Low Serum Bicarbonate Research Articles

Low Serum Bicarbonate and Cardiovascular Disease Risk in Children with CKD

Low Serum Bicarbonate and Cardiovascular Disease Risk in Children with CKD

Characterization of a novel variant in KCNJ16, encoding Kir5.1 channel.

The essential role of the inwardly rectifying potassium channel Kir5.1 (KCNJ16) in controlling electrolyte homeostasis and blood pressure has been demonstrated in human and animal studies. Previous studies have identified several bi-allelic mutations of KCNJ16 in humans, causing severe hypokalemia, renal salt wasting, and disturbed acid-base homeostasis. Here, we identified a novel homozygous variant of KCNJ16, I26T, in an Amish patient affected with polydipsia, developmental delay, and chronic metabolic acidosis with low serum bicarbonate concentration. Subsequently, we generated the rat model with I26T mutation using Dahl salt-sensitive rat (I26T rat) to characterize this variant. The male mutant rats displayed similar blood pressure and electrolyte homeostasis under baseline and with a high salt (4% NaCl) challenge. Blood pH, HCO3 - and renal damage also remained similar between WT and I26T rats after high salt challenge. Additionally, single-channel patch clamp analysis revealed similar channel activity in CHO cells overexpressed with WT and I26T mutant Kir4.1/5.1 channels. In summary, this study reported a novel variant in KCNJ16, namely I26T, which is likely a benign variant and not associated with pathologic phenotype in either human or Dahl salt-sensitive rats, indicating that the type/location of variant should be considered when diagnosing and treating patients with KCNJ16 mutations.

Respiratory Alkalosis Accounts for Nearly Half of Cases of Low Serum Bicarbonate in Patients with Cirrhosis with AKI

Respiratory Alkalosis Accounts for Nearly Half of Cases of Low Serum Bicarbonate in Patients with Cirrhosis with AKI

Pseudohypobicarbonatemia Associated with Profound Hypertriglyceridemia

A case is presented of falsely low serum bicarbonate levels with normal arterial blood gas bicarbonate levels in a patient with high triglyceride (TG) levels. This false phenomenon is explained by the presence of high triglyceride levels. Most laboratories use an enzymatic/photometric or indirect ion-selective electrode method to measure bicarbonate. Hyperlipidemia interferes with photometric analysis due to its light scattering effect. An ABG analyser employs a direct ion-selective electrode method that is free from the errors of a photometric analyser. Currently, several methods are available to eliminate the interference of lipemia and allow accurate measurement of biological quantities. The clinical laboratory must establish a protocol for handling lipemic samples according to the biological quantity to be tested.

Severe respiratory acidosis contributing to refractory hyperkalemia: a case series of COVID-19 patients with renal failure

Introduction: Respiratory acidosis (RA) is not known to cause severe hyperkalemia. However, an exception to this general rule was observed in three patients with severe COVID-19 complicated with renal failure in our center. Objectives: The current study investigated the explanation for hyperkalemia refractory to renal replacement therapy in patients with severe COVID-19 with hypercarbia and renal failure in a tertiary care center. Patients and Methods: In this study, we present a case series of three patients with severe COVID-19 with hypercarbia and dialysis-requiring renal failure who developed persistent hyperkalemia refractory to renal replacement therapy. We studied various causes of persistent hyperkalemia, such as acid‒base disorder, a high turnover state, exogenous administration, rhabdomyolysis, and hypoaldosteronism. Results: All three patients initially presented with episodes of severe hyperkalemia, which were ameliorated after RA was corrected. All of these patients had worsening pulmonary function, after which the hyperkalemia could not be corrected, corresponding to persistent RA. The evidence that there was a contribution of RA to hyperkalemia was further strengthened by the observations of patient 1, in whom the hyperkalemia was only corrected after changing ventilator settings and who was unresponsive to dialysis. We studied the dialysate effluent in patient 3, and the results showed satisfactory removal of potassium with no improvement in the high serum potassium levels. Another interesting finding was that although the dialysate sodium concentration was greater than the serum sodium concentration, there was a decrease in the serum sodium concentration, indicating a reduced movement of sodium into the extracellular space. Conclusion: In our study, metabolic acidosis alone could not explain the high serum potassium levels. Moreover, hyperkalemia was corrected after RA was corrected, indicating that the latter might have been the predominant cause of hyperkalemia in these scenarios. The presence of renal failure and low serum bicarbonate levels might have been the factors contributing to decreased Na+-K+-ATPase activity in the setting of RA, which contributed to severe hyperkalemia in all three patients.

Association of Serum Bicarbonate Level with Mortality in Patients with Acute Kidney Injury: A Retrospective Cohort Study

ABSTRACT Background: Metabolic acidosis due to a decreased level of serum bicarbonate in patients with chronic kidney disease is associated with increased mortality, but the association of serum bicarbonate with outcomes in patients with acute kidney injury (AKI) is uncertain. We investigated the association of serum bicarbonate level with mortality in patients with AKI. Methods: The study cohort consisted of 4800 patients diagnosed with AKI at multiple hospitals between September 17, 2013, and April 14, 2014. Smooth curve fitting, threshold effect analysis, and multiple regression analysis were used to assess the relationship between serum bicarbonate and 14-day mortality (primary outcome) and with intensive care unit (ICU) admission, length of hospitalization, and total hospital costs (secondary outcomes). Results: Multiple regression analysis, adjusting for confounding factors, demonstrated a U-shaped association between serum bicarbonate levels and AKI mortality. The lowest mortality rate was observed in patients with a bicarbonate level of 26.9 mmol/L, while greater rates were observed in those with lower and higher levels. Additionally, patients with AKI exhibiting high serum bicarbonate levels (> 26.9 mmol/L) had a significantly lower rate of ICU admission and a shorter hospital stay compared to those with low serum bicarbonate levels (< 26.9 mmol/L). Conclusion: A serum bicarbonate level of 26–29 mmol/L in patients with AKI is associated with a lower 14-day mortality rate, with the lowest rate observed at a serum bicarbonate level of 26.9 mmol/L. Prospective clinical studies are needed to determine whether optimizing the serum bicarbonate level can decrease mortality in this population.

#2477 Longitudinal serum bicarbonate and mortality risk in older patients with advanced chronic kidney disease: analyses from the EQUAL cohort

Abstract Background and Aims Serum bicarbonate (SBC) disorders have been consistently linked to mortality in chronic kidney disease (CKD) patients. Low SBC levels have been extensively associated with increased mortality in CKD patients, possibly due to the detrimental effects of acidosis on various organs and systems. Likewise, several studies have identified high levels of SBC as a risk factor for mortality in the CKD population. To date, most studies have focused on the association between SBC levels and patient survival during the pre-kidney replacement therapy (KRT) period or the period after KRT initiation, considered separately. None have explored this association across the continuum of CKD (e.g., from pre-KRT to post-KRT start), which is relevant since metabolic acidosis is expected to be managed through dialysis in the KRT population, and thus its clinical outcomes might change after KRT initiation. To provide new insights on this topic, we aimed to explore the relationship between SBC and mortality in advanced CKD during three distinct treatment periods: during the pre-KRT period, during the transition phase surrounding the start of KRT (transition-CKD), and during KRT. Method Using the European QUALity Study on treatment in advanced CKD (EQUAL) cohort, which includes patients aged ≥65 years and eGFR ≤20 ml/min per 1.73 m2 from six European countries, we explored the association between longitudinal SBC and all-cause mortality in three separate CKD populations: pre-KRT, transition-CKD and in the KRT populations, using multivariable time-dependent Cox regression models. The cumulative time-averaged, the cumulative exposure of SBC, and the slope of the SBC trajectory during the pre-KRT phase were calculated and evaluated for association with all-cause mortality in the transition-CKD population. Subgroup analysis were used to evaluate the effect modification by pre-specified variables on the relationship between SBC and mortality. Results We included 1485 patients with a median follow-up of 2.9 (IQR 2.7) years, during which 529 (35.6%) patients died. A U-shaped relationship between SBC levels and all-cause mortality was observed in the pre-KRT population (p = 0.03; Fig.). Low cumulative exposure, defined as the area under the SBC trajectory before KRT initiation, was associated with increased mortality risk after transitioning to KRT (p = 0.01). Similarly, in the KRT population, low SBC levels showed a trend towards increased mortality risk (p = 0.13). We observed effect modification on the relationship between SBC and mortality by subjective global assessment category (p-value for interaction = 0.02) and KRT initiation (p-value for interaction = 0.02). Conclusion Our study has provided important insights into the relationship between SBC and mortality in advanced CKD patients. A U-shaped relationship describes the association between SBC and mortality in the advanced CKD pre-KRT population, whereas in patients that initiate KRT only low SBC levels are associated with an increased mortality risk. Our findings suggest that the relationship between SBC and mortality varies across different stages of CKD and that this relationship is modified by KRT initiation. From this point of view, it would be appropriate to consider a personalized management of acid-base balance disorders based on a comprehensive evaluation of the clinical status of the patient.

Diabetic acidosis with severe fetal hypoxia in pregnancy: Narrative review and case study.

Diabetic ketoacidosis (DKA) in pregnancy could be a disastrous event with increased maternal and perinatal morbidity and mortality. DKA can occur with a normal blood glucose level, known as euglycemic DKA. It particularly affects pregnant women with type I diabetes. Here, we report the case of a 28 year-old primigravid patient, with a diagnosis of type 1 diabetes for 8 years. This patient consulted our department at 29 weeks of gestation with a previous history of headaches, vomiting and diarrhea for 9 h. Blood glucose level was 8.8 mmol/L with a ketone test positive (>15 mg/dL). Blood test showed high anion gap (17.9 mmol/L) with low serum bicarbonate rate (21 mmol/L). Systemic examination and fetal heart rate (FHR) was reassuring. The patient was subsequently discharged. She returned to the clinic 19 h later with further symptoms of nausea, polyuria-polydipsia, asthenia and a weight loss of 4 kg since the day before. Blood sugar was 14.3 mmol/L and a ketone test was strongly positive. Cardiotocography showed fetal tachycardia and repeated late decelerations. A diagnosis of DKA was made and emergency cesarean was performed for fetal distress. At delivery, pH was acidosis (pH: 7.02, lactates: 6.2). The patient was successfully treated with intravenous hydration and insulin. Neonatal evolution was favorable. Pregnant women with type I diabetes can develop euglycemic DKA. Early recognition and prompt treatment could help prevent severe maternal and fetal adverse outcomes. DKA in pregnant women can induce fetal acidosis with abnormal FHR. In this situation, a cesarean can be performed to improve neonatal outcome even inducing a premature delivery. Prolonged pregnancy can lead to irreversible neonatal brain abnormalities.

Serum bicarbonate levels and kidney outcomes in critically ill patients: a prospective cohort study.

The interplay between serum bicarbonate levels and kidney outcomesis not fully understood. We conducted a prospective cohort study in three intensive care units (ICUs) to evaluate the association of serum bicarbonate levels with acute kidney injury (AKI) and kidney function recovery in critically ill patients. A prospective cohort study in three intensive care units (ICUs) was performed. The serum bicarbonate level in the first 24h after ICU admission was categorized as low (< 22mEq/L), normal (22-26mEq/L), or high (> 26mEq/L). Serum creatinine (SCr) levels according to theKDIGOAKI guideline were used for defining AKIwithin the first 7 days of ICU stay. At ICU admission, SCr≥ 1.1for women and ≥ 1.3 mg/dL for men were indicative of impaired kidney function.Mortality outcome was tracked up to 28days, and kidney function recovery was assessed at hospital discharge. A total of 2732 patients (66 ± 19years and 55% men) were analyzed, with 32% having impaired kidney functionat ICU admission. Overall, 26% of patients had low bicarbonate levels, while 32% had high bicarbonate levels. Notably, patients with preserved kidney function showed a lower prevalence of low bicarbonate levels compared to those with impaired kidney function (20% vs. 39%, p < 0.001), while higher rates were observed for high bicarbonate (35% vs. 24%, p < 0.001). Compared with patients with normal serum bicarbonate levels, those with low bicarbonate were 81% more likely to develop AKI (OR = 1.81; 95% CI 1.10-2.99), whereas those with high bicarbonate were 44% less likely (OR = 0.56; 95% CI 0.32-0.98) in the adjusted model for confounders. Neither those with high nor low serum bicarbonate levels were associated with an increased risk of mortality (HR = 1.03; 95% CI 0.68-1.56 and 0.99; 95% CI 0.68-1.42, respectively). In subgroup analysis, regardless of the kidney functionat ICU admission, serum bicarbonate levels were not associated with the development of AKI and all-cause mortality. Regarding kidney function recovery, higher non-recovery rates were found for those with low bicarbonate. In critically ill ICU patients, low bicarbonate levels were associated with the more likely development of AKIand subsequentnon-recovery ofkidney function, while high bicarbonatelevels showed no such association. Therefore, low bicarbonate levels may be considered a risk factor for adverse kidney outcomes in critically ill patients.

Evaluation of the Effect of Fluid and Electrolyte Therapy on Electrolytes and Acidosis Resolution Time in Diabetic Ketoacidosis

Objective: Fluid replacement and insulin infusion are the cornerstones of treatment of diabetic ketoacidosis, but the optimal volume, rate of infusion, and electrolyte content of fluid replacement have been controversial. The aim of this study was to investigate the effects of treatment on pH, bicarbonate (HCO3), anion gap, chloride, and potassium levels as well as time to resolution of acidosis in children with diabetic ketoacidosis. Material and Methods: Ninety-six episodes with diabetic ketoacidosis between January 2015-December 2017 were evaluated. Results: The mean resolution time of acidosis was 13.4±7.1 hours. Anion gap was returned to normal in 68 (70.8%) episodes at the 4th hour of treatment with a mean of 11±4.2 mmol/L. Episodes with potassium phosphate (KPO4) replacement resulted in a faster increase in pH and a significantly shorter resolution time of acidosis (p&amp;lt;0.001). Acidosis persisted at the 16th hour of treatment in episodes with lower pH, lower serum bicarbonate (HCO3) and higher white blood cell (WBC) counts on admission (p&amp;lt;0.001, p=0.003 p=0.033, respectively). Hyperchloremia (Cl/Na ratio &amp;gt; 0.79) was observed in 97% of cases after 8 hours of treatment. Conclusion: Although the value of the anion gap in predicting acidosis is controversial, severe DKA episodes and high white blood cell count at admission; potassium replacement with high amounts of chloride and KCl containing fluids given during treatment have been associated with a longer recovery time of acidosis.

The association between serum chloride and mortality in ICU patients with heart failure: The impact of bicarbonate

ObjectiveTo assess whether serum chloride predicts risk of death in intensive care unit (ICU) patients with heart failure (HF) and the effect of bicarbonate on the efficacy of serum chloride in predicting risk of death in ICU patients. MethodsA total of 9364 HF patients hospitalized in the ICU were enrolled. Patients were divided into hypochloremia (< 96 mEq/L), normal chloride (96–108 mEq/L), and hyperchloremia (> 108 mEq/L) groups. Similarly, we divided the serum bicarbonate level into three groups: low bicarbonate (< 22 mEq/L), medium bicarbonate (22–26 mEq/L), and high bicarbonate (> 26 mEq/L). The outcome of this study was in-hospital mortality. Then, we analyzed the association between abnormal serum chloride and mortality according to the category of serum bicarbonate and assessed the interaction effect. Restricted cubic spline (RCS) was used to show possible nonlinear associations. ResultsIn the overall study population, hypochloremia was associated with a higher risk of in-hospital mortality than normal chloride (odds ratio [OR] 1.54, 95% confidence interval [CI] 1.26–1.86, P < 0.001), hyperchloremia was not significantly related to in-hospital mortality (OR 1.00, 95% CI 0.85–1.19, P = 0.962). However, a linear association between serum chloride and in-hospital mortality was found in the low and normal bicarbonate groups (all P for nonlinear >0.05). ConclusionsHypochloremia is associated with in-hospital mortality and longer hospital stay in critically ill patients with HF. In addition, risk of death in the low and medium serum bicarbonate groups decreased with increasing serum chloride level.

Distinct clinical phenotypes in paediatric cancer patients with sepsis are associated with different outcomes—an international multicentre retrospective study

Identifying phenotypes in sepsis patients may enable precision medicine approaches. However, the generalisability of these phenotypes to specific patient populations is unclear. Given that paediatric cancer patients with sepsis have different host response and pathogen profiles and higher mortality rates when compared to non-cancer patients, we determined whether unique, reproducible, and clinically-relevant sepsis phenotypes exist in this specific patient population. We studied patients with underlying malignancies admitted with sepsis to one of 25 paediatric intensive care units (PICUs) participating in two large, multi-centre, observational cohorts from the European SCOTER study (n=383 patients; study period between January 1, 2018 and January 1, 2020) and the U.S. Novel Data-Driven Sepsis Phenotypes in Children study (n=1898 patients; study period between January 1, 2012 and January 1, 2018). We independently used latent class analysis (LCA) in both cohorts to identify phenotypes using demographic, clinical, and laboratory data from the first 24h of PICU admission. We then tested the association of the phenotypes with clinical outcomes in both cohorts. LCA identified two distinct phenotypes that were comparable across both cohorts. Phenotype 1 was characterised by lower serum bicarbonate and albumin, markedly increased lactate and hepatic, renal, and coagulation abnormalities when compared to phenotype 2. Patients with phenotype 1 had a higher 90-day mortality (European cohort 29.2% versus 13.4%, U.S. cohort 27.3% versus 11.4%, p<0.001) and received more vasopressor and renal replacement therapy than patients with phenotype 2. After adjusting for severity of organ dysfunction, haematological cancer, prior stem cell transplantation and age, phenotype 1 was associated with an adjusted OR of death at 90-day of 1.9 (1.04-3.34) in the European cohort and 1.6 (1.2-2.2) in the U.S. cohort. We identified two clinically-relevant sepsis phenotypes in paediatric cancer patients that are reproducible across two international, multicentre cohorts with prognostic implications. These results may guide further research regarding therapeutic approaches for these specific phenotypes. Part of this study is funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development.

EFFECTS OF ORAL SODIUM BICARBONATE SUPPLEMENTATION ON NUTRITIONAL STATUS OF PATIENTS UNDERGOING MAINTENANCE HEMODIALYSIS

To determine the oral sodium bicarbonate supplementation effects on nutritional status of patients undergoing maintenance hemodialysis. In a Medicine department at Combined Military Hospital, Peshawar, a case-control study was carried on “14-October 2021 to 14-April 2022”. It enrolled patients of ESRD on MHD with low serum bicarbonate levels. Patients were allocated into two groups: an experimental group receiving oral sodium bicarbonate and a control group receiving standard care. Parameters such as mid-thigh circumference, serum bicarbonate, and serum albumin were assessed at baseline and after 3 months, with statistical analysis performed using an independent sample t-test. The intervention group had a notable elevation in serum bicarbonate levels (20.87±1.58 mmol/l) as compared to the control group (18.73±2.38 mmol/l) (P = 0.0001). Furthermore, it was observed that the intervention group had a noteworthy elevation in serum albumin levels after 3 months (4.40±0.28 g/l), as compared to the control group (3.77±0.30 g/l) (P = 0.0001). Additionally, there was a statistically significant rise in the average mid-thigh circumference among participants in the intervention group during the third month, in comparison to those of the control group (41.20±1.70 vs. 39.74±1.27 cm; P = 0.001). Oral sodium bicarbonate supplementation in patients on maintenance hemodialysis significantly increased serum bicarbonate level, serum albumin level and mid-thigh size.

Chest configuration in children and adolescents with infantile nephropathic cystinosis compared with other chronic kidney disease entities and its clinical determinants.

Infantile nephropathic cystinosis (INC) is a systemic lysosomal storage disease causing intracellular cystine accumulation, resulting in renal Fanconi syndrome, progressive kidney disease (CKD), rickets, malnutrition, and myopathy. An INC-specific disproportionately diminished trunk length compared to leg length poses questions regarding the functionality of the trunk. Thus, we prospectively investigated thoracic dimensions and proportions, as well as their clinical determinants in 44 pediatric patients with INC with CKD stages 1-5 and 97 age-matched patients with CKD of other etiology between the ages of 2-17years. A total of 92 and 221 annual measurements of patients with INC and CKD, respectively, were performed, and associations between anthropometric and clinical parameters were assessed using linear mixed-effects models. Patients with INC exhibited altered chest dimensions that were distinct from CKD controls, characterized by markedly increased chest depth to height and chest depth to chest width ratio z-scores (> 1.0), while those of patients with CKD were only mildly affected (z-score within ± 1.0). Ratio z-scores differed significantly between both patient groups from 2-6years of age onward. The degree of chest disproportion in INC patients was significantly associated with both the degree of CKD and tubular dysfunction (e.g., low serum phosphate and bicarbonate) across three different age groups (2-6, 7-12, and 13-17years). Our data show an INC-specific alteration in thoracic shape from early childhood onward, which is distinct from CKD of other etiologies, suggesting early childhood subclinical changes of the musculoskeletal unit of the thoracic cage, which are associated with kidney function. A higher resolution version of the Graphical abstract is available as Supplementary information.

Preoperative renal function in women in Port Harcourt, Nigeria, with major gynecological lesions requiring urological and surgical interventions

Introduction: Preoperative renal function assessment is a prerequisite for many surgical procedures. This is because of the vital function of the kidneys in the regulation of serum electrolytes, and excretion of waste products or by-products of metabolic processes. Materials and Methods: This cross-sectional descriptive study was done at two university teaching hospitals in Port Harcourt, Nigeria, from January 2021 to December 2022. Case files of seventy-two (72) women scheduled for major gynecological surgeries were studied. Data obtained were analyzed using the SPSS, version 20, and the outcome was expressed using frequency tables and charts. Results: The mean age of the women in the study was 37.50 ± 1.22 years. Women with hyponatremias were 9 (12.5%); hypokalemia, 11 (15.3%); hyperkalemia, 3 (4.2%). Thirty-nine patients, 39 (54.2%) had acidosis, low serum bicarbonate (HCO3-). Low blood urea was found in 11 (15.3%) of the women. One of them (1.4%) had elevated blood urea. The rest had normal values. Hypocreatinaemia and hypercreatinaemia were detected in 29 (40.3%) and 2 (2.8%) patients respectively. Conclusion: Electrolyte derangement was found in 40 (55.6%) of the patients preoperatively. This finding suggests that renal function assessment is crucial in the preoperative evaluation of gynecological patients before major gynecological surgeries.

Low carbohydrate intake correlates with trends of insulin resistance and metabolic acidosis in healthy lean individuals.

Both obesity and a poor diet are considered major risk factors for triggering insulin resistance syndrome (IRS) and the development of type 2 diabetes mellitus (T2DM). Owing to the impact of low-carbohydrate diets, such as the keto diet and the Atkins diet, on weight loss in individuals with obesity, these diets have become an effective strategy for a healthy lifestyle. However, the impact of the ketogenic diet on IRS in healthy individuals of a normal weight has been less well researched. This study presents a cross-sectional observational study that aimed to investigate the effect of low carbohydrate intake in healthy individuals of a normal weight with regard to glucose homeostasis, inflammatory, and metabolic parameters. The study included 120 participants who were healthy, had a normal weight (BMI 25 kg/m2), and had no history of a major medical condition. Self-reported dietary intake and objective physical activity measured by accelerometry were tracked for 7 days. The participants were divided into three groups according to their dietary intake of carbohydrates: the low-carbohydrate (LC) group (those consuming <45% of their daily energy intake from carbohydrates), the recommended range of carbohydrate (RC) group (those consuming 45-65% of their daily energy intake from carbohydrates), and the high-carbohydrate (HC) group (those consuming more than 65% of their daily energy intake from carbohydrates). Blood samples were collected for the analysis of metabolic markers. HOMA of insulin resistance (HOMA-IR) and HOMA of β-cell function (HOMA-β), as well as C-peptide levels, were used for the evaluation of glucose homeostasis. Low carbohydrate intake (<45% of total energy) was found to significantly correlate with dysregulated glucose homeostasis as measured by elevations in HOMA-IR, HOMA-β% assessment, and C-peptide levels. Low carbohydrate intake was also found to be coupled with lower serum bicarbonate and serum albumin levels, with an increased anion gap indicating metabolic acidosis. The elevation in C-peptide under low carbohydrate intake was found to be positively correlated with the secretion of IRS-related inflammatory markers, including FGF2, IP-10, IL-6, IL-17A, and MDC, but negatively correlated with IL-3. Overall, the findings of the study showed that, for the first time, low-carbohydrate intake in healthy individuals of a normal weight might lead to dysfunctional glucose homeostasis, increased metabolic acidosis, and the possibility of triggering inflammation by C-peptide elevation in plasma.

No Good Deed: Acidosis in Chronic Kidney and Liver Disease

Studies have shown that low or high serum bicarbonate levels (reflecting metabolic acidosis or alkalosis)are associated with increased all-cause mortality rates in moderate and advanced chronic kidney disease (CKD) cases. Correction of presumed acidosis using sodium bicarbonate, targeting serum levels around 22 mmol/l, has proven beneficial in delaying the progression of the disease and provided mortality benefit. A similar prognostic association may exist between uncorrected metabolic acidosis in chronic liver disease. Correcting it with sodium-containing salts may require more interventions due to increased sodium/fluid load. In patients with liver failure, a naturally alkalotic state, where sodium load is a concern, the impact of this intervention is unclear. This study aims to generate proof of concept through a retrospective chart review in individuals with CKD-related metabolic acidosis and liver cirrhosis. We extrapolate that lowering bicarbonate targets in other clinical scenarios like liver failure, pregnancy, and cardiac failure may be prudent and will lead to a lower sodium load.

Increasing Serum Bicarbonate is Associated With Reduced Risk of Adverse Kidney Outcomes in Patients with CKD and Metabolic Acidosis

Low serum bicarbonate at a single point in time is associated with accelerated kidney decline in patients with chronic kidney disease (CKD). We modeled how changes in serum bicarbonate over time affect incidence of adverse kidney outcomes. We analyzed data from Optum's deidentified Integrated Claims-Clinical data set of US patients (2007-2019) with≥1 year of prior medical record data, CKD stages G3 to G5, and metabolic acidosis (i.e., index serum bicarbonate 12 to<22 mmol/l). The primary predictor of interest was the change in serum bicarbonate, evaluated at each postindex outpatient serum bicarbonate test as a time-dependent continuous variable. The primary outcome was a composite of either a≥40% decline in estimated glomerular filtration rate (eGFR) from index or evidence of dialysis or transplantation, evaluated using Cox proportional hazards models. A total of 24,384 patients were included in the cohort with median follow-up of 3.7 years. A within-patient increase in serum bicarbonate over time was associated with a lower risk of the composite kidney outcome. The unadjusted hazard ratio (HR) per 1-mmol/l increase in serum bicarbonate was 0.911 (95% confidence interval [CI]: 0.905-0.917; P< 0.001). After adjustment for baseline eGFR and serum bicarbonate, the time-adjusted effect of baseline eGFR and other covariates, the HR per 1-mmol/l increase in serum bicarbonate was largely unchanged (0.916 [95% CI: 0.910-0.922; P< 0.001]). In a real-world population of US patients with CKD and metabolic acidosis, a within-patient increase in serum bicarbonate over time independent of changes in eGFR, was associated with a lower risk of CKD progression.

Low Serum Bicarbonate in a Patient With Diabetes Mellitus:: A Quiz

Low Serum Bicarbonate in a Patient With Diabetes Mellitus:: A Quiz

Descriptors of Failed Extubation in Norwood Patients Using Physiologic Data Streaming

The objective of this study is to evaluate the utility of high-frequency physiologic data during the extubation process and other clinical variables for describing the physiologic profile of extubation failure in neonates with hypoplastic left heart syndrome (HLHS) post-Norwood procedure. This is a single-center, retrospective analysis. Extubation events were collected from January 2016 until July 2021. Extubation failure was defined as the need for re-intubation within 48h of extubation. The data included streaming heart rate, respiratory rate, blood pressure, arterial oxygen saturation, and cerebral/renal near-infrared spectroscopy (NIRS). The most recent blood laboratory results before extubation were also included. These markers, demographics, clinical characteristics, and ventilatory settings were compared between successful and failed extubations. The analysis included 311 extubations. The extubation failure rate was 10%. According to univariable analyses, failed extubations were preceded by higher respiratory rates (p = 0.029), lower end-tidal CO2 (p = 0.009), lower pH (p = 0.043), lower serum bicarbonate (p = 0.030), and lower partial pressure of O2 (p = 0.022). In the first 10min after extubation, the failed events were characterized by lower arterial (p = 0.028) and cerebral NIRS (p = 0.018) saturations. Failed events were associated with persistently lower values for cerebral NIRS 2h post-extubation (p = 0.027). In multivariable analysis, vocal cord anomaly, cerebral NIRS at 10min post-extubation, renal NIRS at pre-extubation and post-extubation, and end-tidal CO2 at pre-extubation remained as significant co-variables. Oximetric indices before, in the 10min immediately after, and 2h after extubation and vocal cords paralysis are associated with failed extubation events in patients with parallel circulation.