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Background: Poor nutritional status is common among patients undergoing lower extremity amputation (LEA). In this study, the association between preoperative hypoalbuminemia, a marker for malnutrition, and postoperative mortality in patients undergoing LEA was explored., Methods: Data on patients undergoing LEA between 2005 and 2017 were retrospectively analyzed from the prospectively collected American College of Surgeons National Surgical Quality Improvement Program database. Patients were divided into clinically relevant categories based on their serum albumin level (<2.5, 2.5-3.39, ≥3.4 g/dl) and were further stratified according to amputation level. Operative death was compared across groups and multivariable logistic regression was performed to estimate risk-adjusted odds ratio (AOR)., Results: In 35,383 patients, the rate of 30-day postoperative mortality was 7.6% (n = 2693). Mortality rate was highest in patients with very low albumin levels (11%) as compared to low (6.8%) and normal levels (3.9%). On multivariable analysis, lower albumin levels emerged as a risk-adjusted independent predictor of mortality. After risk-adjustment, patients with very low albumin levels (AOR [95% CI]: 2.25 [1.969-2.56], P < 0.001) and low albumin levels (AOR [95% CI]: 1.42 [1.239-1.616], P < 0.001) had higher odds of mortality when compared to patients with normal albumin levels. On sensitivity analysis, a similar trend was seen in patients undergoing above knee amputation but not in patients undergoing minor amputations., Conclusions: In patients undergoing major LEA, hypoalbuminemia is associated with an increased risk of postoperative mortality in a dose response manner, specifically in above knee amputations. Monitoring and optimizing patients' nutritional status before surgery, when possible, may be warranted and should be further explored., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Introduction: Acute kidney injury (AKI) is a common and serious complication after hip fracture surgery in older adults. Hypoalbuminemia is a known independent risk factor for AKI. However, few studies have investigated the relationship between early postoperative hypoalbuminemia and AKI after hip fracture surgery. Therefore, we sought to determine the incidence of and risk factors for AKI and the effects of early postoperative hypoalbuminemia on AKI incidence after surgery for hip fractures, especially intertrochanteric fractures of the proximal femur., Patients and Methods: In this retrospective cohort study from a single center, we reviewed the medical records of 481 consecutive patients (>60 years) who underwent surgery for intertrochanteric fracture of the proximal femur. Multiple logistic regression was performed to identify independent risk factors for AKI. After determining the cut-off value of the minimal level of postoperative serum albumin during the first two postoperative days, we divided the patients into two groups: group 1 included 251 patients whose minimal early postoperative serum albumin level was <2.9 g/dL during the first two postoperative days; and group 2 included 230 patients whose minimal early postoperative serum albumin level was ≥2.9 g/dL. The incidence of AKI was analyzed using inverse probability of treatment weighting (IPTW), propensity score matching (PSM), and propensity score matching weighting (PSMW) analyses., Results: The incidence of AKI, defined based on the Kidney Disease Improving Global Outcomes criteria, was 11.8% (n = 57). Chronic kidney disease and the minimal early postoperative serum albumin level <2.9 g/dL at any point during the first two postoperative days were independent risk factors for AKI. The IPTW, PSM, and PSMW analyses comparing the incidence of AKI between the two groups revealed that the minimal early postoperative serum albumin level <2.9 g/dL was significantly associated with AKI development (P < 0.001, P = 0.025, and P = 0.011, respectively)., Conclusion: The incidence of postoperative AKI was 11.8%. Our findings demonstrate that early postoperative hypoalbuminemia is an independent risk factor for AKI in patients undergoing surgery for intertrochanteric fracture of the proximal femur., (Copyright © 2018. Published by Elsevier Ltd.)

Background and Aims: Low serum albumin level is reportedly associated with worse clinical outcomes in patients with chronic kidney disease (CKD). However, associations between decreased serum albumin level and outcomes in non-CKD patients with coronary artery disease (CAD) remain unclear. Therefore, we aimed to evaluate the prognostic value of serum albumin concentrations in stable CAD patients with preserved renal function., Methods and Results: We studied 1316 patients with CAD and preserved renal function (estimated glomerular filtration rate ≥60 mL/min/1.73 m 2 ) who underwent their first PCI between 2000 and 2011 and had data available for pre-procedural serum albumin. Patients were assigned to quartiles based on pre-procedural albumin concentrations. The incidence of major adverse cardiac events (MACE), including all-cause death and non-fatal myocardial infarction, was evaluated. Mean albumin concentration was 4.1 ± 0.4 g/dL. During the median follow-up of 7.5 years, 181 events occurred (13.8%). Kaplan-Meier curves revealed that patients with decreased serum albumin concentrations showed a higher event rate for MACE (log-rank, p < 0.0001). Using the highest tertiles (>4.3 g/dL) as reference, adjusted hazard ratios were 1.97 (95% CI, 1.12-3.55), 1.77 (95% CI, 0.99-3.25), and 1.19 (95% CI, 0.68-2.15) for serum albumin concentrations of <3.9, 3.9-4.0, and 4.1-4.3 g/dL, respectively. Decreased serum albumin concentration was associated with MACE even after adjusting for other independent variables (HR, 2.21 per 1-g/dL decrease; 95% CI, 1.37-3.56, p = 0.001)., Conclusion: Decreased serum albumin concentration independently predicted worse long-term prognosis in non-CKD patients after PCI. Pre-procedural serum albumin concentration could offer a useful predictor for patients with CAD and preserved renal function., (Copyright © 2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

The mechanism of edema formation in the nephrotic syndrome has long been a source of controversy. In this review, through the construct of Starling's forces, we examine the roles of albumin, intravascular volume, and neurohormones on edema formation and highlight the evolving literature on the role of primary sodium absorption in edema formation. We propose that a unifying mechanism of sodium retention is present in the nephrotic syndrome regardless of intravascular volume status and is due to the activation of epithelial sodium channel by serine proteases in the glomerular filtrate of nephrotic patients. Finally, we assert that mechanisms in addition to sodium retention are likely operant in the formation of nephrotic edema.

Background & Aims: Malnutrition is common in older persons. However, it is unclear whether malnutrition diagnosed with the Mini Nutritional Assessment (MNA) predicts mortality in older hospitalized patients., Methods: We prospectively studied the impact of the MNA-short form (MNA-SF) and co-morbidities on long-term mortality in 444 patients (mean age 85.3 ± 6.7; 74.0% women) receiving geriatric inpatient care. In a cross-sectional study we studied the interplay between the MNA, nutritional markers and co-morbidities (using the Cumulative Illness Rating Scale, CIRS)., Results: The prevalence of malnutrition and "at risk of malnutrition", defined by MNA-SF, was 25.5 and 50.5% respectively in our prospective study. CIRS scores (HR = 1.09, p < 0.001) and a low BMI (HR = 0.96, p < 0.05), but not the MNA-SF (HR = 0.79 and 0.89 for "at risk" and malnutrition respectively, P = NS), were associated with 4-year mortality. CIRS scores, albumin and other nutritional markers were similar between MNA categories. High CIRS scores and hypoalbuminemia were observed even in patients with normal MNA scores. There was good agreement (>80%) between the MNA-SF and the complete MNA., Conclusions: Malnutrition as diagnosed with the MNA at admission failed to predict long-term mortality in older inpatients, likely due to the overriding impact of co-morbidities and acute disease., (Copyright © 2011 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Oedema is a common clinical manifestation of nephrotic syndrome. However, the pathophysiological mechanism of sodium retention in nephrotic syndrome has been intensely debated for decades. Several clinical and experimental observations argue against the classic or "underfill" hypothesis of oedema formation in nephrotic syndrome. In many patients, oedema formation in nephrotic syndrome is due to the kidney being intrinsically unable to excrete salt and is unrelated to systemic factors (i.e. hypoalbuminaemia, decreased &ldquo;effective&rdquo; arterial blood volume, and secondary hyperaldosteronism). The cortical collecting duct is the nephron site of sodium retention in nephrotic syndrome. Activation of the epithelial sodium channel in the cortical collecting duct is responsible for sodium retention in nephrotic syndrome. In nephrotic syndrome, a defective glomerular filtration barrier allows the passage of proteolytic enzymes or their precursors, which have the ability to activate the epithelial sodium channel, thereby causing the the subsequent sodium retention and oedema.

Study Objective: To determine if animals with abnormally low albumin levels are more susceptible to the effects of hypercapnia on BP compared to normal animals., Design: Prospective, controlled laboratory experiment., Setting: University research laboratory., Animals: Eighteen male Sprague-Dawley rats: 6 rats 10 to 12 weeks old (young Sprague-Dawley [YSD]), 6 rats 6 to 9 months old (old Sprague-Dawley [OSD]), and 6 rats 10 to 12 weeks old (Nagase analbuminemic mutant Sprague-Dawley [NAR])., Methods: Under general anesthesia and paralysis, we varied the Paco(2) by changing the respiratory rate on mechanical ventilation. Mean arterial pressure (MAP) was monitored in a continuous fashion. We obtained arterial blood for blood gas and electrolyte analysis, and nitric oxide (NO) production., Results: OSD rats had reduced serum albumin, while NAR rats were analbuminemic. Although NAR animals had a decreased buffer capacity compared to age-matched control animals (0.010 vs 0.013, p < 0.05), the MAP decreased in an identical fashion in all three groups. NO production increased with hypercapnia but was similar in all three groups. However, NAR rats had consistently higher plasma strong ion gap (2.8 to 4.1 mEq/L greater) compared to either YSD or OSD rats (p < 0.01), and baseline strong ion difference (mean +/- SD) was significantly lower in NAR rats (28.7 +/- 2.1 mEq/L) compared to either YSD rats (33.0 +/- 5.1 mEq/L) or OSD rats (31.2 +/- 5.1 mEq/L) [p < 0.05]., Conclusions: These findings suggest that analbuminemic or hypoalbuminemic rats are not more susceptible to hypercapnia-induced hemodynamic instability. Baseline values for apparent strong ion difference are lower in NA rats consistent with a reduced buffer base resulting from analbuminemia.

Background/aims: Hyperlactatemia with unexplained absence of metabolic acidosis is observed in acute liver failure. In chronic liver disease offsetting metabolic acid-base disorders could be revealed by means of physical-chemical acid-base analysis. The purpose of this study was to determine whether the acidifying effect of lactate is neutralized by the alkalinizing effect of hypoalbuminemia in acute liver failure., Methods: Serial arterial blood samples of 46 consecutive patients with non-paracetamol-induced acute liver failure were studied after admission to a medical ICU in a prospective investigation and compared to healthy controls. Acid-base state was assessed by quantitative physical-chemical analysis., Results: Lactate was increased and albumin was decreased in patients with acute liver failure compared to healthy controls resulting in normal net metabolic acid-base state. The alkalinizing effect of hypoalbuminemia was neutralized by the acidifying effect of elevated lactate. This observation was confirmed in serial analysis during 5 days after admission., Conclusions: The acidifying effect of lactate is neutralized by the alkalinizing effect of hypoalbuminemia in non-paracetamol-induced acute liver failure. The absence of apparent metabolic acidosis in the presence of elevated lactate can be explained by means of the physical-chemical acid-base model.