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PubMed2004

Proximal renal tubular dysfunction in primary distal renal tubular acidosis.

Low-molecular-weight (LMW) proteinuria has been described in patients with primary distal renal tubular acidosis (dRTA). However, other proximal renal tubular dysfunctions have rarely been reported. In this report we describe reversible and multiple proximal renal tubular cell dysfunctions in a patient with dRTA. A 4-year-old girl was admitted to our hospital for investigation of short stature and proteinuria. Laboratory studies revealed a hyperchloremic metabolic acidosis without aciduria, hypokalemia, hypouricemia with uricosuria, hypercalciuria, LMW proteinuria, phosphaturia, and generalized aminoaciduria. The patient was diagnosed as having dRTA with multiple proximal renal tubular dysfunctions. All proximal renal tubular dysfunction subsided 1.5 years after starting alkali therapy. The precise pathogenic mechanisms underlying the development of multiple proximal renal tubular dysfunctions in dRTA remained unclear. However, proximal renal tubular endosomal dysfunction resulting from a profound intracellular acidosis caused by vacuolar H+-ATPase dysfunction or hypokalemic nephropathy might contribute to the development of proximal renal tubular dysfunctions in patients with dRTA.

Acidosis, Renal Tubular↗
PubMed1997

Renal tubular acidosis and osteopetrosis with carbonic anhydrase II deficiency: pathogenesis of impaired acidification.

Renal tubular acidosis with osteopetrosis is an autosomal recessive disorder due to deficiency of carbonic anhydrase II (CAII). A 3.5-year-old Egyptian boy with osteopetrosis and cerebral calcification has a persistent normal anion gap type of metabolic acidosis (plasma pH 7.26) and a mild degree of hypokalemia. A baseline urine pH was 7.0; ammonium (NH4+) excretion was low at 11 mumol/min per 1.73 m2; fractional excretion of bicarbonate HCO3 (FEHCO3) was high at 9% when plasma HCO3 was 20 mmol/l; citrate excretion rate was high for the degree of acidosis at 0.35 mmol/mmol creatinine. Intravenous administration of sodium bicarbonate led to a urine pH of 7.6, a FEHCO3 of 14%, a urine-blood PCO2 difference of 7 mmHg, NH4+ excretion fell to close to nil, and citrate excretion remained at 0.38 mmol/mmol creatinine. Intravenous administration of arginine hydrochloride caused the urine pH to fall to 5.8, the FEHCO3 to fall to 0, the NH4+ excretion rate to rise to 43 mumol/min per 1.73 m2, and citrate excretion to fall to < 0.01 mmol/mmol creatinine. These results show that our patient had a low rate of NH4+ excretion, a low urine minus blood PCO2 difference in alkaline urine, and a low urinary citrate excretion, but only when he was severely acidotic. He failed to achieve a maximally low urine pH. These findings indicate that his renal acidification mechanisms were impaired in both the proximal and distal tubule, the result of his CAII deficiency.

Acidosis, Renal Tubular↗
PubMed1979

Severe mixed metabolic acidosis secondary to rhabdomyolysis.

A patient with severe metabolic acidosis in association with rhabdomyolysis and nonoliguric acute renal failure is presented. Evaluation of his acidosis indicated a large excess of unmeasured anions as well as evidence of a renal acidifying defect. We conclude that the metabolic acidosis seen with myoglobinuric acute renal failure may represent a mixed acid-base disturbance.

Acidosis↗
PubMed1979

Bicarbonate-buffered peritoneal dialysis. An effective adjunct in the treatment of lactic acidosis.

Severe lactic acidosis is associated with poor prognosis. Usually, the patient is treated with massive amounts of intravenous sodium bicarbonate, which in itself carries many undesirable consequences such as fluid overload and hypernatremia. We have successfully used peritoneal dialysis with a bicarbonate-buffered dialysate in the management of severe acidosis. Bicarbonate-buffered peritoneal dialysis provided an unlimited supply of physiologic buffer over a prolonged period without causing hypervolemia or hypernatremia. Furthermore, significant amounts of lactate were removed by dialysis. We, therefore, recommend the use of bicarbonate-buffered peritoneal dialysis as an adjunct in the treatment of severe lactic acidosis.

Acidosis↗
PubMed1980

Methanol poisoning in human subjects. Role for formic acid accumulation in the metabolic acidosis.

Whereas a great deal of information is available on the etiology of methanol poisoning in the monkey, very little study has been made in human subjects. The role of formic acid in methanol toxicity in human subjects has not been established. Two patients have been studied who have presented with the characteristics of methanol poisoning--metabolic acidosis and ocular toxicity. This has made possible a confirmation of the role of formate in the toxic syndrome. Acidosis was very severe in both cases with arterial pH values of about 6.9 and plasma bicarbonate concentrations of 3 meq/liter. A sensitive and specific assay was used to measure formic acid levels in blood and other fluids. Formate accumulation was marked with initial blood levels ranging from 11.1 to 26.0 meq/liter. Decreases in blood bicarbonate concentrations of similar magnitude coincided with the increase in formate. Thus, accumulation of formic acid plays a major part in the acidosis observed in human subjects poisoned with methanol, as has been demonstrated in monkeys. Treatment involving bicarbonate administration, ethanol infusion and hemodialysis, rapidly decreased formate levels in the blood to control values. Methanol concentrations were reduced but to lesser extent than that of formate. Despite the reduction in formate and methanol concentrations in both cases, the treatment was successful in only one of the two patients.

Acidosis↗
PubMed1982

Chronic acidosis with metabolic bone disease. Effect of alkali on bone morphology and vitamin D metabolism.

Chronic metabolic acidosis and osteomalacia developed in two patients following urinary diversion. Good clinical, biochemical, and histologic responses were seen following treatment with alkali alone (vitamin D was not given), despite the presence of markedly impaired glomerular filtration in one of the patients. Plasma 25-hydroxyvitamin D and 1 alpha, 25-dihydroxyvitamin D concentrations were normal before and during treatment in one of the patients and in the other were low before and normal during treatment. The results show that successful treatment of the osteomalacia of chronic acidosis is not necessarily accompanied by changes in the plasma levels of vitamin D metabolites and that even when marked glomerular dysfunction coexists with acidosis and osteomalacia, treatment with alkali may be more appropriate than the administration of vitamin D analogues.

Acidosis↗
PubMed1982

Distal renal tubular acidosis with intact capacity to lower urinary pH.

The sine qua non for the diagnosis of distal renal tubular acidosis requires that the urinary pH cannot decrease maximally during systemic acidosis. A defect in distal acidification however, could also result from a decrease in the capacity (or rate) of distal hydrogen ion secretion. In this type of defect, the ability to lower the urinary pH during acidemia could be preserved as long as a certain capacity for hydrogen ion secretion remained. In this report, we describe four patients with deranged distal urinary acidification, in whom urinary pH was able to decrease (4.99 +/- 0.11) during acidemia. One of the patients had hyperchloremic metabolic acidosis whereas the remaining three were not spontaneously acidotic. In these patients, the defect for distal urinary acidification was disclosed by the inability of the urine-blood pCO2 gradient to increase normally (i.e., above 30 mm Hg) during bicarbonate loading. In contrast, a normal increase in the urine-blood pCO2 gradient was observed in each patient in response to neutral sodium phosphate infusion. The reabsorptive capacity of bicarbonate was not depressed in these patients, which indicated that the acidification process in the proximal nephron was intact. We propose that our four patients had a defect in distal urinary acidification caused by a reduction in the rate of distal hydrogen ion secretion rather than an inability to generate a steep pH gradient across the distal nephron. Our data also suggest that the inability to raise urinary pCO2 normally during sodium bicarbonate loading may be the most sensitive index of decreased distal urinary acidification available.

Acidosis, Renal Tubular↗
PubMed1983

Acute cocaine poisoning. Importance of treating seizures and acidosis.

Cocaine poisoning has increased recently, and survival is rare because of its sudden onset and rapidly fatal course. A patient is described in whom cocaine poisoning developed. This condition was manifest by the findings of acute agitation, diaphoresis, and tachycardia, and was complicated by grand mal seizures, severe respiratory and metabolic acidosis, apnea, and accelerated idioventricular rhythm. After control of the seizures with diazepam and treatment of the acidosis with ventilation and bicarbonate, the ventricular dysrhythmia abated, and the patient made a quick recovery. Recently reported experiments suggest that seizures are a major determinant of lethality in cocaine poisoning. Treatment of the seizures is of prime importance, and correction of the acidosis can normalize cardiac rhythm and function in these critically ill patients.

Acidosis↗
PubMed1982

The development of fetal acidosis in the presence of an abnormal fetal heart rate tracing. I. The average for gestational age fetus.

An abnormal fetal heart rate (FHR) tracing is a sensitive indicator of positivity that disease exists, but the intrinsic predictive value of such a tracing is disappointingly low because of the large number of false positive results. Abnormal FHR tracings, defined as those having a persistent quantitative score of 4 or less, were measured against time and outcome. A baseline fetal scalp blood sample was taken. Twenty fetuses were acidotic at the first blood sample. There were 121 study cases, all of which were greater than 37 weeks' gestational age. All fetuses were average for gestational age. Amniotic fluid was clear, internal FHR tracings were initially normal, and the first pH was normal. A relative acidosis-free interval could be demonstrated during the first 90 to 100 minutes. Following this time period rapid cumulative acidosis was seen, which varied according to the FHR pattern observed. The P50 acidosis values for various patterns were late decelerations, 115 minutes; variable decelerations, 145 minutes; and flat line tracings, 185 minutes.

Acidosis↗
PubMed1990

Severe acidosis and subsequent neurologic status.

To examine the relationship between severe acidosis at birth and evidence of subsequent neurologic dysfunction, a 4-year review was performed encompassing 15,528 neonates. One hundred forty-two (0.91%) of these neonates had an umbilical cord arterial pH less than or equal to 7.05 with a base deficit greater than or equal to mEq/L. Neurologic assessments found 101 of 110 term neonates (91.8%) and 17 of 32 preterm neonates (53.1%) with severe acidosis to be free of neurologic deficits at the time of hospital discharge. Follow-up developmental evaluation data were available for 7 of 9 term neonates and 8 of 15 preterm neonates with abnormal examinations. Although 5 term and 6 preterm infants demonstrated mild developmental delays or mild tone abnormalities in the first year of life, none exhibited a major motor or cognitive abnormality at 12 to 24 months of age. Consequently, acidosis in umbilical cord blood, even when severe, is a poor predictor of subsequent neurologic dysfunction.

Acid-Base Equilibrium↗
PubMed1995

Newborn complications after intrapartum asphyxia with metabolic acidosis in the preterm fetus.

OBJECTIVE: Our purpose was to determine the nature of the complications in preterm newborns after intrapartum fetal asphyxia with metabolic acidosis at delivery. STUDY DESIGN: Thirty-seven preterm fetuses with metabolic acidosis were matched with 37 preterm fetuses with normal blood gas measurements at delivery. A complication score expressed the magnitude of newborn complications during the 10 days after delivery. RESULTS: The mean complication score for the preterm newborns at 32 to 36 weeks in the asphyxia group, 9.6, was significantly greater than that for the control group, 3.1. Fetal asphyxia was associated with severe complications in all systems. The complication scores for the preterm newborns < 32 weeks in the asphyxia group were of the same order as the control group. This may be related in part to a short duration of the asphyxial insult. The Apgar score at 1 minute was a valuable predictor of newborn complications in both the asphyxia and control groups. CONCLUSIONS: Intrapartum fetal asphyxia with metabolic acidosis at delivery is an important factor in the occurrence of severe complications, particularly in the central nervous system, respiratory system, and kidney, of preterm newborns.

Acidosis↗
PubMed1983

Effect of metabolic acidosis on phosphate transport by the renal brush-border membrane.

Metabolic acidosis produces a phosphaturia which is independent of parathyroid hormone or dietary phosphorus intake. To study the underlying mechanism, inorganic phosphate (Pi) and glucose transport were studied in brush-border membrane vesicles prepared from the renal cortex of parathyroidectomized rats gavaged for three days with either 7.5 ml of 1.6% NaCl (control) or 1.5% NH4Cl (acidosis). At killing, blood pH and plasma bicarbonate were 7.36 +/- 0.01 and 21.8 +/- 0.8 mequiv./l, respectively, in control and 7.12 +/- 0.03 (P less than 0.01) and 11.1 +/- 1.2 (P less than 0.01) in acidotic rats. Serum Pi was similar in both groups, while 24 h urine Pi excretion was higher in the acidotic group (P less than 0.01). Peak sodium-dependent uptake of Pi, measured after 1.5 min of incubation, was higher in controls than acidotic rats (4442 +/- 464 vs. 2412 +/- 259 pmol/mg protein, P less than 0.01), whereas peak glucose uptake at 1.5 min was not significantly different between the groups. Equilibrium values for Pi and glucose uptake were similar in the two groups. Km for Pi uptake in the control and acidotic animals were not different, 0.036 and 0.040 mM, respectively. By contrast, Vmax was higher in controls than in the acidotic group, 3.13 vs. 1.15 nmol/mg protein per 15 s. These results suggest that metabolic acidosis directly inhibits Pi uptake by the brush border of the proximal tubule by decreasing the availability of Pi carriers of the renal brush-border membrane.

Acidosis↗
PubMed1985

Inhibition by free radical scavengers and by cyclooxygenase inhibitors of the effect of acidosis on calcium transport by masseter muscle sarcoplasmic reticulum.

In vitro, arachidonic acid depressed calcium transport by sarcoplasmic reticulum (SR) in the homogenate of canine masseter muscle. This effect was inhibited by superoxide dismutase (SOD), a scavenger of the superoxide anion radial ( . O-2), at pH 7.0, and by SOD plus d-mannitol, a scavenger of hydroxyl free radical ( . OH), at pH 5.5. Indomethacin and 2-aminomethyl-4-tert-butyl-6-propionyl phenol (ONO-3144), a compound known to accelerate the conversion of prostaglandin G2 (PGG2) to PGH2 and scavenge free radicals, inhibited the effect of arachidonic acid at both pH 7.0 and pH 5.5. PGG2, but not PGH2, duplicated the effect of arachidonic acid. The effect of PGG2 on SR function was similar to that of exogenous free radicals generated from the xanthine-xanthine oxidase system. Incubation at pH 5.5, in the absence of an exogenous free-radical generating system, depressed SR calcium transport in the homogenate and in isolated SR. This effect in the homogenate was inhibited by indomethacin or by ONO-3144. At 10-min incubation at pH 5.5, SOD partially and temporarily reversed the depressant effect of acidosis. The addition of SOD plus d-mannitol completely reversed the system. d-Mannitol alone was ineffective. Arachidonic acid was able to mimic these effects of acidosis, except that arachidonic acid further depressed isolated SR calcium transport. These results demonstrate that acidosis can depress SR calcium transport in the homogenate of masseter muscle by an oxygen-free radical mechanism by the generation of . O-2 and . OH. Our results also demonstrate that significant oxygen radical generation can occur through the cyclooxygenase pathway of arachidonic acid metabolism at an acidotic pH in the cellular environment outside of the SR of the muscle cell, and seems to be responsible for the generation of the . OH derived from . O-2.

Acidosis↗
PubMed1984

The effect of metabolic acidosis upon autoregulation of cerebral blood flow in newborn dogs.

The radioactive microsphere technique was used in 13 newborn dogs to determine the effect of a metabolic (lactic)acidosis upon cardiac output (CO), cerebral blood flow (CBF), and autoregulation of cerebral blood flow. The animals were mechanically ventilated with supplemental oxygen to ensure normocarbia and hyperoxia throughout the experiments. Baseline cardiac output and cerebral blood flow measurements were made, followed by a lactic acid infusion to maintain pH less than 7.25. Metabolic acidosis produced a 27% fall in cardiac output and no change in cerebral blood flow (19 ml/100 g/min). Autoregulation was tested in 6 of the acidemic puppies by acute volume depletion to reduce blood pressure by 30% of baseline, followed by rapid volume re-expansion of the withdrawn blood. With volume depletion, CO decreased by 38%, and with volume re-expansion CO returned to baseline. The CBF remained at baseline levels with volume depletion but was slightly increased after rapid volume re-expansion. Five acidemic controls maintained CO and CBF constant with time. Thus cerebral autoregulation is preserved in the newborn dogs during metabolic acidosis, although cerebral blood flow was slightly increased following volume re-expansion.

Acidosis↗
PubMed1988

Lactic acidosis and recovery of neuronal function following cerebral hypoxia in vitro.

The rat hippocampal slice preparation was used to study the combined effects of hypoxia and lactic acidosis on neuronal function. Control slices were exposed to a standard hypoxic insult while being perfused with normal artificial cerebrospinal fluid (ACSF). Experimental slices were perfused with ACSF containing 1.0, 2.0, 10.0 or 20.0 mM lactic acid, 30 min before and during the same standard hypoxic insult. Following at 30-min recovery period the ability of these slices to respond to orthodromic stimulation by displaying a population spike (synaptic function) was tested. No significant decreases in the recovery rate of synaptic function were found between control and experimental groups, excluding the combination of 20 mM lactic acid and 10 min hypoxia, where such a decrease was found. The combination of 10 mM lactic acid and 12 min hypoxia brought about an increase in the recovery rate of synaptic function. Thus, the adverse effects attributed to lactic acid in vivo were not seen in the present in vitro study. Neuronal tissue appears to be able to handle excess lactic acid by yet, unknown mechanism (high intracellular buffer capacity?). The suggested in vivo damage due to lactic acidosis could originate in the cerebrovascular system. On the other hand, the possibility that lactic acidosis is harmless under hypoxic conditions should also be considered.

Acidosis, Lactic↗
PubMed1991

Effect of acidosis on lipid peroxidation in brain slices.

Acidification of the incubation medium markedly increased lipid peroxidation of cortical brain slices. Lactic acidosis caused a more extensive lipid peroxidation than did phosphoric acidosis (+35% at pH 6 and +81% at pH 5), probably due to the rapid diffusion of the protonated form of lactic acid across cell membranes. These results support the hypothesis that free radical mechanisms may be involved in the cytotoxicity of acidosis.

Acidosis↗
PubMed1994

Response of cytosolic Ca2+ to hypercapnic acidosis in cultured glomus cells of the adult rabbit carotid body.

The characteristics underlying the response of cytosolic Ca2+ ([Ca2+]i) to hypercapnic acidosis in clusters of cultured glomus cells of the adult rabbit carotid body were evaluated using fura-2 microscopic fluorometry. Application of CO2 by bubbling through both superfusions of bicarbonate-buffered saline and HEPES-buffered saline produced a rapid and sustained increase in [Ca2+]i. The [Ca2+]i response increased correspondingly with a rise in concentrations of CO2 to 20% but at a point between 20 and 50% adapted to CO2 and it decreased its linear assent. The hypercapnic acidosis-induced increase of [Ca2+]i was diminished by removing external Ca2+. Also the [Ca2]i response was reduced in dose-dependent fashion by the addition of the voltage-gated Ca2+ channel blocker D600. An additional response of [Ca2+]i to acetate was also diminished by Ca2+ removal. These results suggest that the [Ca2+]i response to hypercapnic acidosis involves an influx of external Ca2+ through voltage-gated Ca2+ channels.

Acidosis↗