus (2) Google Scholar who reported an association between elevated intra-abdominal pressure (IAP) and day 30 glomerular filtration rate. The authors concluded that the formers are clinically “relevant fluid status indicators” after kidney transplant. Although we congratulate the authors on these novel and important findings, we like to highlight several points. First, the notion that IAP is a surrogate of volume status is unsupported by the literature or authors’ own findings.1Dupont V. Bonnet-Lebrun A.S. Boileve A. et al.A pilot study on the association between early fluid status indicators after kidney transplantation and graft function recovery.Kidney Int Rep. 2022; 7: 1416-1419Abstract Full Text Full Text PDF Scopus (2) Google Scholar,2Dupont V. Debrumetz A. Leguillou A. et al.Intra-abdominal hypertension in early post-kidney transplantation period is associated with impaired graft function.Nephrol Dial Transplant. 2020; 35: 1619-1628https://doi.org/10.1093/ndt/gfaa104Crossref PubMed Scopus (5) Google Scholar More frequent etiologies for elevated IAP in the early postoperative period than volume overload include the following: ileus, obesity, and sliding down in bed from elevated head of bed position.3Hermans M.H. Call E. Failure to reposition after sliding down in bed increases pressure at the sacrum and heels.Wounds. 2015; 27: 191-198PubMed Google Scholar,4Holte K. Kehlet H. Postoperative ileus: a preventable event.Br J Surg. 2002; 87: 1480-1493https://doi.org/10.1046/j.1365-2168.2000.01595.xCrossref Scopus (479) Google Scholar In addition, volume overload severe enough to cause intra-abdominal hydrostatic edema will usually have other signs of generalized edema. Second, as depicted in Figure 1 of Dupont et al.,1Dupont V. Bonnet-Lebrun A.S. Boileve A. et al.A pilot study on the association between early fluid status indicators after kidney transplantation and graft function recovery.Kidney Int Rep. 2022; 7: 1416-1419Abstract Full Text Full Text PDF Scopus (2) Google Scholar IAP further increased between 36 hours and 48 hours, despite a decrease in weight gain and central venous pressure.1Dupont V. Bonnet-Lebrun A.S. Boileve A. et al.A pilot study on the association between early fluid status indicators after kidney transplantation and graft function recovery.Kidney Int Rep. 2022; 7: 1416-1419Abstract Full Text Full Text PDF Scopus (2) Google Scholar This additional elevation in IAP cannot be ascribed to an increased fluid status. Third, we wholeheartedly agree with the authors’ statement elsewhere5Dupont V. Debrumetz A. Wynckel A. Rieu P. [How to explain glomerular filtration rate decrease in intra-abdominal hypertension?]. Comment expliquer la baisse du débit de filtration glomérulaire en cas d’hypertension intra-abdominale?.Nephrol Ther. 2018; 14: 24-28https://doi.org/10.1016/j.nephro.2017.04.005Crossref PubMed Scopus (3) Google Scholar that IAH-induced decrease in glomerular filtration rate is multifactorial and insufficiently understood, with renal venous congestion playing an important, putative, pathophysiological role. In fact, the elevated IAP-mediated compression of the vena cava triggers pooling and increased pressure in upstream venous beds, with a simultaneous underfilling of the heart and ensuing multitude of compensatory mechanism that culminate in renal injury.S1 As a result, renal venous congestion may occur in both extraperitoneally and intraperitoneally grafted kidneys. Last, an additional plausible mechanism for IAP-mediated kidney injury is that elevated IAP subsequently increases intravesical and ureteral pressures and diminishes urinary flow, with resultant kidney injury. The differential diagnosis of elevated IAP is critical. Erroneously attributing elevated IAP to excess fluid may lead to fluid restriction, decreased preload, and exacerbation of acute kidney injury by prerenal azotemia.S1 Volume status is better estimated by CVP, pulmonary artery occlusive pressure, or noninvasively with B-type natriuretic peptide, chest X-ray, or bedside echocardiography. Intraoperatively and in patients on mechanical ventilation, stroke volume and pulse pressure variation (e.g., FloTrac) may be used to guide fluid therapy. Download .pdf (.01 MB) Help with pdf files Supplementary File (PDF) Supplementary Reference. In Reply to “Abdominal Pressure and Fluid Status After Kidney Transplantation”Kidney International ReportsVol. 7Issue 7PreviewWe thank Yehuda and Nicolau-Raducu1 for their commentary on our recent publication.2 They first question the use of intra-abdominal pressure (IAP) as a surrogate of hydration status. We previously established a positive correlation between IAP and both central venous pressure and weight gain in our cohort.3 We also reported that severe intra-abdominal hypertension was associated with higher fluid balance.3 Others have previously revealed a correlation between IAP and other fluid status indicators, such as extravascular lung water index. Full-Text PDF Open AccessA Pilot Study on the Association Between Early Fluid Status Indicators After Kidney Transplantation and Graft Function RecoveryKidney International ReportsVol. 7Issue 6PreviewProgress in short-term kidney graft survival has decreased since 2000 which suggests an unmet need for innovation regarding early kidney graft function optimization.1 Previous studies have revealed that optimal perioperative fluid therapy was associated with a lower incidence of delayed graft function after kidney transplantation.2–4 Contrary to earlier studies, large volume administration is no longer recommended, and an individualized approach is now encouraged to balance the graft perfusion and the possible complications of fluid overload.