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PubMed1983

Effect of hypoxia and hypercapnic acidosis on renal autoregulation in the dog: role of renal nerves.

Previous studies suggest that hypoxia and hypercapnic acidosis exert a renal nerve mediated adverse effect on renal haemodynamic function. We therefore examined the effect of hypoxia and hypercapnic acidosis on renal blood flow and glomerular filtration rate responses to lowering renal perfusion pressure from 125 to 75 mmHg in the anaesthetized dog. To study the role of renal nerves in these responses, paired innervated and denervated kidneys were studied in each animal. Hypoxia (PO2 43 +/- 3 mmHg) affected neither renal blood flow nor glomerular filtration rate responses to decreasing renal perfusion pressure. Hypercapnic acidosis (PCO2 71 +/- 2 mmHg; pH 7.03 +/- 0.01) significantly decreased both renal blood flow and glomerular filtration rate as renal perfusion pressure was lowered. This effect of hypercapnic acidosis could be abolished by renal denervation. These findings suggest that hypercapnic acidosis results in renal nerve stimulation, which prevents the usual decrease in renal afferent arteriolar tone that occurs in response to lowering of renal perfusion pressure.

Acidosis, Respiratory↗
PubMed1991

Skeletal muscle degradation and nitrogen wasting in rats with chronic metabolic acidosis.

1. Chronic metabolic acidosis is associated with impaired growth and negative nitrogen balance, suggesting that it promotes endogenous protein catabolism. 2. Skeletal muscle is the major repository of body protein and is a potential target for stimuli of protein catabolism. 3. This study in vivo examines the effects of chronic metabolic acidosis on the relationship between growth, nitrogen disposal and skeletal muscle catabolism in the rat. 4. Growth, nitrogen utilization and acquisition of body mass were significantly impaired in acidotic animals compared with pair-fed controls. 5. Total nitrogen excretion was significantly increased in acidotic rats despite decreased urea production. The time course of this response to acidosis was synchronous with that of accelerated protein catabolism in skeletal muscle. 6. It is proposed that metabolic acidosis impairs growth by stimulating skeletal muscle protein catabolism. It is suggested that this forms part of a co-ordinated multi-organ homoeostatic response to acidosis, skeletal muscle and down-regulated urea production supplying the nitrogen required for renal ammoniagenesis.

Acidosis↗
PubMed2004

Metformin and lactic acidosis: cause or coincidence? A review of case reports.

OBJECTIVE: Metformin has been associated with the serious side-effect lactic acidosis. However, it remains unclear whether the use of metformin was a cause or a coincidence in lactic acidosis. DESIGN: A literature search of the Index Medicus (1959-66) and of the databases Embase, Medline, Medline Express (1966-99) was performed using the keywords metformin, biguanides and lactic acidosis. All articles of cases with metformin-induced lactic acidosis (MILA) were cross-referenced. SUBJECTS: Cases were included for analysis if they met the following criteria: serum pH < or =7.35, lactate concentration > or =5 mmol L(-1). INTERVENTION: A forum of six experts in intensive care medicine independently categorized the cases in MILA unlikely (score 0), possible MILA (score 1) or probable MILA (score 2). MAIN OUTCOME MEASURES: Statistical analysis included the paired interobserver agreement (kappa) and multivariate regression analysis. RESULTS: Of 80 reported cases, 33 were excluded because of insufficient quality. The forum scores of the remaining 47 cases were distributed normally with a mean score of 7 (range 2-10). The kappa-value was 0.041 (SD = 0.24, range -0.514, 0.427). Neither lactate concentration nor mortality correlated with serum metformin concentrations. CONCLUSIONS: Given the low interobserver agreement and the lack of any relationship between metformin levels and outcome parameters, the concept that there is a simple, causal relationship between metformin use and lactic acidosis in diabetic patients has to be reconsidered.

Acidosis, Lactic↗
PubMedDate not supplied

A review of the effects of correction of acidosis on nutrition in dialysis patients.

Metabolic acidosis is a condition that is commonly encountered in both chronic renal failure (CRF) and in end-stage renal disease (ESRD). Known complications and surmised consequences associated with the acidosis of renal disease include bone lesions, depression of myocardial contractility, and growth retardation. Conversely the correction of acidosis in children with renal tubular acidosis improves growth velocity. This is also the case in children with CRF. The conclusion drawn from this study was that the correction of metabolic acidosis improved serum albumin concentrations in patients on hemodialysis and that this correction also induced a decrease in the nPCR.

Acidosis↗
PubMed2001

Topiramate and metabolic acidosis in pediatric epilepsy.

PURPOSE: Topiramate (TPM) has been widely used as an adjunctive therapy for treating epilepsy. TPM is reported to have multiple mechanisms of action, including inhibition of carbonic anhydrase, which may result in metabolic acidosis from decreased serum bicarbonate (HCO3-). METHODS: Clinical data from 30 children who received TPM as adjunctive therapy for medically refractory epilepsy were reviewed at Children's Hospital, Boston. Serum HCO3- levels were assessed before, during, and after discontinuing TPM (n = 9). When multiple data were available, mean values were used for analysis. RESULTS: Of the 30 patients, 21 had a >10% decrease in HCO3- levels. The mean decrease in HCO3- among the 21 patients was 4.7 mEq/L, and maximum was 10 mEq/L. No clinical symptoms occurred, and HCO3- supplement was not needed, except for one patient who developed tachypnea from worsened acidosis after prolonged status epilepticus during a suspected viral illness. Among the 21 patients, TPM was discontinued in seven children because of a lack of efficacy, and in two because of anorexia. After discontinuing TPM, the serum HCO3- returned to the previous level before starting TPM in all nine. CONCLUSIONS: Decreased HCO3- levels occurred in the majority of patients reviewed, usually only to a small to moderate extent, but by 8 and 10 mEq/L in two cases. In patients at risk for acidosis, the decrease in HCO3- may cause significant consequences, such as severe acidosis or renal calculi. Monitoring HCO3- levels before and during TPM therapy may be indicated, especially with conditions that predispose to acidosis.

Acidosis↗
PubMed2000

D-lactic acidosis 23 years after jejuno-ileal bypass.

Accumulation of D-lactate after gastrointestinal surgery, particularly jejuno-ileal bypass, is an uncommon and often misdiagnosed clinical disturbance. The syndrome may be complicated by dizziness, ataxia, confusion, headache, memory loss, and aggressive behavior. Serum chemistries are often deceptive because the anion gap is frequently normal in spite of severe metabolic acidosis. Moreover, the urine anion gap may be positive, incorrectly suggesting a defect in renal net acid excretion. Indeed, the combination of a normal anion gap metabolic acidosis and positive urine anion gap may erroneously suggest a diagnosis of renal tubular acidosis. Importantly, all reported cases of D-lactic acidosis secondary to bypass surgery have been encountered within 5 to 10 years following the surgery. Here we present an unusual case of D-lactic acidosis (complicated by encephalopathy) presenting 23 years after a jejuno-ileal bypass procedure. The patient was initially diagnosed with a drug intoxication secondary to benzodiazepines. Ultimately, the diagnosis of D-lactate encephalopathy was established after challenging the patient with a carbohydrate load. Thus, administration of 40 kcal/kg over 16 hours reproduced the clinical syndrome and was accompanied by a marked increment in serum and urine D-lactate concentration. The patient had sustained resolution of her symptoms after treatment with oral vancomycin.

Acidosis, Lactic↗
PubMed2003

Severe renal tubular acidosis in a renal transplant recipient with repeated acute rejections and chronic allograft nephropathy.

Renal tubular acidosis in renal transplant recipients usually is asymptomatic and subclinical. The authors report a case of severe renal tubular acidosis manifested as muscle weakness in a renal transplant recipient. The patient received a renal transplant 30 months ago and had a history of successive episodes of acute rejection during the past 2 months. On admission, arterial blood (arterial blood pH, 7.11; pco(2), 12.8 mm Hg; and bicarbonate, 4 mEq/L [4 mmol/L]) and urine gas analysis were compatible with distal renal tubular acidosis. The graft biopsy findings showed superimposed acute rejection on chronic allograft nephropathy, and immunohistochemical staining and electron microscopic findings showed the reduced immunoactivity of H(+)ATPase pump and anion exchanger 1. The patient was treated successfully with intravenous bicarbonate and oral steroid pulse therapy. This finding suggests that rejection-related renal tubular acidosis should be considered a cause of severely affected metabolic acidosis in renal transplant recipients.

Acidosis, Renal Tubular↗
PubMed1978

[Haemodialysis in the treatment of biguanide-induced lactate acidosis (author's transl)].

Severe lactate acidosis developed in nine diabetics on biguanide. When lactate acidosis was diagnosed all patients had reduced renal function, six being oligoanuric. Pre-existing chronic renal failure as a factor in the development of lactic acidosis was excluded in five patients, normal renal function being restored later. All patients were dialysed, seven surviving. This mortality rate is lower than that reported by others for biguanide-induced lactate acidosis. Rapid biguanide elimination by dialysis was demonstrated both in vitro and in vivo. The in vivo clearance of buformin was 83 +/- 43 ml/min (mean +/- SD, n = 4), that of phenformin 68 +/- 33 ml/min (n = 7). The main advantages of haemodialysis in the treatment of biguanide-induced lactic acidosis are rapid removal of toxic biguanides and excess lactate and the ability to administer sodium bicarbonate adequately without risking hypernatraemia and fluid overload.

Acidosis↗
PubMed2000

[Metformin-induced lactic acidosis].

HISTORY AND ADMISSION FINDINGS: A 62-year-old woman had been found unconscious on her bed. She had to be resuscitated several times in the ambulance on the way to hospital. On admission her pupils were dilated and fixed, the cardiovascular system was unstable. Her rectal temperature was 28 degrees C. She was a diabetic being treated with metformin and glimepiride and was in incipient renal failure (serum creatinine 1.5 mg/dl). She was also in heart failure due to coronary heart disease and was in a debilitated state. INVESTIGATIONS: She had marked lactic acidosis (lactate 45.3 mmol/l; pH 6.6). Toxicological screening tests were negative. TREATMENT AND COURSE: In the absence of a history she was at first treated symptomatically. Conventional management of the lactic acidosis neither corrected the acidosis nor stabilized the circulatory system. Continuous veno-venous haemodialysis with bicarbonate-buffered solutions succeeded in reducing the need for catecholamines. Neurological examination was supplemented by recording acoustic and sensory evoked potentials. Suspected metformin-induced lactic acidosis was confirmed by appropriate tests. Three weeks after admission she was well enough to be transferred to a normal medical ward and ultimately discharged without further complications. CONCLUSION: Metformin should only be prescribed if the contraindications, in particular renal failure are carefully monitored. Severe lactic acidosis should be treated early with continuous veno-venous haemodialysis with bicarbonate-buffered substituting fluids. The good neurological results in this case are probably largely due to the marked hypothermia.

Acidosis, Lactic↗
PubMed1988

The effect of fetal hypoxia and acidosis on the changes in fetal electroencephalogram during labor.

As artefact-free recordings of the fetal brain bioelectric potentials can only be obtained by specially designed electrodes, an electrode for taking electroencephalogram (EEG) and cardiotocogram (CTG), according to the principle of vacuum electrode developed by Rosen and Scibetta, has been designed. The polygraphic technique was used to examine a total of 65 deliveries, divided into two groups. The first group (n = 33) consisted of newborns free of any signs of hypoxia and acidosis, whereas the second group (n = 32) was comprised of newborns with evident clinical and biochemical signs of hypoxia and acidosis. Fetal hypoxia and acidosis were observed to entail some characteristic changes in EEG, that is, a decrease in the frequency and wave amplitude through the appearance of the isoelectric line (ISO) featuring in severe cases of fetal hypoxia and acidosis. The following changes were found to occur during the development of hypoxia and acidosis:hypoxia, a decrease in the EEG frequency and amplitude, preacidosis with the appearance of both early and late decelerations coupled with a significant drop in the oscillation and, eventually, severe variable decelerations accompanied by terminal bradycardia. The time interval between the manifestation of initial signs of a decreasing central nervous system (CNS) activity and changes in the fetal heart rate was found to be about 10 minutes.

Acid-Base Equilibrium↗
PubMed1984

[Lowering the cesarean section rate by exclusion of cardiotocographically suspected acidosis using fetal blood gas analysis].

In 871 deliveries out of a total of 3980 effected during 1980-1982 at the Winterthur Gynaecological Hospital, we found it necessary to perform one or several microanalyses of blood (blood gas analyses) sub partu. Among these, we found retrospectively that in 22 cases the microanalysis of the blood gas had prevented us from performing caesarean section which would have seemed necessary if we had relied on the cardiotocographical findings alone. Micro-analysis of blood gas made it possible to exclude the presence of pre-acidosis or acidosis which would have made Caesarean section imperative; in all these cases, normal delivery via the vagina was achieved, and in no case did this result in severe acidosis. All newborn had a 5-minute Apgar score of 7 and higher. We can conclude from these results, therefore, that the indication for an immediate termination of delivery via Caesarean section should not depend solely on a pathological cardiotocogram; the final decision should be arrived at only after micro-analyses of blood gas have confirmed the presence of foetal pre-acidosis or acidosis.

Acidosis↗
PubMed1982

Incidence of radiographically evident bone disease, nephrocalcinosis, and nephrolithiasis in various types of renal tubular acidosis.

The syndrome of renal tubular acidosis has been categorized into three physiologic types that have different clinical findings and prognostic and therapeutic implications. We reviewed radiographs of the skeleton and kidneys in 92 patients (56 children and 36 adults) with renal tubular acidosis in order to determine whether the radiologic findings could be related to the type of syndrome. Forty-four patients had Type 1 renal tubular acidosis, 18 had Type 2, and 30 had Type 4. Evidence of skeletal abnormalities was uncommon (17 per cent) and was confined to patients who had the Type 2 disorder or azotemia. The children with Type 2 and skeletal abnormalities had rickets; the adults had osteopenia without pseudofractures. Nephrocalcinosis was evident in approximately one fourth of the group (29 per cent) and was restricted to patients with the Type 1 syndrome. In patients with Type 4, osteopenia was evident in 12 per cent, all of whom were azotemic. Our observations indicate that the radiographic manifestations of renal tubular acidosis are influenced by the physiologic type of renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed1998

Mechanisms involved in the acidosis enhancement of the isoproterenol-induced phosphorylation of phospholamban in the intact heart.

Previous experiments have shown that acidosis enhances isoproterenol-induced phospholamban (PHL) phosphorylation (Mundiña-Weilenmann, C., Vittone, L., Cingolani, H. E., Orchard, C. H. (1996) Am. J. Physiol. 270, C107-C114). In the present experiments, performed in isolated Langendorff perfused rat hearts, phosphorylation site-specific antibodies to PHL combined with the quantitative measurement of 32P incorporation into PHL were used as experimental tools to gain further insight into the mechanism involved in this effect. At all isoproterenol concentrations tested (3-300 nM), phosphorylation of Thr17 of PHL was significantly higher at pHo 6.80 than at pHo 7.40, without significant changes in Ser16 phosphorylation. This increase in Thr17 phosphorylation was associated with an enhancement of the isoproterenol-induced relaxant effect. In the absence of isoproterenol, the increase in [Ca]o at pHo 6.80 (but not at pHo 7.40) evoked an increase in PHL phosphorylation that was exclusively due to an increase in Thr17 phosphorylation and that was also associated with a significant relaxant effect. This effect and the phosphorylation of Thr17 evoked by acidosis were both offset by the Ca2+/calmodulin-dependent protein kinase II inhibitor KN-62. In the presence of isoproterenol, either the increase in [Ca]o or the addition of a 1 microM concentration of the phosphatase inhibitor okadaic acid was able to mimic the increase in isoproterenol-induced Thr17 phosphorylation produced by acidosis. In contrast, these two interventions have opposite effects on phosphorylation of Ser16. Whereas the increase in [Ca]o significantly decreased phosphorylation of Ser16, the addition of okadaic acid significantly increased the phosphorylation of this residue. The results are consistent with the hypothesis that the increase in phospholamban phosphorylation produced by acidosis in the presence of isoproterenol is the consequence of two different mechanisms triggered by acidosis: an increase in [Ca2+]i and an inhibition of phosphatases.

Acidosis↗
PubMed2001

Subclinical rumen acidosis as a cause of reduced appetite in newly calved dairy cows in Denmark: results of a poll among Danish dairy practitioners.

A questionnaire survey was conducted among Danish dairy practitioners to investigate reduced appetite and its relation to subclinical rumen acidosis in post partum dairy cows. The 115 practitioners who responded provided service to 325,300 cows representing 46% of the national herd. Results are presented and discussed in relation to the practitioners beliefs regarding occurrence and value of the diagnostic methods used and treatments applied. The most common diagnoses believed to occur were ketosis (26%), rumen acidosis (22%) abomasal disorders (16%), subclinical hypocalcaemia (15%) and milk fever (15%). Subclinical rumen acidosis was considered to be a commonly occurring underlying condition with significant importance as a cause of reduced appetite. Inadequate feeding strategies were considered to be a main cause of subclinical rumen acidosis. However, the veterinary practitioners were apparently reluctant to imply checking of feeding mangement in their diagnostic work. Possibel reasons for this are discussed. According to the national dairy health recording system subclinical rumen acidosis was rarely reported as a diagnosis among attended cases. Apparently, signs and manifestations of the condition were unclear to the practitioners. It is proposed that the discrepancy is partly due to a lack of precise diagnostic tools available to veterinary practitioners at present and partly due to a missing examination of farm specific feeding management.

Acidosis↗
PubMed2002

Multiple myeloma associated with lactic acidosis.

Type B lactic acidosis is rare among patients with malignant diseases. To date only one case report has documented lactic acidosis occurring in a patient with multiple myeloma (MM). Our patient, a 55-year-old black man, was diagnosed with stage IIIA immunoglobulin G-kappa (IgG-kappa) MM in September 1995. He was found to have severe lactic acidosis at the time of second relapse. During the terminal phase of his disease, he required multiple hospitalizations for management of lactic acidosis and other complications of his MM. No other cause of his elevated lactate levels was identified. Although type B lactic acidosis may more commonly occur in patients with leukemia or lymphoma, it may rarely present in patients with rapidly progressive and refractory MM.

Acidosis, Lactic↗
PubMed2005

Burkitt's lymphoma presenting with lactic acidosis and hypoglycemia - a case presentation.

We present what appears to be the first reported case of lactic acidosis and hypoglycemia in an adult patient with Burkitt's lymphoma. Lactic acidosis and hypoglycemia are rare complications of non-Hodgkin's lymphoma (NHL) with only 26 and 8 previous reports, respectively. Two prior cases of Burkitt's lymphoma-induced lactic acidosis have been reported (one child, one adult), both in the absence of hypoglycemia. A 74-year-old man presented with right upper extremity swelling, pleural effusion and axillary lymphadenopathy. Thoracentesis and bone marrow studies revealed Burkitt's lymphoma. On the second day of his hospitalization he developed severe lactic acidosis (pH 7.29, lactate 15.8 mmol/L) and hypoglycemia (27 - 60 mg/dl) resistant to glucose infusions. Serum insulin, proinsulin and C-peptide levels were normal and insulin antibodies were negative. Insulin-like growth factors I and II were low, while thyroid and cortisol studies were normal. The patient's mental status became altered, care was withdrawn and the patient expired. An autopsy revealed significant tumor burden that appeared to spare the liver. An extensive review of the literature demonstrates that NHL-induced lactic acidosis is associated with a mortality rate of 73% at 1 month and 92% overall with the clinical course closely linked to the chemotherapeutic response of the tumor. Furthermore, in contrast to our patient, 90% of previously reported cases were associated with liver involvement.

Acidosis, Lactic↗
PubMed2004

Unusual D-lactic acid acidosis from propylene glycol metabolism in overdose.

OBJECTIVE: To report a case of D-lactic acid acidosis owing to massive oral ingestion of propylene glycol. CASE REPORT: A 72-year old man with known congestive failure was admitted to the ICU with encephalopathy. Twelve hours prior to admission he had erroneously ingested a large amount of propylene glycol (PG). The laboratory revealed high anion gap (anion gap = 27 meq/l) acidosis (arterial pH = 7.16) and an increased osmolal gap. Toxicological analysis revealed a low serum propylene glycol level. Biochemical analysis indicated that very high amounts of D-lactic acid (up to 110 mmol/l), but not of the usual type of L-lactic acid, were responsible for the metabolic acidosis. Hemodialysis was initiated and associated with a decline of both the acidosis and D-lactic acid levels. The patient regained conciousness. CONCLUSION: Ingestion of massive doses of propylene glycol, previously not reported as a cause of D-lactic acidosis, should be added to the differential diagnosis of this rare condition.

Acidosis, Lactic↗
PubMed2002

High anion gap metabolic acidosis in suicide: don't forget metformin intoxication--two patients' experiences.

Lactic acidosis is a well-recognized side effect of metformin, especially in patients with renal failure. Only a few cases of deliberate self-poisoning with metformin have been described in the literature. We report two patients who took a large dose of metformin in an attempt to harm themselves and both of them presented with severe lactic acidosis. The first patient was admitted because of taking large amounts of her father's unknown drug for suicide. Arterial blood gas showed severe metabolic acidosis with high anion gap and blood lactate level which metformin intoxication was documented. She died of multiple organ failure although we provided aggressive management including continuous renal replacement therapy. The second case, a type 2 diabetic patient, was sent to the emergency department after taking 110 tablets of metformin (500 mg). Arterial blood gas showed severe metabolic acidosis with high anion gap and blood lactate level. Hypotension and consciousness disturbance occurred later. After one session of hemodialysis, she recovered completely. In our experiences, metformin intoxication should be suspected when patients presented by wide anion gap metabolic acidosis after suicide attempt by taking drugs. Hemodialysis or continuous renal replacement should be initiated as soon as possible in addition to other supportive care.

Acid-Base Equilibrium↗