Metabolic Acidosis In Patients Research Articles

Impact of allopurinol on metabolic acidosis in patients with chronic kidney disease; a randomized controlledtrial

Introduction: Chronic kidney disease (CKD) is a disabling disease with multiple complications, like, increased serum levels of uric acid due to glomerular filtration rate (GFR) impairment. Objectives: This study was designed to evaluate the effect of allopurinol on metabolic acidosis in patients with renal failure. Patients and Methods: This is a randomized controlled-trial study on 50 patients with CKD stage II-IV, who referred to Qaem and Montaserieh hospitals in Mashhad. Patients were selected and randomly divided into two equal groups of 25 subjects. In addition to standard treatments, the intervention group received 100 mg allopurinol tablet for three months and the control group received placebo. Demographic data were obtained from each individual. Serum uric acid level, creatinine, blood pH and bicarbonate levels were assessed at the initiation of treatment and at the end of the third month. Results: The mean age of patients was 54.04±12.62 years. Allopurinol administration resulted in a significant increase of serum bicarbonate levels and pH (P<0.001 for each) compared to the control group. A significant reduction in uric acid (P<0.05) and an increase in GFR (P<0.05) was observed in both groups. Conclusion: Allopurinol could ameliorate metabolic acidosis, glomerular filtration and uric acid in patients with CKD.

Modern opportunities for the burn shock resuscitation

Burn shock is characterized by significant disturbances of central hemodynamic, the presence of microcirculatory disorders due to primary hypovolemia, stress reaction, mass release of inflammatory response mediators, the development of all types of hypoxia, sharp changes in the acid-base state, blood coagulation, dysproteinaemic changes, electrolyte imbalance and quickly leads to the organ dysfunction and multiple organ failure. In this regard, infusion therapy is important in the treatment of burn patients, aimed at blood rheology improving, tissues microcirculation, acidosis correction. Significant homeostatic disturbances during the burn shock acutely determine the infusion solutions choice problem for the hemodynamic disturbance’s correction. The infusion solutions characteristics of for the correction of hemodynamic disturbances during burn shock have been given. Volume deficit recovery for tissue perfusion support and metabolic acidosis correction can be achieved with crystalloid and colloid solutions. Among plasma substitutes, these are low molecular weight hydroxyethyl starch which replaced dextran and native proteins (albumin, plasma). But crystalloids cause swelling. Dextran are not applied now. Albumin transfusion is indicated only for hypoproteinaemia, and plasma for the coagulation factors deficiency. The role of Rheosorbilact in the correction of hypovolemia and metabolic acidosis in patients with burn disease is shown. The presence in clinical practice of domestic polyionic multifunctional solutions of Rheosorbilact gives a positive impetus to the development of new infusion therapy methods.

Veverimer versus placebo in patients with metabolic acidosis associated with chronic kidney disease: a multicentre, randomised, double-blind, controlled, phase 3 trial

Patients with advanced chronic kidney disease lose the capacity to fully excrete endogenous acid, resulting in chronic metabolic acidosis that increases the risk of disease progression and causes muscle catabolism and bone resorption. Veverimer, a non-absorbed, counterion-free, polymeric drug, selectively binds and removes hydrochloric acid from the gastrointestinal lumen, unlike current oral sodium bicarbonate therapy for metabolic acidosis that only neutralises accumulated acid. We assessed the efficacy and safety of veverimer as a treatment for metabolic acidosis in patients with chronic kidney disease. We did a multicentre, parallel, randomised, double-blind, placebo-controlled study at 37 sites (hospitals and specialty clinics) in Bulgaria, Croatia, Georgia, Hungary, Serbia, Slovenia, Ukraine, and the USA. Eligible participants were patients aged 18-85 years with non-dialysis-dependent chronic kidney disease (estimated glomerular filtration rate of 20-40 mL/min per 1·73 m2) and metabolic acidosis (serum bicarbonate concentration of 12-20 mmol/L). Patients were randomly assigned (4:3) to veverimer 6 g/day or placebo for 12 weeks while they consumed their typical diet. Both drugs were taken as oral suspensions in water with lunch. Randomisation was done by study site personnel with a computer-generated randomisation code with balanced permuted blocks (block size of seven) and stratified by baseline bicarbonate (≤18 mmol/L vs >18 mmol/L). Patients and investigators were masked to treatment allocation; however, because the appearance of placebo differed from veverimer, a non-masked site staff member who had no other role in the study dispensed, prepared, and supervised dosing of the study drugs. The composite primary efficacy endpoint was the difference (veverimer-placebo) in the proportion of patients achieving at week 12 either an increase of 4 mmol/L or more from baseline in serum bicarbonate concentration or serum bicarbonate in the normal range of 22-29 mmol/L, assessed in the modified intention-to-treat population (all patients with a baseline and at least one post-baseline serum bicarbonate value). Patients fasted for at least 4 h (consuming only water) before measurements of bicarbonate. Safety was assessed in all patients who received any amount of study drug. This trial is registered with ClinicalTrials.gov, number NCT03317444. Between Sept 26, 2017, and Feb 9, 2018, we randomly assigned 124 participants to veverimer and 93 to placebo. The composite primary endpoint was met by 71 (59%) of 120 patients in the veverimer group versus 20 (22%) of 89 patients in the placebo group (a difference of 37%, 95% CI 23-49; p<0·0001). The most common body system in which adverse events in the veverimer group occurred was gastrointestinal; of these, non-treatment limiting diarrhoea was the most common event (11 [9%] vs three [3%] in the veverimer and placebo groups, respectively). The most common treatment-related adverse events were gastrointestinal (diarrhoea, flatulence, nausea, and constipation) occurring in 16 (13%) patients with veverimer and five (5%) patients with placebo. Two deaths occurred during the study, both in the placebo group (unstable angina and pneumonia). Veverimer effectively and safely corrected metabolic acidosis. Longer-term studies are warranted to assess the effects of veverimer on physical functioning and to assess other deleterious consequences of metabolic acidosis including progression of chronic kidney disease and bone health. Tricida.

Correction

Topiramate (TMP) is a broad-spectrum anticonvulsant drug used to treat a wide variety of seizure disorders, for migraine prophylaxis, and for many other indications. An important side effect of TMP is metabolic acidosis, which is mediated by renal tubular defects. TMP inhibits carbonic anhydrase, an enzyme that is necessary for acid handling in the proximal renal tubule. Patients can present with asymptomatic serum electrolyte derangements, acute change in mental status, hyperventilation, cardiac arrhythmias, or other sequelae of metabolic acidosis and associated respiratory compensation. If taken chronically, TMP can cause renal stone formation, bone mineralization defects, and several other effects secondary to changes in serum and urine pH and electrolytes. There is no well-studied way to prevent metabolic acidosis in patients taking TMP, but physicians should be vigilant when prescribing this drug to patients with the history of renal diseases and other comorbidities, and aware of this potential etiology of metabolic acidosis. We present a literature review of the underlying mechanisms involved in the development of renal tubular acidosis secondary to TMP and its clinical consequences.

Type II Renal Tubular Acidosis Secondary to Topiramate: A Review.

Topiramate (TMP) is a broad-spectrum anticonvulsant drug used to treat a wide variety of seizure disorders, for migraine prophylaxis, and for many other indications. An important side effect of TMP is metabolic acidosis, which is mediated by renal tubular defects. TMP inhibits carbonic anhydrase, an enzyme that is necessary for acid handling in the proximal renal tubule. Patients can present with asymptomatic serum electrolyte derangements, acute change in mental status, hyperventilation, cardiac arrhythmias, or other sequelae of metabolic acidosis and associated respiratory compensation. If taken chronically, TMP can cause renal stone formation, bone mineralization defects, and several other effects secondary to changes in serum and urine pH and electrolytes. There is no well-studied way to prevent metabolic acidosis in patients taking TMP, but physicians should be vigilant when prescribing this drug to patients with the history of renal diseases and other comorbidities, and aware of this potential etiology of metabolic acidosis. We present a literature review of the underlying mechanisms involved in the development of renal tubular acidosis secondary to TMP and its clinical consequences.

Blood Gas Analysis in Neonatal Tetanus

We reviewed the results of arterial blood gas analysis in 127 patients with neonatal tetanus on admission, and in 52 of such patients on the day before they died. All patients were hospitalized at the Department of Child Health, Cipto Mangunkusumo Hospital, Jakarta. On admission, most patients showed uncompensated metabolic acidosis. The mortality of patients wjth pH ofless than 7 was 100%. There was no significant difference between the mortality of patients with pH 7.35-7.45 and those with pH of less than 7.35. Analysis of acid-base balance indicated that ventilatory fw1ure was the most common finding in 52 patients who subsequently died. We recommend using intravenous fluid containing a combination of 5% dextrose and sodium bicarbonate with 4 : 1 (vol/vol) ratio from the fust day of hospitalization to reduce the possibility of the development of ongoing metabolic acidosis in patients with neonatal tetanus. Maintaining adequate ventilation is mandatory ln such patients.

PENDEKATAN STEWART DALAM pH DARAH YANG MENDASARI ASIDOSIS METABOLIK

Metabolic acidosis is the most frequent acid-base disorder in patients of the Intensive Care Unit. By conventional approach based onpH value, [HCO3–], and base deficit (BD) from blood gas analyzer (BGA) measurement are often inappropriate with the clinical stateand inadequate in explaining the mechanism of the metabolic acidosis. The Stewart approach states that the blood pH is determinedby a strong ion difference (SID), the carbon dioxide tension (pCO2), the total concentration of non-volatile weak acid. The Stewartapproach may give a better understanding of the mechanisms that underlie the metabolic acidosis. The purpose of this study is to knowthe correlation of blood pH value measurement from BGA and calculation based on Stewart approach and identifying the mechanismsthat underlie a metabolic acidosis. In this study an analytic observational cross-sectional method was used. The examined subjectsconsisted of 71 patients who were admitted with a metabolic acidosis at the ICU from July up to August 2007. All patients were measuredfor their blood pH, pCO2, [HCO3–], BD, sodium, potassium, calcium, magnesium, chloride, lactate, albumin, and phosphate. The resultwas reported as the mean and standard deviation. The data were analyzed by Pearson's correlation test and linier multiple regression.Statistical significance was determined at p &lt; 0.05. The mean values of blood pH measurement from BGA and blood pH calculationbased on the Stewart approach were 7.33 (0.11) and 7.49 (0.11) (r = 0.681; p &lt; 0.001). Most patients had two underlying mechanisms ofmetabolic acidosis. Hyperlactatemia was present in 61.8%, hyperchloremia was present in 58.2% of patients. Based on this study so far,by using the Stewart approach there is an excellent and significant correlation between the blood pH measurement from BGA and bloodpH calculation. Hyperlactatemia and hyperchloremia are the main causes of the metabolic acidosis in patients of the ICU ward.

Assessing Propylene Glycol Toxicity in Alcohol Withdrawal Patients Receiving Intravenous Benzodiazepines: A One-Compartment Pharmacokinetic Model.

While some case reports indicate that high doses of propylene glycol (PG) may result in metabolic acidosis, there has been no large-scale study that evaluatedthe risk of metabolic acidosis in patients receiving PG-containing benzodiazepines for acute alcohol withdrawal. This study was undertaken to evaluate the potential toxicity of PG in patients with acute alcohol withdrawal treated with intermittent intravenous bolus doses of diazepam and/or lorazepam. This is a retrospective case study using data collected from 18 randomly selected patients receiving one or both of these medications per a modified Clinical Institute Withdrawal Assessment for Alcohol (CIWA) Class 3 protocol. Plasma levels of PG were estimated using a one-compartment pharmacokinetic model. Only two patients had an elevated anion gap compared to their baseline value with one also experiencing a significant increase in serum creatinine. No increases in serum osmolarity were noted. Analysis showed that the benzodiazepine dose received was a good predictor of the estimated PG concentration (r=0.6), but was poorly correlated with the anion gap. No significant correlation was found with the creatinine clearance or serum creatinine. Patients receiving several daily doses were at higher risk of developing an anion gap (r=0.33), but the estimated maximum PG concentration did not correlate with the anion gap or serum concentration. It does not appear that intermittent bolus administration of intravenous benzodiazepines for alcohol withdrawal influenced renal function or anion gap regardless of number of administered doses, amount of PG received, or the estimated PG concentration.

Prevalence of hemolysis and metabolic acidosis in patients with circulatory failure supported with extracorporeal life support: a marker for survival?

Elevated levels of plasma free hemoglobin (fHb) indicate red blood cell (RBC) damage. The aim of this study was to analyze the prevalence of hemolysis and metabolic acidosis in patients on extracorporeal life support (ECLS) and to investigate whether it is a marker for outcome. This retrospective analysis included 215 adult patients with cardiac failure treated with ECLS. The cohort was divided into three groups: ECLS (1) during ongoing cardiopulmonary resuscitation (CPR, n = 110); (2) after CPR with return of spontaneous circulation and sustained cardiogenic shock (n = 45); (3) in severe cardiogenic shock without previous CPR (n = 60). Lactate, arterial pH value and fHb were measured daily before (pre-fHb) and during ECLS. CPR caused a pronounced increase in pre-fHb (group1, 318 (138/586) mg/L; group2, 212 (107/439) mg/L; group3, 79 (53/232) mg/L; p < 0.001). Within 24 hours on ECLS, fHb declined significantly. Compared to group 3 without CPR, group1 and 2 had a lower pH value (group1, 7.10 (6.93/7.20); group2, 7.21 (7.16/7.27); group3, 7.28 (7.20/7.35); p < 0.001), and an increased lactate level (group1, 88 (55/129) mg/dL; group2, 76 (36/111) mg/dL; group3, 52 (25/83) mg/dL; p < 0.0001). Multivariante analysis showed that pre-fHb had no prognostic value for survival. Only a low pre-lactate was a surrogate marker for successful weaning (p < 0.0001) and discharge from hospital (p = 0.0028). CPR was associated with a strongly increased fHb irrespective of ECLS. Implantation of ECLS did not aggravate hemolysis but instead decreased it within 24 hours. In this study low pre-fHb had no predictive value for survival.

Acid-base disorders after orthotopic bladder replacement: comparison of an ileal neobladder and an ileal conduit

Objectives: For many years, creation of an orthotopic neobladder after cystectomy has been popular. In the present study, we measured the extent of metabolic acidosis in patients with ileal neobladders compared with ileal conduits and defined risk factors for development of metabolic acidosis.Methods: We retrospectively studied 95 patients, who underwent radical cystectomy and urinary diversion to treat invasive bladder cancer from January 2001 to December 2014 at Hallym University Kangnam Sacred Heart Hospital, through investigation of acid-base balance, serum electrolyte levels and renal function one month and one year after operation.Results: One month after the operation, metabolic acidosis was found from 18 patients (31.0%) in an ileal neobladder group and from 4 (14.8%) in an ileal conduits group. One year after the operation, the numbers became 11 (22.9%) and 2 (10.0%), respectively. However, there was not a statistical difference. The blood biochemical profiles of the two groups did not differ significantly after urinary diversion. Logistic analysis revealed that lower estimated glomerular filtration rate (eGFR) was associated with metabolic acidosis at one month (odds ratio, OR = 0.94 [0.91–0.97]; p < 0.001) and one year (OR = 0.94 [0.92–0.97]; P = 0.001) after urinary diversion. In multivariate analysis, lower eGFR is a significant risk factor for metabolic acidosis at one month.Conclusions: Patients with ileal neobladders and conduits are at the similar risk of metabolic acidosis. A close association between renal function and development of metabolic acidosis was observed, especially stronger in an early period after operation.

Acid retention with reduced glomerular filtration rate increases urine biomarkers of kidney and bone injury

Diets high in acid of developed societies that do not cause metabolic acidosis in patients with chronic kidney disease nevertheless appear to cause acid retention with associated morbidity, particularly in those with reduced glomerular filtration rate. Here we used a rat 2/3 nephrectomy model of chronic kidney disease to study induction and maintenance of acid retention and its consequences on indicators of kidney and bone injury. Dietary acid was increased in animals eating base-producing soy protein with acid-producing casein and in casein-eating animals with added ammonium chloride. Using microdialysis to measure the kidney cortical acid content, we found that nephrectomized animals had greater acid retention than sham-operated animals when both ate the soy diet. Each increment in dietary acid further increased acid retention more in nephrectomized than in sham rats. Nephrectomized and sham animals achieved similar steady-state daily urine net acid excretion in response to increments in dietary acid but nephrectomized animals took longer to do so, contributing to greater acid retention that was maintained until the increased dietary acid was stopped. Acid retention was associated with increased urine excretion of both N-acetyl-β-D-glucosaminidase and deoxypyridinoline, greater in nephrectomized than control rats, consistent with kidney tubulointerstitial and bone matrix injury, respectively. Greater acid retention in nephrectomized than control animals was induced by a slower increase in urinary net acid excretion rate in response to the increment in dietary acid and also maintained until the dietary acid increment was stopped. Thus, acid retention increased biomarkers of kidney and bone injury in the urine, supporting untoward consequences to these two tissues.

Hyperglycemic, high anion-gap metabolic acidosis in patients receiving SGLT-2 inhibitors for diabetes management

Sodium-glucose cotransporter-2 inhibitors (SGLT-2i) are a class of antidiabetic medications that improve glycemic control via inhibiting the reabsorption of filtered glucose and are approved for use in type 2 diabetes (T2DM). These drugs have recently been associated with euglycemic diabetic ketoacidosis (DKA). An increasing number of cases of SGLT-2i-associated DKA have occurred in patients with T2DM. Herein, we describe five episodes of hyperglycemic DKA in four type 2 diabetes patients receiving SGLT-2i therapy. Risk for ketoacidosis in our case series was mediated predominately by reduction of insulin dose and insulinopenia. None of the patients reported a history of low carbohydrate diet or alcohol use, and all but one patient had negative glutamic acid decarboxylase antibodies. Resolution of DKA in SGLT-2i treated patients took longer than for T1DM patients with DKA based on literature data. The mechanisms by which SGLT-2i are associated with ketoacidosis are not fully understood and likely involve hyperglucagonemia and other factors. Further studies are needed to elucidate the precise mechanism.

The frequency and severity of metabolic acidosis related to topiramate.

ObjectiveWe planned a cross-sectional analysis to determine the frequency and severity of metabolic acidosis in patients taking topiramate while awaiting craniotomy.MethodsEighty patients (18 – 65 years) taking topiramate to control seizures while awaiting elective craniotomy were enrolled. Any signs of metabolic acidosis or topiramate-related side effects were investigated. Blood chemistry levels and arterial blood gases, including lactate, were obtained. The severity of metabolic acidosis was defined according to base excess levels as mild or moderate.ResultsBlood gas analysis showed that 71% (n = 57) of patients had metabolic acidosis. The frequency of moderate metabolic acidosis was 56% (n = 45), while that of mild metabolic acidosis was 15% (n = 12). A high respiratory rate was reported in only 10% of moderately acidotic patients.ConclusionsIn patients receiving topiramate, baseline blood gas analysis should be performed preoperatively to determine the presence and severity of metabolic acidosis.

Con: Higher serum bicarbonate in dialysis patients is protective.

Metabolic acidosis is often observed in advanced chronic kidney disease, with deleterious consequences on the nutritional status, bone and mineral status, inflammation and mortality. Through clearance of the daily acid load and a net gain in alkaline buffers, dialysis therapy is aimed at correcting metabolic acidosis. A normal bicarbonate serum concentration is the recommended target in dialysis patients. However, several studies have shown that a mild degree of metabolic acidosis in patients treated with dialysis is associated with better nutritional status, higher protein intake and improved survival. Conversely, a high bicarbonate serum concentration is associated with poor nutritional status and lower survival. It is likely that mild acidosis results from a dietary acid load linked to animal protein intake. In contrast, a high bicarbonate concentration in patients treated with dialysis could result mainly from an insufficient dietary acid load, i.e. low protein intake. Therefore, a high pre-dialysis serum bicarbonate concentration should prompt nephrologists to carry out nutritional investigations to detect insufficient dietary protein intake. In any case, a high bicarbonate concentration should be neither a goal of dialysis therapy nor an index of adequate dialysis, whereas mild acidosis could be considered as an indicator of appropriate protein intake.

Prevalence and severity of metabolic acidosis in patients on maintenance hemodialysis in India

Aim: Metabolic acidosis is a feature of chronic kidney disease (CKD) due to the reduced capacity of the kidney to synthesize ammonia and excrete hydrogen ions. Among the many goals of hemodialysis (HD), the role in correction of metabolic acidosis is an important one. To assess the prevalence and severity of metabolic acidosis in the Indian patients of CKD, who are on maintenance HD (MHD). Methods: This is a cross-sectional study on 35 patients conducted at two centers in Western part of India. The demographic, clinical, and laboratory assessments were done on chronic stable patients receiving MHD. The prevalence and severity of metabolic acidosis were evaluated. Results: Metabolic acidosis was found in 22 out of 35 patients (62.85%), with mean predialysis serum pH and HCO 3 of 7.32 ± 0.083 and 20.37 ± 4.94 mmol/L, respectively. Conclusion: Metabolic acidosis is significantly prevalent in patients on MHD in India.

A profile of metabolic acidosis in patients with sepsis in an Intensive Care Unit setting

Context:Metabolic acidosis is frequently found in patients with severe sepsis. An understanding of types of acidosis in sepsis and their evolution over the course of treatment may give us insight into the behavior of acid–base balance in these patients.Aims:To describe at Intensive Care Unit (ICU) admission and over the first 5 days the composition of metabolic acidosis in patients with sepsis and to evaluate and compare acidosis patterns in survivors and nonsurvivors.Settings and Design:A prospective study conducted at Amrita Institute of Medical Sciences, Kochi, Kerala, in the Department of Internal Medicine.Subjects and Methods:Seventy-five consecutive patients admitted in the medical ICU with sepsis and metabolic acidosis were assessed. Arterial blood gas and serum electrolytes were measured during the first five days of admission or until death, renal replacement or discharge supervened.Statistical Analysis:To test the statistical significance of the difference in mean values of different study variables at day 1 and last day between survivors and non survivors, Mann–Whitney U-test was applied. To test the statistical significance of the difference in mean changes in different study parameters from day 1 to last day, paired t-test was done in the survivor group and Mann–Whitney U-test in the non survivor group.Results:Regardless of survival status, on day 1 of admission, 37 had High Anion Gap metabolic acidosis (HAGMA), 21 had predominant lactic acidosis (LA), 8 had Normal anion gap metabolic acidosis (NAGMA), and 9 had both HAGMA and LA [Figure 1]. When we compared this to the last day, 25 had HAGMA, 3 had LA, 3 had both HAGMA and LA, and 22 patients had resolution of acidosis. Sixty–four patients survived for up to 5 days of admission. Fifteen of these patients underwent hemodialysis on the day of admission itself in view of HAGMA. The remaining 49 comprised of HAGMA (31), Lactic acidosis (12), and a combination (6) on day 1. On the last day in this group, 25 had HAGMA, 2 had LA, and 22 patients had resolution of acidosis. In survivors, over the observation period, changes seen were: mean pH: 7.25–7.34 (P < 0.001), mean serum bicarbonate: 13.9 mEq to 17.2 mEq (P < 0.001), and mean serum lactate: 3.18–1.9 (P = 0.002). The changes in serum albumin and pCO2 were not significant. Eleven patients in the study population succumbed. Seven patients underwent hemodialysis on day 1 and the remaining four were followed up for more than 1 day. On day 1, 7 had lactic acidosis and 5 had HAGMA. Over the observation period, changes seen were mean pH: 7.15–7.14, mean serum lactate: 6.3–7.3 mEq.Conclusions:In patients with sepsis and septic shock, high anion gap metabolic acidosis is the dominant blood gas anomaly. Fall in lactate levels over the first 5 days of admission is a good prognostic marker of survival. Evolution of the blood gas profile over time suggests that a fall in lactate levels and a rise in bicarbonate levels correlate with a better outcome. The role of the anion gap as a prognostic marker holds promise and further studies are needed in this regard.

Prevalence and severity of metabolic acidosis in patients on maintenance hemodialysis in India

Prevalence and severity of metabolic acidosis in patients on maintenance hemodialysis in India

The effect of lanthanum carbonate on metabolic acidosis in patients with chronic kidney disease stage IV, V and V-D.

Hyperphosphatemia and metabolic acidosis are frequently encountered in advanced chronic kidney disease (CKD) patients. Correction of metabolic acidosis in patients with advanced CKD leads to a decrease in the progression of renal impairment and improves nutritional outcomes. Lanthanum carbonate is used for control of hyperphosphatemia. This study evaluated the effect of lanthanum carbonate on metabolic acidosis in CKD IV-V patients and in patients on dialysis. Retrospective data of patients in whom lanthanum carbonate therapy was initiated were collected from 2009 to 2013 in a single dialysis center. Of the 79 patients in whom lanthanum carbonate was introduced, 51 patients were included in the analysis. Of the 51 patients, 39 patients received chronic hemodialysis, two patients received peritoneal dialysis therapy, and 10 patients had stage IV-V CKD not on dialysis. The primary outcome was the serum bicarbonate change after the introduction of lanthanum carbonate. There was a significant increase in mean serum bicarbonate concentration of 2.79 mmol/L (p ≤ 0.001) compared to baseline. The increase remained in the CKD IV-V patients (2.50 mmol/L, p = 0.005) and in the patients on dialysis (2.81 mmol/L, p < 0.001). Serum bicarbonate remained higher (p > 0.05) than baseline up to 6 months after lanthanum carbonate introduction. In this study, lanthanum carbonate introduction increased serum bicarbonate concentration in a small sample of CKD IV-V patients and in patients on dialysis. Further studies are needed to confirm this effect and investigate whether the correction of metabolic acidosis by using lanthanum carbonate in CKD IV-V patients can improve clinical outcomes.

Development of Metabolic Acidosis after Neobladder Reconstruction

Objectives: Metabolic acidosis frequently develops in patients after neobladder reconstruction. However, the incidence of metabolic acidosis in patients with neobladder and the factors associated with the development of metabolic acidosis have not been well elucidated. We aimed to investigate the incidence and the potential predictors for the development of metabolic acidosis after neobladder reconstruction with intestinal segment. Methods: We included patients who underwent neobladder reconstruction using intestinal segment at Ewha Womans University Mokdong Hospital between January 1, 2005 and December 31, 2014. A subgroup of patients according to the time of metabolic acidosis occurrence was further analyzed in order to characterize predictors for metabolic acidosis. Results: Metabolic acidosis was encountered in 79.4% of patients with neobladder during follow up period. When patients were divided into 2 groups according to anion gap (AG), total CO2 (18.9±2.1 mEq/L vs. 20.0±1.3 mEq/L, P=0.001) and chloride (106.6±4.9 mE/L vs. 109.4±3.6 mEq/L, P 12 and AG≤12. Furthermore, when patients were divided into 3 groups; patients with metabolic acidosis at postoperative day (POD) 1; from POD 2 to 14 days; after 14 days, there was significant difference among those subgroups. Conclusion: Our study showed the rate of metabolic acidosis in patients underwent neobladder reconstruction and the difference between patients with metabolic acidosis and those without metabolic acidosis for the first time in Korea. In the future, well designed prospective study will be needed to prevent metabolic acidosis after neobladder reconstruction. (Ewha Med J 2015;38(3):98-105) Received May 6, 2015 Accepted July 2, 2015

Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rate

Alkali therapy of metabolic acidosis in patients with chronic kidney disease (CKD) with plasma total CO2 (TCO2) below 22 mmol/l per KDOQI guidelines appears to preserve estimated glomerular filtration rate (eGFR). Since angiotensin II mediates GFR decline in partial nephrectomy models of CKD and even mild metabolic acidosis increases kidney angiotensin II in animals, alkali treatment of CKD-related metabolic acidosis in patients with plasma TCO2 over 22 mmol/l might preserve GFR through reduced kidney angiotensin II. To test this, we randomized 108 patients with stage 3 CKD and plasma TCO2 22-24 mmol/l to Usual Care or interventions designed to reduce dietary acid by 50% using sodium bicarbonate or base-producing fruits and vegetables. All were treated to achieve a systolic blood pressure below 130 mm Hg with regimens including angiotensin converting enzyme inhibition and followed for 3 years. Plasma TCO2 decreased in Usual Care but increased with bicarbonate or fruits and vegetables. By contrast, urine excretion of angiotensinogen, an index of kidney angiotensin II, increased in Usual Care but decreased with bicarbonate or fruits and vegetables. Creatinine-calculated and cystatin C-calculated eGFR decreased in all groups, but loss was less at 3 years with bicarbonate or fruits and vegetables than Usual Care. Thus, dietary alkali treatment of metabolic acidosis in CKD that is less severe than that for which KDOQI recommends therapy reduces kidney angiotensin II activity and preserves eGFR.