Low Serum Bicarbonate Levels Research Articles

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.

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.

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.

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.

LBODP029 Pseudohypobicarbonatemia In The Setting Of Diabetic Ketoacidosis And Severe Hypertriglyceridemia

Abstract Background Severe hypertriglyceridemia is a rare complication of diabetic ketoacidosis (DKA); however, the resulting spuriously low measurements of serum bicarbonate ("pseudohypobicarbonatemia") are less well known. Clinical Case A healthy 15-year-old female presented to the emergency department with polydipsia, polyuria, and abdominal pain. She had a normal BMI and a sibling with type 1 diabetes (T1D). Labs demonstrated serum glucose of 351 mg/dL, serum ketones of 3.4 mmol/L, serum bicarbonate of &amp;lt;5 mmol/L, anion gap of &amp;gt;23 mmol/L, and triglycerides of &amp;gt;21,000 mg/dL. Serum lipase was normal at 70 units/L. She was admitted for protocolized DKA treatment with intravenous fluids and regular insulin drip. Hospital day 2, serum bicarbonate remained very low (7 mmol/L) despite declining ketones (1.9 mmol/L), decreasing anion gap (15 mmol/L), normal chloride (112 mEq/L), and normal lactic acid (1.3 mmol/L). A spurious lab was suspected, so bicarbonate was calculated from a venous blood gas (VBG) which showed a pH of 7.28 and a bicarbonate of 16.2 mmol/L at a time when serum bicarbonate was 7 mmol/L. Serial BMPs and VBGs were trended, with the serum bicarbonate consistently 7-10 mmol/L lower than the blood gas bicarbonate. Her ketoacidosis resolved, yet she remained hospitalized for continued IV regular insulin drip (max 0.3 units/kg/h) for treatment of severe hypertriglyceridemia. On hospital day 7, triglycerides fell below 500mg/dL. She never developed pancreatitis. She was discharged home on multiple daily injection insulin and a low-fat diet. Her triglyceride level two weeks later was 173 mg/dL. Diabetes autoantibodies returned positive, confirming a diagnosis of T1D. Clinical Lessons This case demonstrates that very high triglycerides can occur with pediatric DKA and cause a falsely low serum bicarbonate level, also known as "pseudohypobicarbonatemia". This is due to chemistry panel analyzers using absorbance to estimate bicarbonate levels, which makes them susceptible to triglyceride interference. In contrast, blood gas analyzers use the Henderson-Hasselbalch equation to calculate bicarbonate, thus, are not vulnerable to the same triglyceride interference. This is especially relevant in pediatrics, as triglyceride levels may not be routinely checked for patients in DKA, so massive elevation may be missed. It is also pertinent for centers where serum bicarbonate levels may be trended to monitor for DKA resolution, instead of blood gases. If the serum bicarbonate level remains low in a patient with DKA and resolving ketosis, a blood gas may be obtained as another way of looking at the acid/base status. If there is a discrepancy between the two measurements, triglycerides should be assessed, as this could change management and prevent complications such as pancreatitis. Presentation: No date and time listed

Low Serum Bicarbonate Levels Increase the Risk of All-Cause, Cardiovascular Disease, and Cancer Mortality in Type 2 Diabetes.

The evidence regarding bicarbonate status and mortality among diabetes is scarce. The purpose of this study was to investigate the associations of bicarbonate concentrations with risk of all-cause, cardiovascular disease (CVD), and cancer mortality among patients with type 2 diabetes (T2D). This study included 8163 adult diabetic patients from the National Health and Nutrition Examination Survey (NHANES), 1999 to 2018. Death outcomes were ascertained by linkage to National Death Index records through 31 December 2019. The Cox proportional-risk model was used to estimate hazard ratios (HR) and 95% CIs for mortality from all causes, CVD, and cancer. The mediating effects of 11 metabolic, cardiovascular, and renal biomarkers were evaluated using a logistic regression model within a counterfactual framework. During 8163 person-years of follow-up, 2310 deaths were documented, including 659 CVD deaths and 399 cancer deaths. After multivariate adjustment, lower serum bicarbonate levels were significantly linearly correlated with higher all-cause, CVD, and cancer mortality: The risk of all-cause death increased by 40%, the risk of CVD death increased by 48%, and the risk of cancer death increased by 84% compared with the normal group (all P < .05). Altered levels of estimated glomerular filtration rate explained 12.10% and 16.94% of the relation between serum bicarbonate with all-cause and CVD mortality, respectively. Total cholesterol mediated 4.70% and 10.51% of the associations of all-cause and CVD mortality, respectively. Lower serum bicarbonate concentrations were significantly associated with higher all-cause, CVD, and cancer mortality. These findings suggest that maintaining adequate bicarbonate status may lower mortality risk in individuals with T2D.

Pseudohypobicarbonatemia in a patient with amyloidosis.

We report a case of a patient who had critically low serum bicarbonate (HCO3 -) levels ranging from 8 to 11mmol/L on repeated venous measurements using an enzymatic/photometric assay. This prompted hospitalization and treatment with intravenous sodium bicarbonate (NaHCO3) followed by oral NaHCO3. He was evaluated for potential causes of high anion gap metabolic acidosis without any etiology found. He continued to have low serum HCO3 - levels despite maintenance oral NaHCO3 therapy and was referred for a second opinion where further laboratory work was pursued. An arterial blood gas was obtained, which revealed normal whole blood pH and HCO3 - levels. A different enzymatic/photometric assay revealed a normal serum HCO3 - level at 21mmol/L. Additional workup revealed paraproteinemia, which was thought to interfere with the enzymatic process by which his serum HCO3 - was measured, resulting in erroneous values.

Admission Serum Bicarbonate Predicts Adverse Clinical Outcomes in Hospitalized Cirrhotic Patients.

A low serum bicarbonate (SB) level is predictive of adverse outcomes in kidney injury, infection, and aging. Because the liver plays an important role in acid-base homeostasis and lactic acid metabolism, we speculated that such a relationship would exist for patients with cirrhosis. To assess the prognostic value of admission SB on adverse hospital outcomes, clinical characteristics were extracted and analyzed from a large electronic health record system. Patients were categorized based on admission SB (mEq/L) into 7 groups based on the reference range (22–25) into mildly (18–21), moderately (14–17), and severely (<14) decreased groups and mildly (26–29), moderately (30–33), and severely (>30) increased groups, and the relationship of SB category with the frequency of complications (acute kidney injury/hepatorenal syndrome, portosystemic encephalopathy, gastrointestinal bleeding, ascites, and spontaneous bacterial peritonitis) and hospital metrics (length of stay [LOS], admission to an intensive care unit [ICU], and mortality) was assessed. A total of 2,693 patients were analyzed. Mean SB was 22.9 ± 4.5 mEq/L. SB was within the normal range (22–25 mEq/L) in 1,072 (39.8%) patients, and 955 patients (36%) had a low SB. As the SB category decreased, the incidence of complications progressively increased (p < 0.001). Increased MELD-Na score and low serum albumin also correlated with frequency of complications (p < 0.001). As the SB category decreased, LOS, ICU admission, and mortality progressively increased (p < 0.001). On multivariate analysis, the association of decreased SB with higher odds of complications, LOS, ICU admission, and mortality persisted. Conclusion. Low admission SB in patients with cirrhosis is associated with cirrhotic complications, longer LOS, increased ICU admissions, and increased hospital mortality.

A Rare Case of Metformin Associated Lactic Acidosis in a Type 2 Diabetic Patient With No Known Contraindications for Metformin Prescription - a Diagnostic Conundrum!

Introduction: Metformin is a biguanide drug primarily inhibits hepatic gluconeogenesis and improves insulin sensitivity. Lactic acidosis is a rare complication of metformin. The incidence of Metformin-associated lactic acidosis (MALA) is 6.3 per 100,000 patient-years. Metformin raises lactate levels by inhibiting the conversion of lactate and pyruvate into glucose, shunting towards anaerobic glycolysis. Although, MALA is a reported side effect, metformin is still identified as the drug of choice for Type 2 DM. Here we present a case of MALA in a Type 2 Diabetic patient to shed light on this controversial dilemma. Case Presentation: A 56-year-old African-American male with Type 2 DM and diabetic retinopathy presented after a fall and generalized weakness. Upon arrival, his blood sugar was 22 mg/dL. Patient was vitally stable with signs of dehydration. Home medications includes Metformin 1000 mg twice daily and Glipizide. Laboratory results showed an anion gap metabolic acidosis of 18 mmol/L, Lactic acid was 6.5 mmol/L with repeat of 7.6 mmol/L. Creatinine was 6.0 mg/dL with a BUN of 89 mg/dL. Baseline creatinine from 1 year prior was 1.3–1.5 mg/dL with GFR of 52 mL/min. Hemoglobin A1c was 5.9%. Sodium bicarbonate infusion in 5% dextrose in water. The patient clinically improved with closure of the anion gap and resolution of the metabolic acidosis. Metformin level was 10 mcg/mL. He was discharged on basal insulin and discontinued Metformin and Glipizide. Discussion: Metformin is the first line treatment of Type 2 DM due to its safety. The most common adverse events of Metformin include nausea, bloating, and diarrhea. MALA is a rare, yet serious side effect with a reported mortality of 45%. Higher mortality was associated with increased age, lower arterial pH, and need for mechanical ventilation and vasopressor medicationsThe following criteria should raise concern for MALA in patients with history of Metformin use; elevated lactate level, high anion gap, severe acidosis, low serum bicarbonate level and a history of renal insufficiency. Our patient met the above criteria. The treatment approach for MALA includes adequate supportive measures and correction of acidosis with the acceleration of lactic acid metabolism. Ultimately, if there is no improvement with the aforementioned strategies, then the next step is elimination of the offending agent by renal excretion or dialysis. Fortunately our patient improved with intravenous hydration and did not require advanced intervention. This case highlights the importance of the early recognition of MALA in a patient with unexplained anion gap acidosis and history of Metformin use as even with no risk factors, an episode of gastroenteritis can be enough to impair renal function which increases the risk of MALA. More importantly, it is crucial to educate patients to withhold Metformin in the setting of acute illness and volume contraction to prevent MALA.

Obesity and the Risk of Low Bicarbonate: A Cohort Study

Rationale & ObjectiveAcid retention may occur in the absence of overt metabolic acidosis; thus it is important to identify populations at risk. Because obesity may alter renal acid-base handling, we sought to determine whether overweight and obesity are associated with increased risk for low serum bicarbonate levels, suggesting metabolic acidosis.Study DesignRetrospective cohort study.Setting & ParticipantsAdult patients (n = 96,147) visiting outpatient clinics in the Bronx, NY, between January 1, 2010, and December 31, 2015.PredictorBody mass index (BMI).OutcomeLow serum bicarbonate level (≤23 mEq/L).Analytical ApproachLongitudinal analyses were conducted using mixed-effects models to examine associations of BMI with serum bicarbonate levels over time and Cox proportional hazards models to examine associations of BMI with incident low bicarbonate levels.ResultsDuring a median follow-up of 4.4 (interquartile range, 2.3-6.3) years, patients had a median of 8 serum bicarbonate measurements and 34,539 patients developed low bicarbonate levels. Higher BMI was associated with progressively lower serum bicarbonate levels, with attenuation of the association in the highest BMI groups, suggesting a J-shaped relationship. Compared with the reference group (BMI, 18.5 to <25 kg.m2), patients with BMIs of 25 to <30, 30 to <35, 35 to <40, and ≥40 kg/m2 had HRs for incident low bicarbonate levels of 1.10 (95% CI, 1.05-1.14), 1.16 (95% CI, 1.11-1.21), 1.20 (95% CI, 1.14-1.26), and 1.15 (95% CI, 1.09-1.22). Results were similar after adjustment for serum urea nitrogen level and exclusion of patients with diabetes, hypertension, or estimated glomerular filtration rates < 60 mL/min/1.73 m2.LimitationsArterial pH measurements were unavailable.ConclusionsHigher BMI is independently associated with progressively greater risk for developing low serum bicarbonate levels, indicating likely metabolic acidosis. Further research should explore the causes of low bicarbonate levels in patients with overweight and obesity.

Pseudo Metabolic Acidosis in the Setting of Hypertriglyceridemia: A Case Report

Low serum bicarbonate, with or without an elevated anion gap, can indicate metabolic acidosis. High anion gap metabolic acidosis is due to the unmeasured anions. Hypertriglyceridemia can also be associated with spuriously low serum bicarbonate levels due to lab interference. We present a 44-year-old woman who presented with anion gap metabolic acidosis in the presence of severe hypertriglyceridemia

METFORMIN ASSOCIATED LACTIC ACIDOSIS

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Metformin is the most commonly used oral hypoglycemic agent to treat Type 2 Diabetes Mellitus owing to its favorable safety profile. Although metformin is renally cleared, drug levels generally remain within the therapeutic range and lactate concentrations are not substantially increased when used in patients with mild to moderate chronic kidney disease. However, the situation is different when a patient has acute renal insufficiency with progressively worsening kidney function. Here, we present a case of severe Metformin-associated lactic acidosis. CASE PRESENTATION: A 66-year-old Hispanic man with type-2 diabetes on metformin, hypertension, coronary artery disease and chronic back pain presented to our hospital with 2 days of altered mental status and worsening back pain. Initial physical examination was unremarkable except for tachycardia with a heart rate of 156. In the emergency department, laboratory abnormalities included initial blood sugar of 62, creatinine of 11, anion gap of 41 and lactate of 18, bicarbonate of 6 and pH of 6.7 on arterial blood gas. The patient worsened after transfer to critical care unit with acute development of hypoxia and hypotension and had to be intubated and started on mechanical ventilation and vasopressors. Differential diagnosis at this point was broad and it was thought that hypotension, acidemia, and severe metabolic derangement could be consistent with septic shock vs metformin-associated lactic acidosis. Patient was started on broad spectrum antibiotics and a nephrology consult was obtained and the patient was dialyzed within few hours after the placement of temporary dialysis catheter. Patient's pH improved to 7.2 after 1 session of dialysis and vasopressors requirement went down as well. The patient was extubated on day 4 and renal function improved over the coming days as well. DISCUSSION: The overall incidence of lactic acidosis in metformin users is generally low and varies across studies from approximately 3-10 per 100,000 person-years [1]. The overall mortality rate of Metformin associated lactic acidosis is 25.4% according to the study by Renda et al. [2]. Mortality is associated with the extent of acidosis while acute renal failure is associated with a low mortality. It is crucial to maintain a high suspicion of this complication in the differential diagnosis at the earliest stage for patients with metabolic acidosis and history of metformin use. CONCLUSIONS: Lactic acidosis resulting from metformin toxicity should be suspected in any patient who has all of the following five criteria: (1) a history of metformin use; (2) a markedly elevated lactate level (> 15 mmol/L) with a large anion gap (> 20); (3) severe acidemia (pH 7.1); (4) a very low serum bicarbonate level (< 10 mmol/L); and (5) a history of renal insufficiency. Education of both patients and providers to avoid metformin when there is a risk of renal failure is crucial. Reference #1: https://jamanetwork.com/journals/jama/article-abstract/2084896 Reference #2: https://www.ncbi.nlm.nih.gov/pubmed/23436666/ DISCLOSURES: No relevant relationships by Anam Hassan, source=Web Response No relevant relationships by Muhammad Hasham Sarwar, source=Web Response

Low Serum Bicarbonate and CKD Progression in Children.

Studies of adults have demonstrated an association between metabolic acidosis, as measured by low serum bicarbonate levels, and CKD progression. We evaluated this relationship in children using data from the Chronic Kidney Disease in Children study. The relationship between serum bicarbonate and a composite end point, defined as 50% decline in eGFR or KRT, was described using parametric and semiparametric survival methods. Analyses were stratified by underlying nonglomerular and glomerular diagnoses, and adjusted for demographic characteristics, eGFR, proteinuria, anemia, phosphate, hypertension, and alkali therapy. Six hundred and three participants with nonglomerular disease contributed 2673 person-years of follow-up, and 255 with a glomerular diagnosis contributed 808 person-years of follow-up. At baseline, 39% (237 of 603) of participants with nonglomerular disease had a bicarbonate level of ≤22 meq/L and 36% (85 of 237) of those participants reported alkali therapy treatment. In participants with glomerular disease, 31% (79 of 255) had a bicarbonate of ≤22 meq/L, 18% (14 of 79) of those participants reported alkali therapy treatment. In adjusted longitudinal analyses, compared with participants with a bicarbonate level >22 meq/L, hazard ratios associated with a bicarbonate level of <18 meq/L and 19-22 meq/L were 1.28 [95% confidence interval (95% CI), 0.84 to 1.94] and 0.91 (95% CI, 0.65 to 1.26), respectively, in children with nonglomerular disease. In children with glomerular disease, adjusted hazard ratios associated with bicarbonate level ≤18 meq/L and bicarbonate 19-22 meq/L were 2.16 (95% CI, 1.05 to 4.44) and 1.74 (95% CI, 1.07 to 2.85), respectively. Resolution of low bicarbonate was associated with a lower risk of CKD progression compared with persistently low bicarbonate (≤22 meq/L). In children with glomerular disease, low bicarbonate was linked to a higher risk of CKD progression. Resolution of low bicarbonate was associated with a lower risk of CKD progression. Fewer than one half of all children with low bicarbonate reported treatment with alkali therapy. Long-term studies of alkali therapy's effect in patients with pediatric CKD are needed.

Lower serum bicarbonate is associated with an increased risk of acute kidney injury.

Lower serum bicarbonate levels are associated with an increased risk of kidney disease progression. Whether lower serum bicarbonate levels are associated with an increased risk of developing acute kidney injury (AKI) is unclear. We included 8393 patients from the Systolic Blood Pressure Intervention Trial (SPRINT) that had baseline serum bicarbonate levels and complete data available. AKI was a predetermined adjudicated adverse event that was determined by hospital admission and discharge records with AKI as a recorded diagnosis. Serum bicarbonate was examined in clinically significant cutoffs ≤ 24, 25-28 and > 28mEq/L, with 25-28mEq/L as the reference group. Cox proportional hazard models were used to examine the association between serum bicarbonate and development of AKI. The mean (SD) age, estimated glomerular filtration rate (eGFR), and serum bicarbonate level at baseline were 68 (9) years, 77 (23) ml/min/1.73m2 and 26.3 (2.6) mEq/L, respectively. Participants with serum bicarbonate levels ≤ 24mEq/L were more likely to be male and to have lower baseline eGFR. After a median follow-up time of 3.3years, 293 participants developed AKI. More patients in the lower bicarbonate group developed AKI (6.1% vs 2.8% in the 25-28mEq/L and 2.1% in the > 28mEq/L). A bicarbonate level ≤ 24mEq/L was associated with a significantly increased risk of AKI compared to those with a bicarbonate level of 25-28mEq/L after full adjustment (HR 1.42, 95% CI 1.1-1.8). Lower serum bicarbonate levels are an independent risk factor for the development of AKI.

1481. A Study for Risk Factors of Acute Kidney Injury in Leptospirosis in a Tertiary Health Center in South India

BackgroundLeptospirosis is the most widespread zoonotic disease in the world. In India, it is endemic in coast lined states. Renal failure is a severe complication with mortality approaching 22%, early recognition of which helps clinicians in acting fast. This study aimed to investigate the predictors of Acute Kidney Injury (AKI) in LeptospirosisMethodsThis is a prospective, case–control study done in a tertiary care center in Southern India carried out between October 2017 and December 2018. Patients with confirmed Leptospirosis as per CDC 2013 and Faine’s criteria (2012) having AKI as per KDIGO criteria were defined as cases. Subjects without AKI were controls. Demographic, clinical and laboratory data were compared between the groups and analyzed. Logistic regression was performed to analyze the possible risk factors associated with AKI in Leptospirosis.ResultsA total of 329 subjects met the inclusion criteria of the study. 187 patients with AKI (CASES) and 142 patients without AKI (CONTROLS) were studied. Patients with AKI were older, (mean age- 46.99 ± 13.21 vs. 42.99 ± 15.15 years) had longer hospital stay (9.04 ± 5.62 vs. 6.27 ± 3.27 days) had higher SOFA (7.97 ±2.9 vs. 3.37 ± 2.6) and APACHE 2 scores (14.37±5.93 vs. 4.66 ± 4.4), lower mean arterial pressure (84.01 ± 14.45 vs. 89.01 ± 10.63 mmHg; P = 0.001) lower serum bicarbonate level (21.70 ± 2.35 vs. 18.73 ± 3.78 mEq/dL; P < 0.001). Factors like serum lactate, AST, ALT had no significant difference between the groups. Serovar identification was done in 88 patients, of which 57 had AKI. Australis (16.7%), Pyrogenes (16.7%) and Grippotyphosa (11.1%) were the commonest serovars isolated. Serovar most commonly associated with AKI was Pyrogenes (17.5%)Predictors for AKI were jaundice (P = 0.01, OR 2.25; CI 1.21 –3.26), vomiting (P = 0.017, OR 1.9, CI 1.12- 3.26) Hypotension (P = 0.02, OR = 12.3, CI 1.85 – 107.2), tachypnea (P = 0.006, OR = 2.55, CI 1.11- 3.24), leukocytosis (P < 0.001, OR 5.45, CI 1.86- 4.89), thrombocytopenia (P < 0.001, OR 6.49, CI 2.33 – 6.75)ConclusionIdentification of features like hypotension, tachypnea, acidosis, leukocytosis, thrombocytopenia, the occurrence of serovar Pyrogenes should alert the clinician on risk of developing AKIDisclosures All authors: No reported disclosures.

Serum Bicarbonate as a Surrogate for pH in Hemodialysis: A Pilot Study

Rationale & ObjectiveExcess morbidity and mortality are associated with both high and low serum bicarbonate levels in epidemiologic studies of patients with end-stage kidney disease (ESKD) receiving hemodialysis. The Kidney Disease Outcomes Quality Initiative (KDOQI) recommends modifying dialysate bicarbonate concentration to achieve a predialysis serum bicarbonate level ≥ 22 mmol/L, measured as total carbon dioxide (CO2). This practice assumes that total CO2 is an adequate surrogate for acid-base status, yet its surrogacy performance is unknown in ESKD. We determined acid-base status at the beginning and end of hemodialysis using total CO2 and pH and tested whether total CO2 is an appropriate surrogate for acid-base status.Study DesignPilot study.Setting & Participants25 veterans with ESKD receiving outpatient hemodialysis.Tests ComparedpH, calculated bicarbonate level, and total CO2.OutcomesThe proportion of paired samples for which total CO2 misclassified acid-base status according to pH was determined. Bias of total CO2 was evaluated using Bland-Altman plots, comparing it to calculated bicarbonate.ResultsAmong 71 samples, mean pH was 7.41 ± 0.03 predialysis and 7.48 ± 0.05 postdialysis. Compared with interpretation of full blood gas profiles, 9 of 25 (36%) participants were misclassified as acidemic using predialysis total CO2 measures alone (total CO2 < 22 mmol/L but pH ≥ 7.38); 1 (4%) participant was misclassified as alkalemic (total CO2 > 26 mmol/L but pH ≤ 7.42). Among paired samples in which predialysis total CO2 was < 22 mmol/L, the corresponding pH was acidemic (< 7.38) in just 3 of 13 (23%) instances.LimitationsSmall, single-center, entirely male cohort.ConclusionsA majority of participants became alkalemic during routine hemodialysis despite arriving with normal pH. 10 of 25 (40%) participants’ acid-base status was misclassified using total CO2 measurements alone; the majority of predialysis total CO2 values that would trigger therapeutic modification according to practice guidelines did not have acidemia when assessed using pH. Efforts to improve dialysis prescription require recognition that total CO2 may not be reliable for interpreting acid-base status in hemodialysis patients.

THE PERFECT STORM: A CASE OF THYROID STORM AND RAPIDLY FATAL RHABDOMYOLYSIS SECONDARY TO INFLUENZA PNEUMONIA

SESSION TITLE: Wednesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Life-threatening end-organ damage secondary thyroid storm and rhabdomyolysis is often recognized late in patients presenting with sepsis. We present a case of rapidly fatal and refractory rhabdomyolysis and thyroid storm in a patient with influenza pneumonia. CASE PRESENTATION: A 41 year old male non-adherent to medical therapy for hyperthyroidism presented to the emergency department (ED) with chest pain and viral prodrome of one day duration. Vitals were remarkable for pulse of 127. A CXR (Figure 1) demonstrated bilateral pulmonary infiltrates, influenza swab was negative and labs were notable for a low serum bicarbonate (HCo3) level, elevated creatinine and liver function tests, bandemia, and an undetectable TSH. IV fluids and broad spectrum antimicrobials for presumed bacterial pneumonia were initiated. On hospital day 2, his labs were suggestive of worsening acidosis and rapidly progressive renal failure. The patient developed acute respiratory distress requiring emergent intubation and was transferred to the medical intensive care unit (MICU) where he suffered a PEA arrest upon arrival. ROSC was achieved followed by initiation of renal replacement therapy (RRT) along with methimazole, stress dose steroids, and lugol’s iodine solution for presumed thyroid storm. Empiric oseltamivir was added. Creatine kinase (CK) was 742,150. Over the course of 24 hours, his hyperkalemia continued to worsen requiring simultaneous use of two CRRT machines and therapeutic plasma exchange (TPE). Emergent thyroidectomy was considered, however the patient was deemed too unstable. An extended virus respiratory NAAT confirmed influenza-A. His hyperkalemia and thyroid hormone levels remained refractory to maximal medical management. On hospital day 3 he sustained another PEA arrest and died. DISCUSSION: Thyroid storm is a life-threatening condition with mortality nearing 100% in untreated individuals. The diagnosis is made clinically utilizing biochemical evidence of a hyperthyroid state and the Burch and Wartosky criteria, usually in the background of an inciting event such as influenza pneumonia as in this patient. Beyond standard interventions aimed at reducing production, secretion or peripheral conversion of thyroid hormone, this patient underwent TPE. We also highlight the relative insensitivity (∼80%) of nasopharyngeal influenza testing and the importance of empiric therapy when clinical equipoise and pre-test probability are high. CONCLUSIONS: Clinicians must maintain a high index of suspicion for influenza infection despite negative viral testing in the correct clinical setting maintaining a low threshold to initiate empiric oseltamivir. Thyroid storm, if suspected, should likewise be treated empirically before awaiting biochemical confirmation. This case highlights multi-organ failure and severe refractory metabolic derangements that occur in such a scenario. Reference #1: Carroll R, Matfin G. Endocrine and metabolic emergencies: thyroid storm. Ther Adv Endocrinol Metab. 2010;1(3):139-45. Reference #2: Karanikolas M, Velissaris D, Karamouzos V, Filos KS. Thyroid storm presenting as intra-abdominal sepsis with multi-organ failure requiring intensive care. Anaesth Intensive Care. 2009 Nov;37(6):1005-7. PubMed PMID: 20014610. Reference #3: Ba JH, Wu BQ, Wang YH, Shi YF. Therapeutic plasma exchange and continuous renal replacement therapy for severe hyperthyroidism and multi-organ failure: A case report. World J Clin Cases. 2019 Feb 26;7(4):500-507. DISCLOSURES: No relevant relationships by Mark Barash, source=Web Response No relevant relationships by Toni-Denise Espina, source=Web Response No relevant relationships by Kristi Maso, source=Web Response no disclosure on file for Tyler Qiu