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PubMed1998

D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms.

This report describes a case of d-lactic acidosis observed by the authors and then reviews all case reports of d-lactic acidosis in the literature in order to define its clinical and biochemical features and pathogenetic mechanisms. The report also reviews the literature on metabolism of d-lactic acid in humans. The clinical presentation of d-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings. Development of the syndrome requires the following conditions 1) carbohydrate malabsorption with increased delivery of nutrients to the colon, 2) colonic bacterial flora of a type that produces d-lactic acid, 3) ingestion of large amounts of carbohydrate, 4) diminished colonic motility, allowing time for nutrients in the colon to undergo bacterial fermentation, and 5) impaired d-lactate metabolism. In contrast to the initial assumption that d-lactic acid is not metabolized by humans, analysis of published data shows a substantial rate of metabolism of d-lactate by normal humans. Estimates based on these data suggest that impaired metabolism of d-lactate is almost a prerequisite for the development of the syndrome.

Acidosis, Lactic↗
PubMed1981

Treatment of lactic acidosis.

Severe lactic acidosis is often associated with poor prognosis. Recognition and correction of the underlying process is the major step in the treatment of this serious condition. Intravenous administration of sodium bicarbonate has been the mainstay in the treatment of lactic acidosis. Aggressive use of this therapeutic modality, however, can lead to serious complications and should therefore be considered with caution. Peritoneal dialysis and hemodialysis provide large amounts of alkali without causing the hypernatremia or hypervolemia commonly associated with bicarbonate infusion. Peritoneal dialysis with bicarbonate-based dialysate, in particular, appears to be an ideal means of delivering physiologic buffer. Administration of methylene blue was initially thought to increase lactate metabolism by altering the cellular oxidative state. Its subsequent clinical use, however, showed little efficacy. Sodium nitroprusside has been advocated for the treatment of some forms of lactic acidosis as a method of alleviating regional hypoperfusion. Insulin therapy has been found to be quite useful in the treatment of phenformin-associated lactic acidosis and is recommended in this setting. Since dichloroacetate activates pyruvate dehydrogenase and enhances lactate metabolism, it may be a useful adjunct in the treatment of lactic acidosis.

Acidosis↗
PubMed1995

Epinephrine-induced lactic acidosis in the setting of status asthmaticus.

A relationship between intravenous epinephrine infusion and the development of lactic acidosis has been well described. We report a temporal association between the administration of subcutaneous epinephrine and the development of lactic acidosis in the setting of status asthmaticus. A 20-year-old woman with a history of asthma came to the emergency service in acute respiratory distress and was treated with subcutaneous epinephrine. Six hours later, serial arterial blood gas studies revealed the onset of a primary metabolic acidosis. Additional diagnostic studies revealed a serum lactate level of 9.5 mumol/L. The lactic acidosis resolved within 15 hours. The patient never exhibited signs of hypotension, hypoxemia, or sepsis, and other potential etiologies for lactic acidosis were excluded. We believe the events of this case constitute a new observation and theorize a mechanism of peripheral vasoconstriction and transient tissue hypoperfusion mediated by the subcutaneous epinephrine.

Acidosis, Lactic↗
PubMed2002

Metformin-associated lactic acidosis after elective cervical spine fusion: a case report.

STUDY DESIGN: A case of metformin-associated lactic acidosis after elective spinal surgery is reported. OBJECTIVE: To inform spinal surgeons of this potentially fatal side effect and make them aware that metformin should be stopped 48 hours before surgery. SUMMARY OF BACKGROUND DATA: Metformin is a commonly used oral hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus. A rare side effect of metformin is lactic acidosis, which has a 50% mortality rate. Risk factors for metformin-associated lactic acidosis include renal, hepatic, and cardiac failure. Two cases have been reported in postsurgical patients. No cases of this disorder have been reported after orthopedic procedures. METHODS: A patient who developed metformin-associated lactic acidosis after cervical spinal fusion is presented. RESULTS: Recognition of the cause and aggressive medical management led to resolution of the lactic acidosis. Subsequent surgery was uneventful when metformin was discontinued more than 48 hours before surgery. CONCLUSION: Spinal surgeons should be aware of this preventable, potentially fatal side effect and stop metformin 48 hours before surgery.

Acidosis, Lactic↗
PubMed2003

Acidosis downregulates leptin production from cultured adipocytes through a glucose transport-dependent post-transcriptional mechanism.

Metabolic acidosis, a common feature of uremia, has a well documented wasting effect on skeletal muscle. In contrast, the effect of metabolic acidosis on adipose tissue is unknown. Serum levels of the adipocyte hormone leptin have been shown to be lower in acidotic uremic rats when compared with uremic controls. This study investigated the effect of acidosis on leptin protein secretion and leptin gene expression. This was studied in vitro by means of 3T3-L1 cultured adipocytes. Leptin secretion was decreased at an acid pH of 7.1 compared with a control pH of 7.5 (1277 versus 1950 pg/well/48 h, P < 0.05). In contrast, acidosis did not affect leptin mRNA content. Glucose transport was reduced by 39% at pH 7.1 at 24 h, which was comparable in magnitude with the inhibition of leptin secretion at the same pH. The glucose transport inhibitors cytochalasin B (0.5 to 50 micro M) and phloretin (0.05 to 0.25 mM) mimicked the effect of acidosis and reduced leptin secretion in a dose-dependent fashion (P < 0.02). Dose-response curves for the inhibition of glucose uptake showed that decreasing glucose transport to the same extent as with acid was sufficient to drive down leptin secretion, independently of changes of leptin mRNA. Acid decreases leptin secretion from 3T3-L1 adipocytes through a post-transcriptional mechanism via changes in glucose transport. This starvation-like response may be physiologically important in conditions such as uremia to prevent excessive energy expenditure.

3T3 Cells↗
PubMed2003

Fatal lactic acidosis during antiretroviral therapy.

OBJECTIVE: To describe the first pediatric case of fatal lactic acidosis in an antiretroviral-treated child with human immunodeficiency virus (HIV) infection. DESIGN: Case report. SETTING: Pediatric intensive care unit. PATIENTS: A patient with fatal antiretroviral therapy-associated type B lactic acidosis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We report the case of a 5-yr-old girl with HIV infection, receiving ritonavir, stavudine, and didanosine, who presented with a 10-day history of nausea and vomiting. Severe lactic acidosis was found. Her clinical condition worsened, with progressive increase in serum lactate, despite aggressive supportive therapy, including intravenous alkali and continuous arteriovenous hemodiafiltration. CONCLUSIONS: Fatal lactic acidosis is a complication of antiretroviral therapy in pediatric HIV patients, which has not been previously reported in children. Early recognition of mitochondrial dysfunction in these patients could prevent the development of fatal lactic acidosis.

Acidosis, Lactic↗
PubMed2005

Severe lactic acidosis complicating metformin overdose successfully treated with high-volume venovenous hemofiltration and aggressive alkalinization.

OBJECTIVE: In this report of a near-fatal metformin ingestion successfully treated with alkalinization and high-volume hemofiltration, we discuss the management of severe lactic acidosis and demonstrate that early aggressive intervention resulted in a positive outcome. DESIGN: Case report. SETTING: A tertiary pediatric intensive care unit. PATIENT: The patient was a healthy 14-yr-old female found by a sibling following a seizure of unknown duration, thought to be secondary to hypoglycemia as a consequence of a self-ingestion of metformin, atenolol, and diclofenac. She responded well to advanced resuscitation but progressively developed severe lactic acidosis, bradycardia, and hypotension in addition to persistent hypoglycemia. The peak lactate level was 37.5 mmol/L with an albumin corrected anion gap of 65 mmol/L. INTERVENTIONS: She was treated with high-volume venovenous hemofiltration and aggressive alkalinization therapy. The latter facilitated control of severe acidosis, whereas the hemofiltration removed the ingested drugs in addition to endogenously produced lactate precipitated by metformin. CONCLUSIONS: In this case, early and aggressive treatment of the acidosis and cardiovascular compromise with inotropes, venovenous hemofiltration, and large doses of sodium bicarbonate in metformin overdose resulted in a successful outcome even in the presence of severe acidosis and very high lactate levels.

Acidosis, Lactic↗
PubMed2003

The synergistic effects of hypoxia/reoxygenation or tissue acidosis and bacteria on intestinal epithelial cell apoptosis.

BACKGROUND: Clinical data indicate that gut perfusion deficits must be rectified within 24 hours after traumatic injury to decrease organ failure and death. Ischemia/reperfusion injury to the gut causes enterocyte apoptosis (Apo), which may contribute to intestinal barrier failure. The temporal response of enterocyte Apo to acidosis and hypoxia/reoxygenation (H/R) in vitro is unknown. The purpose of this study was to examine the effect of various time points of acidosis or H/R on enterocyte apoptosis and monolayer integrity in an in vitro model. METHODS: Caco-2 cell monolayers were made acidic (Dulbecco's modified Eagle's medium, pH 6.9) by hydrochloric acid or exposed to 95% nitrogen/5% carbon dioxide (hypoxia) and then 21% oxygen (reoxygenation). Escherichia coli C-25 were added to the apical media in subsets. Apo and necrosis were quantified by flow cytometry. Permeability was determined by fluorescein isothiocyanate-dextran. Transepithelial electrical resistance (TEER) indexed monolayer. RESULTS: Extracellular acidosis and C-25 significantly increased apoptosis of Caco-2 cells at 18 hours (extracellular acidosis [EC] + C-25, 14.5 +/- 3.0; control, 3.8 +/- 0.8; p < 0.001 by analysis of variance). Similarly, the H/R + C-25 group showed a significant increase in apoptosis at 12 hours (H/R + C-25 vs. control, 22.86 +/- 2.12 vs. 3.74 +/- 0.7; p < 0.001 by analysis of variance). The permeability difference was not significant for EC + C-25 versus control at 18 hours (0.68 +/- 0.25 vs. 0.43 +/- 0.0.0.36, respectively; p > 0.05). The H/R + C-25 group had a profound increase in permeability over control at 12 hours (10.8 +/- 0.5 vs. 2.1 +/- 0.3, respectively; p < 0.001). The TEER was significantly lowered for EC versus control at 18 hours (458 +/- 1.5 vs. 468 +/- 8.2) and at 0, 6, and 18 hours for EC + C-25 (409 +/- 28.1, 443 +/- 16.8, and 438 +/- 8.9 vs. 455 +/- 6.5, 467 +/- 6.5, and 469 +/- 8.2, respectively). There was no significant change in the H/R and H/R + C-25 groups. CONCLUSION: Synergism of H/R or tissue acidosis and bacteria caused increased Apo, TEER, and permeability in vitro.

Acidosis↗
PubMed2004

Uncompensated metabolic acidosis: an underrecognized risk factor for subsequent intubation requirement.

BACKGROUND: There are no published reports identifying an inadequate ventilatory response to metabolic acidosis as a predictor of impending respiratory failure. Metabolic acidosis should induce a respiratory alkalosis in which the partial pressure of carbon dioxide (Paco2) is (1.5 [HCO3-] + 8) +/- 2. This study examined the relation between inadequate ventilatory compensation and intubation among trauma patients. METHODS: A retrospective chart review was performed for trauma patients admitted between January 1999 and December 2000. Age, gender, Injury Severity Score and combined Trauma and Injury Severity Score, chest injury, history of cardiac or pulmonary disease, partial pressure of oxygen (Pao2), Paco2, Glasgow Coma Score, respiratory rate, systolic blood pressure, base deficit, and ability to compensate were analyzed with respect to intubation and need for ventilator support. RESULTS: Of 140 patients with metabolic acidosis, 45 ultimately were intubated. The mean Paco2 for the unintubated patients was 34 +/- 7 mm Hg, as compared with 41 +/- 11 mm Hg for the intubated patients (p < 0.001). Only injury severity and ability to compensate for metabolic acidosis were independent predictors of intubation. Patients with inadequate compensation were 4.2 times more likely to require intubation when control was used for the Injury Severity Score (95% confidence interval, 1.8-9.7; p < 0.001). CONCLUSIONS: Inability to mount an adequate hyperventilatory response to metabolic acidosis is associated with an increased likelihood of respiratory failure and a need for ventilatory support. Recognition of this relation should lead to closer monitoring of patients with this condition, and could help to avert unforeseen crisis intubations. This observation needs to be validated in a prospective study.

Acidosis↗
PubMed2003

Cerebrovascular vasodilation to extraluminal acidosis occurs via combined activation of ATP-sensitive and Ca2+-activated potassium channels.

Albeit controversial, it has been suggested by several authors that nitric oxide (NO) serves as a permissive factor in the cerebral blood flow response to systemic hypercapnia. Potassium channels are important regulators of cerebrovascular tone and may be modulated by a basal perivascular NO level. To elucidate the functional targets of the proposed NO modulation during hypercapnia-induced vasodilation, the authors performed experiments in isolated, cannulated, and pressurized rat middle cerebral arteries (MCA). Extracellular pH was reduced from 7.4 to 7.0 in the extraluminal bath to induce NO dependent vasodilation. Acidosis increased vessel diameter by 35 +/- 10%. In separate experiments, ATP-sensitive potassium channels (KATP) were blocked by extraluminal application of glibenclamide (Glib), Ca2+-activated potassium channels (KCa) by tetraethylammonium (TEA), voltage-gated potassium channels (Kv) by 4-aminopyridine, and inward rectifier potassium channels (KIR) by BaCl2. Na+-K+-ATP-ase was inhibited by ouabain. Application of TEA slightly constricted the arteries at pH 7.4 and slightly but significantly attenuated the vasodilation to acidosis. Inhibition of the other potassium channels or Na+-K+-ATP-ase had no effect. Combined blockade of KATP and KCa channels further reduced resting diameter, and abolished acidosis induced vasodilation. The authors conclude that mainly KCa channels are active under resting conditions. KATP and KCa channels are responsible for vasodilation to acidosis. Activity of one of these potassium channel families is sufficient for vasodilation to acidosis, and only combined inhibition completely abolishes vasodilation. During NO synthase inhibition, dilation to the KATP channel opener pinacidil or the KCa channel opener NS1619 was attenuated or abolished, respectively. The authors suggest that a basal perivascular NO level is necessary for physiologic KATP and KCa channel function in rat MCA. Future studies have to elucidate whether this NO dependent effect on KATP and KCa channel function is a principle mechanism of NO induced modulation of cerebrovascular reactivity and whether the variability of findings in the literature concerning a modulatory role of NO can be explained by different levels of vascular NO/cGMP concentrations within the cerebrovascular tree.

Acidosis↗
PubMed1975

The effect of propranolol and phentolamine on serum gastrin concentration in response to respiratory acidosis in normal man.

Serum gastrin concentration and basal acid secretion were studied in normal subjects under the influence of respiratory acidosis induced by CO2 rebreathing. During the intragastric instillation of 100 ml/h 0.5 M bicarbonate a significant increase of gastrinaemia from 133 to 158 pg/ml (p less than 0.01) occurred in ten subjects during respiratory acidosis (pCO2 62 torr, pH 7.25). Under the intragastric instillation of 100 ml/h 0.1 N HCl the rise of gastrin concentration in response to CO2 rebreathing (pCO2 68 torr, pH 7.20) was not significant. The relationship between the decrease of pH and the increase of the gastrin concentration was shifted in the direction of a greater systemic acidosis compared to the results performed in the presence of a neutral intragastric pH. 50 mug/kg propranolol intravenously produced a decrease of gastrin concentrations from 145 to 127 pg/ml (p less than 0.01) and a total suppression of hypergastrinaemia in response to CO2 rebreathing, suggesting activation of beta-cell receptors in respiratory acidosis. The infusion of phentolamine in a dose of 0.6 to 1.8 mg/min. resulted in a rise of gastrin concentration from 140 to 165 pg/ml (p less than 0.01) which was not further elevated during respiratory acidosis. The basal acid secretion showed a significant rise in response to CO2 rebreathing, which was abolished by the administration of propranolol.

Acidosis, Respiratory↗
PubMed2004

Do risk factors for lactic acidosis influence dosing of metformin?

BACKGROUND: Metformin is commonly prescribed to treat type 2 diabetes mellitus, however it is associated with the potentially lethal condition of lactic acidosis. Prescribing guidelines have been developed to minimize the risk of lactic acidosis development, although some suggest they are inappropriate and have created confusion amongst prescribers. The aim of this study was to investigate whether metformin dose was influenced by the presence of risk factors for lactic acidosis. METHODS: The study was prospective, and retrieved information from patients admitted to hospital who were prescribed metformin at their time of admission. RESULTS: Eighty-three patients were included in the study, 60 of whom had a least one risk factor for lactic acidosis. Of those 60 patients, 78.3% had a dose adjustment, with renal impairment, hepatic impairment, surgery and use of radiological contrast media--the risk factors most likely to result in a dose adjustment. When dose adjustments did occur, metformin was withheld on 88.7% of occasions. CONCLUSION: Metformin dose was influenced by the presence of risk factors for lactic acidosis, although it was dependent upon the number and particular risk factor/s present.

Acidosis, Lactic↗
PubMed1995

Effects of propranolol pretreatment on cerebral blood flow, oxygen uptake and catecholamines during metabolic acidosis following E. coli endotoxin in dogs.

After an intravenous injection of E. coli endotoxin in dogs a decrease in cerebral blood flow (CBF) and an increase in cerebral metabolic rate of oxygen (CMRo2) have been shown to occur. In metabolic acidosis following endotoxin CMRo2 increased with decreasing pH. A possible explanation for the increased CMRo2 after endotoxin and metabolic acidosis seems to be a damage of the blood-brain barrier (BBB) by endotoxin. This gives possibilities for a leakage of hydrogen ions and circulating monoamines from the blood to the brain, thus affecting the cerebral blood flow and metabolism. The effects of an E. coli endotoxin injection on CBF and CMRo2 during metabolic acidosis and beta-adrenoceptor blockade were studied in eight anaesthetized dogs. All the dogs were pretreated with propranolol (PPL), per os 12.5 mg.kg-1 twice a day for one week. Metabolic acidosis (pH 7.01-7.30) was achieved by an intravenous infusion of hydrochloric acid. Endotoxin E. coli lipopolysaccharide O 111:B 4 was given as an intravenous injection of 1 mg.kg-1 bodyweight over a 5 min period. Another five animals, published earlier, with the same experimental protocol but without PPL, constituted a control group. After endotoxin no increase in CMRo2 or CBF was observed with increasing acidosis in the PPL-group. In the control group, after endotoxin, both CBF and CMRo2 increased with decreasing pH. This resulted in a significant difference in both CBF and CMRo2 between the groups in the pH range 7.01-7.15. The present results indicate that the increase in CMRo2 and CBF with metabolic acidodis in endotoxinaemia is mediated via beta-adrenoceptors.

Acidosis↗
PubMed2000

Renal tubular acidosis associated with zonisamide therapy.

PURPOSE: We sought to report a previously undescribed adverse effect, renal tubular acidosis associated with zonisamide (ZNS) therapy. METHODS: Ammonium chloride, bicarbonate, and furosemide loading tests were performed in an epileptic patient with metabolic acidosis and episodic hypokalemia who was treated with ZNS. RESULTS: Distal renal tubular acidosis was diagnosed. On reexamination 7 weeks after ZNS had been replaced with phenytoin, the renal tubular acidosis disappeared. CONCLUSIONS: This case indicates, for the first time, that ZNS might be a potential cause of renal tubular acidosis. Blood gases and serum electrolytes should be measured in patients undergoing ZNS therapy.

Acidosis, Renal Tubular↗
PubMed2002

Metabolic acidosis up-regulates PTH/PTHrP receptors in UMR 106-01 osteoblast-like cells.

BACKGROUND: Metabolic acidosis results in skeletal demineralization by multiple mechanisms. One of these involves the inorganic phase of bone by which hydrogen ion is buffered by bone carbonate. In addition, the cellular components of bone participate by the induction and repression of several skeletal genes. Previous studies have suggested that the action of parathyroid hormone (PTH), a major regulator of bone turnover, might be altered by acidosis. The present studies were designed to test directly, in vitro, whether acidosis altered the effects of PTH in UMR 106-01 osteoblast-like cells. METHODS: Studies were conducted in confluent cultures of UMR 106-01 cells in modified Eagle's medium (MEM) with 5% fetal bovine serum (FBS) at pH values varying from 7.4 to 7.1 by addition of HCl. After time periods of 4 to 48 hours, cells were tested for cyclic AMP generation in response to PTH. PTH binding and PTH/PTHrP receptor mRNA levels were determined by radioligand binding assay and Northern analysis respectively. RESULTS: After 48 hours, decreases in pH from 7.4 to 7.1 resulted in a progressive increase in PTH-stimulated cyclic-AMP generation from 1978 +/- 294 to 4968 +/- 929 pmol/culture/5 min (P < 0.05). Basal cyclic AMP concentrations were unchanged. PTH binding increased 1.5- to twofold. Competitive inhibition binding revealed an increase in receptor number supported by up-regulation of PTH/PTHrP receptor mRNA up to twofold from control levels. CONCLUSIONS: These findings demonstrate that metabolic acidosis stimulates the response to PTH in UMR 106-01 osteoblast-like cells by a mechanism that involves an increase in the levels of PTH/PTHrP receptor mRNA. Thus, the skeletal response to acidosis that includes an increase in bone resorption may result, at least in part, from an increase in PTH/PTHrP receptors leading to an enhanced effect of PTH on bone.

Acidosis↗
PubMed1986

Ammonium chloride induced acidosis and aldosterone secretion in the goat.

Responses to 30-min intraduodenal infusion of NH4Cl (total amount 75 mmol) were studied in conscious goats. The infusion caused an immediate, transient rise in plasma aldosterone concentration (PA) from a mean of 78 to 221 pmo l-1. As expected, the NH4Cl administration also induced metabolic acidosis, initially subjected to partial respiratory compensation. The acidosis did not become fully developed until 1 h after cessation of the infusion, when PA had almost returned to its initial level. Renal compensation of the acidosis was shown by acidification of the urine and reduced Na excretion being most pronounced 1-2 h post-infusion. During the infusion blood haemoglobin concentration and the haematocrit increased by 25 and 13%, respectively, without simultaneous increase in plasma protein concentration and with persisting ear vasodilatation, indicating a mobilization of stored erythrocytes in the absence of a general increase in sympathetic tone. The results suggest that the reduction of blood pH is not the cause of the increase in PA occurring in association with NH4Cl-induced metabolic acidosis, but leave open the possibility that this increase may be due to some centrally mediated or direct adrenal influence of NH+4. As regards the apparent NH4Cl-induced mobilization of stored erythrocytes, it is suggested that such a response may play a role in the defence against acidosis by increasing the buffering capacity of the circulating blood.

Acid-Base Equilibrium↗
PubMed2005

Influence of pre-exercise acidosis and alkalosis on the kinetics of acid-base recovery following intense exercise.

The purpose of this study was to measure the recovery kinetics of pH and lactate for the conditions of pre-exercise acidosis, alkalosis, and placebo states. Twelve trained male cyclists completed 3 exercise trials (110% workload at VO2max), ingesting either 0.3 g/kg of NH4Cl (ACD), 0.2 g/kg of Na+HCO3- and 0.2 g/kg of sodium citrate (ALK), or a placebo (calcium carbonate) (PLAC). Blood samples (heated dorsal hand vein) were drawn before, during, and after exercise. Exercise-induced acidosis was more severe in the ACD and PLAC trials (7.15 +/- 0.06, 7.21 +/- 0.07, 7.16 +/- 0.06, P < 0.05, for ACD, ALK, PLAC, respectively). Recovery kinetics for blood pH and lactate, as assessed by the monoexponential slope constant, were not different between trials (0.057 +/- 0.01, 0.050 +/- 0.01, 0.080 +/- 0.02, for ACD, ALK, PLAC, respectively). Complete recovery of blood pH from metabolic acidosis can take longer than 45 min. Such a recovery profile is nonlinear, with 50% recovery occurring in approximately 12 min. Complete recovery of blood lactate can take longer than 60 min, with 50% recovery occurring in approximately 30 min. Induced alkalosis decreases metabolic acidosis and improves pH recovery compared to acidodic and placebo conditions. Although blood pH and lactate are highly correlated during recovery from acidosis, they recover at significantly different rates.

Acid-Base Equilibrium↗
PubMed1997

Hyperammonaemia with distal renal tubular acidosis.

The case is reported of an infant with hyperammonaemia secondary to severe distal renal tubular acidosis. A clinical association between increased concentrations of ammonia in serum and renal tubular acidosis has not previously been described. In response to acidosis the infant's kidneys presumably increased ammonia synthesis but did not excrete ammonia, resulting in hyperammonaemia. The patient showed poor feeding, frequent vomiting, and failure to thrive, but did not have an inborn error of metabolism. This case report should alert doctors to consider renal tubular acidosis in the differential diagnosis of severely ill infants with metabolic acidosis and hyperammonaemia.

Acidosis, Renal Tubular↗