Effects of oral alkali drug therapy on clinical outcomes in pre-dialysis chronic kidney disease patients: a systematic review and meta-analysis.

BACKGROUND: Metabolic acidosis accelerates the progression of chronic kidney disease (CKD) and increases the mortality rate. Whether oral alkali drug therapy benefits pre-dialysis CKD patients is controversial. We performed a meta-analysis of the effects of oral alkali drug therapy on major clinical outcomes in pre-dialysis CKD patients. METHODS: We systematically searched MEDLINE using the Ovid, EMBASE, and Cochrane Library databases without language restriction. We included all eligible clinical studies that involved pre-dialysis CKD adults and compared those who received oral alkali drug therapy with controls. RESULTS: A total of 18 eligible studies, including 14 randomized controlled trials and 4 cohort studies reported in 19 publications with 3695 participants, were included. Oral alkali drug therapy led to a 55% reduction in renal failure events (relative risk [RR]: 0.45; 95% confidence interval [CI]: 0.25-0.82), a rate of decline in the estimated glomerular filtration rate (eGFR) of 2.59 mL/min/1.73 m2 per year (95% CI, 0.88-4.31). There was no significant effect on decline in eGFR events (RR: 0.34; 95% CI: 0.09-1.23), proteinuria (standardized mean difference: -0.32; 95% CI: -1.08 to 0.43), all-cause mortality events (RR: 0.90; 95% CI: 0.40-2.02) and cardiovascular (CV) events (RR: 1.03; 95% CI: 0.32-3.37) compared with the control groups. CONCLUSION: Based on the available and low-to-moderate certainty evidence, oral alkali drug therapy might potentially reduce the risk of kidney failure events, but no benefit in reducing all-cause mortality events, CV events, decline in eGFR and porteninuria.

Destoxificação e perfil nutricional da torta de mamona destoxificada por diferentes soluções alcalinas / [Detoxification and nutritional profile of the detoxified castor by different alkaline solutions]

Objetivou-se avaliar a destoxificação da torta de mamona bruta (TMB), por meio de dois produtos alcalinos em diferentes concentrações, e seus efeitos sobre a composição química, a degradabilidade in situ da MS e o fracionamento de proteínas. Utilizou-se o hidróxido de cálcio [Ca(OH)2] e o hidróxido de sódio (NaOH) em duas concentrações (60 e 90 gramas), diluídos em quatro quantidades de água (1.000; 1.500; 2.000 e 2.500mL de água por quilo de TMB). Observou-se que, das diferentes concentrações utilizadas, somente a utilização de 90 e 60 gramas de Ca(OH)2 e NaOH, respectivamente, conseguiu destoxificar 100% da TMB, ambas diluídas em 2.000mL de água. Por outro lado, ao avaliar o tempo mínimo de contato dos reagentes com a TMB para uma máxima destoxificação, observou-se que três horas de contato é o tempo necessário para os reagentes diminuírem em 100% as proteínas citotóxicas, além de não deixar atividade hemaglutinante nesse material. A destoxificação com o NaOH proporcionou maior degradação das proteínas solúveis e da matéria seca, favorecendo a disponibilização do nitrogênio não proteico, estando sua aplicação em escala industrial na dependência de estudos sobre viabilidade operacional e econômica.(AU)

This study aimed to evaluate the detoxification of crude castor (DCC) through two alkaline products in different concentrations and their effects on the chemical composition, in situ degradability of DM and the fractionation of proteins. We used the calcium hydroxide [Ca(OH)2] and sodium hydroxide (NaOH) in two concentrations (60 and 90 grams) diluted in 4 quantities of water (1,000; 1,500; 2,000 and 2,500ml of water per kilo of DCC). It was observed that in the different concentrations used, only the use of 90 and 60 grams of Ca(OH)2 and NaOH, respectively managed to detoxify 100% of the DCC, both diluted in 2,000ml of water. On the other hand, when assessing the minimum time of contact of the reagents with the DCC for maximum detoxification, it was observed that with three hours of contact is the time required for the reagents decrease in 100% of the cytotoxic proteins, in addition to not leave haemagglutinating activity in this material. The detoxification with NaOH provided greater degradation of soluble proteins and degradation of dry matter, favoring the provision of non-protein nitrogen, while its application on an industrial scale is in the dependence of studies on operational feasibility and cost.(AU)

Assessment of conservative dietary management as a method for normalization of 24-h urine pH in stone formers.

Low urine pH is a metabolic risk factor for stone formation. While medical therapy is typically prescribed (as urinary alkalinization), patients typically prefer dietary modifications. We aimed to assess capacity to alter urine pH with dietary management alone. We analyzed a retrospective cohort of stone formers seen between 2000 and 2015 with multiple 24-h urine collections (24hUC). Patients ≥ 18 years old with low urine pH (< 6.0) were included; those prescribed alkalinizing agents or thiazides were excluded. Demographic data, 24hUC parameters, and medications were abstracted. 24hUC was utilized to calculate gastrointestinal alkali absorption (GIAA). The primary outcome was urine pH ≥ 6.0 on second 24hUC. Predictors were selected utilizing multivariable logistic regression. The database consisted of 2197 stone formers; 224 of these met inclusion criteria. On second 24hUC, 124 (55.4%) achieved a favorable pH ≥ 6.0. On univariable analysis, a second pH ≥ 6.0 was associated with high initial pH, low initial sulfate, younger age, increase in citrate/GIAA/urine volume, and decrease in ammonium (P < 0.02). On multivariable analysis, high initial pH (OR = 23.64, P < 0.001), high initial GIAA (OR = 1.03, P = 0.001), lower initial sulfate (OR = 0.95, P < 0.001), increase in urine volume (OR = 2.19, P = 0.001), increase in GIAA (OR = 8.6, P < 0.001), increase in citrate (OR = 2.7, P = 0.014), decrease in ammonium (OR = 0.18, P < 0.001), and younger age (OR = 0.97, P = 0.025) were associated with a second pH ≥ 6.0. The analysis demonstrated a corrected AUC of 0.853. These data suggest that certain dietary recommendations (increases in urine volume, citrate, GIAA, and decreased acid load) may normalize urine pH in a select group of patients. This may allow urologists to counsel patients with low urine pH on possibility of success with dietary modification alone.

Effects of Treatment of Metabolic Acidosis in CKD: A Systematic Review and Meta-Analysis.

BACKGROUND AND OBJECTIVES: Metabolic acidosis is associated with progression of CKD and has significant adverse effects on muscle and bone. A systematic review and meta-analysis was conducted to evaluate the benefits and risks of metabolic acidosis treatment with oral alkali supplementation or a reduction of dietary acid intake in those with CKD. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: MEDLINE, Embase, and Cochrane CENTRAL were searched for relevant trials in patients with stage 3-5 CKD and metabolic acidosis (<22 mEq/L) or low-normal serum bicarbonate (22-24 mEq/L). Data were pooled in a meta-analysis with results expressed as weighted mean difference for continuous outcomes and relative risk for categorical outcomes with 95% confidence intervals (95% CIs), using a random effects model. Study quality and strength of evidence were assessed using Cochrane risk of bias and the Grading of Recommendations Assessment, Development and Evaluation criteria. RESULTS: Fourteen clinical trials were included (n=1394 participants). Treatment of metabolic acidosis with oral alkali supplementation or a reduction of dietary acid intake increased serum bicarbonate levels (14 studies, 1378 patients, mean difference 3.33 mEq/L, 95% CI, 2.37 to 4.29) and resulted in a slower decline in eGFR (13 studies, 1329 patients, mean difference -3.28 ml/min per 1.73 m2, 95% CI, -4.42 to -2.14; moderate certainty) and a reduction in urinary albumin excretion (very-low certainty), along with a reduction in the risk of progression to ESKD (relative risk, 0.32; 95% CI, 0.18 to 0.56; low certainty). Oral alkali supplementation was associated with worsening hypertension or the requirement for increased antihypertensive therapy (very-low certainty). CONCLUSIONS: Low-to-moderate certainty evidence suggest that oral alkali supplementation or a reduction in dietary acid intake may slow the rate of kidney function decline and potentially reduce the risk of ESKD in patients with CKD and metabolic acidosis.

Distal renal tubular acidosis secondary to vesico-ureteric reflux: A case report with review of literature.

Vesicoureteric reflux (VUR) is the most common congenital anomaly of the urinary tract that occurs in 30%-50% of children presenting with recurrent urinary tract infections. Long-standing untreated VUR results in renal scarring and hydronephrotic changes ultimately leading to chronic renal failure and arterial hypertension. However, it may also result in diffuse tubulopathy compromising the concentrating capacity of tubules and urinary acidification defects. Renal tubular dysfunction should be considered in all children with VUR presenting with failure to thrive, rickets, bony deformity/pain, hypokalemia, and metabolic acidosis. We report such a case of a 16-year-old male adolescent who presented with rickets, failure to gain weight and height, bony pains, and muscle weakness with a history of VUR. On investigation, he was found to have normal anion gap metabolic acidosis with hypokalemia suggestive of distal renal tubular acidosis. He responded well to oral alkali and potassium replacement therapy.

Alkaline water improves exercise-induced metabolic acidosis and enhances anaerobic exercise performance in combat sport athletes.

Hydration is one of the most significant issues for combat sports as athletes often use water restriction for quick weight loss before competition. It appears that alkaline water can be an effective alternative to sodium bicarbonate in preventing the effects of exercise-induced metabolic acidosis. Therefore, the main aim of the present study was to investigate, in a double blind, placebo controlled randomized study, the impact of mineral-based highly alkaline water on acid-base balance, hydration status, and anaerobic capacity. Sixteen well trained combat sport athletes (n = 16), were randomly divided into two groups; the experimental group (EG; n = 8), which ingested highly alkaline water for three weeks, and the control group (CG; n = 8), which received regular table water. Anaerobic performance was evaluated by two double 30 s Wingate tests for lower and upper limbs, respectively, with a passive rest interval of 3 minutes between the bouts of exercise. Fingertip capillary blood samples for the assessment of lactate concentration were drawn at rest and during the 3rd min of recovery. In addition, acid-base equilibrium and electrolyte status were evaluated. Urine samples were evaluated for specific gravity and pH. The results indicate that drinking alkalized water enhances hydration, improves acid-base balance and anaerobic exercise performance.

Superior Efficacy of Lipid Emulsion Infusion Over Serum Alkalinization in Reversing Amitriptyline-Induced Cardiotoxicity in Guinea Pig.

BACKGROUND: Tricyclic antidepressants (TCAs) are a major cause of fatal drug poisoning due to their cardiotoxicity. Alkalinization by sodium bicarbonate (NaHCO3) administration, the first-line therapy for TCA-induced cardiotoxicity, can occasionally yield insufficient efficacy in severe cases. Because most TCAs are highly lipophilic, lipid emulsion may be more effective than alkalinization. However, it remains to be determined whether lipid emulsion is more beneficial than alkalinization in reversing amitriptyline-induced cardiotoxicity. METHODS: Hemodynamic variables were recorded from in vivo guinea pig models and Langendorff-perfused hearts. Whole-cell patch-clamp experiments were conducted on enzymatically isolated ventricular cardiomyocytes to record fast sodium currents (INa). Lipid solutions were prepared using 20% Intralipid. The pH of the alkaline solution was set at 7.55. We assessed the effect of lipid emulsion on reversing amitriptyline-induced cardiotoxicity, in vivo and in vitro, compared to alkalinization. The data were evaluated by Student t test, 1-way repeated-measures analysis of variance, or analysis of covariance (covariate = amitriptyline concentration); we considered data statistically significant when P < .05. RESULTS: In the in vivo model, intervention with lipids significantly reversed the amitriptyline-induced depression of mean arterial pressure and prolongation of QRS duration on electrocardiogram more than alkalinization (mean arterial pressure, mean difference [95% confidence interval]: 19.0 mm Hg [8.5-29.4]; QRS duration, mean difference [95% confidence interval] -12.0 milliseconds [-16.1 to -7.8]). In the Langendorff experiments, perfusion with 1% and 2% lipid solutions demonstrated significant recovery in left ventricular developed pressure (LVdevP), maximum change rate of increase of LVdevP (dP/dtmax) and rate-pressure product compared with alkaline solution (LVdevP [mm Hg], alkaline 57 ± 35, 1% lipid 94 ± 12, 2% lipid 110 ± 14; dP/dtmax [mm Hg/s], alkaline 748 ± 441, 1% lipid 1502 ± 334, 2% lipid 1753 ± 389; rate-pressure product [mm Hg·beats·minute], alkaline 11,214 ± 8272, 1% lipid 19,025 ± 8427, 2% lipid 25,261 ± 4803 with analysis of covariance). Furthermore, lipid solutions (0.5%-4%) resulted in greater recovery of hemodynamic parameters at 3 µM amitriptyline. Amitriptyline inhibited INa in a dose-dependent manner: the half-maximal inhibitory concentration (IC50) was 0.39 µM. The IC50 increased to 0.75 µM in the alkaline solution, 3.2 µM in 1% lipid solution, and 6.1 µM in 2% lipid solution. Furthermore, the lipid solution attenuated the use-dependent block of sodium channels by amitriptyline more than alkaline solution. On 30 consecutive pulses at 1 Hz, the current decreased to 50.1 ± 2.1, 60.3 ± 1.9, and 90.4% ± 1.8% in standard, alkaline, and 1% lipid solution, respectively. Even 0.5% lipid solution showed greater effects than the alkaline solution in all experiments. CONCLUSIONS: Lipid emulsion significantly suppressed amitriptyline-induced INa, inhibition, which was likely related to the marked improvement in hemodynamic status observed in vivo and in isolated perfused hearts. These results suggest the superiority of lipid emulsion as the first-line therapy for TCA-induced cardiotoxicity compared to alkalinization therapy.

Diet-induced acidosis and alkali supplementation.

Western diet, high in protein-rich foods and poor in vegetables, is likely to be responsible for the development of a moderate acid excess leading to metabolism deregulation and the onset or worsening of chronic disturbances. Available findings seem to suggest that diets with high protein/vegetables ratio are likely to induce the development of calcium lithiasis, especially in predisposed subjects. Moreover, some evidence supports the hypothesis of bone metabolism worsening and enhanced bone loss following acid-genic diet consumption although available literature seems to lack direct and conclusive evidence demonstrating pathological bone loss. According to other evidences, diet-induced acidosis is likely to induce or accelerate muscle wasting or sarcopenia, especially among elderlies. Furthermore, recent epidemiological findings highlight a specific role of dietary acid load in glucose metabolism deregulation and insulin resistance. The aim of this review is to investigate the role of acid-genic diets in the development of the mentioned metabolic disorders focusing on the possible clinical improvements exerted by alkali supplementation.

Neovascular growth in an experimental alkali corneal burn model.

OBJECTIVE: To analyse the length and area of corneal surface occupied by vessels, and their location in an experimental model of alkali burn-induced corneal neovascularization. METHODS: An injury to the central cornea of the right eye in 91 Sprague-Dawley rats was induced using a silver nitrate pencil. The rats were divided in 7 groups that were sacrificed 2, 4, 6, 8, 10, 12 and 14 days post-injury, and then perfused with a mixture of Chinese ink in PBS -phosphate buffer saline-. Corneas were flat-mounted processed and divided in 4 quadrants. Corneal neovascular growth parameters (length and area) and the location of these vessels were performed blind. The results were statistically analysed. RESULTS: Neovascular growth was observed from day 2, reaching its maximum peak in length and area on the 12th day post-injury. A slight reduction in corneal neovascularization was observed after this day. The vessels were initially located in the middle third of the stroma and tended to be observed in the anterior third during the course of the experiment. CONCLUSIONS: Neovascularisation was observed on day 2 post-injury in all sectors of corneal surface. Neovascular growth was uniform during the experiment. Neovessels were located in the middle and anterior third of the cornea.

A higher alkaline dietary load is associated with greater indexes of skeletal muscle mass in women.

UNLABELLED: Conservation of muscle mass is important for fall and fracture prevention but further understanding of the causes of age-related muscle loss is required. This study found a more alkaline diet was positively associated with muscle mass in women suggesting a role for dietary acid-base load in muscle loss. INTRODUCTION: Conservation of skeletal muscle is important for preventing falls and fractures but age-related loss of muscle mass occurs even in healthy individuals. However, the mild metabolic acidosis associated with an acidogenic dietary acid-base load could influence loss of muscle mass. METHODS: We investigated the association between fat-free mass (FFM), percentage FFM (FFM%) and fat-free mass index (FFMI, weight/height²), measured using dual-energy X-ray absorptiometry in 2,689 women aged 18-79 years from the TwinsUK Study, and dietary acid-base load. Body composition was calculated according to quartile of potential renal acid load and adjusted for age, physical activity, misreporting and smoking habit (FFM, FFMI also for fat mass) and additionally with percentage protein. RESULTS: Fat-free mass was positively associated with a more alkalinogenic dietary load (comparing quartile 1 vs 4: FFM 0.79 kg P < 0.001, FFM% 1.06 % <0.001, FFMI 0.24 kg/m² P = 0.002), and with the ratio of fruits and vegetables to potential acidogenic foods. CONCLUSIONS: We observed a small but significant positive association between a more alkaline diet and muscle mass indexes in healthy women that was independent of age, physical activity and protein intake equating to a scale of effect between a fifth and one half of the observed relationship with 10 years of age. Although protein is important for maintenance of muscle mass, eating fruits and vegetables that supply adequate amounts of potassium and magnesium are also relevant. The results suggest a potential role for diet in the prevention of muscle loss.

Alkaline salts to counteract bone resorption and protein wasting induced by high salt intake: results of a randomized controlled trial.

High sodium chloride (NaCl) intake can induce low-grade metabolic acidosis (LGMA) and may thus influence bone and protein metabolism. We hypothesized that oral potassium bicarbonate (KHCO(3)) supplementation may compensate for NaCl-induced, LGMA-associated bone resorption and protein losses. Eight healthy male subjects participated in a randomized trial with a crossover design. Each of two study campaigns consisted of 5 d of dietary and environmental adaptation followed by 10 d of intervention and 1.5 d of recovery. In one study campaign, 90 mmol KHCO(3)/d were supplemented to counteract NaCl-induced LGMA, whereas the other campaign served as a control with only high NaCl intake. When KHCO(3) was ingested during high NaCl intake, postprandial buffer capacity ([HCO(3)(-)]) increased (P = 0.002). Concomitantly, urinary excretion of free potentially bioactive glucocorticoids [urinary free cortisol (UFF) and urinary free cortisone (UFE)] was reduced by 14% [∑(UFF,UFE); P = 0.024]. Urinary excretion of calcium and bone resorption marker N-terminal telopeptide of type I collagen was reduced by 12 and 8%, respectively (calcium, P = 0.047; N-terminal bone collagen telopeptide, P = 0.044). There was a trend of declining net protein catabolism when high NaCl was combined with KHCO(3) (P = 0.052). We conclude that during high salt intake, the KHCO(3)-induced postprandial shift to a more alkaline state reduces metabolic stress. This leads to decreased bone resorption and protein degradation, which in turn might initiate an anticatabolic state for the musculoskeletal system in the long run.

Multiple biological complex of alkaline extract of the leaves of Sasa senanensis Rehder.

Previous studies have shown anti-inflammatory potential of alkaline extract of the leaves of Sasa senanensis Rehder (SE). The aim of the present study was to clarity the molecular entity of SE, using various fractionation methods. SE inhibited the production of nitric oxide (NO), but not tumour necrosis factor-α by lipopolysaccharide (LPS)-stimulated mouse macrophage-like cells. Lignin carbohydrate complex prepared from SE inhibited the NO production to a comparable extent with SE, whereas chlorophyllin was more active. On successive extraction with organic solvents, nearly 90% of SE components, including chlorophyllin, were recovered from the aqueous layer. Anti-HIV activity of SE was comparable with that of lignin-carbohydrate complex, and much higher than that of chlorophyllin and n-butanol extract fractions. The CYP3A inhibitory activity of SE was significantly lower than that of grapefruit juice and chlorophyllin. Oral administration of SE slightly reduced the number of oral bacteria. When SE was applied to HPLC, nearly 70% of SE components were eluted as a single peak. These data suggest that multiple components of SE may be associated with each other in the native state or after extraction with alkaline solution.

Citrate, malate and alkali content in commonly consumed diet sodas: implications for nephrolithiasis treatment.

PURPOSE: Citrate is a known inhibitor of calcium stone formation. Dietary citrate and alkali intake may have an effect on citraturia. Increasing alkali intake also increases urine pH, which can help prevent uric acid stones. We determined citrate, malate and total alkali concentrations in commonly consumed diet sodas to help direct dietary recommendations in patients with hypocitraturic calcium or uric acid nephrolithiasis. MATERIALS AND METHODS: Citrate and malate were measured in a lemonade beverage commonly used to treat hypocitraturic calcium nephrolithiasis and in 15 diet sodas. Anions were measured by ion chromatography. The pH of each beverage was measured to allow calculation of the unprotonated anion concentration using the known pK of citric and malic acid. Total alkali equivalents were calculated for each beverage. Statistical analysis was done using Pearson's correlation coefficient. RESULTS: Several sodas contained an amount of citrate equal to or greater than that of alkali and total alkali as a lemonade beverage commonly used to treat hypocitraturic calcium nephrolithiasis (6.30 mEq/l citrate as alkali and 6.30 as total alkali). These sodas were Diet Sunkist Orange, Diet 7Up, Sprite Zero, Diet Canada Dry Ginger Ale, Sierra Mist Free, Diet Orange Crush, Fresca and Diet Mountain Dew. Colas, including Caffeine Free Diet Coke, Coke Zero, Caffeine Free Diet Pepsi and Diet Coke with Lime, had the lowest total alkali (less than 1.0 mEq/l). There was no significant correlation between beverage pH and total alkali content. CONCLUSIONS: Several commonly consumed diet sodas contain moderate amounts of citrate as alkali and total alkali. This information is helpful for dietary recommendations in patients with calcium nephrolithiasis, specifically those with hypocitraturia. It may also be useful in patients with low urine pH and uric acid stones. Beverage malate content is also important since malate ingestion increases the total alkali delivered, which in turn augments citraturia and increases urine pH.

Deposition of 18-MEA onto alkaline-color-treated weathered hair to form a persistent hydrophobicity.

A technology for the deposition of a persistent hydrophobicity to alkaline-color-treated weathered hair surfaces using 18-MEA (18-methyleicosanoic acid) is presented. Two approaches were examined in order to make 18-MEA bind tightly to the alkaline-color-treated weathered hair surface. One was to apply 18-MEA as an acid form and the other was to apply 18-MEA as a salt or complex. It was found that the combination of 18-MEA with specific cationic surfactants [stearoxypropyldimethylamine (SPDA) and docosyldimethylamine (DSDA)] makes the alkaline-color-treated weathered hair surface hydrophobic and that its hydrophobicity is maintained even after shampooing. Characterization of adsorbed layers of 18-MEA/SPDA on a mica surface, as a possible hydrophilic surface model, was performed using atomic force microscopy (AFM) and angle-resolved X-ray photoelectron spectroscopy (AR-XPS). The results revealed that 18-MEA/SPDA formed a layer with high wear resistance, with an alkyl chain, the hydrophobic moiety, oriented at an angle of around 25 degrees to the air interface.

Effect of modified alkaline supplementation on bone metabolic turnover in rats.

This study aims to determine the effects of a high protein diet and alkaline supplementation on bone metabolic turnover in rats. Eight-week-old male Sprague-Dawley rats were investigated by bone status, including bone mineral density (BMD) and biomechanical markers from blood and urine. Thirty rats were randomly divided into three groups and treated for 8 weeks as follows: baseline control group (n. 10, C), high-protein supplemented diet group (n. 10, chronic acidosis, CA group) and supplemented chronic acidosis (n.10, SCA). Diet-treated rats were fed an acidic high-protein diet and the supplementation consisted in a modified alkaline formula (Basenpulver, NaMed, Italy). At the end of the experimental period, the rats were sacrificed, blood samples were drawn and femur and tibia were removed for analysis of bone mineral density (BMD) by dual energy X-ray absorptiometry (DEXA). In the CA group, 24-hour urinary calcium (Ca) and phosphorus (P) excretion were increased 2.1-fold (p<0.05 vs normal diet controls) as well as kidney weight. However, serum Ca and P concentration, as well as urinary Dpd excretion were not significantly changed. Femural and tibial BMD was significantly decreased in the CA group (p<0.05), but alkaline supplementation prevented such phenomenon (p<0.05 vs CA). These results suggest that blood Ca and P concentrations in chronic acidosis condition during the 12-week supplementation might be maintained by hypercalciuria and hyperphosphaturia at the expenses of bone structure. However, modified alkaline supplementation is able to prevent such derangements.

The potential of dental-protective chewing gum in oral health interventions.

BACKGROUND: The authors provide an overview of chewing gum as a delivery vehicle for dental-protective agents, highlighting xylitol and its potential application in caries-prevention programs for children. TYPES OF STUDIES REVIEWED: The authors reviewed selected clinical investigations and previous reviews associated with chewing gum containing substances such as calcium, bicarbonate, carbamide, chlorhexidine, fluoride and xylitol and their effects on reducing caries. They searched the MEDLINE database by using the key words "dental caries," "oral health," "calcium," "bicarbonate," "carbamide," "chlorhexidine," "fluoride" and "xylitol." RESULTS: Chewing gum is being used as a delivery vehicle for substances such as calcium, bicarbonate, carbamide, chlorhexidine, fluoride and xylitol to improve oral health and reduce caries. These substances exhibit properties that are protective of the oral environment and mediate common oral diseases. The debate for advocating xylitol use in caries prevention is advancing; however, chewing gum use by young schoolchildren in the United States is hindered by choking hazard concerns and lack of specific xylitol dosing recommendations. CLINICAL IMPLICATIONS: The use of chewing gum containing dental-protective substances, particularly xylitol, in caries-prevention programs can reduce the tooth decay epidemic. Chewing gum use by children in the school setting should be reconsidered.

[Acute renal failure due to sulfadiazine crystalluria]. / Insuficiencia renal aguda por depósito de cristales de Sulfadiacina.

Focal necrotizing encephalitis due to Toxoplasma gondii infection represents one of the most common opportunistic infection in patients with the acquired inmunodeficiency syndrome (AIDS), and the treatment is commonly with a combination sulphadiazine, and pyrimethamine. A major side effect of sulfadiazine therapy is the occurrence of crystallization in the urinary collecting system. We report a patient with AIDS and Toxoplasmic encephalitis treated with sulfadiazine who developed acute renal failure. Renal ultrasound demonstrated echogenic areas within the renal parenchyma, presumed to be sulfa crystals. Renal failure and ultrasound findings resolved rapidly with hydratation and administration of alkali. Patients infected with AIDS frequently have characteristic that increase intratubular crystal precipitation and they require treatment with one or more of the drugs that are associated with crystal-induced renal failure. Controlled alkalinization of the urine and high fluid intake are recommended for prophylaxis of crystalluria. The literature concerning crystalluria and renal failure due to sulfadiazine is reviewed.

Cystinuria in children and young adults: success of monitoring free-cystine urine levels.

Medical treatment of cystinuria is often disappointing. Patients undergo frequent surgery, which is often followed by early relapse. The aim of our study was to evaluate the efficacy of medical treatment of cystinuria, to prevent formation or to reduce the numbers and dimensions of renal stones. Twenty cystinuric patients were treated with a combined approach, including cystine-binding drugs. Free and bound urine cystine levels were measured every 4 months. Drug dosage was adjusted to maintain free urine cystine level below 100 micromol/mmol creatinine. Eighteen patients completed the study; detection of new stones was reduced from 0.28 per year to 0.03 per year, and, in six patients, the numbers and dimensions of pre-existing renal stones were reduced. Surgery was required in one subject, and no relapse was observed 12 months afterwards. The dosage required to achieve target levels was closely correlated with patient body weight: older children required a lower dose. Medical management of cystinuria is feasible. The treatment must be personalised in children, as the amount of drug required is strictly dependent on body size.

[Pathophysiology and diagnosis of renal tubular acidosis]. / Pathophysiologie und Diagnostik renal tubulärer Azidosen.

Intrinsic defects in tubular transport mechanisms of the kidney may cause impairment of urinary acidification or a loss of base equivalents, thereby inducing systemic metabolic acidosis. Different types of this disorder termed renal tubular acidosis (RTA) can be distinguished based on the localization of the disturbance along the nephron (proximal vs. distal) and their association with potassium transport (hypo-/hyperkalemic). Except for the proximal type RTA results in positive acid balance and negatively impacts on bone metabolism and the formation of kidney stones. The diagnosis is based on analysis of acid/base status, urinary pH and determination of ammonium excretion after an oral acid load. Both functional defects of specific tubular transport mechanisms and global impairment of renal tubular function can be causative of RTA. Their therapy is based on treatment of the primary disease process and correction of acidosis by alkali supplementation.

Immunostimulatory effects of the anionic alkali mineral complex Barodon on equine lymphocytes.

Previous studies have shown that the anionic alkali mineral complex BARODON has an immunoenhancing effect on pigs as an adjuvant and as a nonspecific immunostimulant. Likewise, the equine immune system has been defined with various monoclonal antibodies specific to equine leukocyte differentiation antigens to determine the possibility of enhancing equine resistance to respiratory diseases and promoting other immunostimulatory effects with the application of BARODON. Compared with the control group, after 3 weeks of treatment, BARODON-treated groups showed higher proportions of cells (P < 0.05) expressing major histocompatibility complex class II and CD2, CD4(+), CD4(+) CD25(+), CD8(+), and CD8(+) CD25(+) T lymphocytes, dendritic cells, and surface immunoglobulin M(+) B lymphocytes in peripheral blood, as well as enhanced cell proliferative responses with phytohemagglutinin and increased phagocytic activity against Streptococcus equi and Staphylococcus aureus strains with high antibiotic resistance, the bacteria frequently identified as etiologic agents of equine respiratory diseases at the Seoul Race Park in Seoul, Korea. This study shows that BARODON may act as an immunostimulator and can be an effective alternative to antimicrobial feed additives for nonspecific improvements in equine immune responses, particularly against respiratory diseases.