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PubMedDate not supplied

Renal tubular acidosis. Pathophysiology and diagnosis.

The pathophysiology of renal tubular acidosis is slowly being unraveled, which has implications for the traditional classification of the condition. Nonetheless, the diagnosis of renal tubular acidosis is still easy to establish, and identification of the specific pathophysiological subtype is relatively straightforward. The diagnostic information required usually includes only urinary pH and sodium, potassium, and chloride concentrations and serum potassium level. The urinary pH is not a diagnostic test for renal tubular acidosis, but it serves to distinguish between the various subtypes.

Acidosis, Renal Tubular↗
PubMed1977

[The clinical picture of lactate acidosis. 1 : Lactate metabolism].

The definition of lactate acidosis (lactic acidosis) is discussed. The metabolism of lactate and pyruvate are described. An increase in lactate concentration should be called lactic acidemia (lactate emia). This increase in lactate concentration can be caused either by an increased production (primarily by the so-called peripheral tissues) or by a decreased utilization (by the liver or by the kidneys). Therefore, various metabolic alterations can cause lactate acidosis.

Acidosis↗
PubMed1976

[Effect of arterial hypoxia and acidosis on fibrillation threshold in the cat heart in vivo].

The influence of severe arterial hypoxia and acidosis on the fibrillation threshold was checked in 22 cats. Two groups were formed: in 10 cats (group I) acidosis was produced by 2-N lactic acid infusion; in the second group of 12 animals the respirator was turned off for 60 seconds, thus producing a low arterial PO2. If hypoxia and acidosis were severe enough, the fibrillation threshold was significantly lowered in either group. The pathophysiological mechanisms of these findings are discussed.

Acidosis↗
PubMed1996

Type B lactic acidosis in an AIDS patient treated with zidovudine.

Human immunodeficiency virus type 1 (HIV 1) infection has been shown to cause myopathy. Zidovudine, a nucleoside analogue, has also been shown to cause myopathy in HIV-infected patients. Dalakas et al., were unable to distinguish the myopathy associated with HIV infection from the toxic mitochondrial myopathy caused by zidovudine. In a recent report, Chattha et al., described seven patients with Acquired Immunodeficiency Syndrome (AIDS) who developed type B lactic acidosis. Four of these patients were treated with zidovudine. A 100% mortality over a period of 15 months was observed. Zidovudine disrupts the mitochondrial deoxyribonucleic acid (DNA) that encodes for the respiratory chains, inhibiting the transport of lactate into the mitochondria. This may cause the accumulation of lactate in the cytoplasm, producing a severe metabolic acidosis. We present an AIDS patient with servere type B lactic acidosis which could have been associated with, or precipitated by, zidovudine.

Acidosis, Lactic↗
PubMed1997

The search for the uremic toxin: the case for metabolic acidosis.

Much effort has been expended on determining which compound, hormone or metabolic condition causes the uremic syndrome. Byproducts of protein metabolism that can cause uremic symptoms, including loss of lean body mass, have been a focus of research but specific toxins have been difficult to identify. Evidence is provided that implicates metabolic acidosis as the prime signal initiating muscle wasting in uremia since it activates branched-chain ketoacid dehydrogenase and the ubiquitin proteasome pathway. These responses degrade the essential branched chain amino acids and protein in muscle, leading to loss of muscle mass. Correction of the metabolic acidosis with sodium bicarbonate supplements has significant therapeutic implications for uremic patients with even mild degrees of metabolic acidosis.

Acidosis↗
PubMed1997

[Lactic acidosis and hepatic mitochondrial changes during a treatment with zidovudine].

Adverse effects of zidovudine, which mainly result in myopathies and hematological disorders, could be due to multitissular mitochondrial toxicity of the drug. During zidovudine treatment, most cases of lactic acidosis have been attributed to mitochondrial myopathy. We report a case of hepatocellular failure with lactic acidosis in a 33 year-old patient with the human immunodeficiency virus infection and treated with zidovudine for 8 months. Liver biopsy showed massive macrovacuolar steatosis and ultrastructural mitochondrial abnormalities similar to those previously described in the skeletal muscle. This is the second reported case of lactic acidosis and hepatocellular failure which is probably related to hepatic mitochondrial dysfunction caused by zidovudine.

Acidosis, Lactic↗
PubMed1998

Type-II renal tubular acidosis and ventricular tachycardia in a horse.

A 14-year-old Arabian mare was admitted for lethargy, anorexia, and low fecal output. On the basis of laboratory, physical examination, and electrocardiographic findings, diagnoses of type-II renal tubular acidosis (RTA), impaction of the large colon, and ventricular tachycardia were made. Diagnosis of type-II RTA was based on measurement of a low fractional excretion value for potassium and fractional excretion value for sodium within the reference range. In contrast, horses with type-I RTA have high fractional excretion values for sodium and fractional excretion values for potassium within reference ranges. Treatment consisted of intravenous and oral administration of sodium bicarbonate, intravenous administration of fluids, and oral administration of mineral oil and docusate sodium. Acidosis improved, and ventricular tachycardia resolved with resolution of acidosis. Oral administration of bicarbonate was continued after discharge. The mare had several relapses, which were associated with anorexia and low intake of supplemental bicarbonate. The mare was found dead 2 months after discharge.

Acidosis, Renal Tubular↗
PubMed1998

[Systemic effects of ruminal acidosis following ruminal drinking in dairy calves. A retrospective analysis of 293 cases].

In a retrospective study the data of 293 young calves (age upon admission less than four weeks) with evidence of ruminal drinking (rumen pH < 6.0) were analyzed for possible associations between ruminal acidosis and various parameters of systemic acid-base metabolism (blood pH, blood levels of HCO3- and L-lactate, as well as anion gap). On the basis of the degree of ruminal acidosis (pH < 5.0/ > or = 5.0) and evidence of diarrhea, the animals were assigned to one of four groups. The results indicate that severe ruminal acidosis leads to disturbances of systemic acid-base metabolism in young calves, too. With additional diarrhea, those disturbances can be complex.

Acid-Base Equilibrium↗
PubMed1998

Hyperkalemic renal tubular acidosis induced by trimethoprim/sulfamethoxazole in an AIDS patient.

A patient with the acquired immunodeficiency syndrome (AIDS) and sickle cell anemia presented to the University of Wisconsin Hospital on two separate occasions with pneumocystis carinii pneumonia (PCP). On both occasions he was treated with high-dose intravenous trimethoprim/sulfamethoxazole (TMP/SMX). Several days into each treatment course he developed hyperkalemia and systemic acidosis consistent with hyperkalemic renal tubular acidosis (RTA). The abnormalities resolved in the first instance with the addition of amphotericin B while continuing TMP/SMX, and in the second upon discontinuation of the TMP/SMX. While an increasing number of cases with TMP/SMX-induced hyperkalemia have been reported, hyperkalemic RTA is an uncommon complication of TMP/SMX therapy, occurring in patients with predisposing factors for acidosis such as aldosterone defects, medullary dysfunction and renal insufficiency.

AIDS-Related Opportunistic Infections↗
PubMed1994

[Metabolic acidosis--a diagnostic challenge].

Metabolic acidosis can be caused by a variety of pathological conditions, but intoxication with ethylene glycol or methanol should be suspected in cases of a combined increase of osmolal and anion gaps. The determination of the gaps is based on readily available laboratory tests, and the results is known soon after the blood sample is taken. This procedure is of particular interest for hospitals where specific analyses for methanol and ethylene glycol are not available, since calculation of the gap can give an early indication of what treatment to use. Therefore, the gaps should be calculated as a routine in patients with metabolic acidosis of unknown origin. The authors describe the principles for calculating and using the gaps, and report three cases which illustrate their usefulness in practice.

Acidosis↗
PubMed1993

Mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes (MELAS): clinical, radiological, pathological, and genetic observations.

We reviewed 10 patients (5 males, 5 females) with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes. The age of symptom onset ranged from 3 months to 12 years. All had lactic acidosis, multiple stroke-like events with secondary neurological deficits, radiological changes of progressive brain infarction, and muscle biopsy showing ragged-red fibers. In patients with earlier onset of symptoms (< 2 yr), involvement tended to be more diffuse, with failure to thrive and early onset of delayed development. Patients whose symptoms appeared later tended to have focal neurological deficits with migraine-like headache, and a rate of cognitive regression reflecting the rapidity of disease progression. Radiological changes included multiple areas of infarction with initial predilection for parietal occipital areas, progressing to generalized atrophy. Pathological findings in muscle biopsies included type 1 fiber predominance, ragged-red fibers, increased intermyofibrillar lipid deposition, and abnormal mitochondria. Four patients showed mitochondrial DNA tRNA mutation at position 3,243. No difference was noted in clinical, radiological, or pathological findings in patients with and without this mutation, suggesting that multiple sites of point mutation may give rise to mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes.

Base Sequence↗
PubMed1993

Physicochemical effects of acidosis on bone calcium flux and surface ion composition.

Net calcium flux (JCa) from bone in vitro is pH dependent. When pH falls below 7.40, through a reduction in [HCO3-], there is both physicochemical and cell-mediated JCa. To characterize the physicochemical effect of acidosis on bone we inhibited the bone-resorbing cells (osteoclasts) with the specific inhibitor calcitonin and studied the effect of acidosis on JCa and bone ion composition using an analytic high-resolution scanning ion microprobe. Neonatal mouse calvariae were cultured for 48 h in physiologically neutral pH medium (Ntl, pH = 7.41, [HCO3-] = 25 nM) or in medium that modeled metabolic acidosis (Met, pH = 7.10, [HCO3-] = 12), each with or without calcitonin (CT, 3 x 10(-9) M). There was net calcium efflux in Ntl (JCa = 631 +/- 36 nmol per bone per 48 h), which increased in Met (1019 +/- 53, p < 0.01); CT inhibited JCa in Ntl (-54 +/- 11, p < 0.01 versus Ntl), which increased in Met (197 +/- 15, p < 0.01 versus Ntl + CT). In the presence of CT the increase in JCa in Met versus Ntl represents physiochemical bone dissolution. The Ntl bone surface (approximately 2 nm in depth) was rich in Na compared to Ca (Na/Ca = 11.9, count/s of detected secondary ions), which fell in Met (Na/Ca = 6.0, p < 0.05); CT caused a further reduction of Na/Ca (3.1, p < 0.01 versus Ntl and versus Met), which was not altered in Met (2.6, p < 0.05 versus Ntl + CT).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Effects of external acidosis on HERG current expressed in Xenopus oocytes.

We investigated effects of external acidosis on HERG current expressed in Xenopus oocytes. HERG current was rapidly and reversibly suppressed by external acidosis in a voltage-independent manner. The slope conductance was decreased from 143 +/- 11 to 93.4 +/- 6.8 microS by changing external pH (pH(o)) from 7.6 to 6.0 (P<0.05). Steady-state activation was shifted by about 20 mV in a depolarized direction with a change from pH(o) 7.6 to 6.0, while steady-state inactivation was not significantly changed. Activation time constants were increased, deactivation and recovery time constants were decreased, while those of inactivation showed no significant change. When external K(+) concentration ([K(+)](o)) was increased from 2 mM to 10 mM, a ratio of slope conductance at pH(o) 6.0 to pH(o) 7.6 was significantly smaller in 2 mM (pH(o) 6.0/pH(o) 7.6 = 0.65 +/- 0.04) than in 10 mM[K(+)](o) (0.83 +/- 0.06, P<0.05). The changes in activation, deactivation and recovery from inactivation were not affected by change in [K(+)](o). The results indicated that external acidosis suppressed HERG current mainly by shifting the voltage-dependence of the activation and deactivation kinetics, and partly by decreasing slope conductance. Moreover, the reduction of HERG current could be partly antagonized with increasing [K(+)](o).

Animals↗
PubMed1996

Molecular mechanisms of acidosis-mediated damage.

The present article is concerned with mechanisms which are responsible for the exaggerated brain damage observed in hyperglycemic animals subjected to transient global or forebrain ischemia. Since hyperglycemia enchances the production of lactate plus H+ during ischemia, it seems likely that aggravation of damage is due to exaggerated intra- and extracellular acidosis. This contention is supported by results showing a detrimental effect of extreme hypercapnia in normoglycemic rats subjected to transient ischemia or to hypoglycemic coma. Enhanced acidosis may exaggerate ischemic damage by one of three mechanisms: (i) accelerating free radical production via H(+)-dependent reactions, some of which are catalyzed by iron released from protein bindings by a lowering of pH, (ii) by perturbing the intracellular signal transduction pathway, leading to changes in gene expression or protein synthesis, or (iii) by activating endonucleases which cause DNA fragmentation. While activation of endonucleases must affect the nucleus, the targets of free radical attack are not known. Microvessels are considered likely targets of such attack in sustained ischemia and in trauma; however, enhanced acidosis is not known to aggravate microvascular dysfunction, or to induce inflammatory responses at the endothelial-blood interface. A more likely target is the mitochondrion. Thus, if the ischemia is of long duration (30 min) hyperglycemia triggers rapidly developing mitochondrial failure. It is speculated that this is because free radicals damage components of the respiratory chain, leading to a secondary deterioration of oxidative phosphorylation.

Acid-Base Equilibrium↗
PubMed1989

Glucose metabolism and acidosis in the metabolic penumbra of rat brain.

The characterization of tissue acid-base status related to the penumbral zone of increased glucose consumption surrounding a focal cerebral ischemic lesion may suggest therapeutic techniques to maximize tissue survivability from stoke. We measured local cerebral metabolic rate for glucose (1 CMRglc) and an index of brain tissue pH (pHt) concurrently and characterized their interaction in a model of focal cerebral ischemia in rats in a double-label autoradiographic study, using [14C]2-deoxyglucose and [14C]dimethyloxazolidinedione. Computer-assisted digitization and analysis permitted the simultaneous quantification of the two variables on a pixel-by-pixel basis in the same brain slices. Hemispheres ipsilateral to intravascular tamponade-induced middle cerebral artery occlusion showed areas of normal, depressed, and elevated glucose metabolic rate (as defined by an interhemispheric asymmetry index) after 2 hr of ischemia. Regions of increased 1 CMRglc showed moderate acidosis (6.87 +/- 0.05), while regions of normal glucose metabolic rate showed normal pHt (pH +/- SD = 6.98 +/- 0.05) and regions of decreased 1 CMRglc showed severe acidosis (6.69 +/- 0.11). A repeated-measures analysis of variance found these values to differ from each other at the P less than 0.0005 significance level. The finding of moderate acidosis coupled with increased 1 CRMglc in the metabolic penumbra suggests that the excess protons may result from the anaerobic dissociation of ATP synthesis and hydrolysis.

Adenosine Triphosphate↗
PubMed2004

Peritoneal pH during laparoscopy is dependent on ambient gas environment: helium and nitrous oxide do not cause peritoneal acidosis.

BACKGROUND: Little is know about the effects of different insufflation gases on peritoneal pH during laparoscopy. However, these changes may influence the intracellular signalling system, resulting in altered cell growth or adhesiveness. The aim of this study was to determine the effects of carbon dioxide (CO(2)), nitrous oxide (N(2)O), and helium (He) on parietal and visceral peritoneal pH. The effect of different intraabdominal pressures on parietal and visceral peritoneal pH was also examined. METHODS: We conducted both an ambient gas study and a pressure study. For the ambient gas study, 20 pigs were divided into the following four groups: (a) CO(2), (b) He, (c) N(2)O, and (d) abdominal wall lift (Lift) laparoscopy. Parietal and visceral peritoneal pH were measured at 15 min intervals for 180 min. For the pressure study, 15 pigs were divided into the following three groups: (a) CO(2), (b) He, (c) N(2)O laparoscopy. Baseline values were established for parietal and visceral peritoneal pH. Intraabdominal pressure was then increased stepwise at 1-mmHg intervals to 15 mmHg. After pressure was maintained for 15 min at each setting, parietal and visceral peritoneal pH were measured. RESULTS: Ambient gas environment was the major determinant of parietal peritoneal pH. Carbon dioxide caused parietal peritoneal acidosis. Helium, N(2)O, and Lift caused alkalotic parietal peritoneal pH. Intraabdominal pressure had a minor effect on parietal peritoneal pH. At higher intraabdominal pressure (12-15 vs 5-8 mmHg), CO(2) caused a slight decrease in parietal peritoneal pH, whereas N(2)O and He caused a slight increase in parietal peritoneal pH. Visceral peritoneal pH remained relatively unaffected during all studies. CONCLUSIONS: Parietal peritoneal pH during laparoscopy was highly dependent on the ambient gas environment. The effect of intraabdominal pressure on parietal peritoneal pH was of minor significance. Carbon dioxide caused a slight worsening of parietal peritoneal acidosis at higher intraabdominal pressure, whereas, N(2)O, He, and Lift did not cause parietal peritoneal acidosis.

Animals↗
PubMed2004

Effects of acidosis on ventricular myocyte shortening and intracellular Ca2+ in streptozotocin-induced diabetic rats.

We have investigated the effects of acute acidosis on ventricular myocyte shortening and intracellular Ca2+ in streptozotocin (STZ)-induced diabetic rat. Shortening and intracellular Ca2+ were measured in electrically stimulated myocytes superfused with either normal Tyrode solution pH adjusted to either 7.4 (control solution) or 6.4 (acid solution). Experiments were performed at 35-36 degrees C. At 8-12 weeks after treatment, the rats that received STZ had lower body and heart weights compared to controls, and blood glucose was characteristically increased. Contractile defects in myocytes from diabetic rat were characterized by prolonged time to peak shortening. Superfusion of myocytes from control and diabetic rats with acid solution caused a significant reduction in the amplitude of shortening; however, the magnitude of the response was not altered by STZ treatment. Acid solution also caused significant and quantitatively similar reductions in the amplitude of Ca2+ transients in myocytes from control and diabetic rats. Effects of acute acidosis on amplitude of myocyte contraction and Ca2+ transient were not significantly altered by STZ treatment. Altered myofilament sensitivity to Ca2+ and altered mechanisms of sarcoplasmic reticulum Ca2+ transport might partly underlie the acidosis-evoked reduction in amplitude of shortening in myocytes from control and STZ-induced diabetic rat.

Animals↗
PubMed1991

Ischemic brain slice glucose utilization: effects of slice thickness, acidosis, and K+.

Brain slices of varying thickness were used to modify retention of metabolic products in an in vitro model of ischemia. Past and present results reveal increased anaerobic glycolysis in 660-microns slices with accumulation of lactate as slice thickness reaches 1,000 microns. Brain slice glucose utilization and lactate content were measured in buffers of various extracellular K+ levels and pH in 540-, 660-, and 1,000-microns slices. Acidosis suppresses glucose utilization at all slice thicknesses without affecting tissue lactate. Studies of 2-deoxyglucose metabolites establish that the suppression of glucose utilization by acidosis is due entirely to inhibition of glucose phosphorylation without any effect on glucose uptake into tissue. The inhibition is reversible after 45 min at pH 6.1. The experiments with acidosis also suggest that persistent energy demands continue to stimulate phosphofructokinase despite the low pH so that glycolysis continues, with potential for injury. Increasing K+ increases glucose utilization and tissue lactate at all three thicknesses. Correlations of glucose utilization with lactate accumulation support the possibility that high K+ may exert a dual influence on the tissue metabolism, not only stimulating glucose utilization by inducing depolarization but also by influencing the removal of metabolic products.

Animals↗