sodium-bicarbonate and Kidney-Failure--Chronic

Individuals with CKD are at a higher risk of cardiovascular morbidity and mortality. Acidosis is positively correlated with CKD progression and elevated systolic BP. Sodium bicarbonate is an efficacious treatment of acidosis, although this may also increase systolic BP. In this systematic review and meta-analysis, we summarize the evidence evaluating systolic BP and antihypertensive medication change (which may indicate systolic BP change) in response to sodium bicarbonate therapy in individuals with CKD.. Medical Literature Analysis and Retrieval System Online, Excerpta Medica database, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, Cochrane Central Register of Controlled Trials, and World Health Organization (WHO) trials registry databases were searched for randomized control trials where sodium bicarbonate was compared with placebo/usual care in CKD stage G1-5 non-dialysis-dependent populations. Random effects meta-analyses were used to evaluate changes in systolic BP and BP-modifying drugs after sodium bicarbonate intervention.. Fourteen randomized control trials (2110 individuals, median follow-up 27 [interquartile range 97] weeks, mean age 60 [SD 10] years, mean systolic BP 136 [SD 17] mm Hg, mean eGFR 38 [SD 10] ml/min, mean serum bicarbonate 22 [SD 4] mmol/L) were eligible for inclusion. Meta-analysis suggested that sodium bicarbonate did not influence systolic BP in individuals with CKD stage G1-5. Results were consistent when stratifying by dose of sodium bicarbonate or duration of intervention. Similarly, there was no significant increase in the use of antihypertensive medication or diuretics in individuals taking sodium bicarbonate, whereas there was a greater decrease in antihypertensive medication use in individuals taking sodium bicarbonate compared with controls.. Our results suggest, with moderate certainty, that sodium bicarbonate supplementation does not adversely affect systolic BP in CKD or negatively influence antihypertensive medication requirements.

Topics: Acidosis; Antihypertensive Agents; Blood Pressure; Humans; Hypertension; Kidney Failure, Chronic; Middle Aged; Sodium Bicarbonate

Clinical studies of the last 15 years have shown the benefit of pharmacological interventions on the progression of chronic kidney disease, confirming the concept of nephroprotection. Pharmacological blockade of the renin angiotensin system remains the cornerstone of the nephroprotective treatment but the benefits and limitations are now better defined. The RAS blockers are all the more efficient than the proteinuria is abundant and nephroprotection is obtained in proportion to the reduction in proteinuria. Combinations of ACEI+ARA are not validated and their use should be considered only under the supervision of a specialist when optimal monotherapy has failed. The target blood pressure has been the subject of recent controversies, particularly in type 2 diabetic patients with nephropathy. The target should be individualized based on the main risk, renal or cardiovascular. Recent maneuvers have also shown a nephroprotective effect, including the correction of metabolic acidosis with sodium bicarbonate.

Topics: Acidosis; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Blood Pressure; Combined Modality Therapy; Diabetic Nephropathies; Disease Progression; Drug Therapy, Combination; Humans; Kidney Failure, Chronic; Randomized Controlled Trials as Topic; Risk Factors; Sodium Bicarbonate; Survival Rate

Contrast media induced nephropathy is a common complication, particularly in high risk patients, such as patients with chronic kidney disease (CKD) and diabetes. The majority of studies show an increased in-hospital mortality and an unfavourable long-term prognosis after manifestation of contrast media induced nephropathy. The course and the potential risk factors of this type of acute renal failure are known. Therefore, an effective prophylaxis should allow to prevent this complication. In low risk patients oral or intravenous volume expansion is probably sufficient combined with the withdrawal of non-steroidal anti-inflammatory drugs. In high risk patients additional prophylactic measures are needed but their efficacy is not clearly defined. Therefore, heterogeneous recommendations exist. Hydration reduces (afferent) renovasoconstriction, the tubuloglomerular feedback, the tubulotoxic effects of contrast media (via dilution) and the oxygen radical formation. The optimal composition, timing and amount of fluid which should be administered to the patients remain unclear. Most studies show that intravenous administration of volume is more effective than oral fluid intake. The majority of studies found a benefit of isotonic sodium bicarbonate in comparison to isotonic saline solutions, even if meta-analyses displayed only a positive trend for sodium bicarbionate due to the heterogeneity of the data. Controversies exist for N-acetylcysteine, vitamin C, fenoldopam, theophylline or statins. Due to low cost and low side effects, N-Acetylcysteine is widely used. Theophyllin (given intravenously 30 minutes before contrast media injection) is renoprotective, particularly in intensive care unit patients. Very important is the reduction of contrast media volume (if possible <30 ml for diagnostic procedures and <100 ml for interventions). Iso-osmolar and low-osmolar contrast media may have a comparable low risk for the induction of contrast media induced nephropathy. This risk is probably higher after intra-arterial as compared to intravenous administration of contrast media. Controversies exist with respect to the reduction of contrast media induced nephropathy and mortality by prophylactic hemodialysis or hemofiltration. A possible benefit of these procedures consists probably for patients with advanced chronic kidney disease (stage 5). With the further increase of investigations using contrast media, with the further increase in vascular interventions, in age and

Topics: Acetylcysteine; Acute Kidney Injury; Algorithms; Contrast Media; Creatinine; Critical Care; Fluid Therapy; Glomerular Filtration Rate; Hospital Mortality; Humans; Kidney Failure, Chronic; Osmolar Concentration; Renal Dialysis; Risk Factors; Sodium Bicarbonate; Theophylline

Acute renal dysfunction after radiocontrast in patients with pre-existing renal impairment is not uncommon and is associated with significant morbidity and mortality. Isotonic sodium bicarbonate solution was first reported to reduce radiocontrast nephropathy in 2004. This first study was, however; limited by its small sample size and as such, the use of isotonic sodium bicarbonate to prevent radiocontrast nephropathy is still not widely used by many anaesthetists and intensivists. We meta-analysed relevant randomised controlled studies sourced from the Cochrane Controlled Trial Register (2007 issue 4), EMBASE and MEDLINE databases (1966 to April 15, 2008) without any language restriction. The use of isotonic sodium bicarbonate was associated with a significant reduction in risk of an incremental rise in serum creatinine concentration 25% above baseline (relative risk 0.22, 95% confidence interval [CI]: 0.11 to 0.44, P < 0.0001; 2 = 0%) and had a protective effect on the absolute change in serum creatinine concentration (weighted-mean-difference -9.4 micromol/l, 95% CI: -17.2 to -1.7, P = 0.02; F = 0%) and creatinine clearance (weighted-mean-difference 3.7 ml/min, 95% CI: 0.55 to 6.80, P = 0.02; F = 57.1%) after radiocontrast. The incidence of acute renal failure requiring dialysis was low (1.4%) and was not significantly different after the use of isotonic sodium bicarbonate (relative risk 0.59, 95% CI: 0.15 to 2.42, P = 0.47; F = 0%). With the limited data available, isotonic sodium bicarbonate appears to be safe and very effective in reducing radiocontrast nephropathy in patients with mild pre-existing renal impairment. A large randomised controlled study is needed to confirm whether isotonic bicarbonate can improve patient centred clinical outcomes.

Topics: Acute Kidney Injury; Adult; Contrast Media; Creatinine; Humans; Isotonic Solutions; Kidney Failure, Chronic; Randomized Controlled Trials as Topic; Sodium Bicarbonate

Poisoning with flecainide acetate is rare and associated with a high mortality. This usually occurs after massive ingestion but can also be observed during therapeutic overdose in patients with renal failure or with amiodarone therapy. The prognostic depends on the haemodynamic and rhythmic effects of the overdose one sign of which is widening of the QRS complexes. Major sodium bicarbonate or lactate infusion is the generally prescribed treatment. The authors report one case of a patient with renal failure on amiodarone who survived a severe flecainide acetate overdose.

Topics: Aged; Amiodarone; Anti-Arrhythmia Agents; Atrial Flutter; Biological Availability; Calcium Gluconate; Charcoal; Combined Modality Therapy; Consciousness Disorders; Diabetic Nephropathies; Drug Interactions; Drug Therapy, Combination; Flecainide; Heart Block; Hemofiltration; Humans; Hypertension; Hypotension; Intestinal Pseudo-Obstruction; Kidney Failure, Chronic; Male; Poisoning; Pulmonary Edema; Renal Dialysis; Respiration, Artificial; Sodium Bicarbonate; Sodium Channel Blockers; Uremia

Topics: Animals; Catecholamines; Emergency Service, Hospital; Humans; Hyperkalemia; Insulin; Kidney Failure, Chronic; Potassium; Practice Guidelines as Topic; Renal Dialysis; Sodium Bicarbonate

Metabolic acidosis increases protein degradation resulting in muscle wasting and a negative nitrogen balance. The branched-chain amino acids serve as useful markers of these changes and their catabolism is increased in acidosis, particularly for the spontaneous acidosis associated with renal failure. As a result, the neutral nitrogen balance is compromised and malnutrition results. Glucocorticoids mediate these changes through the recently discovered ATP-dependent ubiquitin-proteasome pathway. Therapy necessitates correction of the underlying acidosis either through adjustment of the alkalinity of the dialysate for the patient on dialysis or through dietary protein restriction and sodium bicarbonate supplements for the predialysis patient.

Topics: Acidosis; Amino Acids, Branched-Chain; Dietary Proteins; Humans; Kidney Failure, Chronic; Muscle Proteins; Proteins; Sodium Bicarbonate; Ubiquitins

Follow-up of a previously reported family with dominantly inherited adult onset hypophosphatemic osteomalacia with Fanconi syndrome and diabetes mellitus has shown that both the proposita and her affected sister have developed renal glomerular failure. We describe the evolution of renal failure in this family and discuss the possible mechanisms involved. The development of renal tubular acidosis in this condition further impairs renal function and we suggest that correction of systemic acidosis might improve renal function and prevent further decline in these patients.

Topics: Acidosis, Renal Tubular; Adolescent; Adult; Bicarbonates; Child; Child, Preschool; Diabetes Complications; Diabetes Mellitus; Fanconi Syndrome; Female; Follow-Up Studies; Humans; Kidney Failure, Chronic; Male; Osteomalacia; Pedigree; Phosphates; Sodium; Sodium Bicarbonate

Guidelines advise periprocedural saline hydration for prevention of contrast induced-acute kidney injury (CI-AKI). We analysed whether 1-hour sodium bicarbonate hydration administered solely prior to intra-arterial contrast exposure is non-inferior to standard periprocedural saline hydration in chronic kidney disease (CKD) patients undergoing elective cardiovascular diagnostic or interventional contrast procedures.. We performed an open-label multicentre non-inferiority trial between 2011-2014. Patients were randomized to 1 hour pre-procedure sodium bicarbonate hydration (250 ml 1.4%, N = 168) or 4-12 hours saline hydration (1000 ml 0.9%, N = 165) prior to and following contrast administration (2000 ml of saline total). Primary outcome was the relative serum creatinine increase (%) 48-96 hours post contrast exposure. Secondary outcomes were: incidence of CI-AKI (serum creatinine increase>25% or >44μmol/L), recovery of renal function, the need for dialysis, and hospital costs within two months follow-up.. Mean relative creatinine increase was 3.1% (95%CI 0.9 to 5.2%) in the bicarbonate and 1.1% (95%CI -1.2 to 3.5%) in the saline arm, mean difference 1.9% (95%CI -1.2 to 5.1%, p-non-inferiority <0.001). CI-AKI occurred in 11 (6.7%) patients randomized to sodium bicarbonate and 12 (7.5%) to saline (p = 0.79). Renal function did not fully recover in 40.0% and 44.4% of CI-AKI patients, respectively (p = 0.84). No patient required dialysis. Mean costs for preventive hydration and clinical preparation for the contrast procedure were $1158 for sodium bicarbonate vs. $1561 for saline (p < 0.001).. Short hydration with sodium bicarbonate prior to elective cardiovascular diagnostic or therapeutic contrast procedures is non-inferior to standard periprocedural saline hydration in CKD patients with respect to renal safety and results in considerable healthcare savings.. Netherlands Trial Register (http://www.trialregister.nl/trialreg/index.asp), Nr NTR2699.

Topics: Acute Kidney Injury; Aged; Aged, 80 and over; Cardiovascular System; Contrast Media; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Sodium Bicarbonate; Sodium Chloride

Non-thyroidal illness syndrome (NTIS) is common among patients with advanced chronic kidney disease (CKD) and is strongly associated with poor prognosis. However, it remains unclear in how to correct this disorder and this study aimed to evaluate the effectiveness of sodium bicarbonate (SB) and N-acetyl-cysteine (NAC) for correcting NTIS status.. Patients with CKD stage 3-4 were single-blind, placebo-controlled treated with placebo, SB, or NAC for 18 weeks. The primary end points were the correction of NTIS and the occurrence of end-stage renal disease (ESRD). The secondary point was the change in estimated glomerular filtration rate (eGFR) after the follow-up.. The Kaplan-Meier survival analysis showed significant lower correcting ratio of NTIS in control group compared with SB group [Hazard ratio (HR) 0.19, 95 % confidence interval (CI) 0.04-0.89, p = 0.035] and NAC group (HR 0.09, 95 % CI 0.02-0.38, p = 0.001), and increased ESRD risk in control group than in SB group (HR 1.97, 95 % CI 1.02-3.84, p = 0.045) and NAC group (HR 5.50, 95 % CI 2.23-13.57, p < 0.001). The Cox regression analysis demonstrated significantly different effectiveness of placebo, SB and NAC on NTIS correction and ESRD risk, p < 0.05, respectively. Variance analysis displayed a greater reduction in eGFR in controls than in SB (p = 0.044) and NAC group (p < 0.001).. SB and NAC are effective in promoting the recovery from NTIS status and delaying the deterioration of renal function in advanced CKD patients.

Topics: Acetylcysteine; Chi-Square Distribution; China; Disease Progression; Euthyroid Sick Syndromes; Female; Glomerular Filtration Rate; Humans; Kaplan-Meier Estimate; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Proportional Hazards Models; Renal Insufficiency, Chronic; Risk Factors; Single-Blind Method; Sodium Bicarbonate; Time Factors; Treatment Outcome

Hydration to prevent contrast-induced acute kidney injury (CI-AKI) induces a diagnostic delay when performing computed tomography-pulmonary angiography (CTPA) in patients suspected of having acute pulmonary embolism.. To analyze whether withholding hydration is non-inferior to sodium bicarbonate hydration before CTPA in patients with chronic kidney disease (CKD).. We performed an open-label multicenter randomized trial between 2009 and 2013. One hundred thirty-nine CKD patients were randomized, of whom 138 were included in the intention-to-treat population: 67 were randomized to withholding hydration and 71 were randomized to 1-h 250 mL 1.4% sodium bicarbonate hydration before CTPA. Primary outcome was the increase in serum creatinine 48-96 h after CTPA. Secondary outcomes were the incidence of CI-AKI (creatinine increase > 25%/> 0.5 mg dL(-1) ), recovery of renal function, and the need for dialysis within 2 months after CTPA. Withholding hydration was considered non-inferior if the mean relative creatinine increase was ≤ 15% compared with sodium bicarbonate.. Mean relative creatinine increase was -0.14% (interquartile range -15.1% to 12.0%) for withholding hydration and -0.32% (interquartile range -9.7% to 10.1%) for sodium bicarbonate (mean difference 0.19%, 95% confidence interval -5.88% to 6.25%, P-value non-inferiority < 0.001). CI-AKI occurred in 11 patients (8.1%): 6 (9.2%) were randomized to withholding hydration and 5 (7.1%) to sodium bicarbonate (relative risk 1.29, 95% confidence interval 0.41-4.03). Renal function recovered in 80.0% of CI-AKI patients within each group (relative risk 1.00, 95% confidence interval 0.54-1.86). None of the CI-AKI patients developed a need for dialysis.. Our results suggest that preventive hydration could be safely withheld in CKD patients undergoing CTPA for suspected acute pulmonary embolism. This will facilitate management of these patients and prevents delay in diagnosis as well as unnecessary start of anticoagulant treatment while receiving volume expansion.

Topics: Aged; Angiography; Contrast Media; Creatinine; Female; Fluid Therapy; Humans; Kidney Failure, Chronic; Lung; Male; Middle Aged; Multidetector Computed Tomography; Sodium Bicarbonate; Tomography, X-Ray Computed; Treatment Outcome; Venous Thrombosis; Water

Citrate has anticoagulative properties and favorable effects on inflammation, but it has the potential hazards of inducing hypocalcemia. Bicarbonate dialysate (BHD) replacing citrate for acetate is now used in chronic haemodialysis but has never been tested in postdilution online haemodiafiltration (OL-HDF).. Thirteen chronic stable dialysis patients were enrolled in a pilot, short-term study. Patients underwent one week (3 dialysis sessions) of BHD with 0.8 mmol/L citrate dialysate, followed by one week of postdilution high volume OL-HDF with standard bicarbonate dialysate, and one week of high volume OL-HDF with 0.8 mmol/L citrate dialysate.. In citrate OL-HDF pretreatment plasma levels of C-reactive protein and β 2-microglobulin were significantly reduced; intra-treatment plasma acetate levels increased in the former technique and decreased in the latter. During both citrate techniques (OL-HDF and HD) ionized calcium levels remained stable within the normal range.. Should our promising results be confirmed in a long-term study on a wider population, then OL-HDF with citrate dialysate may represent a further step in improving dialysis biocompatibility.

Topics: Adult; Aged; Anticoagulants; Citric Acid; Dialysis Solutions; Feasibility Studies; Female; Hemodiafiltration; Hemodilution; Humans; Italy; Kidney Failure, Chronic; Male; Middle Aged; Pilot Projects; Sodium Bicarbonate; Treatment Outcome; Young Adult

Although the mechanism of muscle wasting in end-stage renal disease is not fully understood, there is increasing evidence that acidosis induces muscle protein degradation and could therefore contribute to the loss of muscle protein stores of patients on hemodialysis, a prototypical state of chronic metabolic acidosis (CMA). Because body protein mass is controlled by the balance between synthesis and degradation, protein loss can occur as result of either increased breakdown, impaired synthesis, or both. Correction of acidosis may therefore help to maintain muscle mass and improve the health of patients with CMA. We evaluated whether alkalizing patients on hemodialysis might have a positive effect on protein synthesis and on nutritional parameters.. Eight chronic hemodialysis patients were treated daily with oral sodium bicarbonate (NaHCO(3)) supplementation for 10-14 days, yielding a pre-dialytic plasma bicarbonate concentration of 28.6 +/-1.6 mmol/l. The fractional synthesis rates (FSR) of muscle protein and albumin were obtained by the L-[(2)H(5)ring]phenylalanine flooding technique.. Oral NaHCO(3 )supplementation induced a significant increase in serum bicarbonate (21.5 +/- 3.4 vs. 28.6 +/- 1.6 mmol/l; p = 0.018) and blood pH (7.41 vs. 7.46; p = 0.041). The FSR of muscle protein and the FSR of albumin did not change significantly (muscle protein: 2.1 +/- 0.2 vs. 2.0 +/- 0.5% per day, p = 0.39; albumin: 8.3 +/- 2.2 vs. 8.6 +/- 2.5% per day, p = 0.31). Plasma concentrations of insulin-like growth factor 1 decreased significantly (33.4 +/- 21.3 vs. 25.4 +/- 12.3 nmol/l; p = 0.028), whereas thyroid-stimulating hormone, free thyroxin and free triiodothyronine did not change significantly and nutritional parameters showed no improvement.. In contrast to other findings, raising the blood pH of dialysis patients was not associated with a positive effect on albumin and muscle protein synthesis, or nutritional and endocrinal parameters.

Topics: Administration, Oral; Adult; Aged; Blood Chemical Analysis; Blood Proteins; Female; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Protein Biosynthesis; Renal Dialysis; Sodium Bicarbonate

Bicarbonate supplementation preserves renal function in experimental chronic kidney disease (CKD), but whether the same benefit occurs in humans is unknown. Here, we randomly assigned 134 adult patients with CKD (creatinine clearance [CrCl] 15 to 30 ml/min per 1.73 m(2)) and serum bicarbonate 16 to 20 mmol/L to either supplementation with oral sodium bicarbonate or standard care for 2 yr. The primary end points were rate of CrCl decline, the proportion of patients with rapid decline of CrCl (>3 ml/min per 1.73 m(2)/yr), and ESRD (CrCl <10 ml/min). Secondary end points were dietary protein intake, normalized protein nitrogen appearance, serum albumin, and mid-arm muscle circumference. Compared with the control group, decline in CrCl was slower with bicarbonate supplementation (5.93 versus 1.88 ml/min 1.73 m(2); P < 0.0001). Patients supplemented with bicarbonate were significantly less likely to experience rapid progression (9 versus 45%; relative risk 0.15; 95% confidence interval 0.06 to 0.40; P < 0.0001). Similarly, fewer patients supplemented with bicarbonate developed ESRD (6.5 versus 33%; relative risk 0.13; 95% confidence interval 0.04 to 0.40; P < 0.001). Nutritional parameters improved significantly with bicarbonate supplementation, which was well tolerated. This study demonstrates that bicarbonate supplementation slows the rate of progression of renal failure to ESRD and improves nutritional status among patients with CKD.

Topics: Acidosis; Administration, Oral; Blood Proteins; Creatinine; Dietary Proteins; Disease Progression; Female; Humans; Kaplan-Meier Estimate; Kidney Failure, Chronic; Male; Middle Aged; Nutritional Status; Serum Albumin; Sodium Bicarbonate; Treatment Outcome

Contrast-induced acute kidney injury (CI-AKI) is one of the leading causes of hospital-acquired acute kidney injury. Multiple clinical studies have proposed several preventive strategies.. To examine the efficacy of sodium bicarbonate compared with sodium chloride and oral N-acetylcysteine (NAC) for preventive hydration after cardiac catheterization.. We conducted a prospective, single-center trial. Patients with chronic kidney disease (CKD) stage III-IV undergoing cardiac catheterization were allocated to receive either an infusion of 0.9% sodium chloride and oral NAC or 154 mEq/L sodium bicarbonate. MAIN: Outcome measure CI-AKI, defined as an increase of 25% or 0.3 mg/dL or more in plasma creatinine within 2 days of contrast administration.. Ninety-three patients were allocated to one of the two groups: 42 patients in the saline plus NAC group and 51 patients in the bicarbonate group. There were no statistically significant differences between the groups in the most important clinical and procedural characteristics. Baseline plasma creatinine levels, estimated glomerular filtration rate, incidence of diabetes mellitus, hypertension, congestive heart failure, and contrast medium volume were similar. Mean plasma creatinine concentration was 1.76 +/- 0.54 mg/dL in the saline and NAC group and 1.9 +/- 1 mg/dL in the bicarbonate group (P = 0.23). The rate of CI-AKI was 9.8% in the bicarbonate group and 8.4% in the saline plus NAC group. No patient required renal replacement therapy.. Hydration with sodium bicarbonate is not more effective than hydration with sodium chloride and oral NAC for prophylaxis of CI-AKI in patients with CKD stage III-IV undergoing cardiac catheterization.

Topics: Acetylcysteine; Aged; Cardiac Catheterization; Contrast Media; Creatine; Dehydration; Female; Free Radical Scavengers; Glomerular Filtration Rate; Humans; Kidney Diseases; Kidney Failure, Chronic; Male; Prospective Studies; Regression Analysis; Risk Assessment; Sodium Bicarbonate; Sodium Chloride; Statistics as Topic

Contrast-induced nephropathy is associated with increased in-hospital and long-term adverse clinical outcomes.. To investigate whether hydration with sodium bicarbonate improves long-term clinical outcomes compared with sodium chloride, patients with chronic kidney disease undergoing an emergent coronary procedure were enrolled in a randomized clinical trial with > or = 1 year of follow-up. The 59 patients with chronic kidney disease (serum creatinine concentration > 1.1 mg/dl or estimated glomerular filtration rate < 60 ml/min) were randomly assigned to receive a 154 mmol/L intravenous infusion of either sodium bicarbonate (n = 30) or sodium chloride (n = 29). The electrolytes were given as a bolus of 3 ml.kg(-1).h(-1) for 1 h before the administration of contrast, followed by an infusion of 1 ml.kg(-1).h(-1) for 6 h during and after the procedure. During a mean follow-up period of 15.9+/-4.5 months, the incidence of renal replacement therapy or death was significantly lower in the sodium bicarbonate group than in the sodium chloride group (3% vs 21%, respectively; p = 0.037).. Hydration with sodium bicarbonate reduces the incidence of renal replacement therapy and death in patients with chronic kidney disease undergoing an emergent coronary procedure.

Topics: Aged; Aged, 80 and over; Contrast Media; Creatinine; Emergencies; Female; Follow-Up Studies; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Male; Sodium Bicarbonate; Sodium Chloride; Survival Analysis; Survivors

Acidosis causes malnutrition in peritoneal dialysis (PD) patients. The effect of oral bicarbonate in PD patients with Kt/V <2.1 has not been studied. We randomly assigned 60 PD patients with acidosis and Kt/V <2.1 to oral sodium bicarbonate (0.9 g thrice daily) or placebo. Patients were followed for 12 mo. We compared their nutritional status, including subjective global assessment (SGA) score and normalized protein nitrogen appearance (NPNA), hospitalization and all-cause mortality. Treatment with oral bicarbonate resulted in a higher plasma bicarbonate level at 4 wk (27.8 +/- 2.6 versus 24.7 +/- 3.9 mmol/L, P = 0.002), and the difference persisted until 52 wk. Bicarbonate treatment had a significant effect on the change in overall SGA score (repeated measures ANOVA, P = 0.0003). The overall SGA score of the treatment group was higher than the placebo group at 24 wk (5.07 +/- 0.94 versus 4.40 +/- 1.00, P = 0.015), and the difference persisted thereafter. NPNA rose in the treatment group (1.17 +/- 0.32 to 1.28 +/- 0.26 g/kg per d, P = 0.034), but declined in placebo group (1.13 +/- 0.25 to 1.03 +/- 0.28 g/kg per d, P = 0.054). The treatment group had a shorter hospitalization than the placebo group (8.4 +/- 17.7 versus 16.8 +/- 21.7 d/yr; P = 0.02). Mortality was not significantly different. Although our trial has limited statistical power, we find that in PD patients with mild acidosis and Kt/V <2.1, oral sodium bicarbonate probably improve nutritional status and reduce the duration of hospitalization.

Topics: Acidosis; Administration, Oral; Aged; Bicarbonates; Body Weight; Dialysis; Female; Follow-Up Studies; Humans; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Nitrogen; Nutritional Status; Peritoneal Dialysis; Placebos; Random Allocation; Renal Dialysis; Sodium Bicarbonate; Time Factors

Fifteen children with chronic renal failure from early infancy who did not require renal replacement therapy were followed for 3 years. Chronic renal failure was defined as a serum creatinine at or above 1 mg/dl for the entire 1st year of life. These patients were treated conservatively with diet and supplements of sodium bicarbonate and sodium chloride, calcium and vitamin D. Erythropoietin was given to 5 patients. Neither nasogastric nor gastrostomy tube feeding was used, and none of the patients received recombinant human growth hormone. We analyzed length, weight, and head circumference at 3, 12, 24, and 36 months of age. All three variables displayed a significant drop in the first 3 months, but remained stable for the whole observation period thereafter. At the age of 3 years, the patients' mean values of length, weight, and head circumference standard deviation score were -1.96, -1.37, and -1.07, respectively. Height velocity during the 1st, 2nd, and 3rd year was 22.2, 10.9, and 7.6 cm per year, respectively. The first two figures and the cumulative height velocity are significantly better than those from a large cohort of chronic renal failure patients collected by the European Study Group for Nutritional Treatment of Chronic Renal Failure in Childhood; here the corresponding figures of height velocity were 12.3, 8.3, and 7.6 cm per year. Median serum calcium, phosphate, parathyroid hormone, and albumin levels remained within normal limits for the entire study period. Therapy-resistant hyperparathyroidism occurred in 1 patient and radiological signs of renal osteodystrophy in 4 patients. Kidney length, as measured by ultrasonography, showed almost no growth.

Topics: Age Factors; Body Height; Body Weight; Bone and Bones; Calcium; Child, Preschool; Creatinine; Diet, Protein-Restricted; Female; Follow-Up Studies; Glomerular Filtration Rate; Humans; Infant; Infant, Newborn; Kidney; Kidney Failure, Chronic; Male; Radiography; Sodium Bicarbonate; Sodium Chloride; Vitamin D

Serum albumin concentration has been strongly associated with risk of death in hemodialysis patients, with mortality increasing as albumin decreases. Metabolic acidosis stimulates protein catabolism and decreases protein synthesis. A study was undertaken to investigate the effect of increasing predialysis serum bicarbonate (HCO3) concentrations on the nutrition of hemodialysis patients as measured by albumin and total lymphocyte count (TLC). Metabolic acidosis was defined as a predialysis serum bicarbonate concentration of < or = 18 mEq/L. Thirty-six hemodialysis patients were enrolled in the study. Each had been stable on hemodialysis for > or = 3 months and each had a mean serum bicarbonate concentration of < or = 18 mEq/L on predialysis monthly laboratory values during the preceding 3 months. The subjects were randomized into 2 groups. The first group consisted of 18 control subjects who were dialyzed on a standard bicarbonate bath of 35 mEq/L. The second group consisted of 18 experimental patients who were dialyzed on a bicarbonate bath of 40 mEq/L. Subjects in the experimental group who had predialysis serum bicarbonate concentrations less than 22 mEq/L after 2 weeks on the higher bicarbonate bath were additionally supplemented with oral sodium bicarbonate at a dosage of 1 mEq/kg dry weight/d. Monthly predialysis laboratory values were checked for all subjects and included serum electrolytes, blood urea nitrogen, calcium, and albumin. TLCs were obtained at the initiation and at the conclusion of the study. Intact parathyroid hormone, blood pressures, and interdialytic weight gains were also followed. The study lasted 16 weeks; 32 subjects completed the study (16 in each group). There were no statistically significant differences between the two groups at the initiation of the study. The serum bicarbonate concentrations were significantly different between the two groups at the end of the study (control HCO3 17.3 +/- 3.2 mEq/L v experimental HCO3 20.2 +/- 2.9 mEq/L; P = 0.01). Serum albumin concentrations and TLCs were not statistically different (P > 0.05) between the two groups at the end of the study (control albumin 3.88 +/- 0.28 g/dL v experimental albumin 3.76 +/- 0.26 g/dL and control TLC 1,780.0 +/- 779.4/mm3 v experimental TLC 2,020.1 +/- 888.0/mm3). Potassium, intact parathyroid hormone, interdialytic weight gain, blood pressures, Kt/Vs, and protein catabolic rates did not differ. We found that the change in serum bicarbonate concentration w

Topics: Acidosis; Administration, Oral; Bicarbonates; Female; Hemodialysis Solutions; Humans; Kidney Failure, Chronic; Leukocyte Count; Male; Middle Aged; Nutritional Status; Outcome Assessment, Health Care; Prospective Studies; Renal Dialysis; Serum Albumin; Sodium Bicarbonate; Time Factors

Hyperkalemia in patients with renal failure is frequently treated with a cation exchange resin (sodium polystyrene sulfonate, hereafter referred to as resin) in combination with a cathartic, but the effect of such therapy on serum potassium concentration has not been established. This study evaluates the effect of four single-dose resin-cathartic regimens and placebo on 5 different test days in six patients with chronic renal failure. Dietary intake was controlled. Fecal potassium output and serum potassium concentration were measured for 12 h. Phenolphthalein alone caused an average fecal potassium output of 54 mEq. The addition of resin caused an increase in insoluble potassium output but a decrease in soluble potassium output; therefore, there was no significant effect of resin on total potassium output. Sorbitol plus resin caused less potassium output than phenolphthalein plus resin. On placebo therapy, the average serum potassium concentration increased slightly (0.4 mEq/L) during the 12-h experiment. This rise was apparently abrogated by some of the regimens that included resin; this may have been due in part to extracellular volume expansion caused by absorption of sodium released from resin. Phenolphthalein regimens were associated with a slight rise in serum potassium concentrations (similar to placebo); this may have been due to extracellular volume contraction produced by high volume and sodium-rich diarrhea and acidosis secondary to bicarbonate losses. None of the regimens reduced serum potassium concentrations, compared with baseline levels. Because single-dose resin-cathartic therapy produces no or only trivial reductions in serum potassium concentration, and because this therapy is unpleasant and occasionally is associated with serious complications, this study questions the wisdom of its use in the management of acute hyperkalemic episodes.

Topics: Analysis of Variance; Cathartics; Chlorides; Dose-Response Relationship, Drug; Drug Therapy, Combination; Feces; Female; Glucose; Humans; Kidney Failure, Chronic; Male; Phenolphthalein; Polystyrenes; Potassium; Renal Dialysis; Resins, Synthetic; Sodium; Sodium Bicarbonate; Sorbitol; Treatment Outcome; Water-Electrolyte Balance

Animal studies suggest that alkalinization and increased intake of free water both serve to decrease the rate of progression in chronic renal failure. However, clinicians have been reluctant to apply either strategy because of concerns regarding volume overload and water intoxication. We tested the effects of 2 1 daily water supplementation, with either an electrolyte-poor or a HCO3-rich (47.5 mmol/1) water in 11 patients with chronic renal failure (creatinine clearance 10 +/- 5 ml/min). The patients were brought into balance on a diet containing 80 mmol/24 h Na+, 80 mmol/24 h Cl- and 70 mmol/24 h K+. After a 3-day equilibration period, the patients were randomized to one or the other regimen for 7 days. After a 3-day washout period, the alternate regimen was given for another 7 days. Neither regimen led to weight gain or hyponatremia. The supplemental 95 mmol/24 h HCO3- lowered the serum Cl- concentration and raised the serum HCO3- concentration, as well as the pH value, to normal. Creatinine clearance and protein excretion were not affected. Serum beta 2-microglobulin concentrations decreased with the NaHCO3-containing water. Na+/H(+)-antiporter activity was not consistently influenced since an order effect of the regimens was apparent. We conclude that 2 1/24 h water and NaHCO3 supplementation is well tolerated, causes no deleterious effects, and may evoke improvement in patients with chronic renal failure.

Topics: Acid-Base Equilibrium; Adult; Aged; Aged, 80 and over; beta 2-Microglobulin; Cross-Over Studies; Double-Blind Method; Female; Fluid Therapy; Humans; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Sodium Bicarbonate; Sodium-Hydrogen Exchangers; Water

Ten patients with acute and 60 with chronic renal failure (both groups having hyperkalaemia), were managed at Kenyatta National Hospital in the medical wards and Renal Unit between August, 1995 and January, 1996. They were divided into seven different treatment groups, each consisting of ten patients. Treatment A glucose 25g i.v. with insulin 10 units i.v., treatment B 50 mmol of 8.4% sodium bicarbonate infusion, treatment C 0.5mg of salbutamol i.v. in 50mls 5% dextrose, treatment D was a combination of treatments A and B, treatment E was a combination of treatment B and C, treatment F was a combination of treatments A and C while treatment G was a combination of treatments A and B and C. Serum potassium was measured, 30 minutes, 1 hour, 2 hours, 4 hours and 8 hours after treatment. Plasma glucose concentration was measured before treatment was given and 1 hour after in all patients. Electrocardiography was done before treatment on all patients and repeated 30 minutes and 1 hour after treatment for the patients with hyperkalaemic changes on the initial recording. All treatment modalities had satisfactory potassium lowering effects. Of the single therapeutic approaches, treatment A and C were equieffective, but better than treatment B (P < 0.001). Amongst the two regimen combinations, treatment D and F were more efficacious than treatment E and all the single therapeutic approaches (P < 0.001). Treatment G was the most efficacious in lowering serum potassium in this study. All treatment modalities had maximum serum potassium lowering effect at 1-2 hours. A fall in plasma glucose concentration was a notable feature of treatments A and D, but significant hypoglycaemia occurred in 20% of patients receiving treatment A and in none on treatment D. The ECG changes of hyperkalaemia did not correlate with serum potassium levels. The normalisation of hyperkalaemic ECG alteration occurred within the first 30 minutes after treatment. In conclusion, combination therapies for hyperkalaemia appear to be more efficacious than single therapeutic approaches. Inclusion of salbutamol seems to protect against insulin induced hypoglycaemia. The maximum potassium lowering effect is observed 1-2 hours of administration of either agents. The potassium reducing effect remains significant compared to baseline values even after 8 hours. If dialysis cannot be instituted early enough it seems reasonable to repeat treatment every 4-6 hours to sustain the effect. Repeated administration

Topics: Acute Kidney Injury; Adolescent; Adrenergic beta-Agonists; Adult; Aged; Aged, 80 and over; Albuterol; Drug Therapy, Combination; Electrocardiography; Glucose Solution, Hypertonic; Humans; Hyperkalemia; Hypoglycemic Agents; Infusions, Intravenous; Insulin; Kidney Failure, Chronic; Middle Aged; Prospective Studies; Single-Blind Method; Sodium Bicarbonate; Sodium-Potassium-Exchanging ATPase

Acute treatment of hyperkalemia in patients with end-stage renal disease requires temporizing measures to shift potassium rapidly from the extracellular to the intracellular fluid compartments until hemodialysis can be initiated. Whereas insulin and albuterol are effective in lowering plasma potassium acutely, bicarbonate by itself is not. Bicarbonate administration may, however, potentiate the effects of insulin and albuterol on plasma potassium. Using a prospective cross-over design, we investigated the acute effects of (1) isotonic bicarbonate, (2) isotonic saline, (3) insulin + bicarbonate, (4) insulin + saline, (5) albuterol + bicarbonate, and (6) albuterol + saline on plasma potassium as well as blood bicarbonate and pH in nondiabetic hemodialysis patients. After obtaining a baseline blood sample, the subjects received one of the six treatment protocols, with plasma potassium measured every 15 minutes over 1 hour. Neither isotonic bicarbonate nor isotonic saline decreased plasma potassium significantly (-0.03 +/- 0.06 mmol/L v -0.01 +/- 0.10 mmol/L at 60 minutes; P = 0.60). Intravenous insulin decreased plasma potassium by a similar degree when given in conjunction with bicarbonate or saline (-0.81 +/- 0.05 mmol/L v -0.85 +/- 0.06 mmol/L at 60 minutes; P = 0.65). Likewise, nebulized albuterol decreased plasma potassium by a similar degree when given with bicarbonate or saline (-0.71 +/- 0.16 mmol/L v -0.53 +/- 0.15 mmol/L at 60 minutes; P = 0.18). The three protocols that included bicarbonate administration resulted in significant increases in blood bicarbonate (P < 0.005) and pH (P < 0.01), whereas the three protocols that included saline did not affect blood bicarbonate or pH. These observations suggest that bicarbonate administration does not potentiate the potassium-lowering effects of insulin or albuterol in hemodialysis patients.

Topics: Adrenergic beta-Agonists; Adult; Aged; Albuterol; Cross-Over Studies; Drug Synergism; Female; Humans; Hydrogen-Ion Concentration; Hyperkalemia; Insulin; Kidney Failure, Chronic; Male; Middle Aged; Potassium; Prospective Studies; Renal Dialysis; Sodium Bicarbonate

Topics: Acetates; Acetic Acid; Adolescent; Adult; Bicarbonates; Blood Pressure; Fatigue; Headache; Humans; Kidney Failure, Chronic; Muscle Cramp; Renal Dialysis; Sodium Bicarbonate; Vomiting

Severe metabolic alkalosis is rarely seen in end stage renal disease (ESRD) patients on long-term hemodialysis. This can be life threatening and mortality is exponentially increased when the pH exceeds 7.60. Persistent vomiting, ingestion of alkali for dyspepsia and pica behavior are all potential causes of such severe metabolic alkalosis. The prevalence of pica is increased in chronic kidney disease and ESRD patients, with ice being the most commonly ingested substance. It can cause a myriad of complications including death, but the diagnosis may be elusive unless the pica behavior is witnessed firsthand by others since patients do not typically disclose their behavior. We present the case of a hemodialysis patient with severe alkalemia, hypernatremia, and excessive interdialytic weight gains resulting in recurrent hospitalizations for fluid overload due to baking soda pica behavior.

Topics: Alkalosis; Humans; Kidney Failure, Chronic; Pica; Renal Dialysis; Sodium Bicarbonate

YES. Long-term sodium bicarbonate therapy slightly slows the loss of renal function in patients with chronic kidney disease (CKD) and may moderately reduce progression to end-stage renal disease (strength of recommendation [SOR]: B, meta-analyses of lower-quality randomized controlled trails [RCTs]). Therapy duration of 1 year or less may not be beneficial (SOR: C, secondary analyses in meta-analyses).

Topics: Bicarbonates; Disease Progression; Female; Humans; Kidney Failure, Chronic; Male; Renal Insufficiency, Chronic; Sodium Bicarbonate

Patients with chronic kidney disease often experience metabolic acidosis. Whether oral sodium bicarbonate can reduce mortality in patients with metabolic acidosis has been debated for years. Hence, this study was conducted to evaluate the utility of sodium bicarbonate in patients who will undergo dialysis therapy. In this study, we investigated the effect of oral sodium bicarbonate therapy on mortality in patients with end-stage kidney disease (ESKD) initiated on dialysis therapy.. We conducted an observational study of patients when they started dialysis therapy. There were 17 centres participating in the Aichi Cohort Study of Prognosis in Patients Newly Initiated into Dialysis. Data were available on patients' sex, age, use of sodium bicarbonate, drug history, medical history, vital data, and laboratory data. We investigated whether patients on oral sodium bicarbonate for more than three months before dialysis initiation had a better prognosis than those without sodium bicarbonate therapy. The primary outcome was defined as all-cause mortality.. The study included 1524 patients with chronic kidney disease who initiated dialysis between October 2011 and September 2013. Among them, 1030 were men and 492 women, with a mean age of 67.5 ± 13.1 years. Of these, 677 used sodium bicarbonate and 845 did not; 13.6% of the patients in the former group and 21.2% of those in the latter group died by March 2015 (p <  0.001). Even after adjusting for various factors, the use of sodium bicarbonate independently reduced mortality (p <  0.001).. The use of oral sodium bicarbonate at the time of dialysis initiation significantly reduced all-cause mortality in patients undergoing dialysis therapy.

Topics: Acidosis; Administration, Oral; Aged; Female; Heart Failure; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prognosis; Propensity Score; Prospective Studies; Renal Dialysis; Renal Insufficiency, Chronic; Sodium Bicarbonate

The dialysate alkali used in hemodialysis to replace low body alkali levels in end stage renal disease (ESRD) patients has changed over time from bicarbonate to acetate and finally back to bicarbonate with a small addition of acetate. The ideal way to replace alkali in dialysis patients remains uncertain. Elsewhere in this issue of the journal, Sargent and Gennari, who have contributed greatly to our understanding of dialysis and acid-base kinetics, suggest that decreasing the currently used concentration of bicarbonate while increasing concentration of acetate in the dialysate may be a much more physiological approach to alkali delivery during hemodialysis. These recommendations are based on results from a series of hemodialysis simulations using mathematical theoretical methods, with the assumption that acetate metabolism will be sufficiently delayed with the higher acetate dialysate and reduce the rate of correction of metabolic acidosis during dialysis. Although valuable in calling attention to the issues surrounding alkali repletion during hemodialysis, these postulations should be tested in clinical trials. We believe, however, that the available evidence suggests that the rate of gain of bicarbonate during dialysis with the higher acetate dialysate would not be slower and that the replacement of some dialysate bicarbonate with acetate will not alter alkali accretion or intradialytic pH.

Topics: Acetates; Alkalies; Buffers; Hemodialysis Solutions; Humans; Kidney Failure, Chronic; Renal Dialysis; Sodium Bicarbonate

Flecainide intoxication is a severe intoxication that can lead to cardiogenic shock. We report on a 68-year-old female patient, who presented with a flecainide intoxication in the setting of renal failure. She was managed with invasive supportive therapy at the ICU and infusion of sodium bicarbonate and intravenous lipid emulsion (ILE, intralipid 20%), after which she made a complete recovery.

Topics: Aged; Anti-Arrhythmia Agents; Bradycardia; Buffers; Cardiotonic Agents; Drug Overdose; Electrocardiography; Fat Emulsions, Intravenous; Female; Flecainide; Humans; Kidney Failure, Chronic; Renal Elimination; Shock, Cardiogenic; Sick Sinus Syndrome; Sodium Bicarbonate; Treatment Outcome

To date, very few studies have been carried out on the associations of pre- and postdialysis acid-base parameters with mortality in hemodialysis patients.. An observational study including cross-sectional and 1-year analyses.. Data from the renal registry of the Japanese Society of Dialysis Therapy (2008-2009), including 15,132 dialysis patients 16 years or older.. Predialysis pH<7.30, 7.30 to 7.34 (reference), 7.35 to 7.39, or ≥7.40 (1,550, 4,802, 6,023, and 2,757 patients, respectively); predialysis bicarbonate level < 18.0, 18.0 to 21.9 (reference), 22.0 to 25.9, or ≥26.0 mEq/L (2,724, 7,851, 4,023, and 534 patients, respectively); postdialysis pH<7.40, 7.40 to 7.44, 7.45 to 7.49 (reference), or ≥7.50 (2,114, 5,331, 4,975, and 2,712 patients, respectively); and postdialysis bicarbonate level < 24.0, 24.0 to 25.9, 26.0 to 27.9 (reference), or ≥28.0 mEq/L (5,087, 4,330, 3,451, and 2,264 patients, respectively).. All-cause and cardiovascular (CV) mortality during the 1-year follow-up.. HRs were estimated using unadjusted models and models adjusted for age, sex, dialysis vintage, history of CV disease, diabetes, weight gain ratio, body mass index, calcium-phosphorus product, serum albumin level, serum total cholesterol level, blood hemoglobin level, single-pool Kt/V, and normalized protein catabolic rate.. Of 15,132 patients, during follow-up, 1,042 died of all causes, including 408 CV deaths. In the adjusted analysis for all-cause mortality, HRs compared to the reference group were significantly higher in patients with predialysis pH≥7.40 (HR, 1.36; 95% CI, 1.13-1.65) and postdialysis pH<7.40 (HR, 1.22; 95% CI, 1.00-1.49). Predialysis pH≥7.40 was also associated with higher risk of CV mortality (HR, 1.34; 95% CI, 1.01-1.79). No association of pre- or postdialysis bicarbonate level with all-cause and CV mortality was observed.. Single measurements of acid-base parameters, short duration of follow-up, small number of CV deaths.. Predialysis pH≥7.40 was associated with significantly elevated risk of all-cause and CV mortality. However, pre- and postdialysis bicarbonate levels were not associated with all-cause and CV mortality. Predialysis pH may be the most appropriate reference for accurate correction of metabolic acidosis in dialysis patients.

Topics: Aged; Cardiovascular Diseases; Cause of Death; Female; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Multivariate Analysis; Renal Dialysis; Risk Assessment; Sodium Bicarbonate

Topics: Cardiovascular Diseases; Female; Humans; Kidney Failure, Chronic; Male; Renal Dialysis; Sodium Bicarbonate

The development of delayed disorders caused by acute ethylene glycol poisoning has been studied in experiments on male rats. These disorders include chronic renal failure and secondary combined immunodeficiency status of the "circulus vitiosus" type. Urgent pharmacological correction was shown to be necessary shortly after the poisoning. The experimental therapy (administration of immunomodulators with various mechanisms of action in addition to conventional antidote treatment with ethanol) resulted in the restoration of nonspecific resistance and both cellular and humoral immunity. Reduction of the urinary system damage after the administration of immunomodulators was observed. The results demonstrated the importance of multiagent immunotherapy for the correction of delayed effects of acute ethylene glycol poisoning.

Topics: Acridines; Animals; Antidotes; Blood Glucose; Creatinine; Cytokines; Dipeptides; Ethanol; Ethylene Glycol; Immunity, Humoral; Immunity, Innate; Immunologic Deficiency Syndromes; Immunologic Factors; Kidney Failure, Chronic; Kidney Function Tests; Lactic Acid; Male; Rats; Rats, Wistar; Sodium Bicarbonate

Dietary alkali slows GFR decline in humans with a moderately reduced glomerular filtration rate (GFR) despite the absence of metabolic acidosis. Similarly, dietary alkali slows GFR decline in animals with 2/3 nephrectomy (Nx), a chronic kidney disease (CKD) model without metabolic acidosis in which GFR decline is mediated by acid (H(+)) retention through endothelin (ET) and mineralocorticoid receptors. To gain insight as to whether this mechanism might mediate GFR decline in humans, we explored whether macroalbuminuric subjects with moderately reduced (CKD stage 2 = 60-90 ml/min; CKD 2) compared with normal estimated GFR (> 90 ml/min; CKD 1), each without metabolic acidosis, have H(+) retention that increases plasma levels of ET-1 and aldosterone. Baseline plasma ET and aldosterone concentrations were each higher in CKD 2 than CKD 1. Baseline dietary H(+) and urine net acid excretion (NAE) were not different between groups, but an acute oral NaHCO₃ bolus reduced urine NAE less (i.e., postbolus urine NAE was higher) in CKD 2 than CKD 1, consistent with greater H(+) retention in CKD 2 subjects. Thirty days of oral NaHCO₃ reduced H(+) retention in CKD 2 but not CKD 1 subjects and reduced plasma ET and aldosterone in both groups but to levels that remained higher in CKD 2 for each. Subjects with CKD stage 2 eGFR and no metabolic acidosis nevertheless have H(+) retention that increases plasma ET and aldosterone levels, factors that might mediate subsequent GFR decline and other untoward vascular effects.

Topics: Aldosterone; Double-Blind Method; Endothelins; Glomerular Filtration Rate; Humans; Kidney; Kidney Failure, Chronic; Patient Selection; Sodium Bicarbonate

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

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Aged, 80 and over; Comorbidity; Diabetes Mellitus, Type 2; Diuretics; Drug Monitoring; Female; Humans; Hypoglycemic Agents; Kidney Failure, Chronic; Lactates; Metformin; Polypharmacy; Renal Dialysis; Sodium Bicarbonate

Topics: Aldosterone; Endothelins; Glomerular Filtration Rate; Humans; Kidney; Kidney Failure, Chronic; Sodium Bicarbonate

A total of 25 Chinese patients aged 6 to 36 months hospitalised at Beijing Children's Hospital due to melamine-induced kidney stones complicated by acute obstructive renal failure in 2008 were included in a study in order to diagnose and treat these special cases more effectively. Feeding history, clinical presentation, ultrasound findings, treatments and effects were summarised. Twelve to seventeen months follow-up was reported also. Ultrasound examination showed that calculi were located at the kidney and ureters. Stones were composed of both uric acid and melamine in a molar ratio of 1.2:1 to 2.1:1. Treatments providing liquid plus alkalisation of urine proved to be effective in helping the patients pass the stones. Surgical intervention was needed in severe cases. Renal function returned to normal in all 25 patients after various durations of therapy. Sixty-eight percent of the patients expelled all of the calculi within 3 months, 90% in 6 months and 95% in 9 months, without sequelae till now. Melamine-contaminated milk formula can cause kidney stones in infants, which should be diagnosed by feeding history, clinical symptoms and ultrasound examination. Composition of the stones was not only of melamine but also uric acid. Providing liquid orally or intravenously plus alkalisation of urine proved to promote the removal of the stones. Follow-up of 12 to 17 months after discharge showed no sequelae.

Topics: Catchment Area, Health; Catheterization; Child, Preschool; China; Cystoscopy; Female; Follow-Up Studies; Food, Formulated; Humans; Infant; Kidney Calculi; Kidney Failure, Chronic; Male; Renal Dialysis; Sodium Bicarbonate; Treatment Outcome; Triazines

The effect of the correction of metabolic acidosis (MA) on serum albumin concentrations (sAlbs) in hemodialysis (HD) patients is controversial. This study evaluated the role of the correction of MA on sAlb concentrations, normalized protein catabolic rate (nPCR), and the effect of the concomitant inflammatory status, in a group of acidotic HD patients.. The correction of MA by oral supplementation with sodium bicarbonate, and the evaluation of its effect on sAlb, nPCR, and high-sensitivity C-reactive protein (hsCRP), were performed in 29 patients on bicarbonate dialysis for a median of 30 months. Other variables included pre-HD arterial pH, serum bicarbonate, serum creatinine, serum Na, body weight, interdialytic weight gain, pre-HD systolic and diastolic blood pressure, and Kt/V.. Serum bicarbonate and pH increased significantly (P < .0001), from 19.1 +/- 0.7 mmol/L to 24.6 +/- 1.1 mmol/L and from 7.33 +/- 0.03 to 7.39 +/- 0.02, respectively (all values with +/- are SD). The nPCR decreased from 1.13 +/- 0.14 g/kg/day to 1.05 +/- 0.14 g/kg/day (P < .0001). The other variables did not change significantly. In 17 patients with high-sensitivity C-reactive protein <10 mg/L, sAlb increased from 3.7 +/- 0.3 g/dL to 4.0 +/- 0.3 g/dL (P < .01), whereas in 12 with high-sensitivity C-reactive protein >or=10 mg/L, sAlb did not change (3.5 +/- 0.17 g/dL vs. 3.4 +/- 0.13 g/dL; P = NS).. Oral sodium bicarbonate supplementation is effective in correcting MA in HD patients and does not affect interdialytic weight gain, plasma Na, and blood pressure. The correction of MA is effective in reducing protein catabolism (nPCR) in both inflamed and less inflamed HD patients, but increases sAlb only in patients without inflammation. In inflamed patients, the correction of MA is not sufficient per se to improve sAlb concentrations.

Topics: Acidosis; Administration, Oral; Bicarbonates; Blood Pressure; C-Reactive Protein; Dietary Proteins; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Nitrogen; Nutrition Disorders; Nutritional Status; Prospective Studies; Renal Dialysis; Serum Albumin; Sodium; Sodium Bicarbonate; Treatment Outcome

Contrast-induced nephropathy (CIN) is associated with adverse outcomes. Strategies for its prevention have been evaluated for patients undergoing invasive coronary and peripheral angiography, including treatment with N-acetylcysteine, sodium bicarbonate, and use of iso-osmolar nonionic contrast. Recently, multidetector computed tomographic angiography (MDCTA) of the coronary and peripheral arteries has been introduced as an accurate method for assessing vascular stenosis and has been widely adopted for assessment of outpatients with suspected coronary artery disease or peripheral arterial disease. To date, the incidence of CIN in outpatients with chronic renal insufficiency (CRI) treated with CIN-preventive strategies undergoing MDCTA remains unknown. Thus, we evaluated the incidence of CIN in outpatients with CRI (creatinine 1.5 to 2.5 mg/dl) undergoing MDCTA using CIN-preventive measures; 400 patients with CRI (78.5% men, mean age 76 years, 41% with diabetes) underwent MDCTA with iodixanol for detection of coronary artery disease or peripheral arterial disease (mean contrast volume 101 cc). CIN was defined as a nonallergic creatinine increase of >0.5 mg/dl. Creatinine levels were obtained before and 3 to 5 days after MDCTA; the average creatinine levels were 1.80 mg/dl and 1.75 mg/dl, respectively (p = NS), with an average change of -0.03 mg/dl. In the study cohort, only 7 patients (1.75%) experienced a creatinine increase >0.5 mg/dl, satisfying the definition of CIN. In conclusion, multivariate analysis, diabetes was the only predictor for CIN (odds ratio 5.9, 95% confidence interval 1.0 to 33.3, p = 0.045). No patient required hemodialysis. In conclusion, in patients with CRI undergoing MDCTA and receiving CIN-preventive measures, the incidence of CIN is low.

Topics: Acetylcysteine; Aged; Angiography; Contrast Media; Coronary Angiography; Creatinine; Female; Humans; Kidney Diseases; Kidney Failure, Chronic; Male; Sodium Bicarbonate; Tomography, X-Ray Computed; Triiodobenzoic Acids

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Electrocardiography; Enalapril; Humans; Hyperkalemia; Hypertension; Kidney Failure, Chronic; Male; Potassium; Renal Dialysis; Sodium Bicarbonate; Sympathomimetics

With longer graft and patient survival, recurrent disease is becoming recognized as an increasingly important contributor to long-term graft loss in renal transplant recipients. However, patients may present for the first time in end-stage renal disease (ESRD) leading to uncertainty as to their underlying diagnosis and the risk of recurrence. The purpose of this study was to describe the features of children who presented for the first time in ESRD and to determine the predictive value of investigations in differentiating diseases with and without a recurrence risk. From 7/99 to 11/04, 13 children presented to our center in ESRD. Their median age was 13.3 yr; 77% were male. The majority were hypertensive (77%) and oligoanuric (69%). All had proteinuria (median urine protein to creatinine ratio [Up/c] 7.0), and 92% had microhematuria. Only seven had small kidneys on ultrasound. All children underwent a serologic work-up and six (46%) were biopsied. Of the 13 children, seven had a glomerular disease; in five the diagnosis was made on biopsy, in one on serologic testing and one by family history. Of the remaining six children, three had non-glomerular diseases: obstructive uropathy in one and primary hyperoxaluria type 1 in two, and 3 had an unknown disease. When patients with glomerular diseases were compared with those with non-glomerular diseases, the two predictors for glomerular disease were a lower serum albumin (p = 0.004) and a higher serum bicarbonate level (p = 0.01). Comparing patients with and without a risk of recurrence, there were no differences between the two groups in any of their demographic, clinical, or biochemical parameters by analysis of variance (including serum albumin or proteinuria). In summary, the vast majority of children presenting in ESRD have hematuria and proteinuria, even with non-glomerular diseases. The significant overlap in clinical features between patients with and without a risk of recurrence emphasizes the need for all children presenting in ESRD to be evaluated extensively so that disease recurrence after transplantation can be anticipated or even prevented.

Topics: Adolescent; Female; Hematuria; Humans; Kidney Failure, Chronic; Kidney Transplantation; Male; Predictive Value of Tests; Proteinuria; Recurrence; Retrospective Studies; Risk Factors; Serum Albumin; Sodium Bicarbonate; Treatment Outcome

Topics: Adult; Alkalosis; Aspirin; Citrates; Drug Combinations; Female; Humans; Iron Deficiencies; Kidney Failure, Chronic; Pica; Renal Dialysis; Seizures; Sodium Bicarbonate

We describe a case of medication induced metabolic alkalosis in a maintenance dialysis patient who developed severe hypotension while undergoing a lactate hemofiltration procedure. A 73-year-old man with ESRD due to renovascular disease was used to ingesting up to 30 grams per day of a non-prescription medication (Effervescent granulare 250 grams, CRASTAN, Pisa Italy) consisting of sodium bicarbonate, citric acid, glucose and lemon flavor. For technical problem lactate hemofiltration was performed and thirty minutes after dialysis was started a severe symptomatic hypotension occurred (blood pressure 65/35 mmHg). Lactate hemofiltration was suspended and one-hour later standard bicarbonate dialysis was performed without any clinical problem. The different mechanisms in acidosis buffering occurring in lactate and bicarbonate hemofiltration were discussed.

Topics: Aged; Alkalosis; Hemodiafiltration; Humans; Hypotension; Kidney Failure, Chronic; Male; Severity of Illness Index; Sodium Bicarbonate

Topics: Alum Compounds; Calcium Sulfate; Causality; Diagnosis, Differential; Electrolytes; Female; Humans; Hyperkalemia; Hypokalemia; Kidney Failure, Chronic; Middle Aged; Pica; Renal Dialysis; Sodium Bicarbonate; Starch

Topics: Aged; Analgesics; Blood Pressure; Female; Homes for the Aged; Humans; Kidney Failure, Chronic; Long-Term Care; Nursing Homes; Renal Dialysis; Sodium Bicarbonate; Sodium, Dietary; Weight Gain

In chronic renal failure, metabolic acidosis is associated with increased whole body protein degradation. In rats this effect of acidosis occurs in skeletal muscle and is associated with increased ubiquitin mRNA expression. This has not been demonstrated in humans.. Six patients with chronic renal failure and acidosis underwent muscle biopsy before and after 1 month's treatment with sodium bicarbonate. RNA was extracted from the biopsy, and the expression of the genes for ubiquitin and the proteasome component, C2, were measured by Northern blotting.. There was no significant difference in the expression of ubiquitin or C2 after bicarbonate treatment. This is contrast with results from animal models of acidosis and some other catabolic conditions in humans. This may reflect the complexity of the ubiquitin-dependent pathway, and it may be that changes in ubiquitin expression are only seen with more severe and/or acute changes in pH.

Topics: Acidosis; Adult; Biopsy; Blotting, Northern; Complement C2; Female; Gene Expression; Humans; Kidney Failure, Chronic; Male; Middle Aged; Muscle, Skeletal; RNA; Sodium Bicarbonate; Treatment Failure; Ubiquitin

Metabolic acidosis (MA) is a frequent complication in advanced chronic renal failure (CRF). Currently, there is good evidence that MA contributes to malnutrition in CRF patients.. We evaluated the effect of correcting MA on nutritional status after 6 months of oral sodium bicarbonate supplementation in 18 patients aged 73 +/- 6 years with CRF to maintain serum bicarbonate levels at 24 +/- 2 mmol/L. The following parameters were measured: dietary record, energy intake, dietary protein intake (DPI), mini-nutritional assessment (MNA), serum albumin level, prealbumin level, prognosis inflammatory and nutritional index (PINI), and protein catabolic rate (nPCR).. No significant changes in body weight or systolic and diastolic blood pressure were observed. Serum albumin and prealbumin levels showed a significant increase. nPCR decreased significantly. DPI, energy intake, PINI, and MNA score did not change significantly. No patient reported side effects or fluid retention during the study.. Correction of MA improves serum albumin and prealbumin concentration, and it is not associated with any significant change in DPI, but induces a decrease in nPCR values. Whereas nPCR may provide an index of protein catabolism, it does not differentiate between dietary sources of protein or net catabolism of endogenous proteins. In the absence of dietary changes, the decrease in nPCR values may be attributed to a decrease in whole body protein degradation.

Topics: Acidosis; Aged; Bicarbonates; Diet Records; Dietary Proteins; Energy Intake; Female; Humans; Kidney Failure, Chronic; Male; Nutrition Assessment; Nutrition Disorders; Nutritional Status; Prospective Studies; Proteins; Renal Dialysis; Serum Albumin; Sodium Bicarbonate

Topics: Child; Enteral Nutrition; Home Nursing; Humans; Kidney Failure, Chronic; Medication Errors; Sodium; Sodium Bicarbonate; Sodium Chloride

To examine the relationship between serum leptin levels (SLL) and metabolic acidosis in patients with chronic renal failure (CRF).. SLL in control patients and in predialysis patients with CRF were measured and compared. SLL before and after correction of acidosis in patients with CRF were also compared.. Twenty-five patients with CRF (10 men and 15 women) aged 51.2 +/- 10.4 years and control patients (healthy subjects, 23 men and 25 women) aged 42.1 +/- 12.6 years were studied.. Five percent sodium bicarbonate (NaHCO(3), 2 to 3 mL/kg) was intravenously infused on the morning of the first day of treatment. NaHCO(3) was taken orally at a dosage of 50 to 200 mg/kg/d for 3 to 5 days thereafter.. SLL before and after NaHCO(3) treatment was measured by radioimmunoassay, and blood gas was measured before and after correction of metabolic acidosis in patients with CRF.. SLL in the normal control group (n = 48) was 10.04 +/- 7.0 ng/mL and was realated to body mass index (BMI) (P =.0331). SLL in men (n = 23) was lower than that in female controls (n = 25, P <.01). SLL in patients with CRF (n = 25) before (plasma HCO(3)(-), 13.03 +/- 3.05 mmol/L) and immediately after improvement of metabolic acidosis (plasma HCO(3)(-), 18.35 +/- 4.21 mmol/L) was 14.52 +/- 9.27 ng/mL and 15.34 +/- 11.89 ng/mL (P >.05), respectively. SLL measured 3 to 5 days after treatment for metabolic acidosis (plasma HCO(3)(-), 20.46 +/- 4.03 mmol/L) was 19.33 +/- 14.58 ng/mL, which was significantly higher than that in the normal control group and that in acidotic patients before NaHCO(3) treatment (P <.01).. SLL in acidotic patients with CRF were comparable to that in control subjects, and SLL was significantly increased after correction of metabolic acidosis in patients with CRF. The preliminary results suggest that hyperleptinemia in patients with CRF may be masked by metabolic acidosis and that metabolic acidosis may inhibit leptin synthesis or secretion. Further studies are needed to clarify the mechanisms.

Topics: Acidosis; Administration, Oral; Adult; Aged; Blood Gas Analysis; Body Mass Index; Case-Control Studies; Female; Humans; Infusions, Intravenous; Kidney Failure, Chronic; Leptin; Male; Middle Aged; Radioimmunoassay; Sex Factors; Sodium Bicarbonate

Topics: Alkalosis; Circadian Rhythm; Humans; Hypertension; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Sleep Apnea Syndromes; Sodium Bicarbonate; Substance-Related Disorders

Metabolic acidosis is almost invariably a consequence of advanced renal failure, although its severity can vary widely. To evaluate the determinants of the severity of metabolic acidosis, with special interest in determining if there is any difference in the prevalence and severity of metabolic acidosis between patients with and without diabetes, 113 predialysis patients with renal failure were studied. Criteria for inclusion onto the study were: creatinine clearance (Ccr)/1.73 m2 less than 30 mL/min, no alkali therapy within the previous 30 days, and the absence of respiratory diseases. Forty-eight patients had diabetes (33 patients with diabetic nephropathy). The following data were analyzed: demographics; cause of renal failure; hematocrit; serum urea, creatinine, uric acid, albumin, glucose, hemoglobin A1c, bicarbonate, sodium, potassium, chloride, calcium, phosphorus, and alkaline phosphatase levels; anion gap; urinary protein excretion; Ccr/1.73 m2; half of the sum of creatinine and urea clearances (Ccr-Cu); protein-equivalent nitrogen appearance (PNA); and whether the patients received diuretics (75 patients), angiotensin-converting enzyme inhibitors (54 patients), and/or calcium channel blockers (55 patients). After the exclusion of eight patients because of hypochloremia (three patients with and five patients without diabetes), mean serum bicarbonate levels were significantly greater in patients with diabetes than in the rest of the patients (20.7 +/- 2.3 v 18.2 +/- 2. 3 mmol/L; P = 0.0001). The mean anion gap (mmol/L) was also significantly less in patients with than without diabetes (19.70 +/- 3.65 v 22.35 +/- 3.64; P = 0.003). Eleven of 105 patients had serum bicarbonate levels of 23 mmol/L or greater (9 patients with and 2 patients without diabetes). Pure elevated anion gap followed by mixed (high anion gap and hyperchloremia) were the most common types of metabolic acidosis observed in both groups. There were no differences in PNA, diuretic treatment, or vomiting history between patients with and without diabetes. By multiple logistic regression analysis, the best determinants for a serum bicarbonate level greater than 19 mmol/L were: the diagnosis of diabetic nephropathy (odds ratio, 0.107; P = 0.0002), Ccr-Cu (odds ratio, 0.824; P = 0. 014), and age (odds ratio, 0.966; P = 0.046). In conclusion, patients with diabetes with advanced renal failure showed a less severe metabolic acidosis, which cannot be explained by gastrointestinal hydrogen

Topics: Acidosis, Renal Tubular; Creatinine; Diabetes Complications; Diabetes Mellitus; Diabetic Nephropathies; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Odds Ratio; Regression Analysis; Sodium Bicarbonate; Urea

Methemoglobinemia may occur after the administration of various drugs, including some local anesthetics. We report a patient with chronic renal failure and ischemic heart disease who developed clinically significant methemoglobinemia after an axillary block with bupivacaine and additional injection of lidocaine in the operative field. Although the two local anesthetics usually do not cause methemoglobinemia, we suspect that the displacement of lidocaine from protein binding by bupivacaine, in combination with metabolic acidosis and treatment with other oxidants, was the reason for the development of methemoglobinemia.

Topics: Acidosis; Alkalies; Anesthetics, Local; Antidotes; Axilla; Bupivacaine; Drug Interactions; Female; Humans; Intraoperative Care; Kidney Failure, Chronic; Lidocaine; Methemoglobinemia; Methylene Blue; Middle Aged; Myocardial Ischemia; Nerve Block; Oxidants; Protein Binding; Sodium Bicarbonate

Topics: Humans; Kidney Failure, Chronic; Pica; Sodium Bicarbonate; Water-Electrolyte Imbalance

Oral sodium bicarbonate (NaHCO3) is widely used to treat acidosis in patients with renal failure. However, no data are available in man on the effects on proximal renal tubular protein catabolism or markers of tubular injury. We have developed methods to allow such studies, and both increased tubular catabolism of 99mTc-labelled aprotinin (Apr*), as well as tubular damage were found in association with increased ammonia (NH3) excretion in patients with nephrotic range proteinuria. We now examine the effects of reducing renal ammoniogenesis, without altering proteinuria, using oral NaHCO3 in 11 patients with mild/moderate renal impairment and proteinuria. Renal tubular catabolism of Apr* was measured before and after NaHCO3 by renal imaging (Kidney uptake, K% of dose) and urinary excretion of free 99mTcO4- (metabolism, Met% of dose/h) over 26 h. Fractional degradation (Frac) was calculated from Met/K (/h). Fresh urine was also analyzed for NH3 excretion every fortnight from 6/52 before treatment. Total urinary N-acetyl-beta-D-glucose-aminidase (NAG) and the more tubulo-specific NAG "A2" were measured. 51CrEDTA clearance and 99mTc-MAG 3 TER were also assessed. After NaHCO3 Met over 26 h was significantly reduced (from 1.3 +/- 0.2% of dose/h to 0.9 +/- 0.1% dose/hr, p < 0.005), as was Frac of Apr* (from 0.06 +/- .006/h to 0.04 +/- 0.005/hr, p < 0.003). NH3 excretion also fell significantly (from 0.9 +/- 0.2 mmol/h to 0.2 +/- 0.05 mmol/h, p < 0.007), as did both total urinary NAG (from 169 mumol/24 h, 74-642 mumol/24 h to 79 mumol/ 24 h, 37-393 mumol/24 h, p < 0.01), and the NAG 'A2' isoenzyme (from 81.5 mumol/24 h, 20-472 mumol/24 h to 35.0 mumol/24 h, 6-388 mumol/24 h, p < 0.001). Proteinuria remained unaltered, and there was no change in blood pressure nor in glomerular haemodynamics. Oral NaHCO3 may thus pro-tect the proximal renal tubule and help delay renal disease progression.

Topics: Acetylglucosaminidase; Administration, Oral; Adult; Ammonia; Aprotinin; Blood Pressure; Chromium Radioisotopes; Edetic Acid; Female; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Kidney Tubules, Proximal; Male; Middle Aged; Nephelometry and Turbidimetry; Organotechnetium Compounds; Proteinuria; Radionuclide Imaging; Radiopharmaceuticals; Sodium Bicarbonate

Uraemia and dialysis are viewed as catabolic processes resulting in malnutrition in chronic renal failure (CRF) patients. To sort out the effects of uraemia, acidosis, and dialysis on protein metabolism, we measured leucine flux in CRF patients before and after initiation of maintenance dialysis.. Whole-body leucine flux was measured by primed-constant infusion of L[1-(13)C] leucine in nine CRF patients longitudinally; twice before and once after initiation of maintenance dialysis (D). Before dialysis, one leucine flux was measured when the patients were acidotic (A), and the other, when acidosis was corrected with NaHCO, (NA). Five normal subjects underwent one single leucine flux measurement to serve as control (N). Both patients and normal subjects consumed a constant diet for 6 days and leucine flux was measured on the 7th day 12 h post-absorption. Diet for the CRF patients was identical during the three periods. Plasma L[1-(13)C] leucine and L[1-(13)C]KIC were measured by gas chromatography/mass spectrometry and expired 13CO2 by isotope ratio spectrometry. Leucine kinetics were calculated using standard equations.. Plasma CO2 levels were 19, 26 and 31 mmol/l in A, NA and D periods respectively. All kinetic results (micromol/kg/h) are presented as means +/- SD in the order of A, NA, D, and N, and CRF values that are statistically different from N are identified (*). The amounts of leucine release from endogenous protein breakdown (Ra or Q) were 101 +/- 12* 95 +/- 9* 113 +/- 22 and 117 +/- 6. Leucine oxidation (C), quantities of leucine irreversibly oxidized to CO2, were 16.5 +/- 5.4, 9.7 +/- 3.7*, 12.3 +/- 3.0*, and 23.2 +/- 3.1. Leucine protein incorporation levels (S) were 85 +/- 10, 85 +/- 8, 101 +/- 19 and 94 +/- 6. The S of 101 in CRF patients at period D was statistically higher than those during A and NA periods.. These data indicate that when acidosis was corrected, CRF patients adapted to lower protein intake by reducing amino-acid oxidation and protein degradation, and maintained protein synthesis at normal levels. Metabolic acidosis impaired the downregulation of amino-acid oxidation. Maintenance dialysis treatment longitudinally restored protein flux to normal and increased protein synthesis. The general notion that uraemia and dialysis are protein catabolic is not supported by this work.

Topics: Acidosis; Case-Control Studies; Female; Humans; Kidney Failure, Chronic; Leucine; Longitudinal Studies; Male; Middle Aged; Nutrition Disorders; Nutritional Status; Peritoneal Dialysis, Continuous Ambulatory; Proteins; Renal Dialysis; Sodium Bicarbonate; Uremia

Topics: Alkalosis; Female; Humans; Kidney Failure, Chronic; Middle Aged; Pica; Renal Dialysis; Sodium Bicarbonate

This study was aimed to evaluate the efficacy of combination therapy of bicarbonate and salbutamol for hyperkalemia in 9 hemodialysis patients. Simultaneous administration of 8.4% sodium bicarbonate (i.v., 2 mEq/kg) for 1/2 hour and salbutamol (15 mg) in nebulized form for 10 min was compared with treatment modality of either bicarbonate or salbutamol alone. Infusion of sodium bicarbonate induced a significant rise in plasma bicarbonate from 17.3 +/- 3.2 to 22.1 +/- 2.4 mEq/L (p < 0.01), but was ineffective in lowering plasma potassium (-0.13 +/- 0.06 mEq/L). As expected, salbutamol significantly lowered plasma potassium (-0.57 +/0 0.03 mEq/L, p < 0.02 vs. basal value) in all except 2 patients. The combined regimen of bicarbonate and salbutamol to a total 9 patients including 2 patients without hypokalemic effect to salbutamol alone revealed a substantially greater fall in plasma potassium (-0.96 +/- 0.08 mEq/L, p = 0.000 vs. either drug alone) accompanied with significant increase in plasma bicarbonate and blood pH. Treatment with salbutamol or the combined regimen produced slight increases in heart rate but not in blood pressure. It is concluded that the combined regimen of bicarbonate and beta(2)-adrenergic agonist (salbutamol) could be recommended as an efficient alternative for severe hyperkalemia in uremic patients, and is suggested that the enhanced transcellular hypokalemic effects of salbutamol in this combined regimen with bicarbonate would be related to the activation of Na-K pump with acute correction of underlying metabolic acidosis.

Topics: Adrenergic beta-Agonists; Adult; Albuterol; Blood Pressure; Drug Therapy, Combination; Female; Heart Rate; Humans; Hydrogen-Ion Concentration; Hyperkalemia; Kidney Failure, Chronic; Male; Middle Aged; Potassium; Sodium Bicarbonate

The case is described of a 29-year-old man with renal failure and recurrent hyperparathyroidism who 3 weeks postparathyroidectomy developed hypocalcemic tetany because he was taking one-half the prescribed dose of calcitriol. He interpreted his symptoms as those of potassium intoxication and self-administered almost 1,500 mEq sodium bicarbonate. The increase in plasma sodium and osmolarity led to increased fluid intake, and at presentation he had an ionized calcium of 0.50 mmol/L, K 5.3 mmol/L, Na 148 mmol/L, total CO2 52.6 mmol/L, pO2 51.2 mm Hg, and pH of 7.61. He had gained 7 kg in weight. All abnormalities were corrected by dialysis, using initially a calcium-free dialyzate with extra calcium infused. The case illustrates the effect of alkalosis in reducing the amount of calcium that exists in ionized form, and it is suggested that complexing of calcium as calcium bicarbonate together with the pH change contributed to the decrease in ionized calcium. It is also an example of the hazards of treating patients who devise their own therapeutic regimens.

Topics: Adult; Alkalosis; Calcitriol; Calcium; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Male; Parathyroidectomy; Postoperative Complications; Renal Dialysis; Self Medication; Sodium Bicarbonate; Tetany

The effects of insulin-like growth factor I (IGF-I) and insulin on glucose metabolism were compared in awake, chronically catheterized rats with chronic renal failure (CRF) and sham-operated, pair-fed controls. In control rats, IGF-I (5 micrograms.kg-1.min-1) and insulin (2 mU.kg-1.min-1) infusions produced similar twofold increases in total body glucose uptake from fasting values under euglycemic conditions (euglycemic clamps). Total body glucose uptake during euglycemic IGF-I clamps at 5 and 10 micrograms.kg-1.min-1 was not different between CRF and control rats. Total body glucose uptake during euglycemic insulin clamps at 2 and 4 mU.kg-1.min-1 was significantly lower in CRF rats compared with corresponding values in control rats. Hepatic glucose production was suppressed by insulin equally but not by IGF-I in both groups. Correction of metabolic acidosis by NaHCO3 partially improved insulin resistance in rats with CRF, whereas an equimolar amount of NaCl had no effect. Thus the capacity of IGF-I infusion to stimulate total body glucose uptake is maintained in CRF rats that are insulin resistant.

Topics: Animals; Blood Glucose; Glucose; Humans; Insulin; Insulin Resistance; Insulin-Like Growth Factor I; Kidney Failure, Chronic; Liver; Male; Rats; Rats, Sprague-Dawley; Recombinant Proteins; Reference Values; Sodium Bicarbonate

In normal humans and in patients with chronic renal failure (CRF), acidosis increases whole-body protein degradation. Correction of acidosis reduces protein degradation. The mechanisms underlying these changes in protein metabolism are unclear. However, one possibility is that dietary protein intake is reduced in acidosis and that this causes increased protein degradation. This possibility has not been tested. In this study the effects of acidosis on protein intake in patients with CRF have been assessed using 7-day weighed dietary inventories in the acidotic state (venous bicarbonate 15.6 +/- 1.0 mmol/L) and following treatment with oral sodium bicarbonate (venous bicarbonate 21.0 +/- 1.4 mmol/L). Protein intake was also derived from urinary nitrogen excretion. There was no significant difference in protein intake calculated from dietary records (1.0 +/- 0.09 g/kg/d v 1.06 +/- 0.1 g/ kg/d) or calculated from urinary nitrogen (1.13 +/- 0.07 g/kg/d v 1.06 +/- 0.06 g/kg/d) between the untreated and bicarbonate-treated states in eight patients with CRF. We conclude that acidosis in CRF patients does not affect dietary protein intake and that dietary changes therefore do not contribute significantly to the changes in protein metabolism seen in acidosis.

Topics: Acidosis; Adult; Aged; Blood Urea Nitrogen; Diet Records; Dietary Proteins; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Middle Aged; Proteins; Sodium Bicarbonate

To test the hypothesis that acidosis contributes to the insulin resistance of chronic renal failure (CRF) and impairs the action of insulin to decrease protein degradation, eight CRF patients were studied using the combined L-[1-13C]leucine-euglycemic clamp technique before (acid) and after (NaHCO3) 4 wk treatment with NaHCO3 (pH: acid 7.29 +/- 0.01 vs. NaHCO3 7.36 +/- 0.01, P < 0.001). Protein degradation (PD) was estimated sequentially from the kinetics of a primed continuous infusion of L-[1-13C]leucine in the basal state and during a hyperinsulinemic euglycemic clamp. Insulin sensitivity was measured during the clamp. The correction of acidosis significantly increased the glucose infusion rate necessary to maintain euglycemia (acid 6.44 +/- 0.89 vs. bicarbonate 7.38 +/- 0.90 mg.kg-1.min-1, P < 0.01) and significantly decreased PD in the basal state (acid 126.4 +/- 8.1 vs. bicarbonate 100.1 +/- 6.9 mumol.kg-1.h-1, P < 0.001). Hyperinsulinemia decreased PD in both studies (acid basal 126.4 +/- 8.1 vs. clamp 96.5 +/- 7.7, P < 0.001; bicarbonate basal 100.1 +/- 6.9 vs. clamp 88.2 +/- 5.5 mumol.kg-1.h-1, P = 0.06), its effect being unaltered by acidosis, with a reduction of 24% before and 12% after the correction of acidosis. In conclusion, acidosis contributes to the insulin resistance of CRF but does not affect the action of insulin on PD.

Topics: Acidosis; Adult; Aged; Amino Acids; Bicarbonates; Blood Pressure; Body Weight; Female; Glucose; Glucose Clamp Technique; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Leucine; Male; Middle Aged; Sodium Bicarbonate

We have evaluated intracellular pH (pHi) and Na+/H+ exchanger activity in peripheral lymphocytes from 16 patients on regular acetate hemodialysis. All the patients were taking oral NaHCO3 supplementation (30 mmol/day), to maintain predialysis arterial blood acid-base status within normal range (pH 7.36 +/- 0.02, PHCO3- 23.3 +/- 1.2 mM, pCO2 40.9 +/- 1.4 mm Hg). pHi was measured, using the fluorescent probe BCECF (2',7'-bis-carboxyethyl-5,6-carboxyfluorescein), both in nominal absence of bicarbonate (Hepes solution, pH 7.4; n = 10) and in the presence of HCO3-/CO2 buffer system (pH 7.4, [HCO3-] 25 mM, pCO2 40 mm Hg; n = 6). Predialysis pHi did not differ from controls when measured in the presence of HCO3-/CO2 (7.28 +/- 0.04 vs. 7.29 +/- 0.04, p = NS), but was lower in dialysis patients than in normal subjects (7.11 +/- 0.04 and 7.20 +/- 0.02, respectively; p < 0.05) when measured in Hepes solution. This suggested that bicarbonate-independent pHi regulation was abnormal in dialysis patients. To further characterize this abnormality of pHi regulation, lymphocytes were exposed to ethylisopropylamiloride, a specific Na+/H+ antiporter inhibitor, in Hepes solution; this maneuver induced a significantly lower decrement in pHi (0.04 +/- 0.04 vs. 0.15 +/- 0.03, p < 0.05) in dialysis patients than in controls, indicating reduced Na+/H+ exchanger activity in the patients. The rate of pHi recovery during the first 30 s after induction of various degrees of cell acidification (pHi range 6.2-7.0), which in the absence of HCO3-/CO2 is dependent on Na+/H+ exchanger activity, was also reduced in the patients as compared to controls (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Amiloride; Cell Separation; Female; Flow Cytometry; Fluoresceins; Fluorescent Dyes; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Sodium Bicarbonate; Sodium-Hydrogen Exchangers; T-Lymphocytes

Topics: Acidosis; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Peritoneal Dialysis; Proteins; Sodium Bicarbonate

Topics: Acidosis; Bicarbonates; Erythropoietin; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Sodium; Sodium Bicarbonate

Plasma catecholamines (noradrenaline, adrenaline, dopamine) and dopamine-beta-hydroxylase were investigated in hypotensive haemodialysis patients treated with different sodium dialysate concentrations in acetate or bicarbonate fluids. The present results suggest that most physiological reactions could be obtained in patients treated with equimolar sodium concentration in blood and dialysis fluids in both kinds of acetate and bicarbonate.

Topics: Acetates; Acetic Acid; Adult; Blood Pressure; Blood Pressure Determination; Dopamine; Dopamine beta-Hydroxylase; Epinephrine; Female; Humans; Kidney Failure, Chronic; Male; Norepinephrine; Renal Dialysis; Sodium Bicarbonate

The effect of correction of acidosis in chronic renal failure (CRF) was determined from the kinetics of infused L-[1-13C]leucine. Nine CRF patients were studied before (acid) and after two 4-wk treatment periods of sodium bicarbonate (NaHCO3) and sodium chloride (NaCl) (pH: acid 7.31 +/- 0.01, NaHCO3 7.38 +/- 0.01, NaCl 7.30 +/- 0.01). Leucine appearance from body protein (PD), leucine disappearance into body protein (PS) and leucine oxidation (O) decreased significantly with correction of acidosis (PD: acid 122.4 +/- 6.1, NaHCO3 88.3 +/- 6.9, NaCl 116.2 +/- 9.1 mumol.kg-1.h-1, acid vs. NaHCO3 P < 0.01, NaHCO3 vs. NaCl P < 0.01, acid vs. NaCl NS; PS: acid 109.4 +/- 5.6, NaHCO3 79.0 +/- 6.3, NaCl 101.3 +/- 7.7 mumol.kg-1.h-1, acid vs. NaHCO3 P < 0.01, NaHCO3 vs. NaCl P < 0.01, acid vs. NaCl NS; O: acid 13.0 +/- 1.2, NaHCO3 9.2 +/- 0.9, NaCl 15.0 +/- 1.9 mumol.kg-1.h-1, acid vs. NaHCO3 P < 0.05, NaHCO3 vs. NaCl P < 0.01, acid vs. NaCl NS). There were no significant changes in plasma amino acid concentrations. These results confirm that correction of acidosis in chronic renal failure removes a potential catabolic factor.

Topics: Acidosis; Adolescent; Adult; Aged; Amino Acids; Bicarbonates; Blood Glucose; Blood Pressure; Body Weight; Female; Hormones; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Oxidation-Reduction; Proteins; Sodium; Sodium Bicarbonate; Sodium Chloride; Urea

The present report describes a rare of a 77-year-old woman who developed encephalopathy and metabolic acidosis associated with hyperammonemia, at the introduction of hemodialysis by chronic renal failure. With the intravenous infusion of HCO3-, levels of acidosis and hyperammonemia decreased rapidly. Concomitantly the disturbance of consciousness was improved. Results of plasma amino acid patterns of pre and post infusion of HCO3- showed improvement of the metabolism of the urea cycle, increased urea synthesis and decreased plasma ammonium levels. The role of the hepatic urea cycle has been considered to be exclusively the elimination of potentially toxic ammonia. In the conventional view, the acid base balance of the body obtains stabilized homeostasis by the function of the principal organs, lungs and kidneys. But, it has been recently shown that urea cycle is an important factor in the maintenance of pH homeostasis, due to regulated metabolism of HCO3-. Both HCO3- and NH4+ are converted to urea indicating the urea cycle's involvement in acid base homeostasis. 2HCO3- + 2NH4+-->urea+CO2+3H2O In this case, with the infusion of HCO3, the metabolism of the urea-cycle was improved and plasma ammonium levels were decreased. This indicates that HCO3- is an important factor for the metabolism of ammonia.

Topics: Acid-Base Equilibrium; Acidosis; Aged; Ammonia; Female; Hepatic Encephalopathy; Humans; Infusions, Intravenous; Kidney Failure, Chronic; Renal Dialysis; Sodium Bicarbonate; Urea

To evaluate the effectiveness of continuous arteriovenous hemodiafiltration (CAVHD) using citrate as the anticoagulant for the treatment of lactic acidosis in patients with renal failure.. Case series with careful monitoring of the clinical course of patients being treated in a medical or surgical ICU.. University hospital ICU.. Two patients with lactic acidosis are described, along with our experience using CAVHD and citrate in other clinical settings.. CAVHD was used to manage renal failure, while a continuous infusion of citrate was administered to maintain patency of the extracorporeal circuit.. Total and ionized serum calcium concentrations and citrate concentrations were monitored.. CAVHD with citrate as the anticoagulant proved to be a convenient means of managing vascular volume, serum electrolyte concentrations, acid-base balance, and replacement renal function requirements in the setting of severe lactic acidosis, oliguric renal failure, and hemorrhagic diathesis.. CAVHD with citrate as the anticoagulant can be recommended as effective therapy for selected patients, but careful monitoring is needed to avoid serious complications.

Topics: Acidosis, Lactic; Adult; Aged; Bicarbonates; Chlorides; Citrates; Citric Acid; Female; Hemofiltration; Humans; Hypernatremia; Kidney Failure, Chronic; Male; Middle Aged; Sodium; Sodium Bicarbonate

Topics: Adult; Aged; Aged, 80 and over; Bicarbonates; Diabetic Ketoacidosis; Erythropoietin; Female; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Sodium; Sodium Bicarbonate

Topics: Abdominal Pain; Adult; Bicarbonates; Child; Dialysis Solutions; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Peritoneal Dialysis; Peritoneal Dialysis, Continuous Ambulatory; Sodium; Sodium Bicarbonate

Ten uremic patients maintained stable on regular dialysis treatment participated in a comparison study of 2 hours' biofiltration and 4 hours' bicarbonate hemodialysis with informed consents. In biofiltration, ultrafiltrate was replaced by a solution consisting of Na 145 mEq/l, HCO3- 100 and Cl 45 at the infusion rate 2.51/hour. Dialysate composition was Na 130-149 mEq/l, K 1.0, Cl 119, Ca 2.5, Mg 0.5, CH3COO- 15 and glucose 200 mg/dl. Hemodiafilter was F80, polysulphone, 1.9 m2, manufactured by Fresenius Co. Ltd. Blood flow rate was 5 ml/min/kg.body.weight to keep urea index (Kt/V) over 1.0. B-A-B' comparison was designed in which B and B' stand for 4 hours' bicarbonate hemodialysis while A for 2 hours' biofiltration, 3 times per week for 2 months, respectively. It was intended to find out if there are aggravations of clinical parameters in A after B and/or improvements in B' after A in view of evaluation of optimum for 2 hours' biofiltration. One patient was withdrawn from biofiltration at 15th treatment in A because of frequent muscular twitchings. Others finished the whole program, thus making drop-out rate 10%. No significant differences were observed in the following parameters between B and A and between A and B': cardiothoratic ratio, pre-treatment blood pressure, human atrial natriuretic hormone, cardiovascular dynamics, total protein, BUN, serum creatinine, uric acid, beta 2 microglobulin, blood counts, blood gas analysis, electrolytes, alkaline-phosphatase, PTH-C, protein catabolic rate (PCR), lipids and liver functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Bicarbonates; Blood Urea Nitrogen; Creatinine; Evaluation Studies as Topic; Female; Hemodynamics; Hemofiltration; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Sodium; Sodium Bicarbonate; Time Factors

The purpose of the study was to evaluate the potassium-lowering effect of hypertonic versus isotonic sodium bicarbonate (NaHCO3) in patients with end-stage renal disease (ESRD) receiving chronic maintenance hemodialysis. Immediately prior to dialysis, we infused isotonic (1.4%, 150 mEq/l) NaHCO3 in H2O (1 mEq/kg body weight over 2 h) to 10 patients with ESRD. Blood was drawn in heparinized tubes, without the use of a tourniquet, from the angioaccess for Na, K, pH, PCO2, HCO3, and osmolality at baseline (x 3) and after 10, 20, 40, 60, 90, 120, and 180 min of infusion. All patients were acidotic (HCO3 13-21 mEq/l, pH 7.25-7.38) prior to the study. In these patients, plasma HCO3 increased by an average of 3 mEq/l, and plasma K decreased by 0.35 mEq/l at 180 min. Plasma osmolality did not change. In 8 patients, a bolus of hypertonic (8.4%, 1,000 mEq/l) NaHCO3 (1 mEq/kg body weight over 5 min) tended to cause a transient increase in plasma HCO3, an increase in plasma osmolality, and minor changes in the K levels (an initial small and transient albeit significant decrease, followed by a tendency to increase). Finally, plasma K tended to increase in patients receiving infusions of either isotonic (n = 6) or hypertonic (n = 6) sodium chloride. Our data do not support the efficacy of the common practice of administering NaHCO3 for the emergency treatment of hyperkalemia in patients with ESRD receiving maintenance dialysis.

Topics: Bicarbonates; Humans; Hydrogen-Ion Concentration; Hypertonic Solutions; Isotonic Solutions; Kidney Failure, Chronic; Male; Osmolar Concentration; Potassium; Sodium; Sodium Bicarbonate

Topics: Bicarbonates; Calcium Gluconate; Education, Medical; Humans; Hyperkalemia; Kidney Failure, Chronic; Nephrology; Renal Dialysis; Sodium; Sodium Bicarbonate; Surveys and Questionnaires; United States

Chronic renal failure is associated with increased protein turnover, and recent evidence suggests that this may be due to the accompanying acidosis. Patients with stable chronic renal failure maintained on protein restriction were given sodium bicarbonate supplementation for 8 weeks. This resulted in improvements in acid-base status, plasma urea and uric acid levels, independent of changes in glomerular filtration rate. Acidosis is a potentially reversible toxic effect of chronic renal failure and its correction produces sustained metabolic benefit.

Topics: Acidosis, Renal Tubular; Adult; Bicarbonates; Blood Glucose; Blood Proteins; Female; Humans; Insulin; Kidney Failure, Chronic; Male; Middle Aged; Sodium; Sodium Bicarbonate; Urea; Uremia

Topics: Bicarbonates; Calcium Gluconate; Humans; Hyperkalemia; Kidney Failure, Chronic; Sodium; Sodium Bicarbonate

The purpose of this study was to evaluate the effects of oral base therapy on selected chemical parameters in chronic hemodialysis patients. Oral base supplements were administered to 20 acidotic chronic hemodialysis patients for one month. Serum bicarbonate levels rose from 18.6 +/- 2.9 to 22.5 +/- 4.0 mEq/L (p less than 0.0005) and pH rose from 7.35 +/- 0.03 to 7.39 +/- 0.04 (p less than 0.0005). Serum ionized calcium levels fell from 5.03 +/- 0.37 to 4.83 +/- 0.34 mg/dL (1.25 +/- 0.09 to 1.21 +/- 0.08 mmol/L) (p less than 0.01), while intact parathyroid hormone (PTH) levels rose from 547 +/- 697 to 619 +/- 776 pg/mL (p less than 0.05). Base therapy did not result in significant changes in serum levels of total calcium, phosphorus, alkaline phosphatase, urea nitrogen, creatinine, total protein, albumin or potassium. If empiric therapy with exogenous base is given to dialysis patients, ionized calcium levels should be closely monitored since changes in calcium supplement or vitamin D therapy may be required to maintain ionized calcium and parathyroid hormone values at the pre-treatment levels.

Topics: Acidosis; Antacids; Bicarbonates; Calcium; Citrates; Citric Acid; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Phosphorus; Renal Dialysis; Sodium; Sodium Bicarbonate

Topics: Acidosis; Adult; Cardiopulmonary Bypass; Hemofiltration; Humans; Kidney Failure, Chronic; Male; Sodium Bicarbonate; Sodium Chloride

In steady state, the acidosis in the majority of 17 uremic patients was characterized by a persistent bicarbonaturia (FEHCO3 ranging between 0% and 17.65%). An NH4Cl loading test in 17 patients revealed two distinct groups: group A (n = 11) with complete disappearance of the urinary bicarbonate loss and a mean UpH of 5.39 +/- 0.10 at a PHCO3 level of 13.3 +/- 0.5 mEq/L; and group B (n = 6) with urinary acidification disturbances with a persistent FEHCO3 ranging between 1.06% and 3.15% and a mean UpH of 6.53 +/- 0.06 at a PHCO3 level of 13.5 +/- 0.7 mEq/L. Between the two groups, there were no differences in CCr, plasma Na, K, Cl, Ca, PO4, PCO2, and aldosterone levels. Calculation of the THCO3/TNa reabsorption ratio over a wide range of PHCO3 levels revealed no differences between the two groups. The mean levels of circulating PTH were significantly higher in group B compared with group A (40.1 +/- 10.8 mU/dL v 19.3 +/- 4.4 mU/dL; P less than .05), and the spontaneous steady-state FENa was more pronounced in group B than in group A (12.1% +/- 1.5% v 4.9% +/- 0.7%; P less than .05). Four patients from group B with a well-documented salt-losing nephropathy (FENa ranging from 10.20% to 15.10%) were submitted to a progressive dietary salt restriction over several weeks. At this stage, the four patients no longer had bicarbonaturia, and the urinary pH decreased to levels between 5.15 and 5.65 during NH4Cl-induced acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acidosis, Renal Tubular; Adult; Aged; Ammonium Chloride; Bicarbonates; Diet, Sodium-Restricted; Homeostasis; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Middle Aged; Parathyroid Hormone; Sodium; Sodium Bicarbonate

Topics: Aluminum Hydroxide; Bicarbonates; Humans; Kidney Failure, Chronic; Sodium; Sodium Bicarbonate; Sodium Chloride; Vitamins

The human end-stage kidney and its experimental analogue, the remnant kidney in the rat, exhibit widespread tubulo-interstitial disease. We investigated whether the pathogenesis of such tubulo-interstitial injury is dependent upon adaptive changes in tubular function and, in particular, in ammonia production when renal mass is reduced. Dietary acid load was reduced in 1 3/4-nephrectomized rats by dietary supplementation with sodium bicarbonate (NaHCO3), while control rats, paired for serum creatinine after 1 3/4 nephrectomy, were supplemented with equimolar sodium chloride. After 4-6 wk, NaHCO3-supplemented rats demonstrated less impairment of tubular function as measured by urinary excretory rates for total protein and low molecular weight protein and higher transport maximum for para-aminohippurate per unit glomerular filtration rate, less histologic evidence of tubulo-interstitial damage, less deposition of complement components C3 and C5b-9, and a lower renal vein total ammonia concentration. Such differences in tubular function could not be accounted for simply on the basis of systemic alkalinization, and differences in tubular injury could not be ascribed to differences in glomerular function. Because nitrogen nucleophiles such as ammonia react with C3 to form a convertase for the alternative complement pathway, and because increased tissue levels of ammonia are associated with increased tubulo-interstitial injury, we propose that augmented intrarenal levels of ammonia are injurious because of activation of the alternative complement pathway. Chemotactic and cytolytic complement components are thereby generated, leading to tubulo-interstitial inflammation. Thus, alkali supplementation reduces chronic tubulo-interstitial disease in the remnant kidney of the rat, and we propose that this results, at least in part, from reduction in cortical ammonia and its interaction with the alternative complement pathway.

Topics: Acid-Base Equilibrium; Ammonia; Animals; Bicarbonates; Complement C3; Complement Pathway, Alternative; Creatinine; Diet; Fluorescent Antibody Technique; Glomerular Filtration Rate; Hemolysis; Kidney Failure, Chronic; Nephrectomy; Proteinuria; Rats; Sodium; Sodium Bicarbonate

Nitrogen and potassium balance studies were conducted in six nondialyzed uremic patients. Each patient was investigated before and after supplementation with sodium bicarbonate and sodium chloride. Every period of the study lasted longer than 1 wk. Each patient had the same calorie and protein intake during the whole study. Urea nitrogen appearance was correlated with protein intake for the assessment of the compliance of patients with their diets. There was a significant decrease of blood urea nitrogen (p = 0.014) of 36% during bicarbonate supplementation and both metabolic balance studies improved significantly (p = 0.0005 and 0.0096). However, there was no significant improvement during sodium chloride administration indicating that the effect of bicarbonate was the result of the correction of metabolic acidosis and not of the expansion of the extracellular volume.

Topics: Acidosis; Adult; Aged; Bicarbonates; Blood Urea Nitrogen; Female; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Male; Middle Aged; Nitrogen; Potassium; Sodium Bicarbonate; Sodium Chloride

Correction of chronic renal acidosis was attempted for 6 weeks in 20 end stage renal failure patients on chronic acetate hemodialysis by means of 6-9 g of sodium bicarbonate given orally by means of gastric juice resistant capsule of 1 g. Normalisation of the inter-dialysis acid base status was obtained without major side effects.

Topics: Acetates; Acidosis; Adult; Aged; Bicarbonates; Humans; Kidney Failure, Chronic; Middle Aged; Sodium Bicarbonate

A case of self-poisoning with ethylene glycol is presented. The metabolic upset induced by ingestion of this substance is discussed and the principles underlying treatment with ethyl alcohol, sodium bicarbonate and renal dialysis are outlined. The practical problems experienced with this therapy are detailed. The need for immediate instigation of treatment and for intensive care are emphasised.

Topics: Aged; Bicarbonates; Critical Care; Ethanol; Ethylene Glycols; Heart Failure; Humans; Kidney Failure, Chronic; Male; Peritoneal Dialysis; Sodium Bicarbonate

The third case in the literature of sodium-losing renal disease due to obstruction is presented. The experimental evidence and limited clinical experience is reviewed which suggests that the sodium loss is due to an inappropriate response in the adaptive processes that are initiated by the loss of functioning nephrons. The immediate treatment is by replacement of sodium but in the long term the condition may be reversed by very cautious reduction in sodium intake. Definitive treatment may be indicated where obstruction is the cause and consequently this should be sought in all cases of salt-losing renal disease.

Topics: Bicarbonates; Female; Humans; Kidney Failure, Chronic; Kidney Tubules; Middle Aged; Sodium; Sodium Bicarbonate; Sodium Chloride; Ureteral Obstruction

In renal failure, absolute calcium excretion is low, but fractional excretion (FE) of filtered load is increased. In order to determine the role of metabolic acidosis in contributing to increased FECa, we have studied thyroparathyroidectomized dogs in a control phase and following the induction of chronic renal failure, both during spontaneous metabolic acidosis and after correction with NaHCO3. FECa was 3.7% in controls and increased to 13.7% in azotemic acidotic dogs (p less than 0.01). After correction of acidosis FENa was not significantly changed, but FECa fell significantly, to 8.1% (p less than 0.01), while glomerular filtration rate, plasma calcium and filtered calcium load were unchanged. Thus although FECa is increased in nonacidotic azotemic dogs, acidosis further enhances calcium excretion by inhibiting renal tubular calcium reabsorption. These effects of metabolic acidosis may contribute to hypocalcemia and bone disease in azotemia.

Topics: Acidosis; Animals; Bicarbonates; Calcium; Dogs; Female; Kidney; Kidney Failure, Chronic; Parathyroid Glands; Sodium Bicarbonate; Thyroidectomy

Topics: Acetates; Bicarbonates; Buffers; Carbon Dioxide; Humans; Hydrogen-Ion Concentration; Infusions, Parenteral; Kidney Failure, Chronic; Renal Dialysis; Sodium Bicarbonate; Systole