Alactic Base Excess, New Potential Marker Associated for Circulatory Stress Due to Hemodialysis, a Pilot Study

Indroduction: Circulatory stress increases mortality in patients with chronic kidney disease in renal replacement therapy by hemodialysis, the measurement of central venous saturation has been proposed as a useful tool for diagnosis but with limitations. We wanted to evaluate a new marker, the alactic base excess, to be applied in all types of hemodialysis patients to help diagnose this clinical condition.Methodology: An observational, analytical, prospective and longitudinal study was carried out in hemodialysis of the Instituto Mexicano del Seguro Social, in León, Guanajuato from May 2020 to June 2021 by determining the alactic base excess. The association of alactic base excess as a marker of circulatory stress in hemodialysis was proposed as a primary end point and mortality at 12 months was evaluated as a secondary end point.Results: An inverse association was found between the alactic base excess with the initial pH (r= -0.303, p= <0.05) and the final lactate (r= -0.297, p= <0.05), in addition to bicarbonate (r= 0.593, p= <0.05) and central venous saturation variability (r= 0.304, p= <0.05). In the analysis by subgroups, both lower tertiles had a higher risk of presenting the adverse event (HR= 0.817, [95% CI 0.21 to 3.05], p= 0.763). No association of mortality was found with the first (HR= 0.95, [95% CI= 0.73 to 1.2], p= 0.687) or final determination (HR= 1, [95% CI= 0.758 to 1.3], p= 0.99).Discussion: In this study we found that the alactic base excess proposed to diagnostic different types of acidosis is capable of identifying small changes related to circulatory stress, regardless of the chronicity of kidney failure, hemodynamic status or hemoglobin concentration, but not related to mortality.Conclusions: Alactic base excess is potentially useful to evaluate circulatory stress in conjunction with other tissue hypoperfusion markers, however it would be necessary to expand the sample size and introduce therapeutic variables to determine its clinical impact.

Renal Perfusion during Hemodialysis: Intradialytic Blood Flow Decline and Effects of Dialysate Cooling

BackgroundResidual renal function (RRF) confers survival in patients with ESRD but declines after initiating hemodialysis. Previous research shows that dialysate cooling reduces hemodialysis-induced circulatory stress and protects the brain and heart from ischemic injury. Whether hemodialysis-induced circulatory stress affects renal perfusion, and if it can be ameliorated with dialysate cooling to potentially reduce RRF loss, is unknown.MethodsWe used renal computed tomography perfusion imaging to scan 29 patients undergoing continuous dialysis under standard (36.5°C dialysate temperature) conditions; we also scanned another 15 patients under both standard and cooled (35.0°C) conditions. Imaging was performed immediately before, 3 hours into, and 15 minutes after hemodialysis sessions. We used perfusion maps to quantify renal perfusion. To provide a reference to another organ vulnerable to hemodialysis-induced ischemic injury, we also used echocardiography to assess intradialytic myocardial stunning.ResultsDuring standard hemodialysis, renal perfusion decreased 18.4% (P<0.005) and correlated with myocardial injury (r=−0.33; P<0.05). During sessions with dialysis cooling, patients experienced a 10.6% decrease in perfusion (not significantly different from the decline with standard hemodialysis), and ten of the 15 patients showed improved or no effect on myocardial stunning.ConclusionsThis study shows an acute decrease in renal perfusion during hemodialysis, a first step toward pathophysiologic characterization of hemodialysis-mediated RRF decline. Dialysate cooling ameliorated this decline but this effect did not reach statistical significance. Further study is needed to explore the potential of dialysate cooling as a therapeutic approach to slow RRF decline.

Persistent Sepsis-Induced Hypotension without Hyperlactatemia: A Distinct Clinical and Physiological Profile within the Spectrum of Septic Shock

Introduction. A subgroup of septic shock patients will never develop hyperlactatemia despite being subjected to a massive circulatory stress. Maintenance of normal lactate levels during septic shock is of great clinical and physiological interest. Our aim was to describe the clinical, hemodynamic, perfusion, and microcirculatory profiles associated to the absence of hyperlactatemia during septic shock resuscitation.Methods. We conducted an observational study in septic shock patients undergoing resuscitation. Serial clinical, hemodynamic, and perfusion parameters were registered. A single sublingual microcirculatory assessment was performed in a subgroup. Patients evolving with versus without hyperlactatemia were compared.Results. 124 septic shock patients were included. Patients without hyperlactatemia exhibited lower severity scores and mortality. They also presented higher platelet counts and required less intensive treatment. Microcirculation was assessed in 45 patients. Patients without hyperlactatemia presented higher PPV and MFI values. Lactate was correlated to several microcirculatory parameters. No difference in systemic flow parameters was observed.Conclusion. Persistent sepsis-induced hypotension without hyperlactatemia is associated with less organ dysfunctions and a very low mortality risk. Patients without hyperlactatemia exhibit less coagulation and microcirculatory derangements despite comparable macrohemodynamics. Our study supports the notion that persistent sepsis-induced hypotension without hyperlactatemia exhibits a distinctive clinical and physiological profile.