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PubMed2000

Transient renal tubular acidosis in pregnancy.

Renal tubular acidosis in pregnancy is a very rare disorder. Most cases are either inherited or secondary to maternal disease or ingestion of toxic chemicals. We report a 22-year-old woman, previously healthy, who presented at 27 weeks of gestation with preterm labor. Investigation revealed renal tubular acidosis with no obvious etiology. Labor was stopped with various tocolytic drugs and her electrolyte imbalance was corrected. She was delivered at 36 weeks, by cesarean for a nonreassuring fetal heart tracing, of an appropriate-for-gestational-age infant weighing 2905 g. Evaluation 3 and 6 months postpartum revealed gradual, but complete resolution of the acidosis and electrolyte abnormality. The infant is now 7 months old, is growing normally with normal electrolytes, and with no evidence of acidosis.

Acidosis, Renal Tubular↗
PubMed2001

Interrelationship between plasma leptin concentration and severity of metabolic acidosis in haemodialysed patients with chronical renal failure.

Patients with chronic renal failure are frequently characterized by malnutrition, hyperleptinaemia and metabolic acidosis. Both hyperleptinaemia and chronic metabolic acidosis are presumed to contribute to the pathogenesis of malnutrition observed in this group of patients. It has been reported, that in vitro adipocytes exposed to acidotic medium decrease leptin secretion. The aim of present study was to analyze the possible impact of uraemic metabolic acidosis on leptinaemia in haemodialysis patients with chronic renal failure. - 94 haemodialysed patients (58 M, 36 F; mean age 45 +/- 1 years) were enrolled in this study. 56 patients were on haemodialysis treatment for one year using an acetate dialysis fluid, while 38 patients were haemodialysed at least for 3 months with a dialysate buffered with bicarbonate. Plasma leptin concentration, blood gases and body composition were assessed in all examined subjects. - Patients haemodialysed with an acetate and bicarbonate buffered dialysate did not differ with respect to body weight, body mass index (BMI), total fat mass (TFM) and plasma leptin concentration. Patients haemodialysed with an acetate buffered dialysate were characterized by a significantly more severe metabolic acidosis than patients on bicarbonate haemodialysis. Patients were divided according to the actual hydrogen ion concentration: over 60 nmol/l, 45-60 nmol/l and below 45 nmol/l. These subgroups did not differ significantly by body weight, BMI and TFM. Only a slightly (not significantly), lower median leptinaemia was found in patients with elevated hydrogen ion concentration. No significant correlation was noticed between blood hydrogen or hydrocarbonate ion concentration respectively and logarithmic values of plasma leptin concentration (tau = 0.025, p = 0.72; tau = - 0.021, p = 0.76 respectively). - From results obtained in this study we may conclude that, blood hydrogen ion concentration does not influence substantially or only moderately to plasma leptin concentration in haemodialysed patients.

Acidosis↗
PubMed1977

Amelioration of metabolic acidosis with fludrocortisone therapy in hyporeninemic hypoaldosteronism.

In four patients with renal hyperchloremic acidosis and hyperkalemia, hyporeninemic hypoaldosteronism and chronic renal insufficiency (glomerular filtration rates of 13, 31, 35 and 44 ml per minute per 1.73 m2), prolonged administration of fludrocortisone increased urinary potassium and net acid excretion, corrected hyperkalemia and substantially ameliorated acidosis. Except in the patient with the lowest glomerular filtration rate, the increased net acid excretion was due mostly to increased ammonium excretion. Urine pH decreased initially in each patient, but in the three patients with the highest filtration rates, it increased subsequently as ammonium excretion increased, indicating that renal ammonia production increased. Urinary ammonium excretion correlated inversely with serum potassium concentration and did not decrease on discontinuation of therapy if hyperkalemia was prevented from recurring. In patients with renal acidosis and hyporeninemic hypoaldosteronism, administration of mineralocorticoid hormone can augment both renal hydrogen-ion secretion and, by correction of hyperkalemia, renal ammonia production, and thereby ameliorate metabolic acidosis.

Acidosis, Renal Tubular↗
PubMed1981

Hyperkalemic distal renal tubular acidosis associated with obstructive uropathy.

We studied renal function in 13 patients with obstructive uropathy and hyperkalemic metabolic acidosis to characterize the pathogenesis of this disorder. Base-line fractional potassium excretion was lower in all patients than in controls with similar glomerular filtration rates. Acetazolamide was given to 11 patients but failed to increase fractional potassium excretion to normal. In five patients, impaired potassium excretion was associated with decreased ammonium excretion, a urinary pH below 5.5 (5.18 +/- 0.07, mean +/- S.E.M.), and aldosterone deficiency. In the remaining eight patients, the urinary pH did not fall below 5.5 (6.4 +/- 0.2) with acidosis, and we failed to lower the urinary pH and increase fractional potassium excretion to normal by administering a mineralocorticoid and sodium sulfate. A syndrome of hyperkalemic distal renal tubular acidosis may occur in patients with obstructive uropathy. In some patients, this syndrome results from a defect in hydrogen and potassium secretion in the distal nephron rather than from aldosterone deficiency. Obstructive uropathy should be included in the differential diagnosis of hyperkalemic acidosis and renal insufficiency.

Acetazolamide↗
PubMed1986

The acidosis of cholera. Contributions of hyperproteinemia, lactic acidemia, and hyperphosphatemia to an increased serum anion gap.

To study the metabolic acidosis that occurs during the diarrhea of cholera, we examined the serum anion gap in 21 patients with hypovolemic shock due to Vibrio cholerae infection. Measurements of serum electrolytes, as well as divalent cations and the anionic contributions of serum proteins, lactate, phosphate, and serum creatinine, were made at the time of admission, after rehydration, and during convalescence. At the time of admission, the mean serum concentration of sodium was 134.8 mmol (meq) per liter, that of chloride was 103.2 mmol per liter, and that of bicarbonate was 11.4 mmol per liter; the mean anion gap was 20.2 mmol per liter. The mean serum creatinine concentration was 2.48 mg per deciliter. The low serum bicarbonate level and the high serum anion gap were corrected by rehydration. The increased serum anion gap was caused by hyperproteinemia, lactic acidemia, and hyperphosphatemia, with anionic contributions to the rise in anion gap estimated as protein, 5.5 meq per liter; lactate, 2.5 meq per liter; and phosphate, 2.5 meq per liter. The hyperproteinemia was attributed to dehydration, the lactic acidemia to shock, and the hyperphosphatemia to acidosis and transient renal failure. The mean concentrations of serum calcium and magnesium were slightly elevated but did not affect the increased anion gap. These results indicate that severe cholera causes acidosis with relatively little change in serum chloride but an increased serum anion gap. The acidosis is more profound than would be expected on the basis of stool losses of bicarbonate, because of superimposed lactic acidemia and renal failure.

Acid-Base Equilibrium↗
PubMed2000

Effect of metabolic acidosis on the insulin-like growth factor-I system and cathepsins B and L gene expression in the kidney.

Prolonged acidemia causes growth retardation and muscle wasting, in part because of reduced food intake, depressed growth hormone secretion, and low serum insulin-like growth factor-I (IGF-I) levels. Paradoxically, in the rat kidney, protein synthesis increases, cathepsin B and L activities decline, protein degradation falls, and the kidneys enlarge. Because IGF-I has been implicated as a cause of renal hypertrophy in a variety of conditions, we examined whether IGF-I could be playing a role in the renal hypertrophy of acidosis. Rats were gavaged with NH4Cl or water for 4 days. Water-gavaged rats either were pair-fed with the NH4Cl-loaded rats (pH 7.15) or were given free access to food and served as controls. After 2 days, kidney weight and IGF-I mRNA levels did not differ between the groups, but kidney IGF-I protein levels were significantly higher in the acidotic rats. After 4 days the kidneys of the acidotic rats were significantly larger than the kidneys in both control groups but the renal IGF-I levels did not differ between the groups. It is notable that renal cathepsin B and L mRNA levels were reduced by 30% to 50% at both times. Thus the transient increase in renal IGF-I protein levels in acidosis, before the onset of hypertrophy, suggests that IGF-I may play a role in initiating kidney growth. Furthermore, it appears that reduced cathepsin B and L gene expression is a cause of the low renal cathepsin activity seen in acidosis. This likely contributes to the depressed renal proteolysis caused by acidosis.

Acid-Base Equilibrium↗
PubMed2001

Prenatal diagnosis of congenital heart disease affects preoperative acidosis in the newborn patient.

OBJECTIVES: Congenital heart disease is the leading cause of death in the first year after birth. Prenatal diagnosis of the disease can optimize the preoperative condition of the patient and may help in the prevention of acidosis. In this retrospective study we compared the occurrence of metabolic acidosis in patients with and without prenatal diagnosis of a congenital heart disease. METHODS: Data of 408 patients who needed an operation for congenital heart disease within 31 days of life were analyzed retrospectively. Arterial blood gases at fixed time intervals and worst blood gas of 81 patients with and 327 patients without a prenatal diagnosis were compared, categorizing the patients on ductus dependency, anticipated univentricular or biventricular repair, and left-sided, right-sided, or no heart obstruction. RESULTS: In the overall group significant differences in lowest pH, lowest base excess, and highest lactate level were found, with metabolic acidosis more common among the patients with a postnatal diagnosis. In the group of patients with ductus-dependent congenital heart disease, the difference between patients receiving a prenatal and those receiving a postnatal diagnosis was more significant than in the group with non-ductus-dependent lesions. Analyzing patients with right-sided, left-sided, and no obstruction separately, significant differences were found in the group with left-sided heart obstruction for lowest pH and base excess and in the group with right-sided heart obstruction for lowest base excess. CONCLUSIONS: Prenatal diagnosis of congenital heart disease minimizes metabolic acidosis in patients with congenital heart disease and may be associated with improved long-term outcome and prevention of cerebral damage among this fragile group of patients, although no significant effect on direct surgical outcome was encountered.

Acidosis↗
PubMed2004

Extracellular acidosis increases neuronal cell calcium by activating acid-sensing ion channel 1a.

Acid-sensing ion channel (ASIC) 1a subunit is expressed in synapses of central neurons where it contributes to synaptic plasticity. However, whether these channels can conduct Ca(2+) and thereby raise the cytosolic Ca(2+) concentration, [Ca(2+)](c), and possibly alter neuronal physiology has been uncertain. We found that extracellular acidosis opened ASIC1a channels, which provided a pathway for Ca(2+) entry and elevated [Ca(2+)](c) in wild-type, but not ASIC1(-/-), hippocampal neurons. Acid application also raised [Ca(2+)](c) and evoked Ca(2+) currents in heterologous cells expressing ASIC1a. Although ASIC2a is also expressed in central neurons, neither ASIC2a homomultimeric channels nor ASIC1a/2a heteromultimers showed H(+)-activated [Ca(2+)](c) elevation or Ca(2+) currents. Because extracellular acidosis accompanying cerebral ischemia contributes to neuronal injury, we tested the effect of acidosis on cell death measured as lactate dehydrogenase release. Eliminating ASIC1a from neurons or treating ASIC1a-expressing cells with the ASIC blocker amiloride attenuated acidosis-induced cell injury. These results indicate that ASIC1a provides a non-voltage-gated pathway for Ca(2+) to enter neurons. Thus, it may provide a target for modulation of [Ca(2+)](c).

Acid Sensing Ion Channels↗
PubMed1984

Na+-H+ exchange activity in renal brush border membrane vesicles in response to metabolic acidosis: The role of glucocorticoids.

Amiloride-sensitive Na+ -H+ exchange activity in brush border membrane vesicles isolated from rat proximal tubule was increased in metabolic acidosis. The enhancement of exchange activity required an intact adrenal gland or glucocorticoid supplements. Ammonium and phosphate excretions were increased during acidosis and these were also largely dependent on an intact adrenal gland or glucocorticoid supplements. Amiloride-insensitive Na+ uptake and passive H+ permeability were not altered by acidosis or the glucocorticoid status of the animal. These findings are consistent with glucocorticoids having an important regulatory role in the kidney by orchestrating the proximal tubular adaptation to metabolic acidosis.

Acidosis↗
PubMed1993

Skeletal troponin C reduces contractile sensitivity to acidosis in cardiac myocytes from transgenic mice.

Depressed contractile function plays a primary role in the pathophysiology of acute myocardial ischemia. Intracellular acidification is an important factor underlying the inhibition of force production in the ischemic myocardium. The effect of acidosis to depress contractility is markedly greater in cardiac as compared to skeletal muscle; however, the molecular basis of this difference in sensitivity to acidosis is not clearly understood. In this report, we describe transgenic mice that express the fast skeletal isoform of troponin C (sTnC) in cardiac muscle. In permeabilized single cardiac myocytes the shift in the midpoint of the tension-pCa relationship (i.e., pCa50, where pCa is -log[Ca2+]) due to lowering pH from 7.00 to 6.20 was 1.27 +/- 0.03 (n = 7) pCa units in control cardiac TnC (cTnC) expressing myocytes and 0.96 +/- 0.04 (n = 11) pCa unit in transgenic cardiac myocytes (P < 0.001). The effect of pH to alter maximum Ca(2+)-activated tension was unchanged by TnC isoforms in these cardiac myocytes. In a reciprocal experiment, contractile sensitivity to acidosis was increased in fast skeletal muscle fibers following extraction of endogenous sTnC and reconstitution with purified cTnC in vitro. Our findings demonstrate that TnC plays an important role in determining the profound sensitivity of cardiac muscle to acidosis and identify cTnC as a target for therapeutic interventions designed to modify ischemia-induced myocardial contractile dysfunction.

Acidosis↗
PubMed2003

Inhibition of glutamine synthetase in the mouse kidney: a novel mechanism of adaptation to metabolic acidosis.

As part of a study on the regulation of renal ammoniagenesis in the mouse kidney, we investigated the effect of chronic metabolic acidosis on glutamine synthesis by isolated mouse renal proximal tubules. The results obtained reveal that, in tubules from control mice, glutamine synthesis occurred at high rates from glutamate and proline and, to a lesser extent, from ornithine, alanine, and aspartate. A 48 h, metabolic acidosis caused a marked inhibition of glutamine synthesis from near-physiological concentrations of both alanine and proline that were avidly metabolized by the tubules; metabolic acidosis also greatly stimulated glutamine utilization and metabolism. These effects were accompanied by a large increase (i) in alanine, proline, and glutamine gluconeogenesis and (ii) in ammonia accumulation from proline and glutamine. In the renal cortex of acidotic mice, the activity of phosphoenolpyruvate carboxykinase increased 4-fold, but that of glutamate dehydrogenase did not change; in contrast with what is known in the rat renal cortex, metabolic acidosis markedly diminished the glutamine synthetase activity and protein level, but not the glutamine synthetase mRNA level in the mouse renal cortex. These results strongly suggest that, in the mouse kidney, glutamine synthetase is an important regulatory component of the availability of the ammonium ions to be excreted for defending systemic acid-base balance. Furthermore, they show that, in rodents, the regulation of renal glutamine synthetase is species-specific.

Acidosis↗
PubMedDate not supplied

Newborn renal tubular acidosis associated with prenatal maternal toluene sniffing.

Sniffing of volatile organic solvents containing toluene, such as acrylic paints, glues, adhesives, paint thinners, varnishes and shoe polishes, has become increasingly frequent in recent years. Renal tubular acidosis is one of a number of human complications reported in the offspring of mothers inhaling toluene during pregnancy. This article reports a case of a premature newborn with renal tubular acidosis probably due to maternal sniffing of paint containing toluene. Characteristics of this condition are described as well as its medical management. With increasing frequency of maternal glue and paint sniffing, more cases of newborn renal tubular acidosis will likely appear. Physicians should be prepared to manage neonatal tubular acidosis that may accompany maternal toluene sniffing in order to lessen newborn morbidity and/or mortality.

Acidosis, Renal Tubular↗
PubMed2001

Whole blood ionized magnesium in neonatal acidosis and preterm infants: a prospective consecutive study.

UNLABELLED: The mineral magnesium is a crucial enzymatic cofactor in the cellular bioenergetic process and alternations in magnesium metabolism may be associated with neurological impairment in newborn infants. Therefore, ionized magnesium (IMg) was measured in 14 newborn infants with acidosis [umbilical arterial cord pH 7.00 +/- 0.06, Apgar score 8.3 +/- 1.6 after 5 min, gestational age (GA) 276 +/- 16 d] and 15 premature infants (umbilical arterial cord pH 7.31 +/- 0.07, GA 236 +/- 12 d). Nineteen healthy mature infants served as controls. Arterial umbilical cord samples were taken immediately after delivery and capillary blood samples were taken 2, 6, 12 and 24 h after delivery by heel stick. IMg was measured by NOVA 8. The results showed an increased umbilical cord blood IMg in infants with acidosis compared with both premature and normal infants (0.58 +/- 0.08 mmol l(-1) vs 0.51 +/- 0.03 mmol l(-1) and 0.49 +/- 0.03 mmol l(-1); p < 0.0001). In infants with acidosis IMg declined significantly 2 h after delivery to 0.49 +/- 0.05 mmol l(-1) (p < 0.0001) and did not show any further significant changes during the first day of life. In premature infants and controls IMg levels were constant during the observation period. CONCLUSION: These findings suggest that elevated IMg is associated with neonatal acidosis.

Acidosis↗
PubMed2006

Long-term management of sevelamer hydrochloride-induced metabolic acidosis aggravation and hyperkalemia in hemodialysis patients.

Sevelamer hydrochloride use in hemodialysis patients is complicated by metabolic acidosis aggravation and hyperkalemia. Rare reports about a short-term correction of this complication have been published. The current authors investigated the long-term correction of metabolic acidosis and hyperkalemia in sevelamer hydrochloride-treated patients at doses adequate to achieve serum phosphate levels within K/DOQI recommendations. The authors followed 20 hemodialysis patients for 24 months in an open-label prospective study. The dialysate bicarbonate concentration was increased stepwise to a maximum 40 mEq/L and adjusted to reach patient serum bicarbonate levels of 22 mEq/L, according to K/DOQI recommendations. Laboratory results for serum bicarbonate, potassium, calcium, phosphate, albumin, alkaline phosphatase, iPTH, cholesterol (HDL-LDL), triglycerides, Kt/V, systolic-diastolic arterial pressure were recorded. Sevelamer hydrochloride-induced metabolic acidosis aggravation and hyperkalemia in hemodialysis patients were corrected, on the long-term, by an increase in dialysate bicarbonate concentration. Further improvement in bone biochemistry was noted with this adequate acidosis correction and parallel sevelamer hydrochloride administration, in sufficiently large doses to achieve K/DOQI phosphate recommendations.

Acidosis↗
PubMedDate not supplied

The hemophagocytic syndrome: titrating continuous hemofiltration to the degree of lactic acidosis.

In 3 cases of severe multiple organ failure due to hemophagocytic lymphohistiocytosis (HLH) in children, the authors demonstrate the utility of continuous hemofiltration in attenuating the consequences of excess cytokine activity, with therapy titrated to the degree of lactic acidosis. HLH was diagnosed in 3 encephalopathic children with multiple organ failure, elevated ferritin (49,396-237,582 pmol/L; or 21,983-105,733 ng/mL), elevated serum triglyceride, and depressed cell lines. One had a known malignancy, one had EBV-associated lymphoproliferative disease, and one was previously healthy. Continuous hemofiltration was initiated, with the ultrafiltrate production rate and countercurrent dialysate flow titrated to metabolic acidosis as reflected by the serum lactate (maximum 3.5 mmol/L or 31.6 mg/dL). Hemofiltration was titrated upward until lactic acidosis resolved, through clearance of lactate or interruption of excess cytokine-driven activity; maximum prescription was 2000 mL/h ultrafiltrate production plus 2500 mL/h dialysate flow. Stability was achieved with hemofiltration, then substantial resolution occurred with treatment according to the HLH-94 protocol (dexamethasone, cyclosporin, VP-16, intrathecal methotrexate). One child succumbed to candidiasis. Another made a full recovery. A third succumbed to his primary malignancy. HLH should be suspected in unexplained or unresolving multiple organ failure. Titration of hemofiltration based on measurable parameters of cellular metabolism (e.g., lactate, base deficit) may stabilize the child with metabolic acidosis long enough to allow proper diagnosis and institution of definitive therapy. Hemofiltration is not a panacea but rather a stabilizing mechanism, with poorly understood effects on interstitial water and solute flux, that facilitates recovery over weeks, not days.

Acidosis, Lactic↗
PubMed2001

In-vitro activation of complement system by lactic acidosis in newborn and adults.

INTRODUCTION: Complement activation occurs secondary to a variety of external stimuli. Lactic acidosis has been previously shown to activate the complement factors C3a and C5a. In the present investigation we examined the differential effect of lactic acidosis on anaphylatoxin levels in cord and adult blood. Furthermore we aimed to determine if the entire complement cascade could be activated by lactic acidosis. METHODS: Cord and adult blood samples (n = 20 each) were collected and incubated for one hour in either untreated condition or with the addition of lactate in two concentrations (5.5 mmol/l vs. 22 mmol/l). Following incubation, levels of C3a, C5a and sC5b-9, and blood gas parameters were determined. RESULTS: Anaphylatoxin (C3a and C5a) and sC5b-9 levels increased with the addition of lactate in a dose-dependent manner in cord and adult blood (C3a: 1 h, 5.5 mmo/l, 22 mmol/l: 418/498/622 microg/l in cord blood; 1010/1056/1381 microg/l in adult blood, p<0,05; similar results were found for C5a and sC5b-9). CONCLUSION: Lactic acidosis leads to an activation of the entire complement system in neonates and in adults. This activation is dose-dependent and more pronounced in adults as compared to neonates.

Acidosis, Lactic↗
PubMed2002

Severe nucleoside-associated lactic acidosis in human immunodeficiency virus-infected patients: report of 12 cases and review of the literature.

Lactic acidosis is a rare but often fatal complication reported in some human immunodeficiency virus (HIV)-infected patients treated with nucleoside-analogue reverse-transcriptase inhibitors. We report a series of 12 patients with HIV infection treated with nucleoside analogues who developed unexplained metabolic acidosis. We have also reviewed 60 additional published cases. The aim of the present study is to describe the clinical picture, prognostic factors, and final outcome for nucleoside-associated lactic acidosis. The mortality rate is high: 33% for our patients, and 57% for the patients described in the literature. In the multivariate analysis, a lactate serum level of >10 mM (odds ratio [OR], 13.23; 95% confidence interval [CI], 2.96-59.25) was the only factor associated with higher mortality. The administration of specific therapy with cofactors against acidosis was associated with a lower mortality (OR, 0.17; 95% CI, 0.04-0.73). We conclude that specific therapy with cofactors may improve the outcome for patients with this syndrome.

Acidosis, Lactic↗
PubMed2002

Lack of correlation between length variation in the DNA polymerase gamma gene CAG repeat and lactic acidosis or neuropathy during antiretroviral treatment.

Antiretroviral therapy, although successful in reducing HIV load and accordingly decreasing the incidence of HIV infection-related symptoms, has its drawbacks in the form of severe side effects. Recognized drug-related side effects are, for example, nausea, fatigue, lactic acidosis, neuropathy, lipodystrophy, and myopathy. Because not all patients experience these side effects, genetic factors could be involved. It is believed that the main toxicity of nucleoside analog drugs is due to a decrease in mitochondrial function, possibly by inhibition of mitochondrial DNA (mtDNA) replication. mtDNA is replicated by a multienzyme complex, the main component of which is the nuclear-encoded DNA polymerase gamma. Presently, the only known variation in the DNA polymerase gamma gene is variation in the number of CAG repeats in the second exon. To investigate whether CAG repeat expansion or mutations in the DNA polymerase gamma (POLG) gene could predispose to peripheral neuropathy or lactic acidosis, we have sequenced part of the second exon of the DNA polymerase gamma gene, containing the CAG repeat, of 59 drug-treated HIV-infected patients, 11 of whom experienced drug-induced neuropathy, and 3 of whom died from lactic acidosis. No correlation was found between numbers of CAG repeats and any of the symptoms. The coding regions of the POLG gene from the three lactic acidosis patients were then completely sequenced, but no mutations were found. In addition, no variation was detected in exons 3, 8, and 19 of seven neuropathy patients and three control subjects without symptoms. These exons were the only sites of amino acid changes between human and chimpanzee POLG genes, and were chosen as targets of tolerated variation.

Acidosis, Lactic↗