sodium-bicarbonate and Diabetes-Mellitus

To document a case of severe metabolic and lactic acidosis secondary to phenformin. This adverse effect has almost been forgotten as 15 years have passed since its withdrawal from the US market.. A 64-year-old man presented with a four-day history of left upper abdominal pain and a one-week history of constipation and diarrhea. His arterial blood gases were pH 6.7, pCO2 2.80 kPa, and pO2 12.00 kPa with 90% oxygen saturation on room air. Serum chemistries indicated an unmeasurable serum bicarbonate concentration, anion gap 52 mmol/L, lactate concentration 29.5 mmol/L, blood urea nitrogen 6.63 mmol/L, creatinine 229.84 mumol/L, and blood glucose 4.35 mmol/L. There were low levels of urine and serum ketones. In the emergency department, he required resuscitation for hypotension and bradycardia. His diagnosis was lactic and ketoacidosis secondary to phenformin. The patient was treated with NaCl 0.9%, sodium bicarbonate, insulin, and hemodialysis. Although he survived the initial insult of lactic and ketoacidosis, his hospital course was complicated and he died on hospital day 105.. Treatment of lactic acidosis is difficult and challenging. The continued availability of phenformin in neighboring countries, and the renewed interest in biguanide therapy for treating diabetes mellitus make it an important diagnosis of exclusion in diabetic patients who present with severe acidosis. Metformin, another biguanide under investigation for the treatment of diabetes mellitus, is associated with a much lower incidence of lactic acidosis than is phenformin.

Topics: Acidosis, Lactic; Diabetes Mellitus; Dichloroacetic Acid; Drug and Narcotic Control; Humans; Insulin; Male; Middle Aged; Phenformin; Renal Dialysis; Sodium Bicarbonate; Sodium Chloride

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

Topics: Acidosis, Lactic; Bicarbonates; Diabetes Complications; Diabetes Mellitus; Humans; Metformin; Renal Dialysis; Sodium; Sodium Bicarbonate

Home monitoring of capillary blood glucose concentrations has changed diabetes care, giving physicians and patients a way to adjust their therapy and achieve better diabetic control. The practical strategies and equipment for home diabetic monitoring are discussed, including the changing role of urine testing and how inexpensive machines may enhance the value of blood glucose monitoring.

Topics: Blood Glucose; Citrates; Citric Acid; Copper Sulfate; Diabetes Mellitus; Drug Combinations; Glucose Oxidase; Glycosuria; Humans; Indicators and Reagents; Ketone Bodies; Monitoring, Physiologic; Peroxidases; Reagent Kits, Diagnostic; Reagent Strips; Sodium Bicarbonate

Metabolic acidosis is a complication of chronic kidney disease (CKD) that increases risk of CKD progression, and causes bone demineralization and muscle protein catabolism. Patients with diabetes are prone to metabolic acidosis and functional limitations that decrease quality of life. Veverimer, an investigational, non-absorbed polymer that binds and removes gastrointestinal hydrochloric acid, is being developed as treatment for metabolic acidosis. This post hoc subgroup analysis evaluated effects of veverimer on metabolic acidosis and physical function among patients with diabetes.. This was a Phase 3, multicenter, randomized, blinded, placebo-controlled trial in 196 patients with CKD (estimated glomerular filtration rate 20-40 mL/min/1.73 m2) and metabolic acidosis who were treated for up to 1 year with veverimer or placebo.. At Week 52, veverimer-treated patients with diabetes (n = 70), had a significantly greater increase in mean serum bicarbonate than the placebo group (n = 57) (4.4 versus 2.9 mmol/L, P < 0.05). Patient-reported limitations of physical function on the Kidney Disease and Quality of Life-Physical Function Domain (e.g. walking several blocks and climbing a flight of stairs) improved significantly in the veverimer versus placebo group (+12.5 versus +0.3, respectively, P < 0.001) as did objective physical performance on the repeated chair stand test (P < 0.0001).. Few interventions for patients with diabetes and CKD have successfully improved quality of life or physical functioning. Our study demonstrated that veverimer effectively treated metabolic acidosis in patients with diabetes and CKD, and significantly improved how these patients felt and functioned.

Topics: Acidosis; Bicarbonates; Diabetes Mellitus; Humans; Polymers; Quality of Life; Renal Insufficiency, Chronic; Sodium Bicarbonate

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

Topics: Acidosis; Aged; Bicarbonates; Diabetes Mellitus; Female; Follow-Up Studies; Humans; Hypoglycemic Agents; Insulin Resistance; Male; Middle Aged; Renal Insufficiency, Chronic; Sodium Bicarbonate

Contrast-induced nephropathy (CIN) is a leading cause of acute renal failure and affects mortality and morbidity. Although the incidence of CIN is quite low in the general population, CIN incidence is significantly increased in patients with diabetes mellitus (DM).. We compared the efficacy of prophylactic use consisting of a saline infusion or a sodium bicarbonate infusion for the prevention of CIN in patients with DM.. A total of 195 DM patients who had unselected renal function were randomized into 2 groups: 101 patients were assigned to saline infusion, and 94 patients were assigned to bicarbonate infusion. The primary end point was the maximum increase in the serum creatinine (SCr) level, whereas the secondary end point was the development of CIN after the procedure.. The maximum increase in SCr levels was significantly lower in the saline group than in the bicarbonate group: -0.03 mg/dL (IQR, -0.09 to 0.10 mg/dL) versus 0.02 mg/dL (IQR, -0.09 to 0.13 mg/dL) (P = 0.014). The rate of CIN was significantly lower in the saline group than in the bicarbonate group (5.9% vs 16%, P = 0.024). In the subset of study participants with a baseline creatinine clearance of less than 60 mL/min, the maximum increase in SCr levels was significantly lower, -0.08 mg/dL (IQR, -0.13 to -0.04 mg/dL), in the saline group than in the bicarbonate group, 0.03 mg/dL (IQR, -0.13 to 0.12 mg/dL) (P = 0.004).. The use of prophylactic hydration with isotonic saline before coronary procedures may decrease SCr levels and reduce the incidence of CIN in patients with DM with unselected renal functions to a greater extent than sodium bicarbonate can.

Topics: Contrast Media; Coronary Angiography; Creatinine; Diabetes Mellitus; Endpoint Determination; Female; Humans; Hydrogen-Ion Concentration; Isotonic Solutions; Kidney Diseases; Male; Middle Aged; Prospective Studies; Sodium Bicarbonate; Sodium Chloride

Sodium bicarbonate has been suggested as a possible strategy for prevention of contrast medium-induced nephropathy, a common cause of renal failure associated with prolonged hospitalization, increased health care costs, and substantial morbidity and mortality.. To determine if sodium bicarbonate is superior to sodium chloride for preventing contrast medium-induced nephropathy in patients with moderate to severe chronic kidney dysfunction who are undergoing coronary angiography.. Randomized, controlled, single-blind study conducted between January 2, 2006, and January 31, 2007, and enrolling 353 patients with stable renal disease who were undergoing coronary angiography at a single US center. Included patients were 18 years or older and had an estimated glomerular filtration rate of 60 mL/min per 1.73 m(2) or less and 1 or more of diabetes mellitus, history of congestive heart failure, hypertension, or age older than 75 years.. Patients were randomized to receive either sodium chloride (n = 178) or sodium bicarbonate (n = 175) administered at the same rate (3 mL/kg for 1 hour before coronary angiography, decreased to 1.5 mL/kg per hour during the procedure and for 4 hours after the completion of the procedure).. The primary end point was a 25% or greater decrease in the estimated glomerular filtration rate on days 1 through 4 after contrast exposure.. Median patient age was 71 (interquartile range, 65-76) years, and 45% had diabetes mellitus. The groups were well matched for baseline characteristics. The primary end point was met in 13.3% of the sodium bicarbonate group and 14.6% of the sodium chloride group (relative risk, 0.94; 95% confidence interval, 0.55-1.60; P = .82). In patients randomized to receive sodium bicarbonate vs sodium chloride, the rates of death, dialysis, myocardial infarction, and cerebrovascular events did not differ significantly at 30 days (1.7% vs 1.7%, 0.6% vs 1.1%, 0.6% vs 0%, and 0% vs 2.2%, respectively) or at 30 days to 6 months (0.6% vs 2.3%, 0.6% vs 1.1%, 0.6% vs 2.3%, and 0.6% vs 1.7%, respectively) (P > .10 for all).. The results of this study do not suggest that hydration with sodium bicarbonate is superior to hydration with sodium chloride for the prevention of contrast medium-induced nephropathy in patients with moderate to severe chronic kidney disease who are undergoing coronary angiography.. clinicaltrials.gov Identifier: NCT00312117.

Topics: Aged; Contrast Media; Coronary Angiography; Diabetes Mellitus; Female; Glomerular Filtration Rate; Humans; Iohexol; Iopamidol; Male; Renal Insufficiency; Renal Insufficiency, Chronic; Risk Factors; Single-Blind Method; Sodium Bicarbonate; Sodium Chloride

The purpose was to determine prognosis of patients presenting extreme acidosis (pH <7) on admission to the intensive care unit (ICU) and to identify mortality risk factors.. We retrospectively analyzed all patients who presented with extreme acidosis within 24 hours of admission to a polyvalent ICU in a university hospital between January 2011 and July 2013. Multivariate analysis and survival analysis were used.. Among the 2156 patients admitted, 77 patients (3.6%) presented extreme acidosis. Thirty (39%) patients suffered cardiac arrest before admission. Although the mortality rate predicted by severity score was 93.6%, death occurred in 52 cases (67.5%) in a median delay of 13 (5-27) hours. Mortality rate depended on reason for admission, varying between 22% for cases linked to diabetes mellitus and 100% for cases of mesenteric infarction (P = .002), cardiac arrest before admission (P < .001), type of lactic acidosis (P = .007), high Simplified Acute Physiology Score II (P = .008), and low serum creatinine (P = .012).. Patients with extreme acidosis on admission to ICU have a less severe than expected prognosis. Whereas mortality is almost 100% in cases of cardiac arrest before admission, mortality is much lower in the absence of cardiac arrest before admission, which justifies aggressive ICU therapies.

Topics: Acidosis; Acidosis, Lactic; Acidosis, Respiratory; Adult; Aged; Diabetes Mellitus; Extracorporeal Membrane Oxygenation; Female; Heart Arrest; Hemorrhage; Hospital Mortality; Hospitalization; Hospitals, University; Humans; Hypoglycemic Agents; Infarction; Intensive Care Units; Male; Mesenteric Ischemia; Metformin; Middle Aged; Multivariate Analysis; Prognosis; Renal Dialysis; Respiration, Artificial; Retrospective Studies; Risk Factors; Severity of Illness Index; Sodium Bicarbonate; Survival Analysis; Vasoconstrictor Agents

Topics: Adrenergic beta-2 Receptor Agonists; Albuterol; Anti-Arrhythmia Agents; Anticonvulsants; Antihypertensive Agents; Antiparkinson Agents; Antipsychotic Agents; Anxiety Disorders; Atropine; Bradycardia; Calcium Chloride; Diabetes Mellitus; Diagnosis, Differential; Drug Therapy, Combination; Humans; Hyperkalemia; Hypertension; Hypoglycemic Agents; Hypolipidemic Agents; Male; Middle Aged; Muscle Weakness; Polypharmacy; Renal Dialysis; Renal Insufficiency; Sodium Bicarbonate; Sodium Chloride

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

We report two diabetic patients who developed lactic acidosis following the use of Buformin. Treatment consisted of mechanical ventilation, massive bicarbonate administration, circulatory support with dopamine and peritoneal dialysis. Despite this, both patients died.

Topics: Acidosis, Lactic; Aged; Bicarbonates; Biguanides; Buformin; Diabetes Mellitus; Diabetic Angiopathies; Dopamine; Humans; Hypertension; Male; Peritoneal Dialysis; Respiration, Artificial; Sodium; Sodium Bicarbonate

Lactic acidosis in diabetics on metformin therapy is rare but still associated with poor prognosis. The authors report here five cases. Three patients were initially with a cardiovascular collapse and all had an acute renal failure. Sodium bicarbonate haemodialysis therapy led to a dramatic improvement. Consciousness and hemodynamic status recovered rapidly. Severe metabolic and blood gases derangements were also rapidly corrected. Plasma metformin removal, appreciated by repeated blood samplings in 3 cases, was satisfactory. All patients survived. However, blood metformin levels remained abnormally high at the end of the dialytic therapy. In conclusion, (1) bicarbonate dialysis is an adequate treatment of lactic acidosis observed in diabetic patients treated with metformin since it rapidly corrects the acid-base disorders and partially removes metformin; (2) the sole accumulation of metformin is not sufficient to explain lactic acidosis since this latter might be corrected in spite of persisting high levels of blood metformin.

Topics: Acidosis, Lactic; Aged; Aged, 80 and over; Bicarbonates; Diabetes Mellitus; Female; Humans; Male; Metformin; Middle Aged; Renal Dialysis; Sodium; Sodium Bicarbonate

Lactic acidosis is a metabolic disturbance characterized by an increase of the production/clearance ratio of lactate. Lactate is a catabolite of glycolysis when this takes place under anaerobic conditions. Clinically LA is characterized by: signs of acidosis, venous blood lactate greater than 5 mMol/l, arterial pH less than 7.25. LA is classified in type A, due to shock, and type B which, in turn, can be divided according to its pathogenesis in B1 correlated to particular pathologies, B2 due to exogenous substances and B3 caused by congenital metabolic diseases. LA is of particular interest in type II diabetes mellitus treated by phenformin. Current therapeutic directions, although suboptimal, are: to eliminate the causes of lactate hyperproduction by maintaining a sufficient efficiency of the cardio-vascular apparatus, to correct acidosis by using alkalinizing solutions, to remove pharmacologically or by dialysis the excess of lactate.

Topics: Acidosis; Bicarbonates; Diabetes Complications; Diabetes Mellitus; Dichloroacetic Acid; Humans; Isotonic Solutions; Lactates; Methylene Blue; Renal Dialysis; Ringer's Solution; Sodium; Sodium Bicarbonate; Tromethamine

Topics: Adolescent; Adult; Aged; Burns, Chemical; Child; Citrates; Citric Acid; Copper Sulfate; Deglutition; Diabetes Mellitus; Drug Combinations; Gastrointestinal Diseases; Glycosuria; Humans; Medication Errors; Middle Aged; Sodium Bicarbonate; Tablets

Topics: Bicarbonates; Blood Proteins; Diabetes Mellitus; Mineral Waters; Sodium Bicarbonate