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PubMed1989

Calcitriol metabolism during chronic metabolic acidosis.

Chronic metabolic acidosis causes a profound disturbance in renal proximal tubule 1OHase activity through perturbation of the normal ionic and hormonal controls of the enzyme activity. A lack of enzyme stimulation in response to hypophosphatemia and a paradoxical response of increased 1OHase activity to increased extracellular phosphorus are the important extracellular markers of deranged P control of 1OHase activity during chronic metabolic acidosis. 1OHase activity is down-regulated during chronic metabolic acidosis by an increase in renal cortical tubule mitochondrial calcium content and a functional abnormality in calcium handling, a reduction in extramitochondrial buffering capacity. There is a defect in PTH regulation of 1OHase during chronic metabolic acidosis, despite PTH levels which are inappropriately normal in relation to ionized hypercalcemia. PTH-directed cAMP accumulation is likely normal as well. Metabolic clearance of calcitriol is increased during chronic metabolic acidosis. Thus, the hormonal stimulus to maintain calcium and phosphorus homeostasis, calcitriol, is so altered by chronic metabolic acidosis that it is easy to understand the profound clinical effects of the acidosis on the skeleton of growing children. Chronic metabolic acidosis has allowed a greater understanding of the complex regulatory physiology that underlies renal proximal tubular 1OHase activity and calcitriol metabolism.

Acidosis, Renal Tubular↗
PubMed1985

[Lactic acidosis treated with thiamine. 3 cases].

Of 3 alcoholic patients with severe lactic acidosis, one had shoshin beriberi; the second--a beer drinker--presented with convulsions associated with hyponatraemia and complicated by rhabdomyolysis and was not thiamine-deficient; the third patient had convulsions associated with Korsakoff's syndrome and was thiamine-deficient. In all three patients treatment with thiamine administered alone corrected the lactic acidosis within less than 4 hours. In patient 1, this result was obtained after symptomatic treatment of shock and lactic acidosis had failed and more than 24 hours before the haemodynamic disorders were corrected. In patient 2, who had no haemodynamic nor haematosis disorders, the lactic acidosis was corrected within 2 hours, i.e. more than 24 hours before neurological improvement developed. In patient 3, the lactic acidosis was also corrected within 2 hours. These results suggest that thiamine should figure among the treatments of lactic acidosis in alcoholic patients. Since thiamine alone is capable of correcting severe lactic acidosis, at least in some of these patients, it deserves to be tried in other types of lactic acidosis.

Acidosis↗
PubMed1985

Familiar hyperkalaemic acidosis.

We evaluated a 26-year-old man with hyperkalaemic acidosis, apparently inherited as an autosomal dominant trait. Type II pseudohypoaldosteronism was suggested by normal aldosterone production and renal sodium conservation. The cause of acidosis in this syndrome is unknown. Both urinary ammonium excretion and bicarbonate threshold were low during hyperkalaemia. After correcting the hyperkalaemia ammonium excretion was normal, but bicarbonate threshold remained low. Maximum bicarbonate reabsorption, urine to blood pCO2 gradients, and minimum urine pH were normal. These findings suggest that hyperkalaemia might contribute to the acidosis by limiting urinary buffer, but that the primary defect is reduced mineralocorticoid effect on hydrogen ion secretion. When the poorly reabsorbed anion, sulphate, was infused, hydrogen ion and potassium secretion were normal. When the relatively reabsorbable anion, chloride, was infused, potassium secretion was decreased. These findings suggest that the attenuated mineralocorticoid effect on hydrogen ion secretion is due to increased reabsorptive avidity for chloride in the distal nephron. To determine if this defect caused resistance to mineralocorticoid we increased mineralocorticoid by dietary sodium restriction and later administered desoxycorticosterone and fludrocortisone. Both endogenous and exogenous mineralocorticoid caused increased net acid excretion and corrected the acidosis, indicating no resistance to mineralocorticoid. Hydrochlorothiazide 50 mg daily promptly corrected the acidosis and the hyperkalaemia by increased urinary potassium excretion. We conclude that the acidosis of type II pseudohypoaldosteronism is due in part to attenuation of the voltage-dependent moiety of mineralocorticoid-driven acidification caused by enhanced distal chloride reabsorption. Suppression of ammoniagenesis by hyperkalaemia exaggerates the acidosis. The acidosis and hyperkalemia are corrected by hydrochlorothiazide.

Acid-Base Equilibrium↗
PubMed1977

Lactic acidosis and ketoacidosis: biochemical and clinical implications.

A case of lactic acidosis presented the opportunity for review of the association between lactic acidosis and ketoacidosis. The diagnosis of lactic acidosis or the combination of lactic acidosis and ketoacidosis is established clinically by the detection of a metabolic acidosis of the "unmeasured anion gap" type in the absence of significant renal failure, poison intake or a strongly positive clinical test for ketones. Before treatment can be planned the biochemical basis of lactic acidosis and ketoacidosis must be understood -- especially the fact that lactic acidosis is not a single disease entity but has many possible causes. Among important considerations is the relation between the blood concentrations of bicarbonate and organic acid anions. After recovery from metabolic acidosis of the unmeasured anion gap type, metabolic alkalosis is common. Decreased bicarbonate excretion plays an important role in the pathogenesis of the latter and may be the result of potassium or chloride loss, or both. The deficits, if present, should be corrected with appropriate therapy.

Acidosis↗
PubMed1996

Renal tubular acidosis in children with vesicoureteral reflux.

PURPOSE: We evaluated renal tubular acidosis in children with primary vesicoureteral reflux. MATERIALS AND METHODS: We studied 18 children 4 to 15 years old to determine age at onset, reflux intensity, and renal scars and volume as possible associated factors of renal tubular acidosis. Patients had normal glomerular filtration rates and no urinary infections for the last 12 weeks, and they had not undergone urological surgery. Urine acidification and alkalization tests were done, and the Mann-Whitney U test was used to assess differences between the groups with and without renal tubular acidosis. RESULTS: A total of 14 patients had unilateral and 4 had bilateral reflux, which varied in severity. All children except 2 had renal scarring. Bilateral renal volume was smaller in the renal tubular acidosis group. Nine patients had distal renal tubular acidosis, including 4 with short stature. CONCLUSIONS: Several patients with vesicoureteral reflux had renal tubular acidosis and some had growth failure. Grades of reflux and renal scarring were similar in patients with and without renal tubular acidosis. A single evaluation of reflux is of slight value for predicting future functional tubular impairment, and the duration of reflux and other associated factors may be more important. Renal tubular acidosis was the main explanation for growth failure in these patients.

Acidosis, Renal Tubular↗
PubMed1996

Extracellular acidosis and chloride channel inhibitors act in the late phase of cellular injury to prevent death.

Extracellular acidosis is cytoprotective in several models against anoxia/hypoxia and a variety of toxicants. The goal of this study was to determine the temporal relationships among toxicant exposure, the initiation of extracellular acidosis, Cl. Influx, Cl- channel inhibition and the onset of cellular death in rabbit renal proximal tubule suspensions. Extracellular acidosis was produced by adding HCl or H2SO4 to renal proximal tubule suspensions to decrease the extracellular buffer pH to 6.4 or by resuspending renal proximal tubules in a pH 6.4 buffer. The initiation of extracellular acidosis 15 min after the mitochondrial inhibitors antimycin A or carbonyl cyanide p-(trifluoromethoxy)-phenylhydrazone addition, a time point in which adenosine triphosphate levels are depleted and intracellular K+ is decreased, ameliorated lactate dehydrogenase release, a marker of necrotic cellular death. The initiation of extracellular acidosis 120 min after the addition of the toxicants tetrafluoroethyl-L-cysteine or t-butyl hydroperoxide decreased lactate dehydrogenase release 120 min later. Increased Cl- influx is an important step during the late phase of toxicant-induced cellular injury. Therefore, we determined if extracellular acidosis cytoprotection was associated with inhibition of Cl- influx and whether the Cl- channel inhibitors indanyloxyacetic acid (1.0 mM). niflumic acid (100 microM) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (100 microM) decreased Cl- influx and cellular death in renal proximal tubules exposed to antimycin A. Indeed, all three Cl- channel inhibitors significantly decreased 38Cl- influx and cellular death. In contrast, extracellular acidosis did not decrease 38Cl- influx but did prevent lactate dehydrogenase release. These results demonstrate that extracellular acidosis cytoprotection occurs during the late phase of cellular injury at a site distal to Cl- influx. Furthermore, the Cl- influx that occurs during the late phase of cellular injury and is critical for cellular swelling and lysis is sensitive to 5-nitro-2-(3-phenylpropyl-amino)-benzoic acid, niflumic acid and indanyloxyacetic acid.

Acidosis↗
PubMed1991

The effect of acidosis on the relationship between Ca2+ and force in isolated ferret cardiac muscle.

1. The relationship between force and intracellular [Ca2+] (monitored using the protein aequorin) has been investigated in papillary muscles isolated from ferret hearts, under control conditions (superfusate pH (pHo) 7.3) and during acidosis (pHo 6.8). 2. At pHo 7.3, increasing bathing [Ca2+] from 0.5 mmol l-1 to 8 mmol l-1 led to an increase in the size of the intracellular calcium transient. At the lower [Ca2+] this was accompanied by an increase in developed force; however, at the higher bathing [Ca2+] developed force reached a plateau. 3. Acidosis (produced by increasing the [CO2] of the gas with which the muscle superfusate was equilibrated) decreased maximum force and shifted the curve relating peak developed force to peak intracellular [Ca2+] to the right. 4. The mechanisms underlying the apparent decrease in the sensitivity of the contractile proteins to Ca2+ were investigated by applying rapid length changes to papillary muscles at control pHo, during acidosis, and after bathing [Ca2+] had been increased to match force during acidosis to that in control. 5. Acidosis decreased the change in force produced in response to a given length change (i.e. decreased muscle stiffness) but when bathing [Ca2+] was increased during acidosis, muscle stiffness returned to control. 6. Acidosis had no effect on muscle stiffness after the induction of rigor in the muscle (produced by metabolic inhibition). 7. It is suggested that in intact cardiac muscle the major effect of a mild acidosis is to decrease the sensitivity of the contractile proteins to Ca2+, hence decreasing the number of bound cross-bridges.

Aequorin↗
PubMed1997

Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acid­base status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acid­base compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.

Journal Article↗
PubMed2004

Hyperchloraemic acidosis: another misnomer?

OBJECTIVE: To review the term hyperchloraemic acidosis. DATA SOURCES: Articles and reviews from peer reviewed journals on acid-base physiology. SUMMARY OF REVIEW: The concept of hyperchloraemic acidosis is well established in medicine and regularly taught to medical students. Unfortunately, it is yet another medical misnomer. Hyperchloraemic acidosis is only likely to exist with normal plasma sodium concentrations. This is because the acidosis is due to a decreased strong-ion-difference rather than the hyperchloraemia alone. If hyponatraemia is present, an identical acidosis can exist without hyperchloraemia; or if hypernatraemia is present there may be hyperchloraemia without acidosis. Even those who cling to the bicarbonate centred approach to acid-base physiology should recognise that describing acid-base changes in terms of chloride alone is less meaningful than considering both the strong cations and the strong anions. For those clinicians, using the Stewart approach the value of the terms "strong ion acidosis" and "strong ion alkalosis" should be readily apparent. CONCLUSIONS: The use of the term hyperchloraemic acidosis is a misnomer as the chloride ion may be elevated or depressed in the absence of an acid bade abnormality.

Journal Article↗
PubMed1994

Greater inhibition of in vitro bone mineralization with metabolic than respiratory acidosis.

At a similar decrement in pH, acidosis produced by lowering the concentration of medium bicarbonate (metabolic acidosis) induces greater net calcium efflux from cultured neonatal mouse calvariae than acidosis produced by increasing the partial pressure of carbon dioxide (respiratory acidosis). This differential effect is due, at least in part, to enhanced cell-mediated bone mineral resorption during metabolic acidosis. To determine the effect of acidosis on osteoblastic bone formation we utilized primary cultures of neonatal mouse calvarial cells which produce calcified nodules in culture. Cells were plated at 4.5 x 10(4) cells/35 mm dish and incubated until confluent (day 9). Nodule formation was then induced by addition of beta-glycerophosphate and ascorbic acid and the cultures were randomly divided and then cultured in control (Ctl, N = 18) medium or in medium simulating metabolic (Met, N = 17) or respiratory (Resp, N = 19) acidosis. Medium was changed and calcium (Ca) measured every 48 hours until day 23. The mean initial medium pH of all Resp cultures (7.186 +/- 0.002) was lower than Met (7.243 +/- 0.006, P < 0.01), which was lower than Ctl (7.502 +/- 0.002, p < 0.01), yet the number of discrete nodules formed in Met (22 +/- 4 nodules/cm2) was lower than Resp (43 +2- 7, P < 0.01), and both were lower than Ctl (88 +/- 6, P < 0.01 vs. both Met and Resp).(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗
PubMed2002

Base deficit does not predict mortality when secondary to hyperchloremic acidosis.

Base deficit has been established as a predictor of mortality and endpoint of resuscitation. We hypothesized that in a significant subset of surgical intensive care patients, base deficit is secondary to hyperchloremic acidosis, and that these patients experience lower mortality than those patients whose base deficits are secondary to other causes. Seventy-five consecutive surgical intensive care patients with base deficits greater than 2.0 were prospectively studied. The etiology of the patients' base deficits was determined by admission laboratory data. Patients were divided into those with hyperchloremic acidosis, and those with acidosis from other causes. Mortality within these groups was compared by Fisher's exact test. Thirty-seven patients (49.3%) had hyperchloremic acidosis. Thirty-three patients (46.7%) had lactic acidosis. Three patients (4%) had base deficits secondary to ketosis, and two patients (2.6%) had base deficits secondary to uremia. There were no significant differences in age, APACHE II scores, or volumes of resuscitation between the hyperchloremic group and the remaining patients. There were four deaths (10.8%) in the hyperchloremic group and thirteen deaths (34.2%) in the remaining patients (P = 0.03). Hyperchloremic acidosis resulted from resuscitation with lactated Ringer's solution in 18 (48.6%) of the hyperchloremic patients. Hyperchloremic acidosis is a common etiology of base deficit in the surgical intensive care unit. It is associated with lower mortality than base deficit secondary to other causes. Moreover, it is frequently induced following resuscitation with lactated Ringer's solution. Failure to properly diagnose this subset of acidotic patients may result in inappropriate clinical interventions due to the erroneous presumption of ongoing tissue hypoxia.

Acid-Base Equilibrium↗
PubMed1988

Effect of metabolic or respiratory acidosis on rabbit renal medullary proton-ATPase.

Distal urinary acidification is thought to be mediated by an H+-ATPase sensitive to N-ethylmaleimide and dicyclohexyl-carbodiimide. We have studied the effect of chronic metabolic acidosis (NH4Cl for 3 days) or respiratory acidosis (inhalation of 10% CO2 for 2 days) on the H+-ATPase of plasma membranes prepared from the medulla. The enzymatic assay for the H+-ATPase was performed in the presence of ouabain and oligomycin and in the absence of Ca. H+-transport activity was assessed by the quenching of acridine orange in the presence of ATP. The 15-25% sucrose gradient fraction was enriched 40-fold in enzymatic activity over the homogenate, and 8-fold in enzymatic activity and 4-fold in H+-transport activity over the fluffy fraction (38,000 X g). Metabolic acidosis (pH less than 7.31) or chronic hypercapnia (PCO2 greater than 66 mmHg; 1 mmHg = 133.3 Pa) was induced for 2-3 days. Both groups showed the same enrichment factor in enzymatic and H+-transport assays as the control rabbits. Enzymatic and H+-transport activities, however, were not different between animals with respiratory acidosis and controls. Kinetic studies failed to disclose an increase in Vmax (673 vs. 702 mumol/(mg protein.min] or a decrease in Km (0.43 vs. 0.48 mM) in chronic hypercapnia as compared with controls. Metabolic acidosis also failed to increase H+-ATPase activity. These data demonstrate that the H+-ATPase of renal medulla does not display the expected increase in activity during acidosis. The role of this H+-ATPase in the adaptation to acidosis remains to be determined.

Acidosis↗
PubMed1990

Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs.

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.

Acidosis↗
PubMed1984

Response of renal NH3 production to chronic respiratory acidosis.

Although chronic metabolic acidosis results in an adaptive increase in the renal capacity to produce NH3, the response to a low pH produced by chronic respiratory acidosis is unknown. Rats were placed in a specially constructed chamber with an ambient CO2 of 10% for 3 days, which increased their PCO2 to 76 +/- 4 mmHg. NH3 production was determined in vitro using both isolated kidneys perfused with 0.5 mM glutamine and cortical tubules incubated with 1 mM glutamine. Conscious rats with chronic respiratory and chronic metabolic acidosis had similar arterial pHs (7.29 +/- 0.01 and 7.31 +/- 0.01), which were significantly lower than controls (7.41 +/- 0.04). NH3 production by kidneys from rats with chronic respiratory acidosis perfused at pH 7.4 did not differ significantly from normal controls (1.13 +/- 0.13 vs. 1.07 +/- 0.17 mumol X min-1 X g-1). By contrast, kidneys from rats with chronic metabolic acidosis produced significantly more NH3 than both these groups (2.73 +/- 0.29 mumol X min-1 X g-1). Cortical tubules from rats with chronic respiratory acidosis also showed no evidence of adaptation in both NH3 (8.8 +/- 0.8 vs. 11.6 +/- 0.8 mumol X min-1 X g-1) and glucose (1.38 +/- 0.08 vs. 1.41 +/- 0.13 mumol X min-1 X g-1) production in comparison with controls, whereas chronic metabolic acidosis stimulated both ammoniagenesis and gluconeogenesis twofold or more. Thus a low systemic pH does not account for the adaptation in the capacity of the kidney to produce either ammonia or glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1993

The effect of respiratory and lactic acidosis on diaphragm function.

The relative effects of respiratory and metabolic acidosis on diaphragm function are not known. To determine these effects, we compared the effects of respiratory and lactic acidosis on the contractile properties of the diaphragm. We estimated diaphragmatic performance from the change in transdiaphragmatic pressure after supramaximal stimulation of the phrenic nerves in an open-chested, casted-abdomen dog. Similarly, we stimulated the gastrocnemius motor nerve and examined force production and relaxation rate to determine if there was a difference in the response of this skeletal muscle. There was a fall in diaphragm performance with respiratory acidosis (77.1 +/- 16.9 cm H2O versus 93.8 +/- 15.0 cm H2O baseline), but not with lactic acidosis (96.7 +/- 15.7 cm H2O versus 93.8 +/- 15.0 cm H2O baseline); and the gastrocnemius was unaffected by either acidosis. The changes with respiratory acidosis were similar to those seen with diaphragmatic fatigue and had similar relaxation rate changes, suggesting that intracellular pH may play a mechanistic role in respiratory muscle fatigue. In addition, the absence of a respiratory acidosis effect on a non-diaphragmatic skeletal muscle's function represents another physiologic difference between the diaphragm and other skeletal muscles.

Acidosis, Lactic↗
PubMed2001

Metabolic acidosis.

Metabolic acidosis occurs in a number of diseases and even certain normal activities such as heavy exercise. It arises from increased endogenous acid production, exogenous acid (or acid-precursor) administration, base losses, and depression of renal acid secretion. Although the magnitude of acidosis is important, the ultimate pathophysiological impact of any metabolic acidosis is defined by the rate of change and the specific cause of the acidosis. This review discusses whole body, organ, and cellular effects of metabolic acidosis, its diagnosis by pathophysiologic categories, and treatment. The diagnosis is made by a synthesis of the clinical history, physical examination, other hematological values, serum and urinary chemistries, and arterial blood gases and electrolytes. Calculation of the anion and osmolal gaps can be effectively used to further narrow the diagnostic possibilities. Supportive care and therapy directed at the cause of the metabolic acidosis are the mainstays of treatment, since most acidotic states will spontaneously correct once the initiating cause is removed or reversed. Theoretical and clinical evidence are discussed for alkalinizing agents, whose use remains controversial except in the treatment of metabolic acidosis associated with hyperkalemia and certain drug or toxin ingestions.

Acidosis↗
PubMed2001

[Activity of elastase and its inhibitors in tissues of aorta and blood serum in various types of acidosis].

In modeling of different types of acidosis (hyperchloraemic, lactate and ketoacidosis in the starvation) at rats the elastase activity, contents of alpha-2 macroglobulin (alpha 2M) and alpha-1 proteinase inhibitor (alpha 1PI) in aorta tissues and blood serum were studied. The obtained results indicate that the degree of disturbance in system elastase-inhibitors depends on expressiveness of parameters changes in system of acid-base state regulation. In modeling of various types of acidosis coefficient inhibitors/elastase is reduced due to different parameters change in aorta, namely decrease of alpha 2M contents--in hyperchloraemic acidosis, increase of elastase activity--in lactat-acidosis, increase of elastase activity and decrease of alpha 2M contents--in ketoacidosis. In blood serum the similar coefficient is reduced due to increase of elastase activity and decrease of alpha 2M contents in hyperchloraemic acidosis and starvation, and, in turn, due to decrease of alpha 2M contents--in lactat-acidosis. The obtained data indicate that one of mechanisms of vascular wall damage in acidosis is disturbance of balance between elastase and its inhibitors in tissues of arteries.

Acidosis↗
PubMedDate not supplied

Renal tubular acidosis in pregnancy: case report and literature review.

Renal tubular acidosis is a rare form of chronic metabolic acidosis, which is either inherited as an autosomal dominant condition (Types 1, 2, and 3) or acquired. Its effects on pregnancy and vice versa are not known, but chronic acidosis may affect fetal bone growth and development. Chronic maternal acidosis may also lead to fetal distress, which should respond to correction of the maternal acidosis. The patient is a 20-year-old gravida 2, para 1-0-0-1, Hispanic female with distal renal tubular acidosis, diagnosed 1 year prior to this pregnancy after suffering from hypokalemic paralysis. During the pregnancy she required steadily increasing doses of potassium and bicarbonate, to maintain electrolyte balance. She delivered a healthy full-term female infant, weighing 2,892 g, with Apgars of 5 and 9 at 1 and 5 min, respectively, following an induction of labor for oligohydramnios. There was no evidence of intrapartum or neonatal distress, and the infant was discharged home with her mother on the first postpartum day in good health. Established renal tubular acidosis, which was adequately treated with bicarbonate and potassium supplementation during pregnancy, had no apparent ill effects on fetal or neonatal well-being in this case.

Acidosis, Renal Tubular↗