Metabolic Acidosis In Patients Research Articles

Prevalence and Correlates of Metabolic Acidosis among Patients with Homozygous Sickle Cell Disease

Very few studies report acid base disorders in homozygous patients with sickle cell anemia (SCA) and describe incomplete renal acidosis rather than true metabolic acidosis, the prevalence of which is unknown and presumably low. This study aimed to assess the prevalence of metabolic acidosis and to identify its risk factors and mechanisms. This study retrospectively analyzed 411 homozygous patients with SCA with a GFR ≥ 60 ml/min per 1.73 m(2), referred in a single center between 2007 and 2012. Acidosis and nonacidosis groups were compared for clinical and biologic data including SCA complications and hemolytic parameters. A subgroup of 65 patients with SCA, referred for a measured GFR evaluation in the setting of sickle cell-associated nephropathy, was further analyzed in order to better characterize metabolic acidosis. Metabolic acidosis was encountered in 42% of patients with SCA, with a higher prevalence in women (52% versus 27% in men; P<0.001). Several hemolytic biomarkers, such as lactate dehydrogenase, were different between the acidosis and nonacidosis groups (P=0.02 and P=0.03 in men and women, respectively), suggesting higher hemolytic activity in the former group. To note, fasting urine osmolality was low in the whole study population and was significantly lower in men with SCA in the acidosis group (392 versus 427 mOsm/kg; P=0.01). SCA subgroup analysis confirmed metabolic acidosis with a normal anion gap in 14 patients, characterized by a lower urinary pH (P<0.02) and no increase in urinary ammonium. Serum potassium, plasma renin, and aldosterone were similar between the two groups and thus could not explain impaired urinary ammonium excretion. These results suggest that the prevalence of metabolic acidosis in patients with SCA is underestimated and related to impaired ammonium availability possibly due to an altered corticopapillary gradient. Future studies should evaluate whether chronic metabolic acidosis correction may be beneficial in this population, especially in bone remodeling.

Etiology and Clinico-biochemical Profile of Patients Admitted to Medicine ICU or Ward with Metabolic Acidosis in Eastern India

Aims: To understand the etiologies and clinical profile of metabolic acidosis in patients � admitted to medicine ICU or ward. To study biochemical parameters a

Propofol infusion associated metabolic acidosis in patients undergoing neurosurgical anesthesia: a retrospective study.

ObjectivePropofol and volatile anesthesia have been associated with metabolic acidosis induced by increased lactate. This study was designed to evaluate changes in pH, base excess (BE), and lactate in response to different anesthetic agents and to characterize propofol infusion-associated lactic acidosis.MethodsThe medical records of patients undergoing neurosurgical anesthesia between January 2005 and September 2012 were examined. Patients were divided into 2 groups : those who received propofol (total intravenous anesthesia, TIVA) and those who received sevoflurane (balanced inhalation anesthesia, BIA) anesthesia. Propensity analysis was performed (1 : 1 match, n=47), and the characteristics of the patients who developed severe acidosis were recorded.ResultsIn the matched TIVA and BIA groups, the incidence of metabolic acidosis (11% vs. 13%, p=1) and base excess (p>0.05) were similar. All patients in the TIVA group who developed severe acidosis did so within 4 hours of the initiation of propofol infusion, and these patients improved when propofol was discontinued.ConclusionsThe incidence of metabolic acidosis was similar during neurosurgical anesthesia with propofol or sevoflurane. In addition, severe acidosis associated with propofol infusion appears to be reversible when propofol is discontinued.

Association between hyperlactatemia and occult cardiac failure in diabetic patients on maintenance hemodialysis

Lactic acidosis as a consequence of high serum lactate levels may deepen the metabolic acidosis in patients with end-stage renal failure. Besides, certain antidiabetic may also cause raised lactate levels in diabetic patients. Therefore, it is obvious that the risk of hyperlactatemia is increased by folds in diabetic patients on chronic hemodialysis program. In this study, it is aimed to evaluate the frequency and the impact of increased serum lactate levels in prevalent diabetic hemodialysis patients. A total of 100 diabetic patients who were under maintenance hemodialysis in five different dialysis centers were included in this study. All biochemical parameters, blood gas measurements, echocardiographic data and antidiabetic treatments were statistically analyzed in terms of serum lactate levels. Out of 100 patients, 12 patients had serum lactate levels over normal limits. When the patients with normal or high serum lactate levels were defined as two different groups, statistical significance was detected between serum lactate levels and serum sodium (p = 0.019), potassium (p = 0.037) and bicarbonate levels (p = 0.028). Moreover, in patients with hyperlactatemia, the ejection fraction value was found significantly low (p = 0.005). The frequency of hyperlactatemia was not rare in prevalent diabetic hemodialysis patients. We additionally found that serum lactate level measurement may particularly help to diagnose the occult cardiac failure. However, further large scale studies are required to define the clinical significance of hyperlactatemia in the end-stage renal failure patients with diabetes mellitus.

Treatment of Metabolic Acidosis in Patients With CKD

Metabolic acidosis is a common complication of chronic kidney disease and is believed to contribute to a number of sequelae, including bone disease, altered protein metabolism, skeletal muscle wasting, and progressive glomerular filtration rate loss. Small trials in animal models and humans suggest a role for alkali therapy to lessen these complications. Recent studies support this notion, although more definitive evidence is needed on the long-term benefits of alkali therapy and the optimal serum bicarbonate level. The role of dietary modification also should be given greater consideration. In addition, potential adverse effects of alkali treatment must be taken into consideration, including sodium retention and the theoretical concern of promoting vascular calcification. This teaching case summarizes the rationale for and benefits and complications of base therapy in patients with chronic kidney disease.

Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease.

Metabolic acidosis may contribute to morbidity and disease progression in patients with chronic kidney disease (CKD). The ratio of dietary protein, the major source of nonvolatile acid, to dietary potassium, which is naturally bound to alkali precursors, can be used to estimate net endogenous acid production (NEAP). We tested the association between estimated NEAP and serum bicarbonate in patients with CKD. NEAP was estimated among 462 African American adults with hypertensive CKD using published equations: NEAP (mEq/d) = -10.2 + 54.5 (protein [g/d]/potassium [mEq/d]). Dietary protein and potassium intake were estimated from 24-hour urinary excretion of urea nitrogen and potassium, respectively. All of the eligible measurements during follow-up were modeled using generalized linear regression clustered by participant and adjusted for demographics, 24-hour urinary sodium, kidney function, and selected medications. Higher NEAP was associated with lower serum bicarbonate in a graded fashion (P trend < 0.001). Serum bicarbonate was 1.27 mEq/L lower among those in the highest compared with the lowest quartile of NEAP (P < 0.001). There was a greater difference in serum bicarbonate between the highest and lowest quartiles of NEAP among patients with stage 4/5 CKD (-2.43 mEq/L, P < 0.001) compared with those with stage 2/3 disease (-0.77 mEq/L, P = 0.01; P-interaction = 0.02). Reducing NEAP, through reduction of dietary protein and increased intake of fruits and vegetables, may prevent metabolic acidosis in patients with CKD.

Metabolic acidosis in patients undergoing liver transplantation

s and Programme: EUROANAESTHESIA 2011: The European Anaesthesiology Congress: Intensive Care Medicine

Evaluation of Metabolic Acidosis in Patients With a Kidney Graft: Comparison of the Bicarbonate-Based and Strong Ion–Based Methods

Background According to the traditional bicarbonate-based approach, metabolic acidosis is highly prevalent in kidney transplant recipients. However, the bicarbonate-based approach has been questioned by intensivists using strong ion difference–based methods. Methods We compared the results obtained by the strong ion–based with the traditional approach based on bicarbonate among a cohort of 83 kidney transplant recipients. Results Fifty-five percent of the patients were acidotic based on venous bicarbonate (<23 mmol/L) and 49% by the use of the effective strong ion difference (SID effective) (<37 mmol/L). Bicarbonate and SID effective were linearly correlated ( r = 0.94; P < .0001), with a slope close to 1. A greater percentage of patients presented with an increase in unexplained anions by the strong ion gap (SIG) than by the anion gap corrected (AG corrected) method (42 vs 32%, respectively). AG corrected and SIG were directly related ( r = 0.919; P < .0001), but the best fit of the relationship was polynomial with a progressively greater effect on SIG with increased AG corrected, suggesting that as anions progressively accumulate, their detection by SIG increases. By multiple regression analysis, plasma chloride, potassium, uric acid, and phosphate predicted blood bicarbonate. Analogously, chloride, potassium and uric acid predicted SID effective. Age was a predictor of changes in AG corrected, whereas age and plasma urea predicted SIG. Conclusions The use of the SID yielded results that were similar to the traditional bicarbonate-based approach. Conversely, SIG appeared to be more sensitive than AG for detection of anion accumulation among patients with a kidney graft.

Defining metabolic acidosis in patients with septic shock using Stewart approach

PurposeThe aim of this study was to define the nature of metabolic acidosis in patients with septic shock on admission to intensive care unit (ICU) using Stewart method. We also aimed to compare the ability of standard base excess (SBE), anion gap (AG), and corrected AG for albumin and lactate (AGcorr) to accurately predict the presence of unmeasured anions (UA). Patients and MethodsThirty consecutive patients with septic shock were prospectively included on ICU admission. Stewart equations modified by Figge were used to calculate the strong ion difference and the strong ion gap (SIG). ResultsMost patients had multiple underlying mechanisms explaining the metabolic acidosis. Unmeasured anions and hyperchloremia were present in 70% of the patients. Increased UA were present in 23% of patients with normal values of SBE and [HCO3−]. In these patients, plasma [Cl−] was significantly lower compared with patients with low SBE and increased UA (103 [102-106.6] vs 108 [106-111] mmol/L; P = .01, respectively). Corrected AG for albumin and lactate had the best correlation with SIG (r² = 0.94; P < .0001) with good agreement (bias, 0, and precision, 1.22) and highest area under the receiver operating characteristic curve (0.995; 95% confidence interval, 0.87-1) to discriminate SIG acidosis. ConclusionsPatients with septic shock exhibit a complex metabolic acidosis at ICU admission. High UA may be present with normal values of SBE and [HCO3−] as a result of associated “relative” hypochloremic alkalosis. Corrected AG for albumin and lactate offers the most accurate bedside alternative to Stewart calculation of UA.

Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis

Objective The objective of the study was to determine if balanced electrolyte solution (BES) prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis (DKA). Methods This is a prospective, randomized, double-blind study. A convenience sample of DKA patients aged 18 to 65 years with serum bicarbonate less than or equal to 15 and anion gap greater than or equal to 16 was enrolled at “Louisiana State University Health Sciences Center-Shreveport" an capitalize Emergency Department over a 24-month period (2006-2008). Patients were randomized to standardized resuscitation with normal saline (NS) or BES (Plasma-Lyte A pH 7.4; Baxter International, Deerfield, IL). Every 2 hours, serum chloride and bicarbonate were measured until the patient's anion gap decreased to 12. An intention-to-treat analysis was performed on patients who met inclusion criteria and received at least 4 hours of study fluid. Chloride and bicarbonate measurements from the BES and NS groups were compared using unpaired and paired Student t tests. Results Of 52 patients enrolled, 45 (22 in BES group and 23 in NS group) met inclusion criteria and received 4 hours of fluid. The mean postresuscitation chloride was 111 mmol/L (95% confidence interval [CI] = 110-112) in the NS group and 105 mmol/L (95% CI = 103-108) in the BES group ( P ≤ .001). The mean postresuscitation bicarbonate was 17 mmol/L (95% CI = 15-18) in the NS group and 20 mmol/L (95% CI = 18-21) in the BES group ( P = .020). Conclusions Resuscitation of DKA patients with BES results in lower serum chloride and higher bicarbonate levels than patients receiving NS, consistent with prevention of hyperchloremic metabolic acidosis.

Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR

Metabolic acidosis often accompanies low glomerular filtration rate and induces secretion of endothelin, which in turn might mediate kidney injury. Here we tested whether treatment of metabolic acidosis in patients with low glomerular filtration rate reduced the progression of kidney disease. Fifty-nine patients with hypertensive nephropathy and metabolic acidosis had their blood pressure reduced with regimens that included angiotensin-converting enzyme inhibition. Thirty patients were then prescribed sodium citrate, and the remaining 29, unable or unwilling to take sodium citrate, served as controls. All were followed for 24 months with maintenance of their blood pressure reduction. Urine endothelin-1 excretion, a surrogate of kidney endothelin production, and N-acetyl-beta-D-glucosaminidase, a marker of kidney tubulointerstitial injury, were each significantly lower, while the rate of estimated glomerular filtration rate decline was significantly slower. The estimated glomerular filtration rate was statistically higher after 24 months of sodium citrate treatment compared to the control group. Hence it appears that sodium citrate is an effective kidney-protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition.

Early anion gap metabolic acidosis in acetaminophen overdose

Purpose The study aimed to determine the incidence and clinical significance of early high (>15 mEq/L) anion gap metabolic acidosis in acetaminophen (APAP) overdose. Methods A retrospective review of a cohort of 74 patients presenting within 24 hours of APAP overdose was conducted. Results Early high anion gap metabolic acidosis was present in 41% of patients on admission and persisted for 1.5 ± 0.1 days. The anion gap was associated with an elevated lactate level (4.5 ± 1 mmol/L) ( r 2 = 0.66, P < .05), which persisted for 1 day. The lactate level increased in proportion to the APAP concentration ( r 2 = 0.75, P < .05). Patients with increased anion gap had a higher incidence of confusion (48% vs 3%; P < .001) and lethargy (39% vs 6%; P = .003). Early high anion gap metabolic acidosis was found in the absence of shock or liver failure. All patients were treated with N-acetylcysteine and, despite the early high anion gap metabolic acidosis, none developed hepatic failure or hypoglycemia. Conclusion Early high anion gap metabolic acidosis in patients with APAP overdose is self-limited and does not predict clinical or laboratory outcomes. Persistent or late metabolic acidosis in the absence of liver failure is not likely due to APAP and should prompt a search for other causes of metabolic acidosis. Finally, APAP overdose should be considered in patients presenting to the emergency department with altered mental status, as this is a treatable condition when detected early.

Hyperchloremic Metabolic Acidosis Due to Deferasirox in a Patient with Beta Thalassemia Major

To report a case of hyperchloremic metabolic acidosis in a patient with beta thalassemia major secondary to treatment with deferasirox due to iron overload. A 58-year-old white female with beta thalassemia major was admitted with fever, fatigue, abnormal liver function test results, and hyperchloremic metabolic acidosis (lactate dehydrogenase 494 U/L, aspartate aminotransferase 167 U/L, alanine aminotransferase 250 U/L, gamma-glutamyl transferase 102 U/L, total bilirubin 3.79 mg/dL, direct bilrubin 2.37, potassium 3.3 mEq/L, PO(2) 81.4 mm Hg, PCO(2) 29.4 mm Hg, HCO(3) 16 mEq/L, pH 7.35, chloride 116 mEq/L, anion gap 7.5 mEq/L). Twenty-five days before admission the patient decided to discontinue treatment with deferoxamine for chronic iron overload and continue treatment with oral deferasirox 1500 mg/day. Despite extended clinical and laboratory examination, no obvious cause of fever, hepatitis, or hyperchloremic metabolic acidosis was revealed. Diagnosis was compatible with tubular dysfunction, drug-induced hepatitis, and hypersensitivity reaction due to deferasirox. All pathological findings were fully reversible and our patient had an excellent outcome. The presence of tubular dysfunction should be considered in any patient with otherwise unexplained hyperchloremic metabolic acidosis. In our patient, other potential causes of metabolic hyperchloremic acidosis were ruled out. Toxic effects of deferasirox are probably caused by chelation of mitochondrial iron, leading to adenosine triphosphate depletion in tubular epithelial cells. Use of the Naranjo probability scale revealed that the adverse reaction was probable. Kidney toxicity may be a major issue in the management of patients receiving deferasirox. Our case indicates a potential risk of renal toxicity with the presence of tubular dysfunction and hyperchloremic metabolic acidosis in patients undergoing treatment with deferasirox.

Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR

Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR

Does Infusion Of Unbalanced Colloid Solutions Influence The Acid Base Status During Liver Transplantation?

Background:The aim of the present study is to investigate the effects of two different unbalanced synthetic colloid solutions on acid-base equilibrium in patients undergoing living donor liver transplantation (LDLT)MethodsForty patients undergoing LDLT were prospectively randomized to receive either 5% human albumin ALB (n=20) or hydroxyethyl starch 6% 130/0.4 HES (n=20). PH, PaCO2, and serum concentrations of sodium, potassium, chloride, lactate, ionized calcium, phosphate, and albumin were measured after induction of anaesthesia, anhepatic phase, and at admission to intensive care unit (ICU). Strong ion difference, strong ion gap, and corrected anion gap were calculated. Results All Patients developed metabolic acidosis during anhepatic phase and at ICU admission. Factors that had contributed to metabolic acidosis were increase in lactate levels, unmeasured anions and hyperphosphatemia. In both groups; serum lactate levels had increased at anhepatic phase and ICU admission. Levels of unmeasured anions during anhepatic phase were 7.7±3.3 mEq/l, and 6.7±4.4 mEq/l among HES and ALB groups respectively). Hyperphosphatemia had occurred among both groups during anhepatic phase and at ICU admission. In HES group, significant decrease in strong ion difference with concomitant decrease in weak plasma acids compared to the albumin group was noticed. Conclusion Both HES 130/0.4 and albumin 5% had led to similar metabolic acidosis in patients undergoing liver transplantation but with great variation in Strong ion difference and weak plasma acid.

Metabolic acidosis in patients with severe sepsis and septic shock: A longitudinal quantitative study

Objective: To describe the composition of metabolic acidosis in patients with severe sepsis and septic shock at intensive care unit admission and throughout the first 5 days of intensive care unit stay. Design: Prospective, observational study. Setting: Twelve-bed intensive care unit. Patients: Sixty patients with either severe sepsis or septic shock. Interventions: None. Measurements and Main Results: Data were collected until 5 days after intensive care unit admission. We studied the contribution of inorganic ion difference, lactate, albumin, phosphate, and strong ion gap to metabolic acidosis. At admission, standard base excess was -6.69 ± 4.19 mEq/L in survivors vs. -11.63 ± 4.87 mEq/L in nonsurvivors (p< .05); inorganic ion difference (mainly resulting from hyperchloremia) was responsible for a decrease in standard base excess by 5.64 ± 4.96 mEq/L in survivors vs. 8.94 ± 7.06 mEq/L in nonsurvivors (p< .05); strong ion gap was responsible for a decrease in standard base excess by 4.07 ± 3.57 mEq/L in survivors vs. 4.92 ± 5.55 mEq/L in nonsurvivors with a nonsignificant probability value; and lactate was responsible for a decrease in standard base excess to 1.34 ± 2.07 mEq/L in survivors vs. 1.61 ± 2.25 mEq/L in nonsurvivors with a nonsignificant probability value. Albumin had an important alkalinizing effect in both groups; phosphate had a minimal acid-base effect. Acidosis in survivors was corrected during the study period as a result of a decrease in lactate and strong ion gap levels, whereas nonsurvivors did not correct their metabolic acidosis. In addition to Acute Physiology and Chronic Health Evaluation II score and serum creatinine level, inorganic ion difference acidosis magnitude at intensive care unit admission was independently associated with a worse outcome. Conclusions: Patients with severe sepsis and septic shock exhibit a complex metabolic acidosis at intensive care unit admission, caused predominantly by hyperchloremic acidosis, which was more pronounced in nonsurvivors. Acidosis resolution in survivors was attributable to a decrease in strong ion gap and lactate levels.

Metabolic acidosis in patients with severe sepsis and septic shock: A longitudinal quantitative study

To describe the composition of metabolic acidosis in patients with severe sepsis and septic shock at intensive care unit admission and throughout the first 5 days of intensive care unit stay. Prospective, observational study. Twelve-bed intensive care unit. Sixty patients with either severe sepsis or septic shock. None. Data were collected until 5 days after intensive care unit admission. We studied the contribution of inorganic ion difference, lactate, albumin, phosphate, and strong ion gap to metabolic acidosis. At admission, standard base excess was -6.69 +/- 4.19 mEq/L in survivors vs. -11.63 +/- 4.87 mEq/L in nonsurvivors (p < .05); inorganic ion difference (mainly resulting from hyperchloremia) was responsible for a decrease in standard base excess by 5.64 +/- 4.96 mEq/L in survivors vs. 8.94 +/- 7.06 mEq/L in nonsurvivors (p < .05); strong ion gap was responsible for a decrease in standard base excess by 4.07 +/- 3.57 mEq/L in survivors vs. 4.92 +/- 5.55 mEq/L in nonsurvivors with a nonsignificant probability value; and lactate was responsible for a decrease in standard base excess to 1.34 +/- 2.07 mEq/L in survivors vs. 1.61 +/- 2.25 mEq/L in nonsurvivors with a nonsignificant probability value. Albumin had an important alkalinizing effect in both groups; phosphate had a minimal acid-base effect. Acidosis in survivors was corrected during the study period as a result of a decrease in lactate and strong ion gap levels, whereas nonsurvivors did not correct their metabolic acidosis. In addition to Acute Physiology and Chronic Health Evaluation II score and serum creatinine level,inorganic ion difference acidosis magnitude at intensive care unit admission was independently associated with a worse outcome. Patients with severe sepsis and septic shock exhibit a complex metabolic acidosis at intensive care unit admission, caused predominantly by hyperchloremic acidosis,which was more pronounced in nonsurvivors. Acidosis resolution in survivors was attributable to a decrease in strong ion gap and lactate levels.

Change in Brain Glucose After Enteral Nutrition in Subarachnoid Hemorrhage

The alteration of brain extracellular glucose after enteral nutrition (EN) remains unclear. In this study, we used brain microdialysis methods to estimate whether the physiologic elevation of plasma glucose following EN affects brain glucose metabolism of aneurysmal subarachnoid hemorrhage (SAH) patients. Brain extracellular glucose, lactate, glycerol, glutamate, and pyruvate were measured with a brain microdialysis probe in 12 patients (mean age: 60.0 y+/-7.8 y) after SAH. The EN was initially administered a mean of 3.2 d after the onset of SAH. All of the measured parameters were estimated before and after EN. Cerebral perfusion pressure did not significantly change after SAH during the study period. Plasma glucose rose significantly after EN (141.4+/-11.6mg/dL before EN versus 183.8+/-26.2mg/dL immediately after EN (P=0.0006), 177.7+/-30.2mg/dL at 2h after EN (P=0.0033)). The brain extracellular glucose before EN (2.5+/-0.92mmol/L) was significantly lower than the levels measured just after (3.49+/-1.0mmol/L, P=0.0186) and 2h after the end of EN (3.70+/-1.0mmol/L, P=0.0053). Brain extracellular concentrations of lactate, glutamate, pyruvate, and glycerol showed no significant changes. Brain extracellular glucose increased after the transient elevation of plasma glucose following EN. These results suggest that brief, physiologic elevations in plasma glucose after EN produced no changes in brain extracellular glutamate concentration or lactate/pyruvate ratio. These data may help determine the plasma glucose levels most effective for avoiding brain metabolic acidosis in patients after SAH. It remains unclear, however, how SAH itself influences these findings.

Influence of Renal Function and Diet on Acid-Base Status in Chronic Kidney Disease Patients

We investigated the influence of potential renal acid load (PRAL) and renal function on the degree of metabolic acidosis in patients with chronic kidney disease (CKD). This was a cross-sectional study. This study was conducted at the Nephrology Outpatient Division of the Hospital Universitário Clementino Fraga Filho (Rio de Janeiro, Brazil). Thirty CKD patients undergoing conservative treatment were divided according to plasma HCO(3)(-) values into acidotic (HCO(3)(-) <or=22 mM, n = 15) and nonacidotic (HCO(3)(-) >22 mM, n = 15). Biochemical, nutritional, and anthropometric parameters and PRAL were measured. The mean of plasma HCO(3)(-) values was 17.7 +/- 2.8 mM in the acidotic group, and 25.1 +/- 2.2 mM in the nonacidotic group. There was no significant difference in mean PRAL values between the acidotic (9.8 +/- 6.4 mEq/day) and nonacidotic (12.7 +/- 10.0 mEq/day) groups, but there was a significant correlation between plasma HCO(3)(-) and creatinine clearance (r = 0.78, P < .0001). Based on the receiver operating characteristic curve, the level of creatinine clearance to begin detection of acidosis was 31.8 mL/min, with a sensitivity and specificity of 86.7%. The acid-base status of this group of CKD patients undergoing conservative treatment was mainly determined by degree of renal insufficiency rather than diet.

Ethylene Glycol Toxicity Presenting with Non‐Anion Gap Metabolic Acidosis

Ethylene glycol classically produces an elevated anion gap metabolic acidosis. We report a series of patients with ethylene glycol toxicity with a component of non-anion gap metabolic acidosis without known associated confounding factors. A retrospective review of Poison Control Center records were searched more than 8 years (2000-2007) for ethylene glycol and antifreeze. Cases were reviewed and excluded for miscoding, information calls, animal exposures, or non-ingestion exposures. The bicarbonate gap, or delta ratio (DR), was calculated using the formula: DR = (AG - 12)/[24 - measured serum where anion gap (AG) = [Na(+)] - [Cl(-)] - , all in mEq/l. Non-anion gap metabolic acidosis was considered present when the DR < 1. Of 254 cases, 175 were excluded. Of the remaining 79 cases, 14 had a component of non-anion gap metabolic acidosis at presentation. Their calculated anion gap was 14-28, and measured serum ranged from 2-20 mEq/l. A normal anion gap was present in two patients who presented with non-anion gap metabolic acidosis. The DR ranged from 0.28-0.95. Seven out of 14 patients with non-anion gap metabolic acidosis had elevated serum [Cl(-)]. In the other cases, no explanation for the non-anion gap metabolic acidosis could be determined. The absence of a significant anion gap elevation in the setting of metabolic acidosis after ethylene glycol ingestion without other confounding factors (such as ethanol, lithium carbonate or bromide) has not previously been recognized. Clinicians should be aware of the potential for non-anion gap metabolic acidosis in patients with ethylene glycol toxicity, and should not exclude the diagnosis in patients who present with a non-anion gap metabolic acidosis. Further study is needed to determine the mechanisms by which this occurs.