Etiology
Type 1 Distal RTA (see Type 1 Distal Renal Tubular Acidosis)
Genetic Disease
- Carbonic Anhydrase I (CA-I) Deficiency/Alteration
- Ehlers-Danlos Syndrome (see Ehlers-Danlos Syndrome)
- Familial Type 1 Distal Renal Tubular Acidosis
- Autosomal Dominant
- Autosomal Recessive
- Hereditary Elliptocytosis (see Hereditary Elliptocytosis)
- Marfan Syndrome (see Marfan Syndrome)
- Medullary Cystic Disease: produces both distal RTA and proximal RTA
- Neuroaxonal Dystrophy
- Osteopetrosis (see Osteopetrosis)
- Sickle Cell Disease (see Sickle Cell Disease)
- Wilson Disease (see Wilson Disease)
Tubulointerstitial Renal Disease
- Chronic Pyelonephritis
- Leprosy (see Leprosy)
- Obstructive Uropathy
- Renal Transplant Rejection (see Renal Transplant)
Nephrocalcinosis Syndromes
- Fabry Disease (see Fabry Disease)
- Hereditary Fructose Intolerance
- Hypercalcemia (see Hypercalcemia)
- Hyperthyroidism (see Hyperthyroidism)
- Milk Alkali Syndrome (see Milk Alkali Syndrome)
- Medullary Sponge Kidney
- Primary Hypercalciuria
- Primary Hyperoxaluria (see Primary Primary Hyperoxaluria)
- Primary/Familial Hyperparathyroidism (see Hyperparathyroidism)
- Sarcoidosis (see Sarcoidosis)
- Vitamin D Intoxication (see Vitamin D)
Autoimmune Disease
- Chronic Active Hepatitis
- Hashimoto’s Thyroiditis (see Hashimoto’s Thyroiditis)
- Primary Biliary Cirrhosis (PBC) (see Primary Biliary Cirrhosis)
- Idiopathic Pulmonary Fibrosis (IPF) (see Idiopathic Pulmonary Fibrosis)
- Rheumatoid Arthritis (RA) (see Rheumatoid Arthritis)
- Sjogren’s Syndrome (see Sjogren’s Syndrome): produces both distal RTA and proximal RTA
- Systemic Lupus Erythematosus (SLE) (see Systemic Lupus Erythematosus)
- Vasculitis (see Vasculitis)
Hypergammaglobulinemic States
- Amyloidosis (see Amyloidosis): produces both distal RTA and proximal RTA
- Cryoglobulinemia (see Cryoglobulinemia)
- Multiple Myeloma (see Multiple Myeloma): produces both distal RTA and proximal RTA
Drugs/Toxins
- Amphotericin B (see Amphotericin)
- Cyclamate
- Nonsteroidal Anti-Inflammatory Drugs (NSAID) (see Nonsteroidal Anti-Inflammatory Drug)
- Ifosfamide (Ifex) (see Ifosfamide): produces both distal RTA and proximal RTA
- Lithium Carbonate (see Lithium)
- Toluene Intoxication (see Toluene)
Other
- Cirrhosis (see Cirrhosis)
- Human Immunodeficiency Virus (HIV)/AIDS (see Human Immunodeficiency Virus): possible etiology
- Idiopathic (Sporadic) Type 1 Distal Renal Tubular Acidosis
Type 2 Proximal RTA (see Type 2 Proximal Renal Tubular Acidosis)
Genetic Disease
- Carbonic Anhydrase II Deficiency
- Cystinosis
- Galactosemia
- Hereditary Fructose Intolerance
- Glycogen Storage Disease Type I
- Lowe Syndrome
- Metachromatic Leukodystrophy
- Methylmalonic Acidemia
- Proximal Tubule Cell Sodium Bicarbonate Co-Transporter (NBCe1) Defect
- Pyruvate Carboxylase Deficiency
- Tyrosinemia
- Wilson Disease (see Wilson Disease): produces both distal and proximal RTA
Renal Interstitial Disease
- Balkan Nephropathy
- Medullary Cystic Disease: produces both distal and proximal RTA
- Renal Transplant Rejection (see Renal Transplant)
- Sjogren’s Syndrome (see Sjogren’s Syndrome)
Carbonic Anhydrase-Related Conditions
- Acetazolamide (Diamox) (see Acetazolamide)
- Physiology: carbonic anhydrase inhibition -> bicarbonate loss in urine
- Carbonic Anhydrase II Deficiency/Osteopetrosis
- Dichlorphenamide (Keveyis) (see Dichlorphenamide)
- Physiology: carbonic anhydrase inhibition -> bicarbonate loss in urine
- Mafenide Acetate (Sulfamylon) (see Mafenide Acetate)
- Mechanism: topical sulfonamide antibiotic (which is rapidly absorbed systemically in burn patients) with carbonic anhydrase inhibitor properties -> bicarbonate loss in urine
- Sulfanilamide
- Topiramate (Topamax) (see Topiramate)
- Mechanism: carbonic anhydrase inhibitor properties -> bicarbonate loss in urine
Dysproteinemias
- Amyloidosis (see Amyloidosis)
- Cryoglobulinemia (see Cryoglobulinemia)
- Light Chain Disease
- Monoclonal Gammopathy of Unclear Significance (MGUS) (see Monoclonal Gammopathy of Unclear Significance)
- Multiple Myeloma (see Multiple Myeloma): produces both distal and proximal RTA
Drugs/Toxins
- Cadmium (see Cadmium)
- Copper (see Copper)
- Gentamicin (see Gentamicin)
- Ifosfamide (Ifex) (see Ifosfamide): produces both distal and proximal RTA
- L-Arginine
- Lead (see Lead)
- Mercury (see Mercury)
- Outdated Tetracycline (see Tetracycline)
- Streptozotocin (see Streptozotocin)
- Tenofovir (Viread) (see Tenofovir)
- Uranium (see Uranium)
- Valproic Acid (see Valproic Acid)
Other
- Chronic Renal Vein Thrombosis (see Renal Vein Thrombosis)
- Idiopathic (Sporadic) Type 2 Proximal Renal Tubular Acidosis
- Malignancies
- Burkitt’s Lymphoma (see Lymphoma)
- Nephrotic Syndrome (see Nephrotic Syndrome)
- Paroxysmal Nocturnal Hemoglobinuria (PNH) (see Paroxysmal Nocturnal Hemoglobinuria)
- Tetralogy of Fallot (see Tetralogy of Fallot)
- Vitamin D Deficiency (see Vitamin D)
- Vitamin D Resistance see Vitamin D)
Type 4 Renal Tubular Acidosis (RTA)/Hypoaldosteronism (see Type 4 Renal Tubular Acidosis and Hypoaldosteronism)
Decreased Aldosterone Synthesis
- Inherited Disorders
- 21-Hydroxylase Deficiency
- Pseudohypoaldosteronism Type 2 (Gordon’s Syndrome)
- Hyporeninemic Hypoaldosteronism
- Advanced Age
- Drug-Induced Hyporeninemic Hypoaldosteronism
- β-Blockers (see β-Adrenergic Receptor Antagonists)
- Calcineurin Inhibitors (see Calcineurin Inhibitors)
- Cyclosporine A (CSA) (see Cyclosporine A)
- Tacrolimus (FK-506, Fujimycin, Prograf, Advagraf, Protopic, Hecoria, Astagraf XL) (see Tacrolimus)
- Nonsteroidal Anti-Inflammatory Drugs (NSAID’s) (see Nonsteroidal Anti-Inflammatory Drug)
- Intrinsic Renal Disease
- Acute Glomerulonephritis with Volume Expansion (see Acute Glomerulonephritis)
- Chronic Kidney Disease (CKD) (see Chronic Kidney Disease): with chronic interstitial nephritis
- Diabetic Nephropathy (see Diabetes Mellitus)
- Drugs
- Angiotensin Converting Enzyme (ACE) Inhibitors (see Angiotensin Converting Enzyme Inhibitors)
- Captopril (Capoten) (see Captopril)
- Enalapril (Vasotec, Enalaprilat) (see Enalapril)
- Fosinopril (Monopril) (see Fosinopril)
- Lisinopril (Zestril) (see Lisinopril)
- Moexipril (Univasc) (see Moexipril)
- Perindopril (Coversyl, Coversum, Preterax, Aceon) (see Perindopril)
- Quinapril (Accupril) (see Quinapril)
- Ramipril (Altace) (see Ramipril)
- Trandolapril (Mavik) (see Trandolapril)
- Angiotensin II Receptor Blockers (ARB’s) (see Angiotensin II Receptor Blockers)
- Candesartan (Atacand) (see Candesartan)
- Fimasartan (Kanarb) (see Fimasartan)
- Irbesartan (Avapro, Aprovel, Karvea) (see Irbesartan)
- Losartan (Cozaar) (see Losartan)
- Olmesartan (Benicar, Olmecip) (see Olmesartan)
- Telmisartan (Micardis) (see Telmisartan)
- Valsartan (Diovan) (see Valsartan)
- Heparins
- Enoxaparin (Lovenox) (see Enoxaparin)
- Heparin (see Heparin)
- Renin Inhibitors
- Aliskiren (Tekturna, Rasilez) (see Aliskiren): renin inhibitor (may cause hyperkalemia when used in combination with ACE inhibitors or ARB’s)
- Angiotensin Converting Enzyme (ACE) Inhibitors (see Angiotensin Converting Enzyme Inhibitors)
- Other
- Severe illness
- Primary Adrenal Insufficiency (see Adrenal Insufficiency)
Aldosterone Resistance
- Inherited Disorders
- Pseudohypoaldosteronism Type 1
- Drugs
- Aldosterone Antagonists
- Drospirenone (Yasmin, Yasminelle, Yaz, Beyaz, Ocella, Zarah, Angeliq) (see Drospirenone)
- Eplerenone (Inspra) (see Eplerenone)
- Spironolactone (Aldactone) (see Spironolactone)
- Epithelial Sodium Channel (ENaC) Antagonists (see Epithelial Sodium Channel Antagonists): these agents act to close sodium channels on the luminal membrane of cells in the collecting tubule (collecting tubule is the site of action of aldosterone)
- Amiloride (see Amiloride)
- Cimetidine (Tagamet) (see Cimetidine)
- Nafamostat: synthetic serine protease inhibitor, used as an anticoagulant
- Pentamidine (see Pentamidine)
- Triamterene (see Triamterene)
- Trimethoprim (see Sulfamethoxazole-Trimethoprim)
- Aldosterone Antagonists
- Other
- Tubulointerstitial Renal Disease
- Amyloidosis (see Amyloidosis)
- Obstructive Uropathy
- Post-Acute Tubular Necrosis (ATN) (see Acute Kidney Injury)
- Sickle Cell Disease (see Sickle Cell Disease)
- Systemic Lupus Erythematosus (SLE) (see Systemic Lupus Erythematosus)
- Tubulointerstitial Renal Disease
Gastrointestinal (GI) Bicarbonate Loss
- Biliary Drainage (Biliary Drain or T-Tube)
- Mechanism: external loss of biliary fluid (biliary fluid contains 35 mmol bicarbonate per L)
- Cholestyramine (see Cholestyramine)
- Mechanism: cationic resin which that is administrated as a chloride salt -> formation of calcium carbonate or the bicarbonate salt of cholestyramine within the gastrointestinal lumen -> increased gastrointestinal bicarbonate loss
- Diarrhea (see Diarrhea)
- Mechanism: gastrointestinal loss of bicarbonate in stool
- Enterovesical Fistula/Colovesical Fistula
- Mechanisms: both require retrograde movement of urine into the intestine
- Urinary Chloride is Exchanged for Bicarbonate by Chloride/Bicarbonate Transporter, Resulting in Bicarbonate Loss in the Stool
- Urinary Urea is Metabolized by Colonic Bacterial Ureases into Ammonium Ions with Ammonium Ion Reabsorption Via Colonic Sodium-Hydrogen Antiporter (as Ammonium Takes the Place of Sodium): result in a net gain of ammonium and chloride ions and a loss of bicarbonate
- Mechanisms: both require retrograde movement of urine into the intestine
- Ileal Conduit (Neobladder) (see Ileal Conduit)
- Epidemiology: since metabolic acidosis is a common complication of ureteroenterostomy, ileal conduits have largely replaced this procedure (however, metabolic acidosis still occurs in 10% of ileal conduit cases, especially in the presence of obstruction)
- Mechanisms
- Intestinal Mucosal Exchange of Urinary Chloride for Bicarbonate: results in urinary bicarbonate loss and hyperchloremia
- Intestinal Mucosal Absorption of Urinary NH4: results in hepatic conversion to NH3 and hydrogen ion
- Increased risk of this occurring when large loop of bowel used to make the neo-bladder, stoma is obstructed, or when sigmoid colonic section is used instead of ileal section
- Laxative Abuse (see Laxative Abuse)
- Mechanism: gastrointestinal loss of bicarbonate in stool
- Oral Calcium Chloride (see Calcium Chloride)
- Epidemiology: with oral administration only
- Mechanism: calcium chloride administered orally is excreted as calcium bicarbonate (due to exchange of the chloride for bicarbonate) -> results in gastrointestinal bicarbonate loss and metabolic acidosis
- Oral Magnesium Sulfate (see Magnesium Sulfate)
- Mechanism: increases gastrointestinal bicarbonate loss
- Pancreaticocutaneous Fistula
- Mechanism: results in external loss of pancreatic fluid (pancreatic fluid contains 115 mmol bicarbonate per L)
- Pancreaticopleural Fistula
- Mechanism: loss of pancreatic fluid into pleural space (pancreatic fluid contains 115 mmol bicarbonate per L)
- Small Intestinal Enterocutaneous Fistula
- Mechanism: external loss of small intestinal fluid (duodenal secretions contain 10 mmol bicarbonate per L, ileal secretions contain 30 mmol bicarbonate per L)
- Ureteroenterostomy/Ureterosigmoidostomy
- Epidemiology: metabolic acidosis is a common complication of ureteroenterostomy
- Mechanism: urinary diversion into the colon -> urinary ammonium is absorbed by the colonic mucosa, resulting in bicarbonate loss in the stool
- Villous Adenoma
- Mechanism: secretion of bicarbonate-rich fluid into the gastrointestinal lumen
Dilutional Metabolic Acidosis
- Rapid Infusion of Bicarbonate-Free (and Lactate-Free) Normal Saline (see Normal Saline)
- Physiology
- Dilutional Metabolic Acidosis Results Predominantly from an Expansion in the Extracellular Fluid Volume by Fluids Which are Bicarbonate-Free or Contain No Organic Acid Salts that Could Potentially Be Metabolized to Bicarbonate (Such as Lactate or Acetate)
- Mechanisms Favoring the Development of Dilutional Metabolic Acidosis
- Narrowing of strong ion difference between sodium and chloride
- Volume expansion -> decreased renal bicarbonate absorption
- Mechanisms Countering the Development of Dilutional Metabolic Acidosis
- Movement of bicarbonate from bone and intracellular stores into the extracellular space
- Binding of hydrogen ions by proteins (albumin, hemoglobin)
- Clinical Significance
- However, in a Dog Model with a 28% Expansion of the Extracellular Volume with Isotonic Saline, the Serum Bicarbonate Only Decreased 10% (Am J Physiol, 1973) [MEDLINE]
- This Suggests that Dilutional Acidosis is Unlikely to Occur Unless Extremely Large Amounts of Bicarbonate-Free Intravenous Fluids are Administered
- However, in a Dog Model with a 28% Expansion of the Extracellular Volume with Isotonic Saline, the Serum Bicarbonate Only Decreased 10% (Am J Physiol, 1973) [MEDLINE]
- Physiology
Other
- Acidic Salt Infusion
- Ammonium Chloride (see Ammonium Chloride): intravenous ammonium chloride is a systemic and urinary acidifying agent, which is converted to ammonia and hydrochloric acid through hepatic oxidation
- Calcium Chloride (see Calcium Chloride): generates hydrogen chloride
- Arginine Hydrochloride: generates hydrogen chloride
- D-Lactic Acidosis with Normal Renal Function (see Lactic Acidosis)
- Mechanism: the proximal tubule sodium/L-lactate co-transporter is stereospecific and does not transport D-lactate
- Therefore, filtered D-lactate is rapidly excreted in the urine (assuming normal renal function)
- Diagnosis: delta anion gap/delta bicarbonate ratio is 1 or <1 (obviously, as the delta anion gap/delta bicarbonate ratio approaches zero, this would be observed as a non-anion gap metabolic acidosis)
- This is in contrast with L-lactic acidosis, where the delta anion gap/delta bicarbonate ratio is typically between 1.1-1.6
- Mechanism: the proximal tubule sodium/L-lactate co-transporter is stereospecific and does not transport D-lactate
- Hydrochloric Acid (HCl) Infusion (see Hydrochloric Acid): hydrogen chloride added to the extracellular space results in replacement of bicarbonate by chloride in an equimolar basis
- Late Phase of Diabetic Ketoacidosis (DKA) (see Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State)
- Mechanism: urinary loss of ketoanions with sodium and potassium -> this is equivalent to a loss of potential bicarbonate, since each ketoanion (if retained) would have consumed a proton and been converted to a new bicarbonate molecule
- Methionine Intoxication (see Methionine)
- Moderate Renal Failure
- Acute Kidney Injury (AKI) (see Acute Kidney Injury)
- Chronic Kidney Disease (CKD) (see Chronic Kidney Disease)
- Mechanisms
- Early Kidney Disease: greater dysfunction in acid excretion than acid anion excretion -> typically have non-anion gap metabolic acidosis or anion gap metabolic acidosis with delta anion gap/delta bicarbonate ratio <1
- Later Kidney Disease: typically have anion gap metabolic acidosis with delta anion gap/delta bicarbonate ratio >1
- Mechanisms
- Total Parenteral Nutrition (TPN) (see Total Parenteral Nutrition)
- Post-Hypocapnic Metabolic Acidosis
- Mechanism
- Chronic Hypocapnia Results in Renal Loss of Bicarbonate
- When Hypocapnia is Remedied (Often in the Setting of Placing the Patient on Mechanical Ventilation, etc), Metabolic Acidosis is Observed Until the Kidney is Able to Compensate by Reabsorbing Bicarbonate
- Mechanism
- Toluene Intoxication (see Toluene)
- May Present as Anion Gap Metabolic Acidosis (see Metabolic Acidosis-Elevated Anion Gap)
- Early in the Course
- With Impaired Renal Function
- May Present as Non-Anion Gap Metabolic Acidosis:
- Late in the Course
- May Present as Anion Gap Metabolic Acidosis (see Metabolic Acidosis-Elevated Anion Gap)
Physiology
Biliary/Duodenal/Pancreatic Secretions are Normally Alkaline
- Biliary/Duodenal/Pancreatic Secretions Serve to Neutralize the Acidity of Gastric Secretions
- Jejunal Mucosal (Luminal) Sodium/Hydrogen Ion Exchanger Normally Functions in Jejunum to Reabsorb Sodium Bicarbonate, Resulting in Normal Stool Having Small Amounts of Bicarbonate
- However, Increased Stool Volume (Diarrhea) Results in Increased Bicarbonate Excretion, Resulting in Metabolic Acidosis
- Jejunal Mucosal (Luminal) Sodium/Hydrogen Ion Exchanger Normally Functions in Jejunum to Reabsorb Sodium Bicarbonate, Resulting in Normal Stool Having Small Amounts of Bicarbonate
Diagnosis
Serum Chemistry
- Serum Bicarbonate: decreased
- Serum Chloride: hyperchloremia
- Anion Gap: normal
- Calculation of Anion Gap = Na – (Cl + HCO3)
- Anion Gap Reflects the Difference Between Unmeasured Cations and Anions (i.e. the Anions in the Blood Which are Not Routinely Measured)
- Calculation of Anion Gap = Na – (Cl + HCO3)
Serum Lactate (see Serum Lactate)
- Normal
Arterial Blood Gas (ABG) (see Arterial Blood Gas)
- Decreased Serum Bicarbonate with Respiratory Compensation
Urine Anion Gap (see Urine Anion Gap)
- Rationale: renal ammonia excretion is the predominant component of renal net acid excretion
- Proximal Tubule: apical Na+/H+ exchanger, NHE-3, is a major mechanism of preferential NH4+ secretion
- Thick Ascending Loop of Henle: apical Na+-K+-2Cl- cotransporter, NKCC2, is a major contributor to ammonia reabsorption and the basolateral Na+/H+ exchanger, NHE-4, appears to be important for basolateral NH4+ exit
- Collecting Duct: major site for renal ammonia secretion, involving parallel H+ secretion and NH3 secretion
- Calculation of Urine Anion Gap = (Urine Na + Urine K) – (Urine Cl)
- Normal Urine Anion Gap: 20 to 90 mEq/L
- On a Typical Western Diet, the Quantity of Sodium and Potassium Absorbed from the Gastrointestinal Tract Exceeds the Quantity of Absorbed Chloride: therefore, renally excreted urine Na and K is greater than the amount of renally excreted urine Cl, making the urine AG positive
- Urine AG >-20 mEq/L (Indicating Increased Renal NH4 Ion Excretion): urine AG becoming more negative indicates gastrointestinal bicarbonate loss
- Diarrhea Results in Gastrointestinal Loss of Na, K, and Non-Chloride Anions (Including Bicarbonate, Butyrate, Citrate, and Lactate)
- Gastrointestinal Loss of Bicarbonate Results in Increased Renal Excretion of Hydrogen Ion (H+) in the Form of Ammonium (NH4+) Chloride: urine chloride serves as a surrogate for NH4 ion excretion
- Hypovolemia occurs with decreased sodium delivery to distal nephron
- Bicarbonate is replaced by chloride in serum (producing hyperchloremia)
- Diarrhea Results in Gastrointestinal Loss of Na, K, and Non-Chloride Anions (Including Bicarbonate, Butyrate, Citrate, and Lactate)
- Urine AG Positive (Indicating Normal-Low Renal NH4 Ion Excretion): indicates altered urinary acidification, suggestive of distal renal tubular acidosis
- Normal Urine Anion Gap: 20 to 90 mEq/L
- Clinical Situations Where the Urine Anion Gap is Unreliable
- Urine Anion Gap is Not Reliable in Neonates: neonates excrete other unmeasured anions at relatively high rates
- Diabetic Ketoacidosis: due to increased urinary excretion of unmeasured non-chloride anions, beta-hydroxybutyrate and acetoacetate -> this alters the relationship between the urine NH4 and urine anion gap
- Toluene Intoxication: due to increased urinary excretion of unmeasured non-chloride anion, hippurate
- Proximal RTA Treated with Alkali Therapy: due to increased urinary excretion of unmeasured non-chloride anion, bicarbonate
- D-Lactic Acidosis: due to increased urinary excretion of unmeasured non-chloride anion, D-lactate
- Pyroglutamic Acidosis: due to increased urinary excretion of unmeasured non-chloride anion, 5-oxoproline
Urine Osmolal Gap
- Rationale: urine osmolal gap performs better as a surrogate of the urine NH4 concentration when urinary ammonium (NH4) ion is excreted with an anion other than chloride (such as beta-hydroxybutyrate, acetoacetate, bicarbonate, or hippurate)
Clinical Manifestations
Pharmacologic Manifestations
Enhanced Effect of Neuromuscular Junction Antagonists (see Neuromuscular Junction Antagonists)
- Physiology
- Acidosis Potentiates the Effect of Neuromuscular Junction Antagonists
- Agents
- Atracurium (Tracrium) (see Atracurium)
- Cisatracurium (Nimbex) (see Cisatracurium)
- Pancuronium (Pavulon) (see Pancuronium)
- Rocuronium (Zemuron) (see Rocuronium)
- Vecuronium (Norcuron) (see Vecuronium)
Renal Manifestations
- Non-Anion Gap Metabolic Acidosis
Treatment
Treat or Remove the Underlying Etiology
- xxxx
Sodium Bicarbonate (see Sodium Bicarbonate)
- xxxx
References
- Effect of isotonic volume expansion on extracellular bicarbonate stores in normal dogs. Am J Physiol. 1973 Sep;225(3):628-36 [MEDLINE]
- Dilution acidosis and contraction alkalosis: review of a concept [MEDLINE]
- Total parenteral nutrition-associated metabolic acidosis. JPEN J Parenter Enteral Nutr. 1986 May-Jun;10(3):306-10 [MEDLINE]
- The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. N Engl J Med. 1988;318(10):594-599 [MEDLINE]
- The delta gap: an approach to mixed acid-base disorders. Ann Emerg Med. 1990;19:1310–1313 [MEDLINE]
- Enterovesical fistula presenting as life-threatening normal anion gap metabolic acidosis. Am J Kidney Dis. 1997 Jul;30(1):131-3 [MEDLINE]
- Management of life-threatening acid-base disorders. First of two parts. N Engl J Med 1998; 338:26-34 [MEDLINE]
- Management of life-threatening acid-base disorders. Second of two parts. N Engl J Med. 1998 Jan 8;338(2):107-11 [MEDLINE]
- Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. Anesthesiology. 1999 May;90(5):1265-70 [MEDLINE]
- Toxicity of methionine in humans. J Nutr. 2006 Jun;136(6 Suppl):1722S-1725S [MEDLINE]
- Severe metabolic acidosis and hypokalemia in a patient with enterovesical fistula. Clin Exp Nephrol. 2007 Sep;11(3):225-9. Epub 2007 Sep 28 [MEDLINE]
- Non–Anion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula. JAOA • Vol 111, No 5, May 2011, 344-345 [MEDLINE]
- Role of NH3 and NH4+ transporters in renal acid-base transport. Am J Physiol Renal Physiol. 2011 Jan;300(1):F11–F23 [MEDLINE]
- Treatment of acute metabolic acidosis: a pathophysiologic approach. Nat Rev Nephrol. 2012 Oct;8(10):589-601. doi: 10.1038/nrneph.2012.186. Epub 2012 Sep 4 [MEDLINE]
- An unrecognised case of metabolic acidosis following neobladder augmentation cystoplasty. Int J Surg Case Rep. 2015;11:129-31. doi: 10.1016/j.ijscr.2015.03.039. Epub 2015 Mar 25 [MEDLINE]