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Diabetic Ketoacidosis
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Routine sodium bicarbonate administration for DKA is not recommended for venous pH ≥6.9 since no benefit in DKA reversal or outcomes has been demonstrated [1, 8–10]. This point is controversial, however, and conditions of diminished cardiac contractility, impaired catecholamine response, dysrhythmias, or severe renal dysfunction may support its use. Some advocate that if, following DKA resolution, a hyperchloremic, non-anion gap metabolic acidosis exists, then sodium bicarbonate infusion should be instituted to hasten replenishment of serum bicarbonate and restore acid-base homeostasis. When implemented, recommendations are for an isotonic solution of 100 mEq sodium bicarbonate (2 ampules 8.4%) in 400 mL sterile water [1], administered over 1–2 hours. Potassium chloride should be added or supplemented when potassium is ≤5.3 mEq/L.
Endogenous Activation and Neurophysiological Functions of Acid-Sensing Ion Channels
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Wei-Zheng Zeng, Yi-Zhi Wang, Tian-Le Xu
Various metabolic reactions such as glycolysis in the cytoplasm and ATP production in mitochondria generate acidic species (11). Metabolic acidosis occurs when either a net increase in the production of nonvolatile acidic species or a loss of bicarbonate from the body overwhelms the mechanisms that regulate acid-base homeostasis, which is referred to as acute or chronic metabolic acidosis, respectively (18). Acute metabolic acidosis, which mainly consists of diabetic ketoacidosis and lactic acidosis (18), most likely results in local acidification that activates ASICs. Extensive studies have identified several endogenous proton sources that act on ASICs. However, more information is needed to clarify the regulation of proton sources during acidosis in the future.
Alternative Tumor-Targeting Strategies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
There is evidence that some tumor microenvironments have a lower pH compared to healthy tissues, as acid-base homeostasis in tumor cells can be perturbed. This has been attributed to increased glucose catabolism resulting in higher levels of lactic acid. However, although tumor cells have a higher level of acid production, they attempt to maintain a normal or alkaline pH relative to normal cells by transporting lactate outside of the cells where it is not cleared as effectively as it would be in healthy tissues due to the poor vasculature and lack of lymphatic drainage. Therefore, due to the limited buffering capacity of the extracellular space, this environment becomes acidic. Tumor cells appear to be able to adapt to this, and in vitro studies have shown that maximum proliferation of some tumor cell types occurs at pH 6.8 compared to the pH 7.3 preferred by healthy cells. Therapeutic approaches have been designed to target this low tumor pH either through pH-activated prodrugs or the pH-triggered release of anticancer agents from nanoparticles, two examples of which are described below.
Utilization of interpretable machine learning model to forecast the risk of major adverse kidney events in elderly patients in critical care
Published in Renal Failure, 2023
Lin Wang, Shao-Bin Duan, Ping Yan, Xiao-Qin Luo, Ning-Ya Zhang
In this study, we utilized the SHAP method to enhance the interpretability of the XGBoost model and identified several key factors that contribute to the risk of MAKE 30 in elderly patients in the ICU. Our analysis identified low platelet count, high baseline estimated glomerular filtration rate, and SOFA score as high-risk factors for MAKE30, which have been previously implicated in the construction of prognostic models for adverse renal outcomes in other populations [3,8,16,17]. Our findings revealed that various demographic and physiological factors, including the APACHE II score, serum creatinine and BUN levels, and SOFA score, are positively associated with the risk of MAKE30. These results suggest that the physiological health status of patients at ICU admission can predict adverse renal outcomes within 30 d. Additionally, our analysis showed that low levels of ‘Arterial blood HCO3’ were linked to a high risk of MAKE30. This may be due to renal compensatory mechanisms for maintaining normal acid-base homeostasis, leading to further renal injury in patients. For example, up-regulating renal endocrine hormones such as angiotensin II, aldosterone, and endothelin-1 by kidney promote renal injury, inflammation, and fibrosis [39,40]. The presence of metabolic acidosis, as indicated by low HCO3- levels, may reflect tubular interstitial disease and poor renal function, leading to an increased risk of AKI [41]. Previous retrospective cohort studies have confirmed this association, and the use of sodium bicarbonate infusion has been explored as a potential intervention to improve kidney and survival outcomes [25,42].
Basic demographic characteristics and prevalence of comorbidities in acute mesenteric ischemia: a systematic review and proportional meta-analysis
Published in Scandinavian Journal of Gastroenterology, 2023
Wenhan Wu, Jia He, Shijian Zhang, Changtong Zeng, Qifa Wang
Surprisingly, the proportion of AMI with kidney disease, chronic kidney disease, and renal failure were also 17.5%, 15.3%, and 14.8%, respectively. This phenomenon appears to be more pronounced in NOMI patients. Numerous studies have demonstrated that chronic kidney disease is at higher risk for perioperative mortality and adverse outcomes [119–121]. This may be related to cardiovascular function, electrolyte and acid-base homeostasis, erythropoiesis, coagulation, and bone metabolism. Fluid management to prevent fluid overload and hypovolemia remains one of the most significant challenges for AMI patients with renal disease. Besides, correction of anemia and the correct use of anesthetics and analgesics during surgery may also minimize unnecessary side effects and thus improve patient outcomes.
Emerging sodium-glucose cotransporter-2 inhibitor therapies for managing heart failure in patients with chronic kidney disease
Published in Expert Opinion on Pharmacotherapy, 2023
Jeffrey Shi Kai Chan, Francesco Perone, Yasmin Bayatpoor, Gary Tse, Amer Harky
In terms of safety, a particularly important and infamous potential adverse effect of SGLT2 inhibitors is ketoacidosis, although it has been shown consistently to be uncommon, with reported incidence rates of 0.6–2.2 events per 1000 person-years [90]. SGLT2 inhibitors have been specifically reported to be associated with the occurrence of euglycaemic diabetic ketoacidosis, an even rarer condition [91]. The Food and Drug Administration labels of both dapagliflozin and empagliflozin recommended withholding these medications for at least three days prior to major surgeries and cautioned their use in the presence of other predisposing factors for ketoacidosis. Although no direct evidence specific to patients with both HF and CKD exists in this regard, CKD is likely to adversely affect acid-base homeostasis, and there does not seem to be any plausible mechanism in which the risks of ketoacidosis would be lower in these patients. It would thus be reasonable to adhere closely to the above recommendations, including temporary withholding of SGLT2 inhibitors in patients with HF and CKD during acute illnesses or other predisposing conditions until the acute physiological stress has subsided.