Explore the vast range of titles available.

Metabolic acidosis can lead to inflammation, tissue damage, and cancer metastasis. Dietary acid load contributes to metabolic acidosis if endogenous acid–base balance is not properly regulated. Breast cancer survivors have reduced capacities to adjust their acid–base balance; yet, the associations between dietary acid load and inflammation and hyperglycemia have not been examined among them. We analyzed data collected from 3042 breast cancer survivors enrolled in the Women’s Healthy Eating and Living (WHEL) Study who had provided detailed dietary intakes and measurements of plasma C-reactive protein (CRP) and hemoglobin A1c (HbA1c). Using a cross-sectional design, we found positive associations between dietary acid load and plasma CRP and HbA1c. In the multivariable-adjusted models, compared to women with the lowest quartile, the intakes of dietary acid load among women with the highest quartile showed 30–33% increases of CRP and 6–9% increases of HbA1c. Our study is the first to demonstrate positive associations between dietary acid load and CRP and HbA1c in breast cancer survivors. Our study identifies a novel dietary factor that may lead to inflammation and hyperglycemia, both of which are strong risk factors for breast cancer recurrence and comorbidities.

Background Correction of metabolic acidosis (MA) with nutritional therapy or bicarbonate administration is widely used in chronic kidney disease (CKD) patients. However, it is unknown whether these interventions reduce insulin resistance (IR) in diabetic patients with CKD. We sought to evaluate the effect of MA correction on endogenous insulin action in diabetic type 2 (DM2) CKD patients. Methods A total of 145 CKD subjects (83 men e 62 women) with DM2 treated with oral antidiabetic drugs were included in the study and followed up to 1 year. All patients were randomly assigned 1:1 to either open-label (A) oral bicarbonate to achieve serum bicarbonate levels of 24–28 mmol/L (treatment group) or (B) no treatment (control group). The Homeostatic model assessment (HOMA) index was used to evaluate IR at study inception and conclusion. Parametric and non-parametric tests as well as linear regression were used. Results At baseline no differences in demographic and clinical characteristics between the two groups was observed. Average dose of bicarbonate in the treatment group was 0.7 ± 0.2 mmol/kg. Treated patients showed a better metabolic control as confirmed by lower insulin levels (13.4 ± 5.2 vs 19.9 ± 6.3; for treated and control subjects respectively; p  < 0.001), Homa-IR (5.9[5.0-7.0] vs 6.3[5.3–8.2]; p  = 0.01) and need for oral antidiabetic drugs. The serum bicarbonate and HOMA-IR relationship was non-linear and the largest HOMA-IR reduction was noted for serum bicarbonate levels between 24 and 28 mmol/l. Adjustment for confounders, suggests that serum bicarbonate rather than treatment drives the effect on HOMA-IR. Conclusions Serum bicarbonate is related to IR and the largest HOMA-IR reduction is noted for serum bicarbonate between 24 and 28 mmol/l. Treatment with bicarbonate influences IR. However, changes in serum bicarbonate explains the effect of treatment on HOMA index. Future efforts are required to validate these results in diabetic and non-diabetic CKD patients. Trial registration The trial was registered at www.clinicaltrial.gov (Use of Bicarbonate in Chronic Renal Insufficiency (UBI) study - NCT01640119 )

Background Globally, the prevalence of chronic kidney disease (CKD) is higher in women than in men; however, women have been historically under-represented in nephrology clinical trials. Metabolic acidosis increases risk of progressive loss of kidney function, causes bone demineralization and muscle protein catabolism, and may be more consequential in women given their lower bone and muscle mass. Veverimer, an investigational, non-absorbed polymer that binds and removes gastrointestinal hydrochloric acid, is being developed as treatment for metabolic acidosis. Methods This was a Phase 3, multicenter, randomised, blinded, placebo-controlled trial in 196 patients with CKD (eGFR: 20–40 mL/min/1.73 m 2 ) and metabolic acidosis who were treated for up to 1 year with veverimer or placebo. We present the findings from a pre-specified subgroup analysis evaluating the effects of veverimer on metabolic acidosis and physical function among women ( N  = 77) enrolled in this trial. Results At week 52, women treated with veverimer had a greater increase in mean (± standard error) serum bicarbonate than the placebo group (5.4 [0.5] vs. 2.2 [0.6] mmol/L; P  < 0.0001). Physical Function reported by patients on the Kidney Disease and Quality of Life – Physical Function Domain, a measure that includes items related to walking, stair climbing, carrying groceries and other activities improved significantly in women randomized to veverimer vs placebo (+ 13.2 vs. -5.2, respectively, P  < 0.0031). Objectively measured performance time on the repeated chair stand test also improved significantly in the veverimer group vs. placebo ( P  = 0.0002). Conclusions Veverimer was effective in treating metabolic acidosis in women with CKD, and significantly improved how they felt and functioned. Trial registration ClinicalTrials.gov Identifier: NCT03390842 . Registered on January 4, 2018.

Aims Cardiovascular (CV) complications are common in chronic kidney disease (CKD). Numerous metabolic disturbances including hyperphosphatemia, high circulating calciprotein particles (CPP), hyperparathyroidism, metabolic acidosis, and magnesium deficiency are associated with, and likely pathogenic for CV complications in CKD. The goal of this feasibility study was to determine whether effervescent calcium magnesium citrate (EffCaMgCit) ameliorates the aforementioned pathogenic intermediates. Methods Nine patients with Stage 3 and nine patients with Stage 5D CKD underwent a randomized crossover study, where they took EffCaMgCit three times daily for 7 days in one phase, and a conventional phosphorus binder calcium acetate (CaAc) three times daily for 7 days in the other phase. Two-hour postprandial blood samples were obtained on the day before and on the 7th day of treatment. Results In Stage 5D CKD, EffCaMgCit significantly increased T50 (half time for conversion of primary to secondary CPP) from baseline by 63% ( P  = 0.013), coincident with statistically non-significant declines in serum phosphorus by 25% and in saturation of octacalcium phosphate by 35%; CaAc did not change T50. In Stage 3 CKD, neither EffCaMgCit nor CaAc altered T50. With EffCaMgCit, a significant increase in plasma citrate was accompanied by statistically non-significant increase in serum Mg and phosphate. CaAc was without effect in any of these parameters in Stage 3 CKD. In both Stages 3 and 5D, both drugs significantly reduced serum parathyroid hormone. Only EffCaMgCit significantly increased serum bicarbonate by 3 mM ( P  = 0.015) in Stage 5D. Conclusions In Stage 5D, EffCaMgCit inhibited formation of CPP, suppressed PTH, and conferred magnesium and alkali loads. These effects were unique, since they were not observed with CaAc. In Stage 3 CKD, neither of the regimens have any effect. These metabolic changes suggest that EffCaMgCit might be useful in protecting against cardiovascular complications of CKD by ameliorating pathobiologic intermediates.

Background Sodium bicarbonate is commonly used to correct metabolic acidosis in pediatric patients, yet its efficacy remains controversial. This study aims to assess its effectiveness in treating non-lactic and lactic metabolic acidosis and its impact at various chloride levels. Methods A retrospective cohort study was conducted by screening pediatric patients diagnosed with metabolic acidosis from a paediatric intensive care database. Patients were categorized into two groups: lactate patients (lactate > 2.0 mmol/L) and non-lactate patients (lactate ≤ 2.0 mmol/L). The risk of death in patients who received sodium bicarbonate was assessed. Results Sodium bicarbonate treatment did not significantly affect in-hospital mortality in either overall lactate patients or non-lactate patients, with adjusted OR of 1.044 (95% CI: 0.829–1.315, p  = 0.714) and 0.838 (95% CI: 0.548–1.281, p  = 0.414), respectively. In lactate patients, those receiving sodium bicarbonate had a higher risk of in-hospital death when chloride was < 107 mmol/L (adjusted OR = 2.195, 95% CI: 1.536–3.135, p  < 0.001), whereas the risk of in-hospital death decreased when chloride was ≥ 113 mmol/L (adjusted OR = 0.365, 95% CI: 0.217–0.614, p  < 0.001). Similar findings were observed in non-lactate patients. Conclusions Sodium bicarbonate treatment does not improve the survival of pediatric patients with lactate or non-lactate metabolic acidosis. However, it can reduce the odds of mortality in pediatric patients with hyperchloremia, regardless of their lactate levels. Prospective studies are needed to further confirm these findings.

Background Overt chronic metabolic acidosis in patients with chronic kidney disease develops after a drop of glomerular filtration rate to less than approximately 25 mL/min/1.73 m 2 . The pathogenic mechanism seems to be a lack of tubular bicarbonate production, which in healthy individuals neutralizes the acid net production. As shown in several animal and human studies the acidotic milieu alters bone and vitamin D metabolism, induces muscle wasting, and impairs albumin synthesis, aside from a direct alteration of renal tissue by increasing angiotensin II, aldosteron and endothelin kidney levels. Subsequent studies testing various therapeutic approaches in very selected study populations showed that oral supplementation of the lacking bicarbonate halts progression of decline of renal function. However, due to methodological limitations of these studies further investigations are of urgent need to ensure the validity of this therapeutic concept. Methods/Design The SoBic-study is a single-center, randomized, controlled, open-label clinical phase IV study performed at the nephrological outpatient service of the Medical University of Vienna. Two-hundred patients classified to CKD stage 3 or 4 with two separate measurements of HCO 3 - of <21 mmol/L will be 1:1 randomized to either receive a high dose of oral sodium bicarbonate with a serum target HCO 3 - level of 24 ± 1 mmol/L or receive a rescue therapy of sodium bicarbonate with a serum target level of 20 ± 1 mmol/L. The follow up will be for two years.The primary outcome is the effect of sodium bicarbonate supplementation on renal function measured by means of estimated glomerular filtration rates (4-variable-MDRD-equation) after two years. Secondary outcomes are change in markers of bone metabolism between groups, death rates between groups, and the number of subjects proceeding to renal replacement therapy across groups. Adverse events, such as worsening of arterial hypertension due to the additional sodium consumption, will be accurately monitored. Discussion We hypothesize that sufficiently balanced acid–base homeostasis leads to a reduction of decline of renal function in patients with chronic kidney disease. The concept of an exogenous bicarbonate supplementation to substitute the lacking endogenous bicarbonate has existed for a long time,but has never been investigated sufficiently to state clear treatment guidelines. Trial registration EUDRACT Number: 2012-001824-36

Background Hyperuricemia and metabolic acidosis have emerged as important risk factors for progression of kidney disease. In this study, we aimed to investigate the effects of allopurinol on metabolic acidosis and endothelial functions in hyperuricemic stage 2–4 chronic kidney disease (CKD) patients. Methods Thirty patients with stage 2–4 CKD and serum uric acid levels over 5.5 mg/dl were included in the study group. They were prescribed 300 mg/day per oral allopurinol treatment for three months. Age- and gender-matched CKD patients ( n  = 30) with similar clinical characteristics were taken as the control group and were not given allopurinol treatment. Endothelial functions were measured via flow-mediated dilatation (∆FMD %) over the forearm. pH and HCO 3 levels in venous blood, Cr clearance and proteinuria levels were calculated in all patients at baseline and in the third month. Results Serum uric acid levels significantly decreased in the study group from 7.9 ± 1.6 to 6.4 ± 1.7 ( p  < 0.001). Cr clearance (from 43.4 ± 20.1 to 51.4 ± 24.9, p  = 0.011), serum bicarbonate levels (from 21.4 ± 3.4 to 23.0 ± 3.4, p  = 0.007) and ΔFMD % values (from 5.8 ± 2.5 to 6.2 ± 2.7, p  = 0.006) increased significantly in the allopurinol group. There were no significant changes except for ∆FMD % values (decreased from 6.27 ± 1.62 to 5.71 ± 1.90, p  = 0.005) in the control group. ∆FMD % variations within the two groups were clearly significant in the repeated ANOVA general linear model. Conclusion We assume that decreasing uric acid levels with allopurinol treatment seems to be helpful in restoring endothelial functions, preventing metabolic acidosis and slowing down the progression of CKD.

Keywords * VA-ECMO * eCPR * Survival * Carbon dioxide * paCO2 * pH Establishing a venoarterial extracorporeal membrane oxygenation (vaECMO) in cardiac arrest is known as extracorporeal cardiopulmonary resuscitation (eCPR). Being a retrospective, observational, single-center study, inherent limitations and biases are to be presumed and findings are to be considered hypothesis generating. [...]data are available however, it might be reasonable to correct both respiratory and metabolic acidosis in eCPR patients. Prognostic factors for extracorporeal cardiopulmonary resuscitation recipients following out-of-hospital refractory cardiac arrest.

Background This study aims to investigate the effects of a modified, balanced crystalloid including phosphate in a perioperative setting in order to maintain a stable electrolyte and acid-base homeostasis in the patient. Methods/design This is a single-centre, open-label, randomized controlled trial involving two parallel groups of female patients comparing a perioperative infusion regime with sodium glycerophosphate and Jonosteril® (treatment group) or Jonosteril® (comparator) alone. The primary endpoint is to maintain a stable concentration of weak acids [A - ] according to the Stewart approach of acid-base balance. Secondary endpoints are measurement of serum phosphate levels, other acid-base parameters such as the strong ion difference (SID), the onset and severity of postoperative nausea and vomiting (PONV), electrolyte levels and their excretion in the urine, monitoring of renal function and glycocalyx components, haemodynamics, amounts of catecholamines and other vasopressors used and the safety of the infusion regime. Discussion Perioperative fluid replacement with the use of currently available crystalloid preparations still fail to maintain a stable acid-base balance and experts agree that common balanced solutions are still not ideal. This study aims to investigate the effectivity and safety of a new crystalloid solution by adding sodium glycerophosphate to a standardized crystalloid preparation in order to maintain a balanced perioperative acid-base homeostasis. Trial registration EudraCT number 201002422520 . Registered on 30 November 2010.

Purpose To evaluate the necessity of chronic alkali therapy in non-complicated orthotopic ileal neobladders with normal renal function. Materials and methods This is a prospective study that included 200 male patients who underwent radical cystectomy and ileal W neobladder for invasive bladder carcinoma between January 1993 and December 2013. The studied patients included 100 consecutive patients who were maintained on regular alkali therapy since surgery and 100 consecutive patients who stopped the use of alkali treatment after initial 3 months postoperative with minimum postoperative observation time of 1 year. All patients had satisfactory function of the reservoirs with normal upper tract. The patients were subjected to blood analysis for creatnine, electrolytes, pH and bicarbonate and urine chemical analysis. The study also included 40 healthy male age-matched volunteers who served as a control group. Results Both groups were comparable as regard age, BMI, follow-up period and surgical technique. There were no significant differences between both groups as regard serum creatnine, electrolytes blood pH and bicarbonate and the mean values were within normal range; however, the neobladder patients are still toward the acidotic side in comparison to healthy volunteers. Also there were no significant differences between both groups of patients as regard urine pH and excretion of electrolytes, calcium, phosphorus and creatnine. Conclusion Patients with non-complicated ileal neobladders with normal upper tract who were not maintained on alkali prophylaxis for long period have a compensated acid base status. Therefore, the prolonged alkali prophylaxis is not mandatory.