Introduction
Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis1.
Humans possess homeostatic mechanisms that maintain acid-base balance (Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis (Figure 1).
Figure 1. Excretion of acid and ways to jeopardize the system.
1. A strong non-volatile acid HA dissociates to release H+ and poses an immediate threat to plasma pH.
2. Bicarbonate buffers the H+ and generates CO2, which is expelled in the lungs and results in depletion of body HCO3-. Non-bicarbonate buffers (collectively referred to as B) carry the H+ until the kidneys excrete it.
3. The kidneys split CO2 into H+ and HCO3- and selectively secrete H+ into the lumen and HCO3- into the blood. In addition, any excess H+ from the body fluid is also excreted.
4. Most H+ excreted in the urine is carried by urinary buffers (UBs).
5. Some organic anions (A) (e.g. lactate, ketoanions) can be metabolized to regenerate the HCO3-. If A is not metabolizable (e.g. phosphate or sulfate), it is excreted in the urine.
* Two possible ways by which metabolic acidosis can occur.
Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories (Figure 2):
1. Drugs as exogenous acid loads
2. Drugs leading to loss of bicarbonate in the gastrointestinal (GI) tract or kidney
3. Drugs causing increased endogenous acid production
4. Drugs that decrease renal acid excretion
Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis.
Figure 2. Mechanisms of drug-induced metabolic acidosis.
1. Increased exogenous ingestion of acidic precursors that are converted into strong acids.
2. Loss of alkali from kidney or GI tract.
3. Increased endogenous production of strong organic acids.
4. Compromised renal net acid excretion by inhibition of the renin-angiotensin-aldosterone system (RAAS), impaired proximal tubule (PT), or distal tubule (DT) H+ secretion.
In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders2, then convert the biochemical diagnosis into a clinical diagnosis with identification of the invading acid/drug3. Next is to review the list of medications by history and record to determine whether any of the drugs are culprits in either the generation or the exacerbation of the disorder. Note that just because a patient has, for example, lactic acidosis and is on a drug that can potentially cause lactic acidosis does not mean that the two are causally related. Finally, if a drug is indeed causing some degree of metabolic acidosis, the clinician should make an appraisal of the benefits from the drug weighed against the severity of the metabolic complication to determine whether cessation of therapy is justified. For example, if a patient with problematic seizures is effectively controlled by topiramate, a mild degree of metabolic acidosis can be more tolerable than seizures.
Drugs resulting in exogenous acid precursors
Non-pharmaceutical agents: toxic alcohols, phenols, and ammonium chloride
Methanol4, ethylene glycol5, diethylene glycol6, and isopropanol7 are volatile alcohols that produce a high plasma osmolar gap (the alcohol itself and the aldehyde metabolite), pure high anion gap metabolic acidosis from their metabolism into strong carboxylic acids such as formic acid (from methanol), and a combination of oxalic, glyoxylic, and glycolic acid (from ethylene/diethylene glycol). Isopropanol alcohol, due to the absence of an alpha-carbon, could only be metabolized to a keto- group and contributes to an osmolar gap but not high anion gap metabolic acidosis in poisoning encounters. Toluene abuse with glue or paint thinner sniffing can cause hippuric metabolic acidosis that presents with a normal plasma anion gap but elevated urinary osmolar gap because of the rapid clearance of hippurate8. Note that the time at which blood is sampled may reveal variable osmolar and anion gap. When the hydroxyl group is metabolized to carboxyl with a low pKa, there will not be an osmolar gap due to the contemporaneous consumption of bicarbonate; however, the metabolite between hydroxyl and carboxyl is an aldehyde, which still contributes to an osmolar gap but not an anion gap.
Ammonium chloride is not usually abused but is used extensively by investigators to study overproduction acidosis and used outside the laboratory9. There is a rise in acid excretion and a fall in serum HCO3- concentration that remains constant after initial drop10,11.
Overproduction acidosis from pharmaceutical agents
The excessive use of amino acids with a net positive charge would result in liberation of H+ during metabolism (arginine and lysine) in parenteral alimentation with inadequate concomitant administration of alkali12. Another example in this category is propylene glycol (1,2-propanediol [PG]), a common hygroscopic and emulsifying agent that is metabolized to lactate13. The U.S. Food and Drug Administration classified PG as GRAS (generally recognized as safe). The recommended maximum daily intake of PG should be less than 25 mg/kg/day (equivalent to 21 mmol/day for a 70 kg person)14. Each drug injection may have very different amounts of PG. Clinically significant toxicity is seen only in rapid, massive, and protracted parenteral administration of high quantities, especially in patients with renal impairment. PG intoxication from intravenous vitamin therapy was reported in pediatric patients who developed stupor15. Intoxication with lactic acidosis and hyperosmolality were found during treatment of schizophrenia16, with the use of intravenous benzodiazepines13,17, etomidate18, nitroglycerin19, and barbiturates20, all with PG as a vehicle. Approximately 55% of PG undergoes oxidation to propionaldehyde and pyruvic, acetic, and lactic acid, while the remainder is excreted unchanged in the urine21,22. Some studies have demonstrated PG-injured proximal tubular cells, leading to impaired renal acidification20,23. Patients with hepatic dysfunction, renal insufficiency, and diabetic ketoacidosis are more susceptible to PG toxicity and development of lactic acidosis24.
Drugs causing external base loss
Renal loss of bicarbonate
Carbonic anhydrases (CAs) are critical enzymes for bicarbonate reabsorption. Acetazolamide is a commonly used CA inhibitor in the treatment of ocular and convulsive disorders. It causes bicarbonaturia and a mild degree of hyperchloremic metabolic acidosis25. There have also been reports of symptomatic anion gap metabolic acidosis associated with acetazolamide therapy in elderly patients26 and in those with impaired renal function26,27 and diabetes mellitus28. Severe metabolic acidosis may result from inhibition of pyruvate carboxylase and mitochondrial damage29. Ocular solution of CA inhibitor-induced acidosis is rare but has been reported30.
Topiramate is approved for the treatment of seizure, as a migraine headache prophylaxis, and for weight loss, with off-label use for bipolar disorder, obesity, neuropathic pain, and smoking cessation31. It inhibits CA II, IV, and XII31. Topiramate generates a mild hyperchloremic metabolic acidosis32,33 but increases urinary pH and drastically lowers urinary citrate excretion, thus increasing the risk for calcium phosphate urolithiasis34,35.
The sulfonamide class of drugs also has CA inhibitory activity. Topical application and absorption over large areas in burn patients can cause extremely high blood levels and systemic CA inhibition36. This results in more than mere renal bicarbonate loss but rather a systemic disequilibrium syndrome.
Gastrointestinal loss of bicarbonate
Cholestyramine is an oral agent for treating hypertriglyceridemia and cholestasis by binding and sequestering bile acids from the entero-hepatic circulation; the non-absorbable complexes are eventually excreted in the stool37. In the GI tract, cholestyramine also binds phosphate, sulfate, and bicarbonate, leading to potential loss of bicarbonate from the body. Under normal conditions, this is easily corrected by renal regeneration of bicarbonate. However, patients with impaired renal function are at risk of hyperchloremic acidosis37–39.
Sevelamer hydrochloride is a non-reabsorbable phosphate binder. Dialysis patients on sevelamer hydrochloride have lower mean serum bicarbonate concentration during and at the end of therapy compared to those treated with calcium acetate40,41. The chloride released upon phosphate stimulates bicarbonate secretion by the gut via chloride-bicarbonate exchange40. This secretion coupled with defective ability to regenerate bicarbonate in renal patients leads to hyperchloremic acidosis. This complication is avoided by using sevelamer carbonate, which binds phosphate and releases carbonate instead42, or by bixalomer, which contains no chloride, and seems to demonstrate equal efficacy of phosphate binding with no evidence of acidosis in clinical trials43,44. Laxative abuse, calcium chloride, and magnesium sulfate could also cause hyperchloremic acidosis because the secreted bicarbonate from the pancreas is trapped by calcium and magnesium45–47 and then excreted in stools.
Drugs causing increased endogenous acid production
Lactic acidosis
Lactic acid is produced under basal metabolic conditions and H+ ions are released. Normally, an equivalent amount of H+ ions is consumed when the liver and renal cortex utilize lactate for gluconeogenesis or oxidize it to water and CO2 so that acid-base balance remains undisturbed (Figure 3). Lactic acidosis is arbitrarily classified into overproduction of lactate (type A), underutilization of lactate (type B), or both48. Type A lactic acidosis is associated with generalized or regional tissue hypoxia, while type B is seen in patients with metabolic abnormalities in malignancy, hepatic dysfunction, diabetes mellitus, congenital enzymatic deficiency, and drugs or toxins45,49. In 1995, metformin replaced phenformin, a notorious inducer of lactic acidosis, and became the primary biguanide used today50. Post marketing safety surveillance revealed no cases of fatal lactic acidosis51. There are still reports of metformin-associated lactic acidosis (MALA)52,53 with proposed mechanisms shown in Figure 3.
Figure 3. Mechanisms of drug-induced lactic acidosis.
1. Metformin inhibits pyruvate carboxylase (PC) → inhibits hepatic gluconeogenesis146 → excess lactate84. Metformin also inhibits complex I of the mitochondrial electron transport chain (ETC)84 → increases NADH/NAD+ ratio → blocks the entry of pyruvate into the tricarboxylic acid (TCA) cycle147. LDH = lactate dehydrogenase
2. In vitro, nucleoside reverse transcriptase inhibitors (NRTIs) inhibit β-oxidation, the tricarboxylic acid (Krebs) cycle, and DNA γ-polymerase → mitochondrial dysfunction and loss of transcription of essential enzymes → hepatic steatosis (increased triglycerides), myopathy, pancreatitis, nephrotoxicity, and lactic acidosis68.
3. Linezolid may cross-react with mammalian cellular processes → disrupts mitochondrial protein synthesis involved in ETC75,148.
4. Propofol may inhibit coenzyme Q and cytochrome C at Complex IV in ETC, and also inhibit mitochondrial fatty acid metabolism88.
5. Isoniazid inhibits metabolism of lactate to pyruvate82.
Most cases of MALA were associated with some underlying conditions such as acute renal failure induced by volume depletion, other potential nephrotoxic agents and concurrent use of radio-contrast media, or hepatic insufficiency54–58. Blood pH and lactate levels are not prognostic in MALA59. Although the incidence of MALA is low, once developed, the mortality can be staggeringly high52, particularly in the critical care setting, so discontinuation is advised in a patient with impending renal and multi-organ failure. Recently, a less restrictive guideline is proposed on metformin usage in patients of stable chronic kidney disease60–63. In general, the mortality of MALA decreased from 50% to 25% from the 1960s to the present64.
Highly active antiretroviral therapy (HAART) has led to dramatic reductions in HIV-associated morbidity and mortality65 (Figure 3). However, lactic acidosis complicated this therapy, especially with the nucleoside and nucleotide reverse transcriptase inhibitor (NRTI)-based regimens: didanosine, stavudine, lamivudine, zidovudine, and abacavir66–71. Combined use of these drugs further increases the risk of lactic acidosis72. Moreover, didanosine73, cidofovir74, lamivudine, and stavudine75 could cause Fanconi syndrome with pan-proximal tubular dysfunction leading to exacerbation of the acidosis and reduction of the plasma anion gap. The mortality of HAART-induced lactic acidosis can be as high as 50%76.
Linezolid is a long-term antibiotic against serious resistant Gram-positive organisms77,78 with adverse effects including bone marrow toxicity, optic/peripheral neuropathy, and lactic acidosis77,79,80. Concurrent use of selective serotonin uptake inhibitors such as citalopram and sertraline may predispose patients to lactic acidosis81,82. The vast majority of lactic acidosis occurred in the elderly and those receiving prolonged treatment, and most resolved upon cessation of linezolid80. Children receiving linezolid appeared to suffer lactic acidosis earlier during treatment83 (Figure 3).
Isoniazid is commonly used to treat tuberculosis84. Dosing more than 300 mg/day can lead to refractory grand mal or localized seizure, coma, and lactic acidosis84–86. Some suggested acidosis stems from excessive muscle activity during refractory seizure86,87, and slow reversal was observed in the postictal period. One proposed mechanism is inhibition of conversion of lactate to pyruvate84,87–89 (Figure 3).
Propofol is commonly used for induction and maintenance of anesthesia, sedation, and interventional procedures. Two cases were reported on propofol-associated severe metabolic acidosis90,91. Risk factors include severe head injury, critical illness, prolonged administration (>48 hours) of large doses (>4 mg/kg/hour, equivalent to 1.6 mmol/hour for a 70 kg person), and inborn errors of fatty acid oxidation90,92 (Figure 3).
Ketoacidosis
Ketosis develops when metabolism of fatty acid exceeds the removal of ketoacids (acetoacetic and β-hydroxybutyric). Typically there is insulin deficiency and/or resistance coupled with elevated glucagon and catecholamine. Glucose utilization is impaired and lipolysis is increased, augmenting the delivery of glycerol, alanine, and fatty acids for ketoacid generation45,93.
Overdose with salicylates in children commonly produces high anion gap acidosis, while adults exhibit a mixed respiratory alkalosis and metabolic acidosis. Metabolic acidosis occurs during salicylate toxicity due to uncoupling of oxidative phosphorylation and interfering with the Krebs cycle45,86, resulting in accumulation of lactic acid and ketoacids in as many as 40% of adult patients with salicylate poisoning45,94,95. The anion gap is mainly composed of ketoanions and lactate, while salicylate anion seldom exceeds 3 mEq/L.
Alcoholic ketoacidosis occurs when ethanol is abused chronically in the setting of poor carbohydrate intake and volume contraction. Ketosis resolves when the ethanol intake is interrupted and the patient is provided with nutrients and fluid, which stimulates insulin secretion and promotes the regeneration of bicarbonate from the metabolism of ketoacid anions45.
Pyroglutamic acidosis
The γ-glutamyl cycle produces glutathione, which is involved in the inactivation of free radicals, detoxification of many compounds, and amino acid transport45,96,97. Acetaminophen can deplete glutathione, leading to increased formation of γ-glutamyl cysteine, which is converted and accumulated as pyroglutamic acid (5-oxoproline)45,97. Patients at risk include those with malnutrition, sepsis, alcohol abuse, underlying liver disease, and/or renal insufficiency96. Acetaminophen ingestion alone may not cause pyroglutamic acidosis, but synergistic interaction between acetaminophen and the other factors as noted above96 can. Concomitant use of other drugs such as aminoglycoside and β-lactam penicillin is reported to increase the risk98.
Drugs causing decreased renal acid excretion
Syndromes of hyper-hypokalemia and reduced distal hydrogen secretion
Both angiotensin II and aldosterone are stimulators of the H+-ATPase α-intercalated cells in the cortical collecting tubule99,100, adding H+ into the urinary luminal. Inhibition of the renin-angiotensin-aldosterone system (RAAS), which leads to secondary inhibition of the H+-ATPase, can lead to decreased H+ secretion and metabolic acidosis. Additionally, inhibition of the RAAS reduces Na+ reabsorption, which reduces the luminal electronegativity and reduces H+ excretion by the H+-ATPase100. The same mechanisms can cause hyperkalemia, which can in turn reduce stimulation of the H+/K+-ATPase101. Hyperkalemia suppresses ammoniagenesis in the proximal tubule, impairs NH4+ transport in the medullary thick ascending limb, and reduces medullary interstitial ammonium concentration, all of which can lower urine acid excretion45,102. Therefore, any drug that affects the RAAS or causes hyperkalemia can increase the risk of metabolic acidosis. These drugs include the following (Figure 4):
- Cyclooxygenase (COX) inhibitors45,103
- β-adrenergic receptor blockers45,104
- Angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), and direct renin inhibitors104–106
- Heparin107 and ketoconazole108,109
- Spironolactone and eplerenone45,110
- Potassium-sparing diuretics: amiloride and triamterene45,110
- Pentamidine and trimethoprim111–113
- Calcineurin inhibitors: cyclosporine and tacrolimus114,115
Figure 4. Mechanisms of drug-induced distal H+ secretion.
1. Cyclooxygenase (COX) inhibitors and β-blockers interfere with release of renin, leading to hyperkalemia with metabolic acidosis43,101.
2. Angiotensin-converting enzyme inhibitors (ACEIs), aldosterone receptor blockers (ARBs), and renin inhibitors all interfere with the renin-angiotensin-aldosterone system (RAAS), causing hyperkalemia with hyperchloremic metabolic acidosis102–104.
3. Heparin105 and ketoconazole106,107 interfere with aldosterone synthesis.
4. Spironolactone and eplerenone block aldosterone receptors43,108.
5. Na+ channel blockers lead to reduced net negative charge in lumen in cortical collecting ducts (CCD), which reduces K+ and H+ excretion and causes hyperkalemia and acidosis43,108–111.
6. Calcineurin inhibitors interfere with Na, K-ATPase in the principal cell decreasing transepithelial K secretion and H+ secretion, cause vasoconstriction of afferent glomerular arterioles, and decrease glomerular filtration rate and alter filtration fraction112,113.
7. Lithium causes a voltage-dependent defect for H+ secretion and decreases H+-ATPase activity114–116.
8. Amphotericin B binds to sterol in mammalian cell membranes106,107 forming intramembranous pores which increase permeability and back diffusion of H+.
When these drugs are administered in combination, there is increased risk for hyperkalemia and metabolic acidosis, especially in patients with diabetes, chronic kidney disease, and liver disease45.
In contrast, patients with classic distal renal tubular acidosis (dRTA) generally have hypokalemic hyperchloremic metabolic acidosis. The metabolic acidosis results from the inability to acidify urine in the distal nephron and impaired excretion of NH4+100. Inherited forms of dRTA have defects in the basolateral HCO3-/Cl- exchanger, B1 or A4 subunits of the H+-ATPase, or CA. Some medications can mimic these defects by altering membrane permeability and causing leaky pathways45. Amphotericin B108,109, lithium116–118, and foscarnet119 are known to cause leak and lead to hypokalemic hyperchloremic metabolic acidosis (Figure 4).
Drugs causing Fanconi syndrome and proximal renal tubular acidosis
The proximal tubule is the initial step in renal acidification and is essential in maintaining acid-base homeostasis by reclaiming 80% of filtered bicarbonate (HCO3-) (Figure 5). Bicarbonate reabsorption occurs by luminal H+ excretion and HCO3- extrusion back into the blood at the basolateral membrane100. CAs catalyze the reaction: CO2 + H2O → HCO3-+ H+. If proximal HCO3- reclamation is impaired, more HCO3- is delivered to the distal tubule, which has limited capacity for HCO3- reabsorption. Bicarbonaturia ensues and net acid excretion decreases, which eventually leads to metabolic acidosis45,120. Generalized proximal tubule dysfunction is termed Fanconi syndrome. Potential drugs that could induce Fanconi syndrome include the following (Figure 5):
- CA inhibitors (e.g. acetazolamide)25.
- Anti-viral/HIV drugs (e.g. lamivudine, stavudine75 and tenofovir121–124). Most tenofovir-induced cases are subclinical125
- Platinum-containing agents (e.g. cisplatin126,127) and DNA alkylating agents (e.g. ifosfamide128–130) are common proximal tubule toxins. Note that cyclophosphamide, structural isomer of ifosfamide, can also cause hemorrhagic cystitis but is not nephrotoxic by producing less chloroacetaldehyde128
- Valproic acids (VPAs)131–133
- Outdated tetracycline134–136
- Aminoglycoside137 accumulation in proximal tubule would lead to nephrotoxicity with an unclear mechanism; however, incidence decreased recently due to a better monitoring strategy138
- Deferasirox139–143
Many other agents such as fumaric acid144, suramin145, and imatinib146 have also been associated with Fanconi syndrome in case reports. This field remained to be further explored as proximal tubule toxicity is common due to the existence of multiple drug transporters at the surface membrane, leading to very high uptake of drugs by this segment147.
Figure 5. Mechanisms of proximal tubule (PT) and drug-induced Fanconi syndrome.
1. CA inhibitors25 cause bicarbonaturia and hyperchloremic metabolic acidosis in the elderly26 and patients with renal failure27 and diabetes28.
2. Antineoplastic platinum-containing agents126,127 and DNA-alkylating agents128–130 damage proximal tubule cells through accumulation and induced cell apoptosis.
3. Anti-viral/HIV drugs75,121–124, valproic acid (VPA)131–133, and outdated tetracycline134–136 interfere with mitochondrial function within proximal tubule cells, leading to tubular dysfunction.
4. Aminoglycosides137,148,149 induce acidosis with unclear mechanisms150.
5. Deferasirox139–143 increases hemodynamic iron removal, causes vacuolization of proximal tubular epithelial cells142, and elevates iron absorption in various organs. All could lead to acidosis.
Conclusion
In summary, metabolic acidosis can occur as a side effect of therapy. Instead of memorizing the catalogue of drugs, clinicians should classify these agents based on their pathophysiologic mechanisms to facilitate the recognition of potential causal relationships. Some of these side effects are inferred from empirical observations, but some have undergone extensive studies to determine the pathogenesis of metabolic acidosis. We hope that this review will intrigue our readers to experience that eureka moment identifying unrecognized explanations for metabolic acidosis in patients or to partake in extending clinical observations to clinical investigations.
Abbreviations
ACEI, Angiotensin-converting enzyme inhibitor; ARB, Aldosterone receptor blocker; CA, Carbonic anhydrase; COX, Cyclooxygenase; dRTA, Distal renal tubular acidosis; FDA, Food & Drug Administration; GRAS, Generally recognized as safe; GI, Gastrointestinal; HAART, Highly active antiretroviral therapy; MALA, Metformin-associated lactic acidosis; NAD, Nicotinamide Adenine Dinucleotide; PG, Propylene glycol; RAAS, Renin-angiotensin-aldosterone system; VPA, Valproic acid.
Competing interests
The authors have no competing interests.
Grant information
The authors are supported by the National Institutes of Health (R01-DK092461, R01 DK081423, R01DK091392, U01-HL111146), the O’Brien Kidney Research Center (P30 DK-079328), and the Charles and Jane Pak Foundation.
Faculty Opinions recommendedReferences
- 1.
Moe OW, Fuster D, Alpern RJ:
Common acid-base disorders. In: Goldman L, Wachter RM, Hollander H, editors. Hosp Med. 2nd ed. Philadelphia: Lippincott, William & Wilkins; 2005; 1055–65.
- 2.
Wiederkehr MR, Moe OW:
Treatment of metabolic acidosis. In: Massry SG, Suki WK, editors. Therapy of Renal Diseases and Related Disorders. 4th ed: Springer; In press, 2011.
- 3.
Moe OW, Fuster D:
Clinical acid-base pathophysiology: disorders of plasma anion gap.
Best Pract Res Clin Endocrinol Metab.
2003; 17(4): 559–74. PubMed Abstract
| Publisher Full Text
- 4.
McMartin KE, Ambre JJ, Tephly TR:
Methanol poisoning in human subjects. Role for formic acid accumulation in the metabolic acidosis.
Am J Med.
1980; 68(3): 414–8. PubMed Abstract
| Publisher Full Text
- 5.
Jacobsen D, Hewlett TP, Webb R, et al.:
Ethylene glycol intoxication: evaluation of kinetics and crystalluria.
Am J Med.
1988; 84(1): 145–52. PubMed Abstract
| Publisher Full Text
- 6.
Vale JA, Buckley BM:
Metabolic acidosis in diethylene glycol poisoning.
Lancet.
1985; 2(8451): 394. PubMed Abstract
| Publisher Full Text
- 7.
Slaughter RJ, Mason RW, Beasley DM, et al.:
Isopropanol poisoning.
Clin Toxicol (Phila).
2014; 52(5): 470–8. PubMed Abstract
| Publisher Full Text
- 8.
Carlisle EJ, Donnelly SM, Vasuvattakul S, et al.:
Glue-sniffing and distal renal tubular acidosis: sticking to the facts.
J Am Soc Nephrol.
1991; 1(8): 1019–27. PubMed Abstract
- 9.
Relman AS, Shelburne PF, Talman A:
Profound acidosis resulting from excessive ammonium chloride in previously healthy subjects. A study of two cases.
N Engl J Med.
1961; 264: 848–52. PubMed Abstract
| Publisher Full Text
- 10.
Lemann J Jr, Lennon EJ, Goodman AD, et al.:
The net balance of acid in subjects given large loads of acid or alkali.
J Clin Invest.
1965; 44(4): 507–17. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 11.
Lemann J Jr, Lennon EJ, Goodman AD, et al.:
The role of fixed tissue buffers in acid-base regulation.
Trans Assoc Am Physicians.
1964; 77: 188–95. PubMed Abstract
- 12.
Tsai IC, Huang JW, Chu TS, et al.:
Factors associated with metabolic acidosis in patients receiving parenteral nutrition.
Nephrology (Carlton).
2007; 12(1): 3–7. PubMed Abstract
| Publisher Full Text
- 13.
Wilson KC, Reardon C, Theodore AC, et al.:
Propylene glycol toxicity: a severe iatrogenic illness in ICU patients receiving IV benzodiazepines: a case series and prospective, observational pilot study.
Chest.
2005; 128(3): 1674–81. PubMed Abstract
| Publisher Full Text
- 14.
Toxicological evaluation of certain food additives with a review of general principles and of specifications. Seventeenth report of the joint FAO-WHO Expert Committee on Food Additives.
World Health Organ Tech Rep Ser.
1974; 539: 1–40. PubMed Abstract
- 15.
Martin G, Finberg L:
Propylene glycol: a potentially toxic vehicle in liquid dosage form.
J Pediatr.
1970; 77(5): 877–8. PubMed Abstract
| Publisher Full Text
- 16.
Cate JC 4th, Hedrick R:
Propylene glycol intoxication and lactic acidosis.
N Engl J Med.
1980; 303(21): 1237. PubMed Abstract
| Publisher Full Text
- 17.
Wilson KC, Reardon C, Farber HW:
Propylene glycol toxicity in a patient receiving intravenous diazepam.
N Engl J Med.
2000; 343(11): 815. PubMed Abstract
| Publisher Full Text
- 18.
Bedichek E, Kirschbaum B:
A case of propylene glycol toxic reaction associated with etomidate infusion.
Arch Intern Med.
1991; 151(11): 2297–8. PubMed Abstract
| Publisher Full Text
- 19.
Demey HE, Daelemans RA, Verpooten GA, et al.:
Propylene glycol-induced side effects during intravenous nitroglycerin therapy.
Intensive Care Med.
1988; 14(3): 221–6. PubMed Abstract
| Publisher Full Text
- 20.
Yorgin PD, Theodorou AA, Al-Uzri A, et al.:
Propylene glycol-induced proximal renal tubular cell injury.
Am J Kidney Dis.
1997; 30(1): 134–9. PubMed Abstract
| Publisher Full Text
- 21.
Ruddick JA:
Toxicology, metabolism, and biochemistry of 1,2-propanediol.
Toxicol Appl Pharmacol.
1972; 21(1): 102–11. PubMed Abstract
| Publisher Full Text
- 22.
Speth PA, Vree TB, Neilen NF, et al.:
Propylene glycol pharmacokinetics and effects after intravenous infusion in humans.
Ther Drug Monit.
1987; 9(3): 255–8. PubMed Abstract
| Publisher Full Text
- 23.
Morshed KM, Jain SK, McMartin KE:
Propylene glycol-mediated cell injury in a primary culture of human proximal tubule cells.
Toxicol Sci.
1998; 46(2): 410–7. PubMed Abstract
| Publisher Full Text
- 24.
Lu J, Zello GA, Randell E, et al.:
Closing the anion gap: contribution of D-lactate to diabetic ketoacidosis.
Clin Chim Acta.
2011; 412(3–4): 286–91. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 25.
Hanley T, Platts MM:
Observations on the metabolic effects of the carbonic anhydrase inhibitor diamox: mode and rate of recovery from the drug's action.
J Clin Invest.
1956; 35(1): 20–30. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 26.
Chapron DJ, Gomolin IH, Sweeney KR:
Acetazolamide blood concentrations are excessive in the elderly: propensity for acidosis and relationship to renal function.
J Clin Pharmacol.
1989; 29(4): 348–53. PubMed Abstract
| Publisher Full Text
- 27.
De Marchi S, Cecchin E:
Severe metabolic acidosis and disturbances of calcium metabolism induced by acetazolamide in patients on haemodialysis.
Clin Sci (Lond).
1990; 78(3): 295–302. PubMed Abstract
| Publisher Full Text
- 28.
Siklos P, Henderson RG:
Severe acidosis from acetazolamide in a diabetic patient.
Curr Med Res Opin.
1979; 6(4): 284–6. PubMed Abstract
| Publisher Full Text
- 29.
Filippi L, Bagnoli F, Margollicci M, et al.:
Pathogenic mechanism, prophylaxis, and therapy of symptomatic acidosis induced by acetazolamide.
J Investig Med.
2002; 50(2): 125–32. PubMed Abstract
| Publisher Full Text
- 30.
Menon GJ, Vernon SA:
Topical brinzolamide and metabolic acidosis.
Br J Ophthalmol.
2006; 90(2): 247–8. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 31.
Mirza N, Marson AG, Pirmohamed M:
Effect of topiramate on acid-base balance: extent, mechanism and effects.
Br J Clin Pharmacol.
2009; 68(5): 655–61. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 32.
Wilner A, Raymond K, Pollard R:
Topiramate and metabolic acidosis.
Epilepsia.
1999; 40(6): 792–5. PubMed Abstract
| Publisher Full Text
- 33.
Stowe CD, Bollinger T, James LP, et al.:
Acute mental status changes and hyperchloremic metabolic acidosis with long-term topiramate therapy.
Pharmacotherapy.
2000; 20(1): 105–9. PubMed Abstract
| Publisher Full Text
- 34.
Welch BJ, Graybeal D, Moe OW, et al.:
Biochemical and stone-risk profiles with topiramate treatment.
Am J Kidney Dis.
2006; 48(4): 555–63. PubMed Abstract
| Publisher Full Text
- 35.
Maalouf NM, Langston JP, van Ness PC, et al.:
Nephrolithiasis in topiramate users.
Urol Res.
2011; 39(4): 303–307. In press. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 36.
Petroff PA, Hander EW, Mason AD Jr:
Ventilatory patterns following burn injury and effect of sulfamylon.
J Trauma.
1975; 15(8): 650–6. PubMed Abstract
| Publisher Full Text
- 37.
Scheel PJ Jr, Whelton A, Rossiter K, et al.:
Cholestyramine-induced hyperchloremic metabolic acidosis.
J Clin Pharmacol.
1992; 32(6): 536–8. PubMed Abstract
| Publisher Full Text
- 38.
Kleinman PK:
Letter: Cholestyramine and metabolic acidosis.
N Engl J Med.
1974; 290(15): 861. PubMed Abstract
| Publisher Full Text
- 39.
Eaves ER, Korman MG:
Cholestyramine induced hyperchloremic metabolic acidosis.
Aust N Z J Med.
1984; 14(5): 670–2. PubMed Abstract
| Publisher Full Text
- 40.
Brezina B, Qunibi WY, Nolan CR:
Acid loading during treatment with sevelamer hydrochloride: mechanisms and clinical implications.
Kidney Int Suppl.
2004; 66(90): S39–45. PubMed Abstract
| Publisher Full Text
- 41.
Qunibi WY, Hootkins RE, McDowell LL, et al.:
Treatment of hyperphosphatemia in hemodialysis patients: The Calcium Acetate Renagel Evaluation (CARE Study).
Kidney Int.
2004; 65(5): 1914–26. PubMed Abstract
| Publisher Full Text
- 42.
Biggar P, Ketteler M:
Sevelamer carbonate for the treatment of hyperphosphatemia in patients with kidney failure (CKD III - V).
Expert Opin Pharmacother.
2010; 11(16): 2739–50. PubMed Abstract
| Publisher Full Text
- 43.
Akizawa T, Origasa H, Kameoka C, et al.:
Randomized controlled trial of bixalomer versus sevelamer hydrochloride in hemodialysis patients with hyperphosphatemia.
Ther Apher Dial.
2014; 18(2): 122–31. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 44.
Hatakeyama S, Murasawa H, Narita T, et al.:
Switching hemodialysis patients from sevelamer hydrochloride to bixalomer: a single-center, non-randomized analysis of efficacy and effects on gastrointestinal symptoms and metabolic acidosis.
BMC Nephrol.
2013; 14: 222. PubMed Abstract
| Publisher Full Text
| Free Full Text
| Faculty Opinions Recommendation
- 45.
DuBose TD:
Disorder of Acid-Base Balance. In: Brenner BM editor. Brenner and Rector's The Kidney. 8th ed. Philadelphia: Saunders; 2007; 505–46.
- 46.
Gennari FJ, Weise WJ:
Acid-base disturbances in gastrointestinal disease.
Clin J Am Soc Nephrol.
2008; 3(6): 1861–8. PubMed Abstract
| Publisher Full Text
- 47.
Haldane JB, Hill R, Luck JM:
Calcium chloride acidosis.
J Physiol.
1923; 57(5): 301–6. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 48.
Madias NE:
Lactic acidosis.
Kidney Int.
1986; 29(3): 752–74. PubMed Abstract
| Publisher Full Text
- 49.
Melvin L, Wesson D:
Lactic Acidosis. In: Dubose TD, Hamm L. Lee, editor. Acid-Base and Electrolyte Disorders: A Companion to Brenner and Rector's The Kidney. Philadelphia: WB Saunders; 2002; 83–5.
- 50.
Lalau JD:
Lactic acidosis induced by metformin: incidence, management and prevention.
Drug Saf.
2010; 33(9): 727–40. PubMed Abstract
| Publisher Full Text
- 51.
Salpeter SR, Greyber E, Pasternak GA, et al.:
Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus.
Cochrane Database Syst Rev.
2010; (4): CD002967. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 52.
Peters N, Jay N, Barraud D, et al.:
Metformin-associated lactic acidosis in an intensive care unit.
Crit Care.
2008; 12(6): R149. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 53.
Almaleki N, Ashraf M, Hussein MM, et al.:
Metformin-associated lactic acidosis in a peritoneal dialysis patient.
Saudi J Kidney Dis Transpl.
2015; 26(2): 325–8. PubMed Abstract
| Publisher Full Text
- 54.
Nyirenda MJ, Sandeep T, Grant I, et al.:
Severe acidosis in patients taking metformin--rapid reversal and survival despite high APACHE score.
Diabet Med.
2006; 23(4): 432–5. PubMed Abstract
| Publisher Full Text
- 55.
Audia P, Feinfeld DA, Dubrow A, et al.:
Metformin-induced lactic acidosis and acute pancreatitis precipitated by diuretic, celecoxib, and candesartan-associated acute kidney dysfunction.
Clin Toxicol (Phila).
2008; 46(2): 164–6. PubMed Abstract
| Publisher Full Text
- 56.
El-Hennawy AS, Jacob S, Mahmood AK:
Metformin-associated lactic acidosis precipitated by diarrhea.
Am J Ther.
2007; 14(4): 403–5. PubMed Abstract
| Publisher Full Text
- 57.
Renda F, Mura P, Finco G, et al.:
Metformin-associated lactic acidosis requiring hospitalization. A national 10 year survey and a systematic literature review.
Eur Rev Med Pharmacol Sci.
2013; 17(Suppl 1): 45–9. PubMed Abstract
| Faculty Opinions Recommendation
- 58.
Scheen AJ, Paquot N:
Metformin revisited: a critical review of the benefit-risk balance in at-risk patients with type 2 diabetes.
Diabetes Metab.
2013; 39(3): 179–90. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 59.
Kajbaf F, Lalau JD:
The prognostic value of blood pH and lactate and metformin concentrations in severe metformin-associated lactic acidosis.
BMC Pharmacol Toxicol.
2013; 14: 22. PubMed Abstract
| Publisher Full Text
| Free Full Text
| Faculty Opinions Recommendation
- 60.
Adam WR, O'Brien RC:
A justification for less restrictive guidelines on the use of metformin in stable chronic renal failure.
Diabet Med.
2014; 31(9): 1032–8. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 61.
Inzucchi SE, Lipska KJ, Mayo H, et al.:
Metformin in patients with type 2 diabetes and kidney disease: a systematic review.
JAMA.
2014; 312(24): 2668–75. PubMed Abstract
| Publisher Full Text
| Free Full Text
| Faculty Opinions Recommendation
- 62.
Venos ES, Sigal RJ:
My patient's diabetic kidney disease has progressed to stage 4; should I discontinue metformin?
Can J Diabetes.
2014; 38(5): 296–9. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 63.
Heaf J:
Metformin in chronic kidney disease: time for a rethink.
Perit Dial Int.
2014; 34(4): 353–7. PubMed Abstract
| Publisher Full Text
| Free Full Text
| Faculty Opinions Recommendation
- 64.
Kajbaf F, Lalau JD:
Mortality rate in so-called "metformin-associated lactic acidosis": a review of the data since the 1960s.
Pharmacoepidemiol Drug Saf.
2014; 23(11): 1123–7. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 65.
Palella FJ, Delaney KM, Moorman AC, et al.:
Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators.
N Engl J Med.
1998; 338(13): 853–60. PubMed Abstract
| Publisher Full Text
- 66.
Gérard Y, Maulin L, Yazdanpanah Y, et al.:
Symptomatic hyperlactataemia: an emerging complication of antiretroviral therapy.
AIDS.
2000; 14(17): 2723–30. PubMed Abstract
- 67.
Sundar K, Suarez M, Banogon PE, et al.:
Zidovudine-induced fatal lactic acidosis and hepatic failure in patients with acquired immunodeficiency syndrome: report of two patients and review of the literature.
Crit Care Med.
1997; 25(8): 1425–30. PubMed Abstract
| Publisher Full Text
- 68.
Bissuel F, Bruneel F, Habersetzer F, et al.:
Fulminant hepatitis with severe lactate acidosis in HIV-infected patients on didanosine therapy.
J Intern Med.
1994; 235(4): 367–71. PubMed Abstract
| Publisher Full Text
- 69.
Goldfarb-Rumyantzev AS, Jeyakumar A, Gumpeni R, et al.:
Lactic acidosis associated with nucleoside analog therapy in an HIV-positive patient.
AIDS Patient Care STDS.
2000; 14(7): 339–42. PubMed Abstract
| Publisher Full Text
- 70.
Kakuda TN:
Pharmacology of nucleoside and nucleotide reverse transcriptase inhibitor-induced mitochondrial toxicity.
Clin Ther.
2000; 22(6): 685–708. PubMed Abstract
| Publisher Full Text
- 71.
Margolis AM, Heverling H, Pham PA, et al.:
A review of the toxicity of HIV medications.
J Med Toxicol.
2014; 10(1): 26–39. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 72.
Bonnet F, Balestre E, Bernardin E, et al.:
Risk factors for hyperlactataemia in HIV-infected patients, Aquitaine Cohort, 1999--2003.
Antivir Chem Chemother.
2005; 16(1): 63–7. PubMed Abstract
- 73.
Crowther MA, Callaghan W, Hodsman AB, et al.:
Dideoxyinosine-associated nephrotoxicity.
AIDS.
1993; 7(1): 131–2. PubMed Abstract
- 74.
Vittecoq D, Dumitrescu L, Beaufils H, et al.:
Fanconi syndrome associated with cidofovir therapy.
Antimicrob Agents Chemother.
1997; 41(8): 1846. PubMed Abstract
| Free Full Text
- 75.
Nelson M, Azwa A, Sokwala A, et al.:
Fanconi syndrome and lactic acidosis associated with stavudine and lamivudine therapy.
AIDS.
2008; 22(11): 1374–6. PubMed Abstract
| Publisher Full Text
- 76.
Falcó V, Rodríguez D, Ribera E, et al.:
Severe nucleoside-associated lactic acidosis in human immunodeficiency virus-infected patients: report of 12 cases and review of the literature.
Clin Infect Dis.
2002; 34(6): 838–46. PubMed Abstract
| Publisher Full Text
- 77.
De Vriese AS, Coster RV, Smet J, et al.:
Linezolid-induced inhibition of mitochondrial protein synthesis.
Clin Infect Dis.
2006; 42(8): 1111–7. PubMed Abstract
| Publisher Full Text
- 78.
Diekema DJ, Jones RN:
Oxazolidinone antibiotics.
Lancet.
2001; 358(9297): 1975–82. PubMed Abstract
| Publisher Full Text
- 79.
Apodaca AA, Rakita RM:
Linezolid-induced lactic acidosis.
N Engl J Med.
2003; 348(1): 86–7. PubMed Abstract
| Publisher Full Text
- 80.
Wiener M, Guo Y, Patel G, et al.:
Lactic acidosis after treatment with linezolid.
Infection.
2007; 35(4): 278–81. PubMed Abstract
| Publisher Full Text
- 81.
Bernard L, Stern R, Lew D, et al.:
Serotonin syndrome after concomitant treatment with linezolid and citalopram.
Clin Infect Dis.
2003; 36(9): 1197. PubMed Abstract
| Publisher Full Text
- 82.
Pea F, Scudeller L, Lugano M, et al.:
Hyperlactacidemia potentially due to linezolid overexposure in a liver transplant recipient.
Clin Infect Dis.
2006; 42(3): 434–5. PubMed Abstract
| Publisher Full Text
- 83.
Ozkaya-Parlakay A, Kara A, Celik M, et al.:
Early lactic acidosis associated with linezolid therapy in paediatric patients.
Int J Antimicrob Agents.
2014; 44(4): 334–6. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 84.
Neff TA:
Isoniazid toxicity: reports of lactic acidosis and keratitis.
Chest.
1971; 59(3): 245–8. PubMed Abstract
| Publisher Full Text
- 85.
Hankins DG, Saxena K, Faville RJ Jr, et al.:
Profound acidosis caused by isoniazid ingestion.
Am J Emerg Med.
1987; 5(2): 165–6. PubMed Abstract
| Publisher Full Text
- 86.
Kreisberg RA, Wood BC:
Drug and chemical-induced metabolic acidosis.
Clin Endocrinol Metab.
1983; 12(2): 391–411. PubMed Abstract
| Publisher Full Text
- 87.
Alvarez FG, Guntupalli KK:
Isoniazid overdose: four case reports and review of the literature.
Intensive Care Med.
1995; 21(8): 641–4. PubMed Abstract
| Publisher Full Text
- 88.
Peters JH, Miller KS, Brown P:
Studies on the metabolic basis for the genetically determined capacities for isoniazid inactivation in man.
J Pharmacol Exp Ther.
1965; 150(2): 298–304. PubMed Abstract
- 89.
Patiala J:
The amount of pyridine nucleotides (coenzymes I and II) in blood in experimental tuberculosis before and during isoniazid treatment.
Am Rev Tuberc.
1954; 70(3): 453–64. PubMed Abstract
- 90.
Kam PC, Cardone D:
Propofol infusion syndrome.
Anaesthesia.
2007; 62(7): 690–701. PubMed Abstract
| Publisher Full Text
- 91.
Marinella MA:
Lactic acidosis associated with propofol.
Chest.
1996; 109(1): 292. PubMed Abstract
| Publisher Full Text
- 92.
Bray RJ:
Propofol infusion syndrome in children.
Paediatr Anaesth.
1998; 8(6): 491–9. PubMed Abstract
| Publisher Full Text
- 93.
Bidani A, Tuazon DM, Heming TA:
Regulation of Whole Body Acid-Base Balance. In: Dubose TD, Hamm L. Lee, editor. Acid-Base and Electrolyte Disorders: A Companion to Brenner and Rector's The Kidney. Philadelphia: WB Saunders; 2002; 1–21.
- 94.
Arena FP, Dugowson C, Saudek CD:
Salicylate-induced hypoglycemia and ketoacidosis in a nondiabetic adult.
Arch Intern Med.
1978; 138(7): 1153–4. PubMed Abstract
| Publisher Full Text
- 95.
Proudfoot AT, Krenzelok EP, Brent J, et al.:
Does urine alkalinization increase salicylate elimination? If so, why?
Toxicol Rev.
2003; 22(3): 129–36. PubMed Abstract
| Publisher Full Text
- 96.
Fenves AZ, Kirkpatrick HM 3rd, Patel VV, et al.:
Increased anion gap metabolic acidosis as a result of 5-oxoproline (pyroglutamic acid): a role for acetaminophen.
Clin J Am Soc Nephrol.
2006; 1(3): 441–7. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 97.
Emmett M:
Acetaminophen toxicity and 5-oxoproline (pyroglutamic acid): a tale of two cycles, one an ATP-depleting futile cycle and the other a useful cycle.
Clin J Am Soc Nephrol.
2014; 9(1): 191–200. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 98.
Croal BL, Glen AC, Kelly CJ, et al.:
Transient 5-oxoprolinuria (pyroglutamic aciduria) with systemic acidosis in an adult receiving antibiotic therapy.
Clin Chem.
1998; 44(2): 336–40. PubMed Abstract
- 99.
Wagner CA, Devuyst O, Bourgeois S, et al.:
Regulated acid-base transport in the collecting duct.
Pflugers Arch.
2009; 458(1): 137–56. PubMed Abstract
| Publisher Full Text
- 100.
Rodríguez-Soriano J:
New insights into the pathogenesis of renal tubular acidosis--from functional to molecular studies.
Pediatr Nephrol.
2000; 14(12): 1121–36. PubMed Abstract
| Publisher Full Text
- 101.
Eiam-Ong S, Kurtzman NA, Sabatini S:
Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium.
J Clin Invest.
1993; 91(6): 2385–92. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 102.
DuBose TD Jr:
Molecular and pathophysiologic mechanisms of hyperkalemic metabolic acidosis.
Trans Am Clin Climatol Assoc.
2000; 111: 122–33; discussion 133–4. PubMed Abstract
| Free Full Text
- 103.
Cheng HF, Harris RC:
Cyclooxygenases, the kidney, and hypertension.
Hypertension.
2004; 43(3): 525–30. PubMed Abstract
| Publisher Full Text
- 104.
Weinberg JM, Appel LJ, Bakris G, et al.:
Risk of hyperkalemia in nondiabetic patients with chronic kidney disease receiving antihypertensive therapy.
Arch Intern Med.
2009; 169(17): 1587–94. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 105.
White WB, Bresalier R, Kaplan AP, et al.:
Safety and tolerability of the direct renin inhibitor aliskiren in combination with angiotensin receptor blockers and thiazide diuretics: a pooled analysis of clinical experience of 12,942 patients.
J Clin Hypertens (Greenwich).
2011; 13(7): 506–16. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 106.
Sakallı H, Baskın E, Bayrakcı US, et al.:
Acidosis and hyperkalemia caused by losartan and enalapril in pediatric kidney transplant recipients.
Exp Clin Transplant.
2014; 12(4): 310–3. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 107.
Preston RA, Hirsh MJ MD, Oster MD Jr, et al.:
University of Miami Division of Clinical Pharmacology therapeutic rounds: drug-induced hyperkalemia.
Am J Ther.
1998; 5(2): 125–32. PubMed Abstract
| Publisher Full Text
- 108.
Ayub M, Levell MJ:
Inhibition of human adrenal steroidogenic enzymes in vitro by imidazole drugs including ketoconazole.
J Steroid Biochem.
1989; 32(4): 515–24. PubMed Abstract
| Publisher Full Text
- 109.
Ohlsson A, Cedergreen N, Oskarsson A, et al.:
Mixture effects of imidazole fungicides on cortisol and aldosterone secretion in human adrenocortical H295R cells.
Toxicology.
2010; 275(1–3): 21–8. PubMed Abstract
| Publisher Full Text
- 110.
Davies DL, Wilson GM:
Diuretics: mechanism of action and clinical application.
Drugs.
1975; 9(3): 178–226. PubMed Abstract
| Publisher Full Text
- 111.
Kleyman TR, Roberts C, Ling BN:
A mechanism for pentamidine-induced hyperkalemia: inhibition of distal nephron sodium transport.
Ann Intern Med.
1995; 122(2): 103–6. PubMed Abstract
| Publisher Full Text
- 112.
Schlanger LE, Kleyman TR, Ling BN:
K+-sparing diuretic actions of trimethoprim: inhibition of Na+ channels in A6 distal nephron cells.
Kidney Int.
1994; 45(4): 1070–6. PubMed Abstract
| Publisher Full Text
- 113.
Velázquez H, Perazella MA, Wright FS, et al.:
Renal mechanism of trimethoprim-induced hyperkalemia.
Ann Intern Med.
1993; 119(4): 296–301. PubMed Abstract
| Publisher Full Text
- 114.
Caliskan Y, Kalayoglu-Besisik S, Sargin D, et al.:
Cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases.
Transplantation.
2003; 75(7): 1069–72. PubMed Abstract
| Publisher Full Text
- 115.
Lea JP, Sands JM, McMahon SJ, et al.:
Evidence that the inhibition of Na+/K+-ATPase activity by FK506 involves calcineurin.
Kidney Int.
1994; 46(3): 647–52. PubMed Abstract
| Publisher Full Text
- 116.
Kim YH, Kwon TH, Christensen BM, et al.:
Altered expression of renal acid-base transporters in rats with lithium-induced NDI.
Am J Physiol Renal Physiol.
2003; 285(6): F1244–57. PubMed Abstract
| Publisher Full Text
- 117.
Roscoe JM, Goldstein MB, Halperin ML, et al.:
Lithium-induced impairment of urine acidification.
Kidney Int.
1976; 9(4): 344–50. PubMed Abstract
| Publisher Full Text
- 118.
Grünfeld JP, Rossier BC:
Lithium nephrotoxicity revisited.
Nat Rev Nephrol.
2009; 5(5): 270–6. PubMed Abstract
| Publisher Full Text
- 119.
Navarro JF, Quereda C, Quereda C, et al.:
Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy.
Am J Kidney Dis.
1996; 27(3): 431–4. PubMed Abstract
| Publisher Full Text
- 120.
Hamm LL, Nakhoul N:
Renal Acidification. In: Brenner BM, editor. Brenner and Rector's The Kidney. Philadelphia: Saunders; 2007; 248–69.
- 121.
Malik A, Abraham P, Malik N:
Acute renal failure and Fanconi syndrome in an AIDS patient on tenofovir treatment--case report and review of literature.
J Infect.
2005; 51(2): E61–5. PubMed Abstract
| Publisher Full Text
- 122.
Hall AM, Hendry BM, Nitsch D, et al.:
Tenofovir-associated kidney toxicity in HIV-infected patients: a review of the evidence.
Am J Kidney Dis.
2011; 57(5): 773–80. PubMed Abstract
| Publisher Full Text
- 123.
Herlitz LC, Mohan S, Stokes MB, et al.:
Tenofovir nephrotoxicity: acute tubular necrosis with distinctive clinical, pathological, and mitochondrial abnormalities.
Kidney Int.
2010; 78(11): 1171–7. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 124.
Lucey JM, Hsu P, Ziegler JB:
Tenofovir-related Fanconi's syndrome and osteomalacia in a teenager with HIV.
BMJ Case Rep.
2013; 2013: pii: bcr2013008674. PubMed Abstract
| Publisher Full Text
| Free Full Text
| Faculty Opinions Recommendation
- 125.
Hall AM, Edwards SG, Lapsley M, et al.:
Subclinical tubular injury in HIV-infected individuals on antiretroviral therapy: a cross-sectional analysis.
Am J Kidney Dis.
2009; 54(6): 1034–42. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 126.
Cachat F, Nenadov-Beck M, Guignard JP:
Occurrence of an acute Fanconi syndrome following cisplatin chemotherapy.
Med Pediatr Oncol.
1998; 31(1): 40–1. PubMed Abstract
| Publisher Full Text
- 127.
Sahni V, Choudhury D, Ahmed Z:
Chemotherapy-associated renal dysfunction.
Nat Rev Nephrol.
2009; 5(8): 450–62. PubMed Abstract
| Publisher Full Text
- 128.
Zamlauski-Tucker MJ, Morris ME, Springate JE:
Ifosfamide metabolite chloroacetaldehyde causes Fanconi syndrome in the perfused rat kidney.
Toxicol Appl Pharmacol.
1994; 129(1): 170–5. PubMed Abstract
| Publisher Full Text
- 129.
Stöhr W, Paulides M, Bielack S, et al.:
Ifosfamide-induced nephrotoxicity in 593 sarcoma patients: a report from the Late Effects Surveillance System.
Pediatr Blood Cancer.
2007; 48(4): 447–52. PubMed Abstract
| Publisher Full Text
- 130.
Leem AY, Kim HS, Yoo BW, et al.:
Ifosfamide-induced Fanconi syndrome with diabetes insipidus.
Korean J Intern Med.
2014; 29(2): 246–9. PubMed Abstract
| Publisher Full Text
| Free Full Text
| Faculty Opinions Recommendation
- 131.
Watanabe T, Yoshikawa H, Yamazaki S, et al.:
Secondary renal Fanconi syndrome caused by valproate therapy.
Pediatr Nephrol.
2005; 20(6): 814–7. PubMed Abstract
| Publisher Full Text
- 132.
Knorr M, Schaper J, Harjes M, et al.:
Fanconi syndrome caused by antiepileptic therapy with valproic Acid.
Epilepsia.
2004; 45(7): 868–71. PubMed Abstract
| Publisher Full Text
- 133.
Endo A, Fujita Y, Fuchigami T, et al.:
Fanconi syndrome caused by valproic acid.
Pediatr Neurol.
2010; 42(4): 287–90. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 134.
Wegienka LC, Weller JM:
Renal tubular acidosis caused by degraded tetracycline.
Arch Intern Med.
1964; 114(2): 232–5. PubMed Abstract
| Publisher Full Text
- 135.
Cleveland WW, Adams WC, Mann JB, et al.:
Acquired Fanconi syndrome following degraded tetracycline.
J Pediatr.
1965; 66(2): 333–42. PubMed Abstract
| Publisher Full Text
- 136.
Montoliu J, Carrera M, Darnell A, et al.:
Lactic acidosis and Fanconi's syndrome due to degraded tetracycline.
Br Med J (Clin Res Ed).
1981; 283(6306): 1576–7. PubMed Abstract
| Publisher Full Text
| Free Full Text
- 137.
Izzedine H, Launay-Vacher V, Isnard-Bagnis C, et al.:
Drug-induced Fanconi's syndrome.
Am J Kidney Dis.
2003; 41(2): 292–309. PubMed Abstract
| Publisher Full Text
- 138.
Banerjee S, Narayanan M, Gould K:
Monitoring aminoglycoside level.
BMJ.
2012; 345: e6354. PubMed Abstract
| Publisher Full Text
- 139.
Grangé S, Bertrand DM, Guerrot D, et al.:
Acute renal failure and Fanconi syndrome due to deferasirox.
Nephrol Dial Transplant.
2010; 25(7): 2376–8. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 140.
Papadopoulos N, Vasiliki A, Aloizos G, et al.:
Hyperchloremic metabolic acidosis due to deferasirox in a patient with beta thalassemia major.
Ann Pharmacother.
2010; 44(1): 219–21. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 141.
Rafat C, Fakhouri F, Ribeil JA, et al.:
Fanconi syndrome due to deferasirox.
Am J Kidney Dis.
2009; 54(5): 931–4. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 142.
Murphy N, Elramah M, Vats H, et al.:
A case report of deferasirox-induced kidney injury and Fanconi syndrome.
WMJ.
2013; 112(1): 177–80. PubMed Abstract
| Faculty Opinions Recommendation
- 143.
Dell'Orto VG, Bianchetti MG, Brazzola P:
Hyperchloraemic metabolic acidosis induced by the iron chelator deferasirox: a case report and review of the literature.
J Clin Pharm Ther.
2013; 38(6): 526–7. PubMed Abstract
| Publisher Full Text
| Faculty Opinions Recommendation
- 144.
Häring N, Mähr HS, Mündle M, et al.:
Early detection of renal damage caused by fumaric acid ester therapy by determination of urinary β2-microglobulin.
Br J Dermatol.
2011; 164(3): 648–51. PubMed Abstract
| Publisher Full Text
- 145.
Rago RP, Miles JM, Sufit RL, et al.:
Suramin-induced weakness from hypophosphatemia and mitochondrial myopathy. Association of suramin with mitochondrial toxicity in humans.
Cancer.
1994; 73(7): 1954–9. PubMed Abstract
| Publisher Full Text
- 146.
François H, Coppo P, Hayman JP, et al.:
Partial fanconi syndrome induced by imatinib therapy: a novel cause of urinary phosphate loss.
Am J Kidney Dis.
2008; 51(2): 298–301. PubMed Abstract
| Publisher Full Text
- 147.
Launay-Vacher V, Izzedine H, Karie S, et al.:
Renal tubular drug transporters.
Nephron Physiol.
2006; 103(3): p97–106. PubMed Abstract
| Publisher Full Text
- 148.
Ghiculescu RA, Kubler PA:
Aminoglycoside-associated Fanconi syndrome.
Am J Kidney Dis.
2006; 48(6): e89–93. PubMed Abstract
| Publisher Full Text
- 149.
Gainza FJ, Minguela JI, Lampreabe I:
Aminoglycoside-associated Fanconi's syndrome: an underrecognized entity.
Nephron.
1997; 77(2): 205–11. PubMed Abstract
| Publisher Full Text
- 150.
Lopez-Novoa JM, Quiros Y, Vicente L, et al.:
New insights into the mechanism of aminoglycoside nephrotoxicity: an integrative point of view.
Kidney Int.
2011; 79(1): 33–45. PubMed Abstract
| Publisher Full Text
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