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PubMed2000

Inherited renal tubular acidosis.

The past few years have witnessed great progress in elucidating the molecular basis of inherited renal tubular acidosis. Consistent with the physiologically defined importance of multiple gene products in urinary acidification, heritable renal tubular acidosis is genetically heterogeneous. Autosomal dominant distal renal tubular acidosis has been associated with a small number of mutations in the AE1 Cl-/HCO3- exchanger although the pathophysiologic mechanisms behind these mutations remain unclear. Rarely, autosomal recessive distal RTA is caused by homozygosity or compound heterozygosity for the loss-of-function mutation AE1 G701D. A larger proportion, often accompanied by hearing loss, is associated with mutations in the ATP6B1 gene encoding the 58 kDa B1 subunit of the vacuolar H+-ATPase. Mutations in the gene encoding the Na+/HCO3- cotransporter, NBC1, have recently been identified in proximal renal tubular acidosis with corneal calcification.

Acidosis, Renal Tubular↗

PubMed1997

Metabolic acidosis.

Metabolic acidosis is a pathophysiologic state that is associated with serious morbidities and mortality. The diagnosis of metabolic acidosis is perplexing for novice and expert advanced practice nurses for many reasons. Its differential diagnosis is broad and includes common and rare, complex disease. The diagnosis of metabolic acidosis is also difficult because it is frequently associated with mixed, acid-base disorders. Its clinical manifestations are often nonspecific or subclinical, which means that its diagnosis is made from laboratory and other diagnostic tests. Timely diagnosis of metabolic acidosis is needed to institute appropriate therapy to avoid negative physiologic effects.

Acidosis↗

PubMed2005

Hypercapnic acidosis does not modulate the severity of bacterial pneumonia-induced lung injury.

OBJECTIVE: Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfusion, endotoxin-induced, and ventilation-induced lung injury. The efficacy of hypercapnic acidosis in bacterial lung infection, a common cause of acute respiratory distress syndrome, is not known. Furthermore, its effect may differ depending on the presence or absence of antibiotic therapy. We investigated whether hypercapnic acidosis-induced by adding CO2 to inspired gas-would protect against acute lung injury induced by pulmonary Escherichia coli instillation in an in vivo model in the presence and absence of effective antibiotic therapy. DESIGN: Prospective randomized animal study. SETTING: University research laboratory. SUBJECTS: Adult male Wistar-Kyoto rats. INTERVENTIONS: The animals were anesthetized and ventilated. In series 1, rats were administered intravenous ceftriaxone (100 mg x kg) and randomized to normocapnia (Normocapnia-ABx; Fico2 0.00, n = 10) or hypercapnia (Hypercapnia-ABx; Fico2 0.05, n = 10) groups. E. coli (8.4 x 10 colony forming units) was instilled intratracheally. Series 2 animals did not receive antibiotics. They were randomized to normocapnia (Normocapnia, n = 10) or hypercapnia (Hypercapnia, n = 10) groups, and intratracheal E. coli was administered. All animals were ventilated for 6 hrs. MEASUREMENTS AND MAIN RESULTS: In series 1, there were no differences between Hypercapnia-ABx and Normocapnia-ABx groups with regard to: (a-a)o2 gradient (mean +/- sem; 215 +/- 13 vs. 252 +/- 22 mm Hg), Pao2, bronchoalveolar lavage neutrophil count, static lung compliance, or histologic injury. Lung bacterial yield was not different between the groups. In series 2, in the absence of antibiotic therapy, there were no differences between Hypercapnia and Normocapnia groups in: (a-a)o2 gradient (mean +/- sem, 345 +/- 25 vs. 332 +/- 23 mm Hg), systemic Pao2, bronchoalveolar lavage neutrophil count, or static lung compliance. Lung bacterial yield was not altered by hypercapnia in either series 1 or 2. CONCLUSIONS: We conclude that hypercapnic acidosis did not alter the magnitude of the lung injury induced by intratracheal E. coli instillation in the presence or absence of antibiotics.

Acidosis, Respiratory↗

PubMed2007

Lactic acidosis in children with acute exacerbation of severe asthma.

This is a retrospective case series reporting lactic acidosis in four pediatric patients with acute severe asthma treated with nebulized beta2-agonists in a pediatric intensive care unit of a tertiary care teaching facility. During treatment with beta2-agonists, these patients developed lactic acidosis with a peak concentration of 5.2 to 13 mmol/l. Lactic acidosis improved within 24 h after discontinuation or decrease in the dosage of beta2-agonists. We conclude that the intensive use of beta2-agonists for acute severe asthma in children may be the primary and significant cause of lactic acidosis.

Acidosis, Lactic↗

PubMed2005

Role of hensin in mediating the adaptation of the cortical collecting duct to metabolic acidosis.

PURPOSE OF REVIEW: The cortical collecting duct is able to secrete HCO3-, a state that can be converted to acid secretion during metabolic acidosis. Bicarbonate secretion in this segment is mediated by beta-intercalated cells whereas alpha-intercalated cells perform acid secretion. During metabolic acidosis, the number of beta-intercalated cells is reduced while that of alpha-intercalated cells increases without a change in the total number of intercalated cells, suggesting conversion of one cell type to another. Using an immortalized intercalated cell line we found that this adaptation is mediated by an extracellular protein named hensin. Hensin is secreted as a monomer which is then polymerized in the extracellular environment by a complex process requiring at least three other proteins. RECENT FINDINGS: We describe that a cyclophilin, via its cis/trans prolyl isomerase activity, is required for this polymerization. This may explain the distal renal tubular acidosis observed with cyclosporin A therapy. In addition, galectin-3 is needed to aggregate the protein. Finally, we recently found that activation of integrins is also necessary for the development of the hensin fiber. Hensin is expressed in all epithelia and deletion of its gene is embryonic lethal at an early stage when the first columnar epithelia develop. SUMMARY: These studies suggest that the response of intercalated cells to metabolic acidosis uses a pathway that is involved in terminal differentiation of columnar epithelia.

Acidosis↗

PubMedDate not supplied

Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure.

Metabolic acidosis, a common condition in patients with renal failure, may be linked to protein-energy malnutrition (PEM) and inflammation, together also known as malnutrition-inflammation complex syndrome (MICS). Methods of serum bicarbonate measurement may misrepresent the true bicarbonate level, since the total serum carbon dioxide measurement usually overestimates the serum bicarbonate concentration. Moreover, the air transportation of blood samples to distant laboratories may lead to erroneous readings. In patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD), a significant number of endocrine, musculoskeletal, and metabolic abnormalities are believed to result from acidemia. Metabolic acidosis may be related to PEM and MICS due to an increased protein catabolism, decreased protein synthesis, endocrine abnormalities including insulin resistance, decreased serum leptin level, and inflammation among individuals with renal failure. Evidence suggests that the catabolic effects of metabolic acidosis may result from an increased activity of the adenosine triphosphate (ATP)-dependent ubiquitin-proteasome and branched-chain keto acid dehydrogenase. In contrast to the metabolic studies, many epidemiologic studies in maintenance dialysis patients have indicated a paradoxically inverse association between mildly decreased serum bicarbonate and improved markers of protein-energy nutritional state. Hence metabolic acidosis may be considered as yet another element of the reverse epidemiology in ESRD patients. Interventional studies have yielded inconsistent results in CKD and ESRD patients, although in peritoneal dialysis patients, mitigating acidemia appears to more consistently improve nutritional status and reduce hospitalizations. Large-scale, prospective randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in malnourished and/or inflamed CKD and maintenance hemodialysis patients. Until then, all attempts should be made to adhere to the National Kidney Foundation Kidney Disease and Dialysis Outcome Quality Initiative guidelines to maintain a serum bicarbonate level in ESRD patients of at least 22 mEq/L.

Acidosis↗

PubMed1993

Effects of acute respiratory acidosis on water and electrolyte transport in the human ileum.

Animal experiments have shown that acute respiratory acidosis stimulates water, Na and Cl absorption and HCO3 secretion in the ileum. The aim of this study was to investigate whether the human ileum also responds to changes in systemic acid-base balance. Seven healthy volunteers (mean age 24, range 21-29 years) underwent segmental ileal perfusion using a multi-lumen tube assembly with a proximal occluding balloon. A 30 cm test segment was perfused under steady state conditions with a plasma-like electrolyte solution containing PEG as a non-absorbable volume marker. After a control period, respiratory acidosis (blood pCO2 56.2 mmHg, pH 7.29 and [HCO3] 26.4 mmol l-1) was induced by CO2-breathing over a period of 50 min. Acute respiratory acidosis stimulated net HCO3 secretion in patients secreting HCO3 and reduced absorption in patients exhibiting net HCO3 absorption. These changes were immediate and appeared to be at least partly reversible. Net water, Na, K and Cl movement were not affected. The data suggest that HCO3 transport in the human ileum responds to acute respiratory acidosis.

Acid-Base Equilibrium↗

PubMed1982

Effect of supramaximal vagal stimulation in combination with hypoxia, respiratory acidosis and deep halothane anaesthesia on cardiovascular function in dogs.

Vagal reflexes are generally recognized as a possible cause of cardiac arrest during anaesthesia. Studies were performed to determine whether hypoxia, respiratory acidosis or deep halothane anaesthesia modify the cardiovascular effect of vagal stimulation (VS) in dogs. The animals were anaesthetized with intravenous urethane and chloralose, and paralysed with metocurine. Normal temperature and arterial blood gas variables were maintained and supramaximal VS was applied to the distal end of both vagus nerves for 5 min. No differences were found in any of the variables measured among the time periods when VS was repeated five times in six control dogs receiving urethane-chloralose basal narcosis only to determine the effects of time. VS resulted in 15 +/- 3 s (mean +/- s.e. mean) of asystole. Heart rate, cardiac output (CO) and mean arterial pressure (MAP) were still significantly decreased (P less than 0.001) and central venous pressure, right atrial pressure, pulmonary capillary wedge pressure (PCW), systemic (SVR) and pulmonary vascular resistance significantly increased (P less than 0.01--P less than 0.001) at the end of stimulation when compared to values before VS in all 24 dogs. Neither hypoxia [PaO2 5.3 kPa (40 mmHg)] nor respiratory acidosis [pH 7.00, PaCO2 10.6 kPa (80 mmHg)] modified these effects of VS. VS during halothane anaesthesia (1.6% end-tidal concentration) resulted in further significant decreases (P less than 0.05--P less than 0.001) in CO, MAP, mean pulmonary arterial pressure, PCW and SVR when compared to VS under basal narcosis. VS under halothane anaesthesia combined with hypoxia or respiratory acidosis did not decrease the cardiovascular parameters as much as VS under halothane anaesthesia alone. VS alone, or in combination with hypoxia or respiratory acidosis, failed to cause persistent asystole.

Acidosis↗

PubMed2005

Intensive care treatment of severe mixed metabolic acidosis.

We report a case of severe metabolic acidosis associated with acute renal failure and septicaemia following treatment with maximal therapeutic doses of metformin and diclofenac. On the second day of intensive care the patient deteriorated with respiratory insufficiency and abdominal pain during continuous renal replacement therapy. A laparoscopy revealed a perforated cholecystitis with abscess formation. The patient regained renal function and recovered. Intake of diclofenac 5 days before this episode could have been the main cause of renal insufficiency and metabolic acidosis in this patient and could also have delayed surgical treatment by masking early clinical signs of perforated cholecystitis. The renal failure may also have caused metformin and lactate to accumulate, contributing to the mixed pattern of metabolic acidosis. This case report describes a mixed organic and non-organic metabolic acidosis associated with acute renal failure, presumably resulting from a combination of drugs and diseases often found in the elderly - metformin for diabetes mellitus and a non-steroidal anti-inflammatory drug for cholecystolithiasis. Acid-base balance and electrolyte changes were rapidly normalized by continuous renal replacement therapy.

Abdominal Abscess↗

PubMed1984

Cholestyramine induced hyperchloremic metabolic acidosis.

The first reported case, in an adult, of cholestyramine induced hyperchloremic metabolic acidosis is a 70 year old female with a two year history of primary biliary cirrhosis confirmed by histologic and immunologic criteria. After taking cholestyramine II sachets twice daily for two months she presented with lethargy, confusion and drowsiness. Examination revealed confusion, jaundice, signs of chronic liver disease, portal hypertension and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis and a urinary pH of 4.85 together with tests of renal acidification, excluded renal tubular acidosis. She received 600 mEq of sodium bicarbonate intravenously over 36 hours by which time her mentation, electrolytes and pH were normal. It is presumed that her hyperchloremic metabolic acidosis was secondary to cholestyramine because of the similarity to pediatric reports; the rapid and lasting response to intravenous sodium bicarbonate; the absence of another etiology; normal serum potassium, chloride and bicarbonate despite continued spironolactone therapy after recovery.

Acidosis↗

PubMed2006

Severe acidosis in patients taking metformin--rapid reversal and survival despite high APACHE score.

BACKGROUND: Metformin has been shown to reduce complications and mortality from Type 2 diabetes mellitus, and is increasingly used to treat this condition. This agent is, however, associated with a rare but serious risk of lactic acidosis. CASE REPORT: We present cases of 10 patients with Type 2 diabetes mellitus who developed acute renal failure and severe lactic acidosis. Despite the severity of their illness, all patients but one survived. CONCLUSIONS: The increasing prevalence of Type 2 diabetes and its treatment with metformin might result in more cases of lactic acidosis. However our case report demonstrates that early and aggressive treatment with haemofiltration can improve outcomes even in the presence of severe acidosis.

APACHE↗

PubMed1989

Acidosis, acetazolamide, and amiloride: effects on 22Na transfer across the blood-brain and blood-CSF barriers.

Sprague-Dawley rats were given treatments, known to decrease 22Na movement into choroid plexus and CSF, to investigate their effect on 22Na transfer across the cerebral capillaries. Acidic salts, acetazolamide, or amiloride was injected intraperitoneally into bilaterally nephrectomized rats, and the rate of 22Na uptake into parietal cortex, pons-medulla, and CSF was determined at 12, 18, and 24 min. Severe acidosis (arterial pH 7.2), produced by HCl injection, decreased the rate of 22Na entry into both brain regions and CSF by 25%, whereas mild acidosis (pH 7.3) from NH4Cl injection reduced brain entry by 18%, but CSF entry by only 10%. Like HCl acidosis, amiloride reduced transport into both brain and CSF by 22%. Penetration of 22Na into parietal cortex was unchanged by acetazolamide, but that into CSF was slowed 30%. Since uptake of 22Na into cortical regions is primarily movement of tracer across the cerebral capillaries when tracer uptake time is less than 30 min, the results indicate that both metabolic acidosis and amiloride decrease Na+ permeativity at the cerebral capillaries as well as at the choroid plexus. Acetazolamide, on the other hand, alters Na+ movement only across the choroidal epithelium.

Acetazolamide↗

PubMedDate not supplied

Severe lactic acidosis treated with prolonged hemodialysis: recovery after massive overdoses of metformin.

We report two cases of severe lactic acidosis due to massive metformin ingestion. The first case was a 37-year-old man who was discovered several hours after ingesting 45 g of metformin. He had severe lactic acidosis (blood pH 6.81, bicarbonate 4 mEq/L, lactate 25.7 mEq/L). Despite intravenous bicarbonate therapy, he decompensated and was placed on a combination of hemodialysis and charcoal hemoperfusion for a continuous time of 25 hours. His hospital course was complicated by acute renal failure requiring a period of intermittent hemodialysis. He has since made a complete recovery. The second case was a 53-year-old man who ingested 50 g of metformin. He also presented with severe lactic acidosis (blood pH 6.85, bicarbonate 3 mEq/L and lactate 28.4 mEq/L) and deteriorated despite intravenous bicarbonate therapy. He was placed on hemodialysis as a continuous therapy for 21 hours. His hospital course was complicated by acute renal failure requiring a period of intermittent hemodialysis. He has subsequently made a complete recovery. Metformin-associated lactic acidosis carries a high mortality rate. Prolonged hemodialysis should be considered as an early treatment option in these cases.

Acidosis, Lactic↗

PubMed2004

Osteal complications as first manifestation in a patient with primary Sjögren's Syndrome and with associated distal tubular acidosis (type 1) and chronic renal insufficiency.

Renal affection is among the complications associated with the Sjögren's Syndrome. Tubulo-interstitial nephritis constitutes the most frequent renal lesion and distal tubular acidosis (Type 1) is the most important clinical manifestation of this tubular dysfunction, although the occurrence of chronic renal insufficiency is not an uncommon finding in the presence of distal renal tubular acidosis. Osteomalacia is a clinical consequence of tubular acidosis caused by buffering of H+ in the bone. We present the case of a woman with osteal complication a year before being diagnosed with primary Sjögren's Syndrome and with distal tubular acidosis and renal insufficiency associated at diagnosis.

Acidosis, Renal Tubular↗

PubMed1988

Vaginally born low-risk preterm infants: fetal acidosis and outcome at 6 years of age.

In a population of vaginally born low-risk preterm infants fetal acidosis (scalp pH less than 7.20) was found in 50% (6 out of 12) of infants of 29-33 weeks' gestational age (Group I) and in 9% (2 of 22) infants of 34-36 weeks' gestational age (Group II). At 6-7 years of age the children underwent a neurodevelopmental examination including a Griffith test. Five out of 6 Group I infants with fetal acidosis and 10 out of 20 Group II infants without fetal acidosis had minor or moderate neurodevelopmental problems. On the Griffith test Group II infants scored below Group I with more coordination and fine motor problems on the tested subscales. Fetal acidosis was more common in very preterm infants but cannot be used per se as a reliable indicator of long-term outcome.

Acidosis↗

PubMed1994

Reversible changes in cerebral activity associated with acidosis in preterm neonates.

Computerized online EEG monitoring in ventilated preterm infants less than 32 weeks' gestation enabled evaluation of the effect of acidosis on cerebral function. All episodes of acidosis were found to be associated with changes in the levels of cerebral activity. In 21 of the 32 episodes, EEG activity returned to pre-acidosis levels after therapeutic intervention. The duration of EEG abnormality was related to the severity of acidosis. However, the time to recovery of the EEG after therapeutic procedures was not related to duration of the EEG change.

Acidosis↗

PubMed1976

Influence of acidosis on noradrenaline-induced vasoconstriction in adipose tissue and skeletal muscle.

Vasoconstriction due to parallel i.a. injections of NA were studied in subcutaneous adipose tissue and gracilis muscle preparations in dogs. The vasoconstrictor response to NA was significantly lower in adipose tissue than in muscle. Only in muscle did acidosis inhibit NA-induced vasoconstriction. The beta-receptor antagonist propranolol increased the vasoconstrictor response in adipose tissue to the level of skeletal muscle. The lack of significant inhibition of NA-induced vasoconstriction in adipose tissue may be due to the simultaneous inhibition of two opposing mechanisms-alpha-adrenergic vasoconstriction and beta-adrenergic vasodilatation. After propranolol acidosis inhibited NA-induced vasoconstriction equally in adipose tissue and muscle. The difference between adipose tissue and muscle may thus be due to a greater importance of a beta-adrenergic vasodilator mechanism in the former tissue. The metabolic response to isoprenaline was inhibited by acidosis, while the direct vasodilatation was unaffected. It is suggested that the beta-adrenergic vasodilator mechanism that is inhibited by acidosis is related to the metabolism of the tissue.

Acidosis, Respiratory↗

PubMed1976

Inhibition of the lipolytic response to nerve stimulation during acidosis.

Acidosis inhibits catecholamine-induced lipolysis in vivo and in vitro. The lipolytic response of canine subcutaneous adipose tissue to short (5 min) nerve stimulations at 4 Hz was, however, not influenced by hypercapnic acidosis (pH 7.0). The steady state outflow of glycerol during a prolonged nerve stimulation at 4 Hz was inhibited by 40 per cent (p less than 0.05) at pH 7.0. Similarly, glycerol outflow during vasodilatation induced by a 4 Hz stimulation in alpha-blocked adipose tissue was inhibited by 37 per cent (p less than 0.05). Post-stimulatory glycerol outflow was, however, not influenced by acidosis. This poststimulatory glycerol outflow, which may represent a complex wash-out phenomenon, forms the largest part of the response to short nerve stimulations. It is suggested that steady state, rather than poststimulatory lipolysis should be studied in order to see the influence of treatments such as acidosis on responses to nerve stimulation.

Acidosis↗