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PubMed1992

Intracellular acidosis in human and experimental brain injury.

Brain tissue acidosis is considered to play a role in the complex sequence of events following traumatic brain injury. This report reviews the experimental and clinical research conducted at the Medical College of Virginia to help clarify the extent of metabolic derangement that occurs and to evaluate the effect of treatment. Experimental injury models in ventilated animals showed that trauma produces a mild brain tissue acidosis that recovers within hours of injury. Hypoxia combined with trauma produces a relative ischemia and exacerbates the acidosis, which eventually resolves with resuscitation. Other studies revealed that CSF lactate measurements should be interpreted with caution, particularly in patients with subarachnoid hemorrhage. The results of two randomized clinical trials testing therapeutic effects of sustained hyperventilation and treatment with tromethamine (THAM) are discussed.

Acidosis↗
PubMed2005

Hepatitis C and didanosine: risk of lactic acidosis.

(1) In patients who are infected with both HIV and hepatitis C virus (HCV), treatment of hepatitis C slightly increases the risk of lactic acidosis associated with antiretroviral treatment, especially when the latter includes didanosine. (2) If a modification in antiretroviral treatment is needed and if treatment for hepatitis C is likely to be necessary, then it is best to avoid didanosine. However, systematic replacement of didanosine is not necessary, given the small magnitude of risk of lactic acidosis. (3) Fatigue, digestive problems, weight loss and dyspnea are signs of lactic acidosis.

Acidosis, Lactic↗
PubMedDate not supplied

Proximal renal tubular acidosis.

The proximal tubule reabsorbs approximately 80% of the filtered load of bicarbonate. Defects in the process of bicarbonate reabsorption result in loss of bicarbonate and proximal renal tubular acidosis. Global proximal tubule dysfunction is known as the Fanconi's syndrome. Both isolated proximal renal tubular acidosis and the Fanconi's syndrome can result from inherited defects or can be acquired. This review will discuss the mechanisms that cause defects in proximal tubule bicarbonate transport as well as the common causes of isolated proximal renal tubular acidosis and the Fanconi syndrome.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Renal tubular acidosis.

Renal tubular acidosis (RTA) is a form of metabolic acidosis due to abnormal alkali (bicarbonate) loss by the kidneys or their failure to excrete net acid. While the latter does occur in chronic renal failure, the term RTA is usually applied only when the glomerular filtration rate is normal or near normal. As well as a cause of metabolic acidosis, RTA often presents as renal stone disease with nephrocalcinosis, rickets/osteomalacia, and growth retardation in children. In this brief review, we have summarized the classification, clinical features and the underlying cell and molecular pathophysiology of RTA. However, despite significant advances in our understanding of the mechanisms of RTA, its treatment is still empirical and based largely on alkali replacement therapy; but its wider significance in renal stone and bone disease is becoming increasingly recognized.

Acidosis, Renal Tubular↗
PubMed1990

[Effect of ulinastatin (UL) on renal function and lactic acidosis during open-heart surgery: comparison with aprotinin (Ap)].

Comparison was made on the renal function and lactic acidosis during cardiopulmonary bypass (CPB) between the group Ul (n = 15) and group Ap (n = 27). A 300,000 u, of ulinastatin was administered intravenously before CPB and 300,000 u, in the prime solution. A 300,000 u, of aprotinin was administered in the prime solution. Urine output during CPB was not significantly different, but the total dose of furosemide administered was less in group Ul and a significant difference (p less than 0.05) was observed in the free water clearance at CPB 1 hr. and 3 hr. postoperatively, -0.83 +/- 0.16 and -1.74 +/- 0.14 in group Ul and -0.43 +/- 0.10, -0.99 +/- 0.14 in group Ap, respectively. Arterial lactate increased as the perfusion time increased but the level at the end of CPB was significantly lower (p less than 0.05) in group Ul and the added 7% NaHCO3 to correct metabolic acidosis during CPB of 29.3 +/- 9.5 ml in group Ul was less than in group Ap of 82.2 +/- 15.2 ml (p less than 0.01). The result suggests the favourable effects of ulinastatin on the renal function and lactic acidosis during CPB.

Acidosis, Lactic↗
PubMed2006

Acid-base profile and predictors of metabolic acidosis in patients undergoing peritoneal dialysis with lactate- and bicarbonate-buffered peritoneal dialysis solutions.

Metabolic acidosis correction is one of the goals of renal replacement therapy. Correction of acidosis in peritoneal dialysis (PD) may be affected by PD modalities such as automated PD (APD) or by new solutions containing a combination of bicarbonate and lactate as a buffer [bicarbonate continuous ambulatory PD (CAPD)]. The aim of the present study was to examine the acid-base status of our PD population and to compare the effects of APD, lactate CAPD, and bicarbonate CAPD on serum bicarbonate levels. We studied 35 stable patients undergoing APD (n = 15), lactate-buffered (35 mEq/L) CAPD (n = 14), and bicarbonate/lactate-buffered CAPD (n = 6) for 48.5 +/- 38.1 months. Most of our patients had serum bicarbonate levels in the normal range. In 3 patients (8%), HCO3 was below 22 mEq/L, and in 8 patients (22%; APD = 2, lactate CAPD = 2, bicarbonate CAPD = 4), HCO3 was above 28 mEq/L. We found no statistically significant correlations between HCO3 serum levels and PD prescription, peritoneal membrane characteristics, or intake of calcium carbonate and sevelamer hydrochloride. Patients on bicarbonate CAPD had higher HCO3 serum levels, but this difference disappeared when corrections for duration of dialysis, residual urine volume, and PD adequacy indices were applied. In the studied PD population, adequate correction of metabolic acidosis was achieved, as reflected in serum bicarbonate levels. We observed no difference in serum bicarbonate levels between APD and lactate CAPD patients. The new bicarbonate-buffered PD solutions are more biocompatible and can result in higher serum bicarbonate levels. However, a significant number of PD patients on bicarbonate-buffered solutions may become alkalotic. The clinical significance of these results needs further examination in prospective studies.

Acid-Base Equilibrium↗
PubMed2006

A high incidence of nucleoside reverse transcriptase inhibitor (NRTI)-induced lactic acidosis in HIV-infected patients in a South African context.

OBJECTIVE: To determine the incidence of and predisposing risk factors for lactic acidosis in HIV-infected patients on antiretroviral drugs in South Africa. DESIGN: Observational case series. SETTING: Sinikithemba HIV Clinic, McCord Hospital, Durban. SUBJECTS: Eight hundred and ninety-one HIV-positive patients on highly active antiretroviral therapy (HAART) during an 18-month period commencing in January 2004. MEASUREMENTS AND RESULTS: Fourteen cases of lactic acidosis (incidence rate of 19 (95% confidence interval (CI): 9-29) cases per 1,000 person-years of treatment) were reported. All cases were female, with a median age of 36 years and a median weight of 81 kg. The median time on HAART before developing lactic acidosis was 7.5 months and the median peak lactate level was 9.3 mmol/l. All cases were on stavudine (d4T), lamivudine (3TC) and 1 non-NRTI. The case mortality rate was 29% (4 patients). CONCLUSIONS: The incidence rate is higher than reported in studies in developed countries. This may be due to d4T, which is recommended as a first-line antiretroviral drug in South Africa. This implication raises the question whether it is an appropriate drug in first-line treatment of patients with predisposing risk factors such as female gender and being overweight.

Acidosis, Lactic↗
PubMedDate not supplied

Acid base equilibrium in experimental acidosis of cows with and without rumen fistula.

Acid base equilibrium in experimental acidosis of cows with and without rumen fistula. Acta Physiol. Pol., 1977, 28, (1): 77-84. Symptoms of acidosis caused by administration of saccharose into the rumen were more significant and lasted longer in the cows without rumen fistula than in those with it. At the peak of acidosis of pH of arterial blood was 7.29 and it was by 0.07 below that in the group of cows with fistula. The alkali reserve was lower by 6 mEq and the bicarbonate level by 5.2. Characteristic differences were observed in oxygen utilization and nitrogen metabolism. Thus, the results obtained in experiments on the cows with rumen fistula do not reflect the normal metabolic processes.

Acid-Base Equilibrium↗
PubMed1991

[Thiamine deficiency as a cause of life threatening lactic acidosis in total parenteral nutrition].

Two patients aged 37 and 44 years developed life-threatening lactic acidosis following abdominal surgery and a period of about 3 weeks of total parenteral nutrition. Septicaemia and hypoxia were excluded as possible causes. Conventional treatment including high doses of buffer agents was unsuccessful. Thiamine (vitamin B1) depletion was suspected as the cause of the metabolic acidosis, and two doses of 400 mg thiamine were given. In both patients, the lactic acidosis improved immediately, and it disappeared following the second dose of thiamine. Both patients were subsequently discharged as symptom-free. As part of the pyruvate-dehydrogenase (PDH) complex, thiamine was capable of improving the life-threatening situation.

Acid-Base Equilibrium↗
PubMed1991

[A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid lactic acidosis].

A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid (CSF) lactic acidosis was reported. A 44-year-old Japanese woman noted tarry stool on July 2, 1988 and was treated with metoclopramide and cimetidine for nausea and vomiting. Hydroxyzine pamoate was also administered for insomnia at 3:10 am and she became comatose with muscle rigidity at 3:40-4:30 am on July 3. Tachycardia and high fever (39.5 degrees C) were evident at 8:00 am on July 4. She was transferred to the Kyushu University Hospital. On admission, serum creatine kinase was elevated to 1640 IU/1; MM fraction was 100%. She was diagnosed as malignant syndrome. Cerebrospinal fluid was normocellular with protein 38 mg/dl and glucose 122 mg/dl. Cerebrospinal fluid lactate increased markedly to 3.43 mmol/l, CSF pH was 7.264, HCO3- 14.4 mEq/l, indicating CSF metabolic acidosis. She became afebrile after the 10th hospital day, and gradually but completely recovered within a month. She was discharged on August 16, 1988. The anti-dopaminergic activity of metoclopramide was considered to be primarily responsible for the development of malignant syndrome in this case. Cerebrospinal fluid lactic acidosis seemed to reflect hyperpyrexia or malignant syndrome induced derangement of the brain metabolism.

Acidosis, Lactic↗
PubMed1991

The relationship between fetal biophysical assessment, umbilical artery velocimetry, and fetal acidosis.

In a prospective study of 62 patients undergoing cesarean delivery before the onset of labor, fetal biophysical assessment and umbilical artery systolic-diastolic ratios (S/Ds) were performed within 3 hours of delivery. There was a significant relationship between the fetal biophysical profile score and cord arterial as well as cord venous pH. However, there was no identifiable relationship between S/D and cord arterial or venous pH. The efficacies of the biophysical components alone (nonstress test [NST] and fetal biophysical profile) and in combination with S/D to predict fetal acidosis were determined. The NST had the best sensitivity (100%) and negative predictive value (100%). The fetal biophysical profile had the best specificity (91%), positive predictive value (62%), and overall efficiency (90%). The S/D had the lowest sensitivity (66%), specificity (42%), positive predictive value (16%), negative predictive value (88%), and overall efficiency (45%). The addition of S/D to the NST or fetal biophysical profile did not improve diagnostic accuracy. These data suggest that the NST should be used as a primary test for the antepartum detection of fetal acidosis, whereas the fetal biophysical profile is a reasonable adjunct test. The umbilical artery S/D, as determined by continuous-wave Doppler velocimetry, has no value as a primary method or an adjunct in the antepartum detection of fetal acidosis.

Acidosis↗
PubMed1990

[Water-electrolyte and acid-base disorders. VIII. Respiratory acidosis].

Acute respiratory acidosis will result from many processes that acutely interfere with the excretion of CO2 by the lungs. CO2 excretion by the lungs can be interfered with by processes that inappropriately decrease minute ventilation, processes that impair the transport of CO2 from the site of production to the lungs for export, and by processes that impair the transfer of CO2 from the blood through the alveolar space to the atmosphere. The underlying clinical syndrome generating the primary hypercapnia will determine the duration of the acidosis as well as the anticipated clinical manifestations attributable to the acidosis.

Acidosis, Respiratory↗
PubMed1978

Lactic acidosis in oat cell carcinoma with extensive hepatic metastases.

Lactic acidosis has been described in patients with leukemia and lymphoma, but its occurrence in other malignant diseases is not documented. We treated two patients with oat cell carcinoma of the lung and extensive liver metastases in whom lactic acidosis developed. Tumor-induced hepatic dysfunction appeared to be a major factor in the pathogenesis of the lactic acidosis observed in these patients.

Acidosis↗
PubMed1990

[Lactic acidosis and hyperlactatemia].

Lactic acidosis is a relatively frequent acid-base disorder in a hospital setting. It is defined by the association of an arterial pH inferior to 7.35 and an arterial lactate level superior to 5 mmol/l. Classically, 2 types of acidosis are distinguished on the basis of their mechanisms of onset: the type A, with evident clinical signs of tissue hypoperfusion and the type B, more are, without apparent hypoxia. This last category is observed in various circumstances such as diabetes, acute liver failure, poisoning and, more rarely, inborn errors of carbohydrate metabolism. Treatment aims primarily at the correction of the cause. The efficacy of sodium bicarbonate is presently debated, considering the risk to worsen hyperlactatemia and to induce hyperosmolarity or rebound alkalosis. The administration of dichloroacetate, an activator of pyruvate dehydrogenase, permits to correct partially the lactic acidosis but is not harmless especially in case of prolonged administration. Other therapeutic modalities are evoked. Arterial lactate level is a reliable prognostic index of shock, because blood values do not depend only of the oxygen debt but also of the efficacy of hepatic and renal lactate uptake. Sequential measurements are recommended.

Acidosis, Lactic↗
PubMed1990

Interorgan glutamine flow regulation in metabolic acidosis.

The flow of glutamine to the kidneys is essential for generating base in response to acid loading yet neither the magnitude nor direction of this flow are normally supportive of renal ammoniagenesis. However, chronic metabolic acidosis sets in motion regulatory systems enhancing flow magnitude as well as redirecting glutamine from the splanchnic bed and ureagenesis to the kidneys for ammoniagenesis and bicarbonate generation. These mechanisms include organ-specific inductions of glutamine synthesizing and hydrolyzing enzymes at the source, muscle, and the destination, kidneys, respectively; organ-specific shifts in fluxes through competing metabolic pathways favoring glutamine formation at the expense of the ureagenic precursor alanine and unique interorgan regulation whereby upstream sites modulate subsequent downstream sites by setting the glutamine loads and the release of glutamine metabolites acting as metabolic signals. These extrarenal regulatory mechanisms act in concert making glutamine available at the expense of ureagenesis. The kidneys draw upon plasma glutamine, despite a 40% reduction in the arterial concentration, generating base in the form of renal venous bicarbonate and excreting nitrogen and protons as ammonium. Underlying this enormous renal extraction is a shift in the uptake mode from a load- to a transport-limited process closely associated with the filtered bicarbonate load. Finally the interorgan glutamine flow set in motion during acidosis can be acutely reversed, revealing a hierarchal interaction of system subserving acid base and nitrogen balance. Thus, the extraordinary responses exhibited in chronic metabolic acidosis provide a superb model for discerning regulatory systems in other physiological as well as pathophysiological conditions.

Acidosis, Renal Tubular↗
PubMed1975

Renal tubular acidosis during therapy for diabetic ketoacidosis.

A young woman presented with typical diabetic ketoacidosis. Five hours after insulin had been given hyperchloremic metabolic acidosis developed. This could not be attributed to gastrointestinal loss of bacarbonate, ingestion of HCI or carbonic anhydrase inhibitor, or the administered fluids and electrolytes. The combination of hyperchloremic metabolic acidosis and a urine pH of 5.6 during acidemia prompted specific studies that established the presence of disorders of renal acidification. A transient defect of hydrogen ion secretion in the distal nephron was suggested by the decrease in urine-blood Pco-2 gradient after administration of sodium bicarbonate. Proximal renal tubular acidosis was indicated by the reduced bicarbonate threshold that persisted for approximately 7 weeks.

Acid-Base Equilibrium↗
PubMed1990

Trimethoprim/sulfamethoxazole-induced renal tubular acidosis.

A child was evaluated for growth failure at the University of California, San Diego. On two occasions the patient had renal bicarbonate wasting, acidosis, and growth failure associated with trimethoprim/sulfamethoxazole (TMP/SMZ) administration. On both occasions, the acidosis resolved and the growth rate normalized following a period without receiving TMP/SMZ. Renal tubular acidosis and growth failure may occur as a result of TMP/SMZ therapy in children.

Acidosis, Renal Tubular↗
PubMed1978

[Metabolic acidosis in chronic renal insufficiency of various etiology].

The renal acidosis may appear by a decrease of the number of nephrons able to function (decrease of the filtrate of the glomerulum) as well as by a selective alteration of the tubular acidification mechanism. In 66 patients with chronic renal insufficiency of different degrees of severity (32 patients with diabetic glomerulosclerosis, 18 patients with chronic glomerulonephritis and 16 patients with chronic pyelonephritis) studies of the parameters of the acid-base-state and the renal insufficiency were carried out. 53 of these patients had a pathologically changed acid-base-state which was most expressed in patients with chronic pyelonephritis. A characteristic relation between the renal function (creatinine clearance) and the change of the pH-values was observed. The regression curve of the pH-values was descending so that in clearance values below 25 ml/min in nearly all patients a pronounced acidosis was present. This could be proved in the patients with pyelonephritis already when higher clearance values were present. The forms of the development of the metabolic acidosis in chronic renal insufficiency are discussed.

Acid-Base Equilibrium↗