Lactic acidosis occurs from an overproduction of lactate or decreased metabolism. It is common in critically ill patients, especially those with hematological conditions such as multiple myeloma, leukemia, and lymphoma. There are two types of lactic acidosis, Type A and Type B, with Type B presenting more commonly in hematological conditions that require prompt diagnosis and treatment of the underlying condition. We present a case of a 43-year-old male with Type B lactic acidosis secondary to stage IV colon cancer with metastasis to the liver. Initial laboratory work was significant for lactic acid of 16.52 mmol/L. Arterial blood gas (ABG) showed pH 7.26, pCO2 21 mmHg, pO2 111 mmHg, and HCO3 9 mEq/L, revealing an anion gap and metabolic acidosis with compensatory respiratory alkalosis. Initially, the patient was treated with aggressive fluid management, IV antibiotics, and sodium bicarbonate; however, his lactic acid continued to rise. The recommendation was made for urgent dialysis. Despite treatments, the prognosis is poor.

While metabolic acidosis is one of the most common complications in patients with chronic kidney disease (CKD), there are several uncommon etiologies that are challenging to diagnose. Here, we describe a patient on peritoneal dialysis who developed high anion gap metabolic acidosis secondary to acquired 5-oxoprolinemia from acetaminophen use. While CKD is a known risk factor for developing this potentially serious complication, this case further highlights how 5-oxoproline accumulation can occur, even with therapeutic dosing of acetaminophen.

Anaerobic exercise decreases systemic pH and increases metabolic acidosis in athletes, altering the acid-base homeostasis. In addition, nutritional recommendations advising athletes to intake higher amounts of proteins and simple carbohydrates (including from sport functional supplements) could be detrimental to restoring acid-base balance. Here, this specific nutrition could be classified as an acidic diet and defined as \'Westernized athletic nutrition\'. The maintenance of a chronic physiological state of low-grade metabolic acidosis produces detrimental effects on systemic health, physical performance, and inflammation. Therefore, nutrition must be capable of compensating for systemic acidosis from anaerobic exercise. The healthy gut microbiota can contribute to improving health and physical performance in athletes and, specifically, decrease the systemic acidic load through the conversion of lactate from systemic circulation to short-chain fatty acids in the proximal colon. On the contrary, microbial dysbiosis results in negative consequences for host health and physical performance because it results in a greater accumulation of systemic lactate, hydrogen ions, carbon dioxide, bacterial endotoxins, bioamines, and immunogenic compounds that are transported through the epithelia into the blood circulation. In conclusion, the systemic metabolic acidosis resulting from anaerobic exercise can be aggravated through an acidic diet, promoting chronic, low-grade metabolic acidosis in athletes. The individuality of athletic training and nutrition must take into consideration the acid-base homeostasis to modulate microbiota and adaptive physiological responses.

Background: The ability of hemoglobin to bind and dissociate oxygen is crucial in delivering oxygen to tissues and is influenced by a range of physiological states, compensatory mechanisms, and pathological conditions. This may be illustrated by the oxyhemoglobin dissociation curve (ODC). The key parameter for evaluating the oxygen affinity to hemoglobin is p50. The aim of this study was to evaluate the impact of hemodialysis on p50 in a group of patients with chronic kidney disease (CKD). An additional goal was to assess the correlation between p50 and the parameters of erythropoiesis, point-of-care testing (POCT), and other laboratory parameters. Methods: One hundred and eighty patients (106 male, 74 female), mean age 62.5 ± 17 years, with CKD stage G4 and G5 were enrolled in this cross-sectional study. Patients were divided into two groups, including 65 hemodialysis (HD) patients and 115 patients not receiving dialysis (non-HD). During the standard procedure of arteriovenous fistula creation, blood samples from the artery (A) and the vein (V) were taken for POCT. The causes of CKD, as well as demographic and comorbidity data, were obtained from medical records and direct interviews. Results: The weekly dose of erythropoietin was higher in HD patients than in non-HD patients (4914 ± 2253 UI vs. 403 ± 798 UI, p < 0.01), but hemoglobin levels did not differ between these groups. In the group of non-HD patients, more advanced metabolic acidosis (MA) was found, compared to the group with HD. In arterial and venosus blood samples, the non-HD group had significantly lower pH, pCO2 and HCO3-. This group had a higher proportion of individuals with MA with HCO3- < 22 mmol/L (42% vs. 24%, p < 0.01). The absolute difference of p50 in arterial and venous blood was determined using the formula Δp50 = (p50-A) - (p50-V). Δp50 was significantly higher in the HD group in comparison to non-HD (0.08 ± 2.05 mmHg vs. -0.66 ± 1.93 mmHg, p = 0,02). There was a negative correlation between pH and the p50 value in arterial (pH-A vs. p50-A, r = -0.56, p < 0.01) and venous blood (pH-V vs. p50-V, r = -0.45, p < 0.01). In non-HD patients, hemoglobin levels correlated negatively with p50 (r = -0.29, p < 0.01), whereas no significant relation was found in HD patients. Conclusions: The ODC in pre-dialysis CKD (non-HD) patients is shifted to the right due to MA, and this is an additional factor influencing erythropoiesis. Hemodialysis restores the natural differences in hemoglobin\'s dissociation characteristics in the arterial and venous circulation.

Diabetic ketoacidosis (DKA) is a severe complication of diabetes mellitus characterized by hyperglycemia, metabolic acidosis, and ketosis. We present a challenging case of euglycemic DKA secondary to fasting and urinary tract infection with acute renal failure in a 50-year-old woman. Despite normal random blood sugar levels, the patient exhibited clinical signs of DKA, leading to further investigation. High anion gap metabolic acidosis with hyperkalemia and abnormal renal function tests were identified. After hemodialysis, serum ketones were found to be highly positive, confirming the diagnosis. Prompt management led to a complete clinical and laboratory resolution. This case underscores the importance of considering DKA in patients with suggestive symptoms, even with normal blood sugar levels.

BACKGROUND: The beneficial effects of oral supplements with alkalinizing agents in patients with chronic kidney disease (CKD) have been limited to the severe stages. We investigated whether two types of supplements, sodium bicarbonate (SB) and potassium citrate/sodium citrate (PCSC), could maintain renal function in patients with mild-stage CKD.
METHODS: This was a single-center, open-labeled, randomized cohort trial. Study participants with CKD stages G2, G3a, and G3b were enrolled between March 2013 and January 2019 and randomly assigned by stratification according to age, sex, estimated glomerular filtration rate (eGFR), and diabetes. They were followed up for 6 months (short-term study) for the primary endpoints and extended to 2 years (long-term study) for the secondary endpoints. Supplementary doses were adjusted to achieve an early morning urinary pH of 6.8-7.2. We observed renal dysfunction or new-onset cerebrovascular disease and evaluated urinary surrogate markers for renal injury.
RESULTS: Overall, 101 participants were registered and allocated to three groups: standard (n = 32), SB (n = 34), and PCSC (n = 35). Two patients in the standard group attained the primary endpoints (renal stones and overt proteinuria) but were not statistically significant. There was one patient in the standard reduced eGFR during the long-term study (p = 0.042 by ANOVA). SB increased proteinuria (p = 0.0139, baseline vs. 6 months), whereas PCSC significantly reduced proteinuria (p = 0.0061, baseline vs. 1 year, or p = 0.0186, vs. 2 years) and urinary excretion of 8-hydroxy-2\'-deoxyguanosine (p = 0.0481, baseline vs. 6 months).
CONCLUSIONS: This study is the first to report supplementation of PCSC reduced intrarenal oxidative stress in patients with mild-stage CKD.

Normal-anion-gap metabolic acidosis (NAGMA) is a common but often under-recognised and poorly understood condition, especially by less-experienced clinicians. In adults, NAGMA might be an initial clue to a more significant underlying pathology, such as autoimmune diseases, hypergammaglobulinemia or drug toxicities. However, identifying the aetiology can be challenging due to the diverse processes involved in the development of acidosis. A better understanding of the pathophysiology of NAGMA can help treating physicians suspect and evaluate the condition early and reach the correct diagnosis. This article provides an overview of renal acid-base regulation, discusses the pathophysiological processes involved in developing NAGMA and provides a framework for evaluation to reach an accurate diagnosis.

UNASSIGNED: It is unclear whether the use of higher dialysate bicarbonate concentrations is associated with clinically relevant changes in the pre-dialysis serum bicarbonate concentration.
UNASSIGNED: The objective is to examine the association between the dialysate bicarbonate prescription and the pre-dialysis serum bicarbonate concentration.
UNASSIGNED: This is a retrospective cohort study.
UNASSIGNED: The study was performed using linked administrative health care databases in Ontario, Canada.
UNASSIGNED: Prevalent adults receiving maintenance in-center hemodialysis as of April 1, 2020 (n = 5414) were included.
UNASSIGNED: Patients were grouped into the following dialysate bicarbonate categories at the dialysis center-level: individualized (adjustment based on pre-dialysis serum bicarbonate concentration) or standardized (>90% of patients received the same dialysate bicarbonate concentration). The standardized category was stratified by concentration: 35, 36 to 37, and ≥38 mmol/L. The primary outcome was the mean outpatient pre-dialysis serum bicarbonate concentration at the patient level.
UNASSIGNED: We examined the association between dialysate bicarbonate category and pre-dialysis serum bicarbonate using an adjusted linear mixed model.
UNASSIGNED: All dialysate bicarbonate categories had a mean pre-dialysis serum bicarbonate concentration within the normal range. In the individualized category, 91% achieved a pre-dialysis serum bicarbonate ≥22 mmol/L, compared to 87% in the standardized category. Patients in the standardized category tended to have a serum bicarbonate that was 0.25 (95% confidence interval [CI] = -0.93, 0.43) mmol/L lower than patients in the individualized category. Relative to patients in the 35 mmol/L category, patients in the 36 to 37 and ≥38 mmol/L categories tended to have a serum bicarbonate that was 0.70 (95% CI = -0.30, 1.70) mmol/L and 0.87 (95% CI = 0.14, 1.60) mmol/L higher, respectively. There was no effect modification by age, sex, or history of chronic lung disease.
UNASSIGNED: We could not directly confirm that all laboratory measurements were pre-dialysis. Data on prescribed dialysate bicarbonate concentrations for individual dialysis sessions were not available, which may have led to some misclassification, and adherence to a practice of individualization could not be measured. Residual confounding is possible.
UNASSIGNED: We found no significant difference in the pre-dialysis serum bicarbonate concentration irrespective of whether an individualized or standardized dialysate bicarbonate was used. Dialysate bicarbonate concentrations ≥38 mmol/L (vs 35 mmol/L) may increase the pre-dialysis serum bicarbonate concentration by 0.9 mmol/L.
UNASSIGNED: On ignore si des concentrations plus élevées de bicarbonate dans le dialysat sont associées à des changements cliniquement significatifs dans le taux de bicarbonate sérique prédialyse.
UNASSIGNED: Examiner l’association entre la prescription de bicarbonate du dialysat et le taux de bicarbonate sérique prédialyse.
UNASSIGNED: Étude de cohorte rétrospective.
UNASSIGNED: Étude réalisée en Ontario (Canada) à partir des données administratives de santé.
UNASSIGNED: Ont été inclus les adultes prévalents qui recevaient une hémodialyse chronique en centre le 1er avril 2020 (n=5 414).
UNASSIGNED: Les sujets ont été regroupés dans les catégories suivantes de concentration en bicarbonate dans le dialysat utilisée dans leur unité de dialyse: individualisée (ajustée selon le taux de bicarbonate sérique prédialyse) ou normalisée (même concentration pour >90% des sujets). La catégorie « standardisée » a été stratifiée selon la concentration: 35 mmol/L, 36 à 37 mmol/L et ≥38 mmol/L. Le principal critère d’évaluation était le taux moyen de bicarbonate sérique prédialyse en ambulatoire au niveau du patient.
UNASSIGNED: Nous avons examiné l’association entre la catégorie de concentration en bicarbonate du dialysat et le taux de bicarbonate sérique prédialyse à l’aide d’un modèle linéaire mixte corrigé.
UNASSIGNED: Pour toutes les catégories de concentration en bicarbonate du dialysat, le taux moyen de bicarbonate sérique prédialyse était dans la plage normale. Dans la catégorie « individualisée », 91% des sujets avaient un taux de bicarbonate sérique prédialyse de ≥22 mmol/L, comparativement à 87% dans la catégorie « standardisée ». Les patients de la catégorie « standardisée » tendaient à avoir un taux de bicarbonate sérique de 0,25 mmol/L (IC 95%: -0,93 à 0,43) inférieur à celui des patients de la catégorie « individualisée ». Comparé aux patients de la catégorie 35 mmol/L, les patients des catégories 36 à 37 mmol/L et ≥38 mmol/L tendaient respectivement à avoir un taux de bicarbonate sérique de 0,70 mmol/L (IC 95%: -0,30 à 1,70) et de 0,87 mmol/L (IC 95%: 0,14 à 1,60) plus élevé. L’âge, le sexe ou les antécédents de maladie pulmonaire chronique n’ont pas semblé modifier l’effet.
UNASSIGNED: Il n’a pas été possible de confirmer directement que toutes les mesures de laboratoire avaient été effectuées avant la dialyse. Les données sur les concentrations de bicarbonate prescrites pour les séances de dialyse individuelles n’étaient pas disponibles, ce qui peut avoir conduit à une classification erronée. De plus, l’observance d’une pratique d’individualisation n’a pas pu être mesurée. Une confusion résiduelle est possible.
UNASSIGNED: Nous n’avons observé aucune différence significative dans les taux de bicarbonate sériques prédialyse, qu’on ait utilisé une concentration individualisée ou standardisée de bicarbonate dans le dialysat. L’utilisation d’un dialysat à ≥38 mmol/L (c. 35 mmol/L) de bicarbonate peut entraîner une hausse de 0,9 mmol/L du taux de bicarbonate sérique prédialyse.

The present study investigated the prevalence of blood chloride (Cl) abnormalities in diarrheic neonatal calves with metabolic acidosis and attempted to identify the most relevant electrolyte abnormality to these abnormalities. A retrospective analysis was conducted on the medical records of 157 diarrheic neonatal calves aged 10.3 ± 4.2 days old with metabolic acidosis. Hypochloremia, normochloremia, and hyperchloremia were observed in 8.9% (14/157), 43.3% (68/157), and 47.8% (68/157), respectively, of diarrheic calves with metabolic acidosis. This distribution remained similar regardless of age (under 8 days or 8 days and older). Furthermore, a multiple logistic regression analysis showed that variations in values for blood sodium [Na (regression coefficients 0.877; 95% confidence interval (CI) 13.977-134.195; P<0.01)], pH (regression coefficients -10.719; 95% CI -19.076- -2.362; P<0.05), and bicarbonate [HCO3- (regression coefficients -0.555; 95% CI -0.820- -0.290; P<0.01)] were associated with blood Cl abnormalities. The present results revealed that blood Na concentrations were more strongly associated with blood Cl concentrations than blood pH and HCO3- values. In the present study, diarrheic calves with hyperchloremia were characterized by normonatremia and extremely severe metabolic acidosis.

Metabolic acidosis is a frequent complication of chronic kidney disease and is associated with a number of adverse outcomes, including worsening kidney function, poor musculoskeletal health, cardiovascular events, and death. Mechanisms that prevent metabolic acidosis detrimentally promote further kidney damage, creating a cycle between acid accumulation and acid-mediated kidney injury. Disrupting this cycle through the provision of alkali, most commonly using sodium bicarbonate, is hypothesized to preserve kidney function while also mitigating adverse effects of excess acid on bone and muscle. However, results from clinical trials have been conflicting. There is also significant interest to determine whether sodium bicarbonate might improve patient outcomes for those who do not have overt metabolic acidosis. Such individuals are hypothesized to be experiencing acid-mediated organ damage despite having a normal serum bicarbonate concentration, a state often referred to as subclinical metabolic acidosis. Results from small- to medium-sized trials in individuals with subclinical metabolic acidosis have also been inconclusive. Well-powered clinical trials to determine the efficacy and safety of sodium bicarbonate are necessary to determine if this intervention improves patient outcomes.