sodium-bicarbonate and Chronic-Disease

Hyperkalemia is a common problem in both inpatients and outpatients. Many disease states (eg, chronic kidney disease) and medications may precipitate hyperkalemia. There are several drugs now available to treat hyperkalemia. Many of these drugs are relatively new. This review provides information regarding drug-induced causes of hyperkalemia and provides detailed information on the medications used to treat this problem.

Topics: Acute Disease; Administration, Intravenous; Adrenergic beta-Agonists; Arrhythmias, Cardiac; Calcium; Cation Exchange Resins; Chronic Disease; Electrocardiography; Glucose; Humans; Hyperkalemia; Hypoglycemia; Hypoglycemic Agents; Insulin; Polymers; Polystyrenes; Potassium; Silicates; Sodium Bicarbonate; Sodium Potassium Chloride Symporter Inhibitors

Chronic metabolic acidosis is a common complication of chronic kidney disease (CKD) and is associated with adverse consequences, such as CKD progression and muscle wasting. We review the findings from recent clinical trials that have examined the effects of sodium bicarbonate therapy and veverimer in patients with CKD and chronic metabolic acidosis.. There are four recent clinical trials on chronic metabolic acidosis of CKD. In a pilot, cross-over study, 6 weeks of sodium bicarbonate therapy improved vascular endothelial function, measured by brachial artery flow-mediated dilation. In a single-center, randomized, open-label study, 6 months of sodium bicarbonate therapy increased muscle mass and lean body mass, and preserved kidney function. The other two clinical trials (phase 1/2 and phase 3 studies) examined the effects of veverimer, which is a hydrochloric acid binder. The phase 3 study showed that 12-weeks of veverimer increased serum bicarbonate levels and might improve physical function. The effects of veverimer on CKD progression, physical function and cardiovascular endpoints as well as its long-term safety are yet to be determined.. Recent studies suggest that sodium bicarbonate therapy may improve vascular endothelial function and muscle mass, and preserve renal function. Veverimer increases serum bicarbonate level and could be a potential new therapeutic option for treating chronic metabolic acidosis.

Topics: Acidosis; Chronic Disease; Clinical Trials as Topic; Humans; Polymers; Renal Insufficiency, Chronic; Sodium Bicarbonate

The combined prophylactic strategy of sodium bicarbonate plus N-acetylsyteine (NAC) seems to be effective in preventing contrast induced acute kidney injury (CI-AKI) in patients at low-to-medium risk. However, in patients at high and very high risk the rate of CI-AKI is still high. In this subset of patients the anticipated advantages of the RenalGuard(tm) System should be investigated. The RenalGuard(tm) System (PLC Medical Systems, Inc., Franklin, MA, USA) is a real-time measurement and real time matched fluid replacement device designed to accommodate the RenalGuard therapy, which is based on the theory that creating and maintaining a high urine output is beneficial by allowing a quick elimination of contrast media, and, therefore, reducing its toxic effects.. The REMEDIAL II trial is a randomised, multicentre, investigator-sponsored trial addressing the hypothesis that the RenalGuard System is superior to the prophylaxis with sodium bicarbonate infusion plus NAC in preventing CI-AKI in high and very high risk patients. Consecutive patients with chronic kidney disease (CKD) and at high to very high risk for CI-AKI, referred to our institutions for coronary and/or peripheral procedures, will be randomly assigned to 1) prophylactic administration of sodium bicarbonate plus NAC (control group) and 2) RenalGuard System treatment (RenalGuard group). All enrolled patients must have an estimated glomerular filtration rate ≤ 30 ml/min/1.73 m2 and/or a contrast nephropathy risk score ≥ 11. In all cases iodixanol (an iso-osmolar, non-ionic contrast agent) will be administered. The primary endpoint is an increase of ≥ 0.3 mg/dL in the serum creatinine concentration 48 hours after the procedure.. The REMEDIAL II trial will give important answers on how to prevent CI-AKI in high and very high risk patients undergoing contrast media exposure.

Topics: Acetylcysteine; Acute Kidney Injury; Biomarkers; Chi-Square Distribution; Chronic Disease; Contrast Media; Creatinine; Diuretics; Drug Therapy, Combination; Equipment Design; Fluid Therapy; Furosemide; Glomerular Filtration Rate; Humans; Italy; Kidney Diseases; Radiography, Interventional; Renal Insufficiency; Research Design; Risk Assessment; Risk Factors; Sodium Bicarbonate; Time Factors; Treatment Outcome; Triiodobenzoic Acids

Metabolic acidosis is a feature of chronic kidney disease (CKD) due to the reduced capacity of the kidney to synthesise ammonia and excrete hydrogen ions. It has adverse consequences on protein and muscle metabolism, bone turnover and the development of renal osteodystrophy. Metabolic acidosis may be corrected by oral bicarbonate supplementation or in dialysis patients by increasing the bicarbonate concentration in dialysate fluid.. To examine the benefits and harms of treating metabolic acidosis in patients with CKD, both prior to reaching end-stage renal disease (ESRD) or whilst on renal replacement therapy (RRT), with sodium bicarbonate or increasing the bicarbonate concentration of dialysate.. We searched CENTRAL (The Cochrane Library, issue 4 2005), Cochrane Renal Group's specialised register (October 2005), MEDLINE (1966 - October 2005) and EMBASE (1980 - October 2005).. Randomised controlled trials (RCTs), crossover RCTs and quasi-RCTs investigating the correction of chronic metabolic acidosis in adults or children with CKD.. Outcomes were analysed using relative risk (RR) and weighted mean difference (MD) for continuous measures.. We identified three trials in adult dialysis patients (n = 117). There were insufficient data for most outcomes for meta-analysis. In all three trials acidosis improved in the intervention group though there was variation in achieved bicarbonate level. There was no evidence of effect on blood pressure or sodium levels. Some measures of nutritional status/protein metabolism (e.g. SGA, NP NA) were significantly improved by correction in the one trial that looked in these in detail. There was heterogeneity of the effect on serum albumin in two trials. Serum PTH fell significantly in the two trials that estimated this, there was no significant effect on calcium or phosphate though both fell after correction. Complex bone markers were assessed in one study, with some evidence for a reduction in bone turnover in those with initial high bone turnover and an increase in low turnover patients. The studies were underpowered to assess clinical outcomes, in the one study that did there was some evidence for a reduction in hospitalisation after correction.. The evidence for the benefits and risks of correcting metabolic acidosis is very limited with no RCTs in pre-ESRD patients, none in children, and only three small trials in dialysis patients. These trials suggest there may be some beneficial effects on both protein and bone metabolism but the trials were underpowered to provide robust evidence.

Topics: Acidosis; Chronic Disease; Hemodialysis Solutions; Humans; Kidney Diseases; Renal Dialysis; Sodium Bicarbonate

Topics: Acetazolamide; Bicarbonates; Carbon Dioxide; Chronic Disease; Humans; Lung Diseases, Obstructive; Medroxyprogesterone; Medroxyprogesterone Acetate; Oxygen; Respiration; Respiration Disorders; Sleep Stages; Sodium Bicarbonate

The aim of this study was to investigate the effects of balneotherapy on chronic low back pain. This is a minimized, follow-up study evaluated according to the analysis of intention to treat. The subjects included in the study were 105 patients suffering from chronic low back pain. The control group (n = 53) received the traditional musculoskeletal pain killer treatment, while the target group (n = 52) attended thermal mineral water treatment for 3 weeks for 15 occasions on top of the usual musculoskeletal pain killer treatment. The following parameters were measured before, right after, and 9 weeks after the 3-week therapy: the level of low back pain in rest and the level during activity are tested using the Visual Analog Scale (VAS); specific questionnaire on the back pain (Oswestry); and a questionnaire on quality of life (EuroQual-5D). All of the investigated parameters improved significantly (p < 0.001) in the target group by the end of the treatment compared to the base period, and this improvement was persistent during the follow-up period. There were no significant changes in the measured parameters in the control group. Based on our results, balneotherapy might have favorable impact on the clinical parameters and quality of life of patients suffering from chronic low back pain.

Topics: Aged; Balneology; Bicarbonates; Chronic Disease; Female; Humans; Low Back Pain; Magnesium; Male; Middle Aged; Mineral Waters; Pain Measurement; Quality of Life; Single-Blind Method; Sodium Bicarbonate

Citric acid has been used for over six decades to induce cough; however the mechanism of its pro-tussive effect is still not fully understood. We assessed the response to inhalation of citric acid at varying levels of acidity to determine if the pH of the solution plays a role in the induction of cough. Data was collected from both healthy volunteers and patients with chronic cough.. 20 chronic cough patients and 20 healthy volunteers were recruited and underwent three cough challenges on separate days. Each visit involved 5 repeated one second inhalations of 300 mM citric acid solution. The concentration of the citrate cation remained constant, but the pH of the solution altered by the addition of sodium bicarbonate to 3, 5 and 6, representing the pK. Two subjects withdrew and were not included in the analysis. Participants were gender matched, each group consisting of 12 females. 74% of chronic coughers coughed at pH 3 (mean coughs 16), 89% coughed at pH 5 (18) and 63% coughed at pH 6 (7). In healthy volunteers, 60% of subjects coughed at pH 3 (9), 30% of subjects coughed at pH 5 (3), and 10% of subjects coughed at pH 6 (0). Thus chronic cough patients coughed more than healthy volunteers and did not exhibit a clear pH concentration response. There was also a greater variability in their response to individual challenges.

Topics: Adult; Aged; Aged, 80 and over; Chronic Disease; Citric Acid; Cough; Double-Blind Method; Female; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Sodium Bicarbonate; Young Adult

The combined prophylactic strategy of sodium bicarbonate plus N-acetylsyteine (NAC) seems to be effective in preventing contrast induced acute kidney injury (CI-AKI) in patients at low-to-medium risk. However, in patients at high and very high risk the rate of CI-AKI is still high. In this subset of patients the anticipated advantages of the RenalGuard(tm) System should be investigated. The RenalGuard(tm) System (PLC Medical Systems, Inc., Franklin, MA, USA) is a real-time measurement and real time matched fluid replacement device designed to accommodate the RenalGuard therapy, which is based on the theory that creating and maintaining a high urine output is beneficial by allowing a quick elimination of contrast media, and, therefore, reducing its toxic effects.. The REMEDIAL II trial is a randomised, multicentre, investigator-sponsored trial addressing the hypothesis that the RenalGuard System is superior to the prophylaxis with sodium bicarbonate infusion plus NAC in preventing CI-AKI in high and very high risk patients. Consecutive patients with chronic kidney disease (CKD) and at high to very high risk for CI-AKI, referred to our institutions for coronary and/or peripheral procedures, will be randomly assigned to 1) prophylactic administration of sodium bicarbonate plus NAC (control group) and 2) RenalGuard System treatment (RenalGuard group). All enrolled patients must have an estimated glomerular filtration rate ≤ 30 ml/min/1.73 m2 and/or a contrast nephropathy risk score ≥ 11. In all cases iodixanol (an iso-osmolar, non-ionic contrast agent) will be administered. The primary endpoint is an increase of ≥ 0.3 mg/dL in the serum creatinine concentration 48 hours after the procedure.. The REMEDIAL II trial will give important answers on how to prevent CI-AKI in high and very high risk patients undergoing contrast media exposure.

Topics: Acetylcysteine; Acute Kidney Injury; Biomarkers; Chi-Square Distribution; Chronic Disease; Contrast Media; Creatinine; Diuretics; Drug Therapy, Combination; Equipment Design; Fluid Therapy; Furosemide; Glomerular Filtration Rate; Humans; Italy; Kidney Diseases; Radiography, Interventional; Renal Insufficiency; Research Design; Risk Assessment; Risk Factors; Sodium Bicarbonate; Time Factors; Treatment Outcome; Triiodobenzoic Acids

We randomized patients with chronic kidney disease (serum creatinine ≥ 1.5 mg/dl or glomerular filtration rate (GFR) <60 ml/min/1.73 m²) in a double-blind fashion to receive saline or sodium bicarbonate prior to and after cardiac or vascular angiography. The primary endpoint was contrast-induced nephropathy (CIN), defined as an increase in serum creatinine by 25% or by 0.5 mg/dl from baseline. Patients with congestive heart failure (CHF), cardiac ejection fraction (EF) <30%, or GFR < 20 ml/min/1.73 m² were excluded. The study was discontinued (after 142 patients were randomized) due to a low incidence of CIN (1.5%). We retrospectively identified all cases of CIN (n = 30) at our institution during the same time period to see if these patients differed from our trial sample. There was no difference in serum creatinine (1.7 ± 0.4 vs. 1.7 ± 0.6 mg/dL), GFR (42.7 ± 9.7 vs. 45.3 ± 3.2 ml/min), incidence of diabetes (51.8% vs. 63.3%), contrast volume (121.7 ± 63.8 vs. 122.7 ± 68.3 ml), ACE inhibitor or angiotensin receptor blocker use (54.0% vs 63.3%), and periprocedure diuretic use (33.1% vs 26.7%). On multivariate analysis, only a cardiac ejection fraction (EF) of less than 40% was significantly associated with CIN (odds ratio, 4.52; 95% confidence interval, 1.30-15.71; P = 0.02). In all, 22/30 patients (73.3%) who developed CIN had at least one or more characteristics that would have excluded their enrollment in our randomized trial including evidence of congestive heart failure (17/30 patients), EF less than 30% (9 patients), age greater than 85 years (2 patients), or advanced renal failure with a baseline GFR of less than 20 cc/min (1 patient). In summary, patients with CKD without evidence of CHF who receive adequate hydration appear to have a very low risk of CIN associated with angiography. A low EF (less than 40%) appeared to be the most significant risk factor for CIN in our population.

Topics: Aged; Chronic Disease; Contrast Media; Double-Blind Method; Heart Failure; Humans; Incidence; Kidney Diseases; Retrospective Studies; Sodium Bicarbonate

Sitz bath is frequently recommended by physicians for a variety of anal disorders including anal fissure. The aim of the present study was to determine whether sitz bath does have any therapeutic properties improving upon a patient's postoperative symptoms after a closed lateral sphincterotomy.. Forty-six patients were randomly assigned to receive analgesics and fiber supplement alone (control patients) or a twice-daily sitz bath along with identical fiber and analgesics (sitz bath group). A 24-h pain score--post-defecation anal burning and symptom improvement--was evaluated on a visual analog scale (VAS).. The groups were equally matched for age, gender distribution, and duration of disease. No significant difference in mean pain score between groups (p = 0.284) was noticed after one week. However, the patients from the control group experienced significant anal burning compared with patients from sitz bath group (p < 0.0001). The improvement score was higher in the sitz bath group when compared with the control group; however, it did not reached a statistically significant level.. Patients after sphincterotomy for anal fissure receiving sitz bath experienced similar levels of pain when compared with those not receiving sitz bath. However, they reported a significant relief in anal burning and a marginally better satisfaction score and no reported adverse side effects.

Topics: Adult; Anal Canal; Anti-Inflammatory Agents, Non-Steroidal; Chronic Disease; Citric Acid; Diclofenac; Drug Combinations; Fissure in Ano; Humans; Hydrotherapy; Pain Measurement; Pain, Postoperative; Plant Extracts; Sodium Bicarbonate; Wound Healing

There are no controlled trials on the efficacy of oral bicarbonate therapy in patients with mild to moderate chronic kidney disease (CKD). This prospective randomized controlled study was done to evaluate the effects of correction of metabolic acidosis on renal functions and bone metabolism in this group of patients.. Forty patients were randomized to treatment with oral bicarbonate or placebo for a period of 3 months. Investigations at baseline included venous pH, bicarbonate, renal functions, serum iPTH, and bone radiology. The treatment group (Group B) received daily oral sodium bicarbonate therapy at a dose of 1.2 mEq/kg of body weight. Their venous blood pH and bicarbonate levels were estimated weekly to keep blood pH near 7.36 and bicarbonate at 22-26 mEq/L by adjusting the dose of sodium bicarbonate. At the end of 3 months, all the tests were repeated in both groups.. After oral bicarbonate therapy (OBT), there was a significant decline in the rise of blood urea level in Group B associated with a sense of well-being in 50% patients. The rise in parathormone (PTH) was six times the baseline value in Group A and only 1.5 times baseline value in Group B, although not statistically significant. There was no significant change in total calcium, phosphorus, alkaline phosphatase, creatinine, total protein, or albumin levels.. Correction of metabolic acidosis in patients with moderate CKD attenuates the rise in blood urea and PTH, which might prevent the deleterious long-term consequences of secondary hyperparathyroidism.

Topics: Acidosis; Adult; Aged; Bone and Bones; Chronic Disease; Female; Humans; Kidney Diseases; Male; Metabolic Diseases; Middle Aged; Prospective Studies; Severity of Illness Index; Single-Blind Method; Sodium Bicarbonate; Urea

Fibre is often recommended as the first-choice treatment but its effects can be uneven. The aim of the study was to compare the clinical efficacy and tolerability of fibre versus lactulose in outpatients with chronic constipation.. In a prospective randomized crossover trial, patients were randomized to receive fibre or lactulose for four weeks. Between treatments, patients had at least one week free of laxatives.. 50 patients, of median age 50 years (range, 18-85) were recruited and 39 patients completed the trial. Compared to fibre, lactulose resulted in significantly higher mean bowel frequency (7.3, 95% CI 5.7 to 8.9 vs. 5.5, 95% CI 4.4 to 6.5; p=0.001) and stool consistency score (3.4, 95% CI 3.1 to 3.7 vs. 2.9, 95% CI 2.5 to 3.3; p=0.018). Scores for ease of evacuation were similar. The frequencies of adverse effects were not significantly different, but greater in the lactulose group. Mean patients' recorded improvement score was significantly higher after taking lactulose than fibre (6.2, 95% CI 5.5 to 7.0 vs. 4.8, 95% CI 4.0 to 5.9; p=0.017). Of the 39 patients who completed the trial, 24 (61.5%) preferred lactulose and 14 (35.9%) preferred fibre.. Lactulose had better efficacy than fibre for chronic constipation in ambulant patients, although both treatments were equally well tolerated in terms of adverse effects.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Chronic Disease; Citric Acid; Constipation; Cross-Over Studies; Drug Combinations; Female; Gastrointestinal Agents; Humans; Lactulose; Male; Middle Aged; Patient Satisfaction; Plant Extracts; Prospective Studies; Sodium Bicarbonate; Treatment Outcome

Polyethylene glycol (PEG) 3350 is a non-absorbable, non-metabolised osmotic agent used in lavage solutions for gut cleansing.. To compare the efficacy of PEG and lactulose in chronic constipation.. A total of 115 patients with chronic constipation entered a multicentre, randomised, comparative trial. They initially received two sachets containing either PEG (13 g/sachet) or lactulose (10 g/sachet) and were given an option to change the dose to one or three sachets/day, depending on response.. Ninety nine patients completed the trial. After four weeks, patients in the PEG group (n=50) had a higher number of stools and a lower median daily score for straining at stool than patients in the lactulose group (n=49). Overall improvement was greater in the PEG group. Clinical tolerance was similar in the two groups, but flatus was less frequently reported in the PEG group. The mean number of liquid stools was higher in the PEG group but the difference was significant only for the first two weeks. There were no serious adverse events and no significant change in laboratory tests in either group. At the end of the study, the number of sachets used by the patients was 1.6 (0.7)/day in the PEG group and 2.1 (0.7)/day in the lactulose group. Sixty one patients completed a further two months open study of one to three sachets PEG daily; there was no loss of efficacy and no serious toxicity.. Low dose PEG 3350 was more effective than lactulose and better tolerated.

Topics: Adult; Aged; Cathartics; Chronic Disease; Constipation; Drug Administration Schedule; Drug Combinations; Female; Follow-Up Studies; Humans; Lactulose; Male; Middle Aged; Polyethylene Glycols; Potassium Chloride; Sodium Bicarbonate; Sodium Chloride; Treatment Outcome

The aim of the present study was to compare the efficacy and safety of a new aluminium-free formulation of alginate with placebo in infants with recurrent gastro-oesophageal reflux. This was a double-blind, randomised, parallel-group study conducted at 25 centres in the UK. Of the 90 paediatric patients recruited in a general practice setting, 42 were randomised to receive alginate and 48 to receive placebo. Infants were assessed before treatment and again after seven and 14 days of treatment. Analyses were based on the last, valid, non-missing observation for each variable for the intent-to-treat (ITT) population of 42 alginate and 46 placebo patients. For the primary efficacy measure (number of vomitting/regurgitation episodes), alginate was significantly superior to placebo (p = 0.009). For the secondary efficacy measure (severity of vomiting), a trend in favour of alginate was observed (p = 0.061). Patients receiving alginate achieved superior assessments of treatment outcome by both investigators (p = 0.008) and parent/guardians (p = 0.002) alike. In addition, alginate achieved a significantly greater reduction in the mean severity of vomiting episodes recorded in a daily diary compared with placebo (p = 0.027) and resulted in more patients having at least 10% symptom-free days (p = 0.027). For none of the variables measured did placebo have a superior effect. More than one-half of all patients experienced some adverse event, although no statistically significant differences were observed between the two treatment groups (p > 0.1), and adverse events accounted for withdrawal in only 12.5% of the patients (alginate, n = 4; placebo, n = 7). Aluminium-free alginate demonstrated superior efficacy over placebo in treating recurrent gastro-oesophageal reflux in paediatric patients. The safety profile of alginate was similar to that of placebo.

Topics: Age of Onset; Alginates; Aluminum Hydroxide; Analysis of Variance; Antacids; Area Under Curve; Chronic Disease; Consumer Product Safety; Double-Blind Method; Drug Combinations; Female; Gastroesophageal Reflux; Humans; Infant; Infant, Newborn; Male; Silicic Acid; Sodium Bicarbonate; Statistics, Nonparametric; Vomiting

Chronic oral malodor is a serious concern for about one-fifth of the North American population, and a field of emerging research interest. The present three studies, one involving gas chromatography and two employing odor judge assessment, examined the efficacy of baking soda and other toothpastes in reducing breath odor. The most common cause of oral malodor is elevated levels of volatile sulfur compounds (VSC's), primarily hydrogen sulfide (H2S) and methyl mercaptan (CH3SH), in the breath. Gas chromatography, an accurate means of measuring breath VSC, was employed to evaluate the breath levels of VSC in 11 men after brushing with baking soda-containing dentifrices with or without the addition of Zn++. Dentifrices with either Zn++ or a concentration of baking soda 20% or greater significantly reduced VSC levels. The addition of Zn++ to baking soda dentifrices enhanced the anti-odor effects. In the first organoleptic study, dentifrices containing 20% baking soda and 30% baking soda demonstrated significantly greater ability to reduce breath odor than a standard sodium fluoride/silica dentifrice. The subjects' baseline mouth odor evaluations, initially rated as strong, declined after brushing with the baking soda toothpastes to a barely detectable level at one hour, then rising to a faint level at two hours and moderate levels at three hours. In the second organoleptic study, a dentifrice containing 65% baking soda demonstrated significantly greater ability to reduce breath odor than a standard sodium fluoride/silica tartar control dentifrice, but did not differ significantly from a standard dentifrice containing 0.76% sodium monofluorophosphate in a dicalcium phosphate dihydrate base. The results of these studies indicate that dentifrices containing 20% or more baking soda can confer a significant odor-reducing benefit for time periods up to three hours.

Topics: Adult; Analysis of Variance; Chromatography, Gas; Chronic Disease; Cross-Over Studies; Dentifrices; Halitosis; Humans; Hydrogen Sulfide; Male; Middle Aged; Sodium Bicarbonate; Sulfhydryl Compounds; Toothbrushing; Zinc Compounds

The efficacy, tolerance and acceptability of lactulose (Duphalac) and ispaghula (Fybogel Orange) were assessed in the treatment of chronic constipation in adults. In an open, prospectively randomised, parallel group study, 124 patients with a history of constipation for more than three weeks were treated with either 15 ml bd of lactulose (increasing to 60 ml daily if necessary) or one sachet bd of ispaghula. Over the four-week treatment period both treatments were shown to be effective, and numbers of concurrent effects were similar between the two groups. Differences were demonstrated with regard to acceptability in favour of lactulose.

Topics: Bicarbonates; Chronic Disease; Citrates; Citric Acid; Constipation; Drug Combinations; Humans; Lactulose; Middle Aged; Patient Acceptance of Health Care; Plant Extracts; Prospective Studies; Sodium Bicarbonate

Topics: Adolescent; Adult; Aged; Aluminum Hydroxide; Anti-Ulcer Agents; Bismuth; Chronic Disease; Cimetidine; Clinical Trials as Topic; Drug Combinations; Duodenal Ulcer; Endoscopy; Female; Gefarnate; Glycyrrhiza; Humans; Magnesium Hydroxide; Male; Middle Aged; Plant Extracts; Sodium Bicarbonate

Topics: Acidosis; Chronic Disease; Evidence-Based Medicine; Germany; Guideline Adherence; Humans; Practice Guidelines as Topic; Practice Patterns, Physicians'; Prevalence; Renal Dialysis; Risk Factors; Sodium Bicarbonate; Survival Rate; Treatment Outcome

Topics: Acidosis; Child, Preschool; Chronic Disease; Humans; Kidney Failure, Chronic; Male; Sodium Bicarbonate; Treatment Outcome

Metabolic acidosis is a prevalent complication in moderate and late stages of chronic kidney disease (CKD). It is established that the correction of metabolic acidosis may improve metabolic bone disorders and protein degradation in the skeletal muscle, two characteristic complications of patients with advanced CKD. In the last 18 months, three randomized controlled trials have drawn the attention on a novel indication to correct metabolic acidosis in these patients, i.e., halting CKD progression. These data show that sodium bicarbonate, a cheap and easily manageable treatment, may delay the progression of CKD and the need of a renal replacement therapy such as dialysis or kidney transplantation.

Topics: Acidosis; Buffers; Chronic Disease; Disease Progression; Humans; Kidney Diseases; Sodium Bicarbonate

Hyperkalemia generally is attributable to cell shifts or abnormal renal potassium excretion. Cell shifts account for transient increases in serum potassium levels, whereas sustained hyperkalemia generally is caused by decreased renal potassium excretion. Impaired renal potassium excretion can be caused by a primary decrease in distal sodium delivery, a primary decrease in mineralocorticoid level or activity, or abnormal cortical collecting duct function. Excessive potassium intake is an infrequent cause of hyperkalemia by itself, but can worsen the severity of hyperkalemia when renal excretion is impaired. Before concluding that a cell shift or renal defect in potassium excretion is present, pseudohyperkalemia should be excluded.

Topics: Adult; Aldosterone; Chronic Disease; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Glomerular Filtration Rate; Humans; Hyperkalemia; Kidney; Kidney Tubules; Liddle Syndrome; Male; Potassium, Dietary; Renin-Angiotensin System; Sodium Bicarbonate

The short-term outcomes of sodium bicarbonate therapy in preterm infants were investigated by retrospective analysis of 165 of 984 infants who received sodium bicarbonate. The infants treated with sodium bicarbonate were more immature and had greater severity of illness and more adverse outcomes. Sodium bicarbonate therapy did not improve the blood pH.

Topics: Acidosis; Chronic Disease; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Infant, Premature; Infusions, Intravenous; Severity of Illness Index; Sodium Bicarbonate

This study investigated the effects of high-intensity training, with or without induced metabolic alkalosis, on lactate transporter (MCT1 and MCT4) and sodium bicarbonate cotransporter (NBC) content in rat skeletal muscles. Male Wistar rats performed high-intensity training on a treadmill 5 times/wk for 5 wk, receiving either sodium bicarbonate (ALK-T) or a placebo (PLA-T) prior to each training session, and were compared with a group of control rats (CON). MCT1, MCT4, and NBC content was measured by Western blotting in soleus and extensor digitorum longus (EDL) skeletal muscles. Citrate synthase (CS) and phosphofructokinase (PFK) activities and muscle buffer capacity (betam) were also evaluated. Following training, CS and PFK activities were significantly higher in the soleus only (P < 0.05), whereas betam was significantly higher in both soleus and EDL (P < 0.05). MCT1 (PLA-T: 30%; ALK-T: 23%) and NBC contents (PLA-T: 85%; ALK-T: 60%) increased significantly only in the soleus following training (P < 0.01). MCT4 content in the soleus was significantly greater in ALK-T (115%) but not PLA-T compared with CON. There was no significant change in protein content in the EDL. Finally, NBC content was related only to MCT1 content in soleus (r = 0.50, P < 0.01). In conclusion, these results suggest that MCT1, MCT4, and NBC undergo fiber-specific adaptive changes in response to high-intensity training and that induced alkalosis has a positive effect on training-induced changes in MCT4 content. The correlation between MCT1 and NBC expression suggests that lactate transport may be facilitated by NBC in oxidative skeletal muscle, which may in turn favor better muscle pH regulation.

Topics: Alkalosis; Animals; Chronic Disease; Citrate (si)-Synthase; Lactic Acid; Male; Monocarboxylic Acid Transporters; Muscle Proteins; Muscle, Skeletal; Phosphofructokinase-1; Physical Conditioning, Animal; Physical Exertion; Rats; Rats, Wistar; Sodium Bicarbonate; Sodium-Bicarbonate Symporters; Symporters

Chronic metabolic acidosis increases, while alkali feeding inhibits, proximal tubule citrate absorption. The activity of the apical membrane Na+/citrate cotransporter is increased in metabolic acidosis, but is not altered by alkali feeding.. Renal cortical mRNA and brush border membrane protein abundances of sodium/dicarboxylate-1 (NaDC-1), the apical membrane Na+/citrate transporter, were measured.. By immunohistochemistry, NaDC-1 was localized to the apical membrane of the proximal tubule. Chronic metabolic acidosis caused an increase in NaDC-1 protein abundance that was maximal in the S2 segment and that increased with time. Metabolic acidosis also increased NaDC-1 mRNA abundance, but this was first seen at three hours and correlated with the severity of the metabolic acidosis. Alkali feeding had no effect on NaDC-1 protein or mRNA abundance.. Chronic metabolic acidosis increases renal cortical NaDC-1 mRNA abundance and apical membrane NaDC-1 protein abundance, while alkali feeding is without effect on NaDC-1.

Topics: Acidosis; Acids; Acute Disease; Alkalies; Ammonium Chloride; Animals; Carrier Proteins; Chronic Disease; Citrates; Dicarboxylic Acid Transporters; Gene Expression; Kidney Cortex; Kidney Tubules, Proximal; Male; Membrane Proteins; Organic Anion Transporters, Sodium-Dependent; Rats; Rats, Sprague-Dawley; RNA, Messenger; Sodium Bicarbonate; Symporters

The present studies examined the effects of chronic NaCl administration and metabolic alkalosis on NHE-3, an apical Na+/H+ exchanger of the rat medullary thick ascending limb of Henle (MTAL). NaCl administration had no effect on NHE-3 mRNA abundance as assessed by competitive RT-PCR, as well as on NHE-3 transport activity estimated from the Na+-dependent cell pH recovery of Na+-depleted acidified MTAL cells, in the presence of 50 microM Hoe-694, which specifically blocks NHE-1 and NHE-2. Two models of metabolic alkalosis were studied, one associated with high sodium intake, i.e., NaHCO3 administration, and one not associated with high sodium intake, i.e., chloride depletion alkalosis (CDA). In both cases, the treatment induced a significant metabolic alkalosis that was associated with a decrease in NHE-3 transport activity (-27% and -25%, respectively). Negative linear relationships were observed between NHE-3 activity and plasma pH or bicarbonate concentration. NHE-3 mRNA abundance and NHE-3 protein abundance, assessed by Western blot analysis, also decreased by 35 and 25%, respectively, during NaHCO3-induced alkalosis, and by 47 and 33%, respectively, during CDA. These studies demonstrate that high sodium intake has per se no effect on MTAL NHE-3. In contrast, chronic metabolic alkalosis, regardless of whether it is associated with high sodium intake or not, leads to an appropriate adaptation of NHE-3 activity, which involves a decrease in NHE-3 protein and mRNA abundance.

Topics: Adaptation, Physiological; Alkalosis; Animals; Blood; Chlorides; Chronic Disease; Diet; Hydrogen-Ion Concentration; In Vitro Techniques; Loop of Henle; Male; Rats; Rats, Sprague-Dawley; RNA, Messenger; Sodium; Sodium Bicarbonate; Sodium-Hydrogen Exchanger 3; Sodium-Hydrogen Exchangers; Time Factors

The principal clinical signs in 59 milk-fed calves with chronic indigestion were general malaise and depression, poor appetite, poor body condition, dehydration, a dull and scaly hair coat, alopecia and clay-like faeces. All the calves had metabolic acidosis, which was associated with an inability to stand up in more than half of them. There were significant differences in the severity of acidosis between the calves that could stand and those that could not. Other signs in some of the calves were dehydration, leucocytosis, and increased activities of liver enzymes.

Topics: Acidosis; Animals; Anti-Bacterial Agents; Blood Gas Analysis; Cattle; Cattle Diseases; Chronic Disease; Dyspepsia; Female; Fermentation; Liver; Male; Milk; Rumen; Severity of Illness Index; Sodium Bicarbonate; Treatment Outcome; Vitamins

In a previous paper, we showed that an inhibition of amino acid transport across the liver plasma membrane is responsible for the decrease in urea synthesis in acute metabolic acidosis. We have now studied the mechanism responsible for the decline in urea synthesis in chronic acidosis. Chronic metabolic acidosis and alkalosis were induced by feeding three groups of rats HCl, NH4Cl, and NaHCO3 (8 mmol/day) for 7 days. Amino acids and NH4+ were measured in portal vein, hepatic vein, and aortic plasma, and arteriovenous differences were calculated. The rates of urinary urea and NH4+ excretion were also determined. Hepatic amino acid consumption was lower in both HCl and NH4Cl acidosis compared with NaHCO3-fed rats. Glutamine release was not different in the three conditions. Because intrahepatic concentrations of amino acids and intracellular protein degradation were similar under these conditions, it can be concluded that at low blood pH amino acid catabolism may be inhibited and might explain the observed decrease in urea excretion in HCl, but not NH4Cl, acidosis; urea excretion was comparable in the NH4Cl and NaHCO3 groups presumably because the increased NH4+ load in the former group was processed, uninhibited, to urea. Amino acids not used by the liver in acidosis could account for the 25-fold increase in NH4+ excretion in HCl and NH4Cl compared with alkalosis (P < 0.05). These findings indicate that urea synthesis is decreased in chronic HCl acidosis. They show that urea synthesis is controlled in chronic, as in acute, acidosis by amino acid uptake by the liver and/or intrahepatic degradation and that the ornithine cycle per se has only minor control of acid-base homeostasis.

Topics: Acidosis; Alkalosis; Amino Acids; Ammonium Chloride; Animals; Chronic Disease; Female; Hepatic Veins; Hydrochloric Acid; Liver; Portal Vein; Quaternary Ammonium Compounds; Rats; Rats, Wistar; Sodium Bicarbonate; Urea

Experiments on white rats found that both chronic acidosis and chronic alkalosis cause fasting hyperglycemia and decreases glucose tolerance. In hypophysectomized animals, alkalosis causes similar effects and acidosis leads to hypoglycemia. Acute acidosis stimulates insulin and corticotropin secretions acute alkalosis reduces blood insulin and corticotropin levels and increases glucagon concentration. Chronic acidosis and alkalosis decrease insulin secretion and stimulates corticotropin secretion. Glucagon levels remain increased in chronic alkalosis. It has been concluded that primary cause of diabetogenic action of chronic acidosis is glucocorticoid hyperfunction and exhausting stimulation of B cells with glucose. Alkalosis causes a direct inhibitory action on B cells and activates A cells of Langerhans' islets.

Topics: Acid-Base Imbalance; Acidosis; Alkalosis; Ammonium Chloride; Animals; Blood Glucose; Chronic Disease; Diabetes Mellitus, Experimental; Hypophysectomy; Male; Rats; Sodium Bicarbonate

Topics: Adolescent; Antacids; Bicarbonates; Child; Child, Preschool; Chronic Disease; Digestive System Diseases; Drug Combinations; Drug Evaluation; Humans; Magnesium; Magnesium Compounds; Sodium; Sodium Bicarbonate; Sodium Compounds

Intravenous sodium bicarbonate (NaHCO3) infusion test was performed in 26 patients with chronic glomerulonephritis (CGN) and 16 with distal renal tubular acidosis (dRTA) in order to evaluate urinary acidifying capacity in chronic renal diseases. Comparative studies with glomerular filtration were planned, so that the patients with CGN were divided by creatinine clearance (Ccr) into 3 groups (G-I greater than or equal to 70, 30 less than or equal to G-II less than 70, G-III less than 30 ml/min). Proximal tubular bicarbonate (HCO3) reabsorption rate increased in CGN as Ccr decreased. Urine to blood carbon dioxide tension gradient (U-B PCO2) was above 30 mmHg in controls and below 20 mmHg in dRTA. In patients with CGN, urine HCO3 concentration (UHCO3) did not increase during NaHCO3 loading as Ccr decreased. However, U-B PCO2 rose above 20 mmHg, when UHCO3 was above 50 ml/min. Fishberg concentrating test was also performed in 15 patients with CGN and 6 with dRTA so that the relationship between urinary concentrating ability and urine acidification might be evaluated. While both functions were decreased in dRTA, U-B PCO2 in alkaline urine remained above 20 mmHg in CGN associated with moderate renal dysfunction (Ccr greater than or equal to 30 ml/min) despite decreased maximal urine osmolality. Intravenous furosemide (FM) injection test was carried out in 8 patients with chronic renal failure (CRF) and 3 with dRTA. Minimal urine pH fell below 5.5 and net acid excretion (NAE) increased in controls, whereas these responses were not seen in dRTA. In CRF, urine pH generally decreased below 5.5 and those who had a similar response to FM as dRTA, seemed to have more severe disturbance of the distal acidification. In conclusion, U-B PCO2 in alkaline urine and lowered urine pH in FM loading appeared to be a useful index of distal tubular acid excretion in patients with renal dysfunction. In CGN with moderate renal dysfunction (Ccr greater than or equal to 30 ml/min), urinary acidifying capacity remained normal in comparison with decreased urine concentrating ability.

Topics: Acidosis, Renal Tubular; Bicarbonates; Chronic Disease; Furosemide; Glomerular Filtration Rate; Glomerulonephritis; Humans; Hydrogen-Ion Concentration; Kidney Concentrating Ability; Kidney Glomerulus; Sodium; Sodium Bicarbonate

Topics: Administration, Topical; Bicarbonates; Blepharitis; Chronic Disease; Eyelid Diseases; Humans; Sodium; Sodium Bicarbonate

Topics: Administration, Inhalation; Bicarbonates; Bronchi; Bronchitis; Chronic Disease; Expectorants; Female; Humans; Middle Aged; Sodium; Sodium Bicarbonate

Topics: Administration, Inhalation; Adult; Bicarbonates; Bronchitis; Chronic Disease; Expectorants; Female; Humans; Male; Middle Aged; Sodium; Sodium Bicarbonate

The occurrence of respiratory alkalosis and potential benefit derived from treatment were examined in thermostressed 4-week-old broiler chicks. Blood pH was greater (P less than .05) in heat-stressed (32 C) panting birds (7.395) than either nonpanting (7.28) or birds raised at 24 C (7.28). Acute thermostress, obtained by elevating ambient temperature from 32 to 41 C over a 20-min period further elevated (P less than .05) blood pH to 7.521. Chronic heat-stressed broiler chicks suffer from intermittent respiratory alkalosis during panting; with acute heat stress, chicks pant continuously and suffer from alkalosis. Including .5% sodium bicarbonate (NaHCO3) in the diet of birds subjected to chronic heat stress enhanced body weight gain by 9% even though it tended (P less than .10) to increase blood pH in nonpanting birds. Adding .3 or 1% ammonium chloride (NH4Cl) to diets decreased blood pH (P less than .01) to 7.194 and increased (P less than .05) body weight gains by 9.5 and 25%, respectively. Effects appeared linear with NH4Cl dose to 1% NH4Cl, but 3% NH4Cl elevated weight gains by only 8% and precipitated blood acidosis (pH 7.09) in nonpanting birds. Supplementing the 1% NH4Cl diet with .5% NaHCO3 increased weight gains an additional 9%. Manipulating sodium: chloride ratios by addition of calcium chloride increased body weight gain 8% and slightly reduced severity of alkalosis. Data indicate that blood alkalosis limits growth rate of broiler chicks reared under chronic thermostress and that the respiratory alkalosis and weight gain depressions attributed to thermostress can be partially alleviated dietarily.

Topics: Alkalosis, Respiratory; Ammonium Chloride; Animals; Bicarbonates; Blood Chemical Analysis; Body Weight; Calcium Chloride; Carbon Dioxide; Chickens; Chronic Disease; Hot Temperature; Hydrogen-Ion Concentration; Poultry Diseases; Sodium; Sodium Bicarbonate; Stress, Physiological

Topics: Aluminum; Aluminum Hydroxide; Anti-Ulcer Agents; Bismuth; Carbenoxolone; Chronic Disease; Cimetidine; Drug Combinations; Drug Evaluation; Gastric Mucosa; Glycyrrhiza; Humans; Magnesium Hydroxide; Plant Extracts; Plants, Medicinal; Recurrence; Sodium Bicarbonate; Stomach Ulcer; Sucralfate

Previous workers have shown that metabolic acidosis increases the apparent space through which administered bicarbonate is distributed. This finding has been ascribed to the accompanying acidemia and to the consequent availability of a large quantity of hydrogen ion that accumulates on nonbicarbonate tissue buffers during the development of acidosis. To test this hypothesis, bicarbonate space was measured in dogs with a broad range of steady-state plasma [HCO-3] in association with alkalemia as well as with acidemia. Appropriate combinations of pH and plasma [HCO-3] were achieved by pretreating the animals to produce graded degrees of each of the four cardinal, chronic acid-base disorders. Metabolic acidosis (n = 15) was produced by prolonged HCl-feeding; metabolic alkalosis (n = 17) by diuretics and a chloride-free diet; and respiratory acidosis (n = 9) and alkalosis (n = 8) by means of an environmental chamber. Animals with normal acid-base status (n = 4) were also studied. Sodium bicarbonate (5 mmol/kg) was infused over 10 min to the unanesthetized animals; observations were carried out over 90 min. The results obtained from animals with metabolic acid-base disturbances demonstrated an inverse relationship between bicarbonate space and initial plasma pH, confirming the previous findings of others. By contrast, the results obtained in animals with respiratory acid-base disturbances demonstrated a direct relationship between bicarbonate space and initial plasma pH. The pooled data revealed that bicarbonate space is, in fact, quite independent of the initial pH but is highly correlated with the initial level of extracellular [HCO-3]; dogs with low extracellular [HCO-3] (congruent to 10 meq/liter) whether acidemic or alkalemic, have a bicarbonate space that is 25% larger than normal and some 50% larger than in dogs with high extracellular [HCO-3] (congruent to 50 meq/liter). We conclude from these results that the increased bicarbonate space in metabolic acidosis (and respiratory alkalosis) does not reflect the availability of more hydrogen ions for release during bicarbonate administration, but merely evidences the wider range of titration (delta pH) of nonbicarbonate buffers that occurs during alkali loading whenever plasma [HCO-3] is low.

Topics: Acid-Base Equilibrium; Acidosis, Respiratory; Alkalosis, Respiratory; Animals; Bicarbonates; Carbon Dioxide; Chronic Disease; Dogs; Extracellular Space; Female; Hydrogen-Ion Concentration; Sodium Bicarbonate

Topics: Aluminum Hydroxide; Antacids; Calcium; Calcium Carbonate; Chronic Disease; Drug Combinations; Duodenal Ulcer; Fasting; Gastric Acid; Gastrointestinal Contents; Humans; Magnesium Hydroxide; Sodium Bicarbonate

Topics: Bicarbonates; Chronic Disease; Deafness; Glomerulonephritis; Hearing Loss; Humans; Sodium Bicarbonate