UNASSIGNED: The hydrogen ion (H+) mobilization model has been previously shown to provide a quantitative description of intradialytic changes in blood bicarbonate (HCO3) concentration during hemodialysis (HD). The current study evaluated the accuracy of different methods for estimating the H+ mobilization parameter (Hm) from this model.
UNASSIGNED: The study compared estimates of the H+ mobilization parameter using predialysis, hourly during the HD treatment, and postdialysis blood HCO3 concentrations (Hm-full2) with those determined using only predialysis and postdialysis blood HCO3 concentrations assuming steady state conditions (Hm-SS2) during the midweek treatment in 24 chronic HD patients treated thrice weekly.
UNASSIGNED: Estimated Hm-full2 values (0.163 ± 0.079 L/min [mean ± standard deviation]) were higher than, but not statistically different (p = 0.067) from, those of Hm-SS2 (0.152 ± 0.065 L/min); the values of Hm-full2 and Hm-SS2 were highly correlated with a correlation coefficient of 0.948 and a mean difference that was small (0.011 L/min). Further, the H+ mobilization parameter values calculated using only predialysis and postdialysis blood HCO3 concentrations during the first and third HD treatments of the week were not different from those calculated during the midweek treatment.
UNASSIGNED: The H+ mobilization model can be used to provide estimates of the H+ mobilization parameter without the need to measure hourly intradialytic blood HCO3 concentrations.

We determined the association between urine pH and blood acid-base indicators and assessed a urine pH cut-off value to predict severe metabolic acidosis under field conditions in cows fed acidogenic diets. Eighty-six cows were sampled for urine and blood. Urine pH was evaluated immediately after collection, and blood acid-base status was evaluated within 2 hours of collection using a portable blood analyzer. Twenty-five cows were classified as having severe metabolic acidosis (blood pH ≤ 7.4; bicarbonate < 24 mmol/L, base excess ≤ -0.5; PCO2 low to normal concentrations and urine pH between 4.88 and 5.71. There was a positive linear association between urine pH and blood pH (r = 0.46), and between urine pH and base excess (r = 0.74). The area under the ROC curve was 0.91 (CI 95 %= 0.84-0.96; good-excellent test). The optimal cut-off value for urine pH to categorize a cow with severe metabolic acidosis was 5.5 (94 % specificity and 72 % sensitivity). For each 0.1 unit of decrease in urine pH below 5.5, cows were 1.6 times (95 % CI= 1.3-2.1) more likely to exhibit a severe metabolic acidosis. We conclude that a urine pH of 5.5 or less is indicative of more life-threatening metabolic acidosis in dairy cows.

The new ligand 3,3\'-bis(((2-(3,6,9-triaza-1(2,6)-pyridinacyclodecaphane-6-yl)ethyl)amino)methyl)-[1,1\'-biphenyl]-2,2\'-diol (L) has been synthesized and characterized. It contains two pyridinacyclophane macrocycles spaced by a 2,2\'-biphenol moiety. The acid-base behaviour of L as well as its binding properties towards Zn2+ ion have been investigated. This work is inserted in the field of fluorescent ditopic receptors, formed by two polyamines spaced by a aromatic fragments. This ligand represents a new example of a peculiar case of polyamine fluorescent receptor in which the interaction with Zn2+ is translated into a deactivation of the emission. Enough data to describe and explain this unusual behaviour was obtained through potentiometric, UV-Vis, fluorescence and NMR titrations as well as theoretical calculations. This studies have shown that the metal cation is indirectly affecting the emission favouring a conformation in which the fluorophore is at stacking distance from the electron poor pyridine moieties. This gives rise to an oxidative photoinduced electron transfer from the excited state of the fluorophore to the electron-poor Zn2+ coordined pyridine.

Acid-base disorders are currently analyzed and treated using a bicarbonate-centered approach derived from blood studies prior to the advent of digital computers, which could solve computer models capable of quantifying the complex physicochemical nature governing distribution of water and ions between fluid compartments. An alternative is the Stewart approach, which can predict the pH of a simple mixture of ions and electrically charged proteins; hence, the role of extravascular fluids has been largely ignored. The present study uses a new, comprehensive computer model of four major fluid compartments, based on a recent blood model, which included ion binding to proteins, electroneutrality constraints, and other essential physicochemical laws. The present model predicts quantitative respiratory acid-base buffering behavior in the whole body, as well as determining roles of each compartment and their species, particularly compartmental electrically charged proteins, largely responsible for buffering. The model tested an early theory that H+ was conserved in the body fluids; hence, when changing Pco2 states, intracellular buffering could be predicted by net changes in bicarbonate and protein electrical charge in the remaining fluids. Even though H+ is not conserved in the model, the theory held in simulated respiratory disorders. Model results also agreed with a second part of the theory, that ion movements between cells and interstitial fluid were linked with H+ buffering, but by electroneutrality constraints, not necessarily by some membrane-related mechanisms, and that the strong ion difference (SID), an amalgamation of ionic electrical charges, was approximately conserved when going between equilibrium states caused by Pco2 changes in the body-fluid system.NEW & NOTEWORTHY For the first time, a physicochemically based, whole body, four-compartment, computer model was used to study respiratory whole body acid-base buffering. An improved approach to quantify acid-base buffering, previously used by this author, was able to determine contributions of the various compartmental fluids to whole body buffering. The model was used to test, for the first time, three fundamental theories of whole body acid-base homeostasis, namely, H+-conservation, its linkage to ion transport, and strong ion difference conservation.

BACKGROUND: Evidence indicating the optimal treatment protocol for dogs in adrenal crisis is lacking.
OBJECTIVE: Compare outcomes of dogs presented in adrenal crisis treated with either hydrocortisone (HC) continuous rate infusion (CRI) or intermittent dexamethasone (DEX) administration.
METHODS: Thirty-nine client-owned dogs.
METHODS: Multi-institutional retrospective observational study (July 2016-May 2022) including dogs diagnosed with adrenal crisis and with available sequential blood work during hospitalization. Dogs were excluded if already on treatment with exogenous corticosteroids. Outcomes assessed included duration of hospitalization, survival, number of repeat measurements of electrolyte concentrations, and time to normalization of electrolyte and acid-base status.
RESULTS: No significant difference was found between the groups for hospitalization time (P = .41; HC median [range] 48 h [19-105 h]; DEX 57 h [17-167 h]) nor case fatality rate 2/28 in the DEX group and 0/11 in the HC group (P = 1), nor in number of measurements of electrolyte concentrations (P = .90; HC 4 [2-10]; DEX 4.5 [2-15]). No significant differences were found between the 2 treatment groups in time to normalization of serum Na (P = .30; HC 33 h [7-66 h]; DEX 16 h [1.5-48 h]), K (P = .92; HC 17 h [4-48 h]; DEX 16 h [1.25-60 h]) or Na/K ratio (P = .08; HC 17 h [8-48 h]; DEX 26 h [1.5-60 h]).
CONCLUSIONS: This study detected no difference in outcomes for dogs in adrenal crisis treated with either DEX boluses or HC CRIs.

BACKGROUND: Disruption of acid-base homeostasis can lead to many clinical problems. Ammonia excretion by the kidneys is critical to maintaining acid-base homeostasis through bicarbonate production. Measurement of ammonia excretion may help determine if the kidneys are properly functioning in maintaining acid-base balance. Reference intervals are essential tools for clinical decision-making but do not currently exist for urinary ammonia-to-creatinine ratio (UACR) in feline patients.
OBJECTIVE: This study aimed to generate a reference interval (RI) for UACR in healthy adult cats.
METHODS: The study used samples from client-owned adult healthy cats that presented to the University of Florida Primary Care and Dentistry service (n = 92). Physical examination, serum biochemistry, urinalysis, urine ammonia, and creatinine concentrations were measured. Cats were excluded if there were significant abnormalities in their urinalysis or biochemistry panel. The RI for UACR was calculated according to the recommendation of the American Society for Veterinary Clinical Pathology. The UACR was evaluated for correlation with serum bicarbonate, weight, age, and sex.
RESULTS: The RI for UACR was 3.4-20.7 with 90% confidence intervals for the lower and upper limits of (3.0-3.7) and (16.0-23.7), respectively. No significant correlation with age, sex, or weight was found. There was no discernable relationship between serum bicarbonate and UACR.
CONCLUSIONS: Establishing an RI for UACR in healthy adult cats will allow further studies to determine if changes in UACR are observed during specific disease states.

Perioperative acid-base disturbance could be informative regarding the possible slow graft function (SGF) or delayed graft function (DGF) development. There is a lack of data regarding the relationship between perioperative acid-base parameters and graft dysfunction in kidney transplant (KT) recipients. We aim to determine the incidence of graft dysfunction types and the association between them and acid-base parameters. We performed a prospective, cohort study on 54 adults, KT recipients, between 1st of January 2019 and 31st of December 2019. Graft function was defined and classified in three categories: immediate graft function (IGF) (serum creatinine < 3 mg/dL at day 5 after KT), SGF (serum creatinine ≥ 3mg/dL at day 5 or ≥ 2.5mg dL at day 7 after KT) and DGF (the need for at least one dialysis treatment in the first week after kidney transplantation). Among the 54 KT recipients, the incidence of SGF and DGF was 13% and 11.1%, respectively. SGF was significantly associated with lower intraoperative pH (7.26± 0.05 vs 7.35± 0.06, p= 0.004), preoperative and intraoperative base excess (BE) [-7.0 (-10.0 ߝ -6.0) vs -3.4 (-7.8 ߝ - 2.1) mmol/L, p= 0.04 and -10.3 (-11.0 ߝ -9.1) vs -4.0 (-6.3 ߝ - 3.0) mmol/L, p= 0.002, respectively] and serum bicarbonate (HCO3-) (16.0± 2.7 vs 19.3± 3.4 mmol/L, p= 0.01 and 14.1± 1.9 vs 18.8± 3.2 mmol/L, p= 0.002 respectively), compared to IGF. DGF was significantly associated with lower intraoperative values of pH (7.27± 0.05 vs 7.35± 0.06, p= 0.003), BE [-7.1 (-10.9 ߝ -6.1) vs -4.0 (-6.3 ߝ - 3.0) mmol/L, p= 0.02] and HCO3- (15.9± 2.4 vs 18.8± 3.2 mmol/L, p=0.02) compared to IGF. No differences were observed between SGF and DGF patients in any of the perioperative acid-base parameters. In conclusion we found that kidney graft dysfunction types are associated with perioperative acid-base parameters and perioperative metabolic acidosis could provide important information to predict SGF or DGF occurrence.

Individuals with liver disease are susceptible to pathophysiological derangements that lead to kidney dysfunction. Patients with advanced cirrhosis and acute liver failure (ALF) are at risk of developing acute kidney injury (AKI). Hepatorenal syndrome type 1 (HRS-1, also called HRS-AKI) constitutes a form of AKI unique to the state of cirrhosis and portal hypertension. Although HRS-1 is a condition primarily characterized by marked renal vasoconstriction and kidney hypoperfusion, other pathogenic processes, such as acute tubular injury and renal vein congestion, can overlap and further complicate the course of HRS-1. ALF can lead to AKI through mechanisms that involve systemic inflammation, direct drug toxicity, or bile acid-induced tubulopathy. In addition, the growing prevalence of nonalcoholic steatohepatitis is changing the spectrum of chronic kidney disease in cirrhosis. In this installment of AJKD\'s Core Curriculum in Nephrology, we explore the underpinnings of how cirrhosis, ALF, acute cholestasis, and post-liver transplantation can be associated with various forms of acute, subacute, or chronic kidney diseases. We navigate through the recommended therapies for each condition, including supportive care, pharmacological interventions, kidney replacement therapy, and organ transplantation. Finally, key acid-base and electrolyte disorders associated with hepatobiliary disease are also summarized.

The development of acidosis in critically ill patients is considered to be a negative prognostic factor, and when extreme, even incompatible with life. We aimed to test the prognosis of patients with a pH lower than 6.9 on emergency department admission.
A retrospective cohort study in adult patients admitted to two emergency departments with a pH < 6.9 during the first 12 h of admission. Primary outcome was mortality within 24 h from emergency department admission. We performed a regression analysis of clinical and laboratory data in order to identify factors associated with mortality in this population.
We analyzed data of 206 admissions to the emergency departments between 2008 and 2018 with extreme acidosis. pH Values ranged from 6.898 to 6.35 (mean 6.8 and median 6.83). 60 (29%) of the patients survived the first 24 h. 35 patients (58%) of those also survived to hospital discharge, and of them 80% have returned to their previous functional status. Patient\'s age, type of acidosis, cardio-pulmonary resuscitation on arrival, and diagnosis on admission were correlated with survival.
A small but significant portion of patients with extreme acidosis on emergency department admission survive at least to 24 h and until hospital discharge. The clinical decision making should be based on other prognostic factors rather than pH value by itself.

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