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
- 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
- Non-Steroidal Anti-Inflammatory Drugs (NSAID) (see Non-Steroidal Anti-Inflammatory Drug)
- Ifosfamide (see Ifosfamide): produces both distal RTA and proximal RTA
- Lithium Carbonate (see Lithium)
- Toluene Intoxication (see Toluene)
Other
- Cirrhosis (see End-Stage Liver Disease)
- 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, [[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, [[Acetazolamide]])
- Physiology: carbonic anhydrase inhibition -> bicarbonate loss in urine
- Carbonic Anhydrase II Deficiency/Osteopetrosis
- Dichlorphenamide (Keveyis) (see Dichlorphenamide, [[Dichlorphenamide]])
- Physiology: carbonic anhydrase inhibition -> bicarbonate loss in urine
- Mafenide Acetate (Sulfamylon) (see Mafenide Acetate, [[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, [[Topiramate]])
- Mechanism: carbonic anhydrase inhibitor properties -> bicarbonate loss in urine
Dysproteinemias
- Amyloidosis (see Amyloidosis, [[Amyloidosis]])
- Cryoglobulinemia (see Cryoglobulinemia, [[Cryoglobulinemia]])
- Light Chain Disease
- Monoclonal Gammopathy of Unclear Significance (MGUS) (see Monoclonal Gammopathy of Unclear Significance, [[Monoclonal Gammopathy of Unclear Significance]])
- Multiple Myeloma (see Multiple Myeloma, [[Multiple Myeloma]]): produces both distal and proximal RTA
Drugs/Toxins
- Cadmium (see Cadmium, [[Cadmium]])
- Copper (see Copper, [[Copper]])
- Gentamicin (see Gentamicin, [[Gentamicin]])
- Ifosfamide (Ifex) (see Ifosfamide, [[Ifosfamide]]): produces both distal and proximal RTA
- L-Arginine
- Lead (see Lead, [[Lead]])
- Mercury (see Mercury, [[Mercury]])
- Outdated Tetracycline (see Tetracycline, [[Tetracycline]])
- Streptozotocin (see Streptozotocin, [[Streptozotocin]])
- Tenofovir (Viread) (see Tenofovir, [[Tenofovir]])
- Uranium (see Uranium, [[Uranium]])
- Valproic Acid (see Valproic Acid, [[Valproic Acid]])
Other
- Chronic Renal Vein Thrombosis (see Renal Vein Thrombosis, [[Renal Vein Thrombosis]])
- Idiopathic (Sporadic) Type 2 Proximal Renal Tubular Acidosis
- Malignancies
- Burkitt’s Lymphoma (see Lymphoma, [[Lymphoma]])
- Nephrotic Syndrome (see Nephrotic Syndrome, [[Nephrotic Syndrome]])
- Paroxysmal Nocturnal Hemoglobinuria (PNH) (see Paroxysmal Nocturnal Hemoglobinuria, [[Paroxysmal Nocturnal Hemoglobinuria]])
- Tetralogy of Fallot (see Tetralogy of Fallot, [[Tetralogy of Fallot]])
- Vitamin D Deficiency (see Vitamin D, [[Vitamin D]])
- Vitamin D Resistance see Vitamin D, [[Vitamin D]])
Type 4 Renal Tubular Acidosis (RTA)/Hypoaldosteronism (see Type 4 Renal Tubular Acidosis, [[Type 4 Renal Tubular Acidosis]] and Hypoaldosteronism, [[Hypoaldosteronism]])
Decreased Aldosterone Synthesis
- Inherited Disorders
- 21 Hydroxylase Deficiency
- Pseudohypoaldosteronism Type 2 (Gordon’s Syndrome)
- Hyporeninemic Hypoaldosteronism
- Advanced Age
- Drug-Induced Hyporeninemic Hypoaldosteronism
- Beta Blockers (see β-Adrenergic Receptor Antagonists, [[β-Adrenergic Receptor Antagonists]])
- Calcineurin Inhibitors (see Calcineurin Inhibitors, [[Calcineurin Inhibitors]])
- Non-Steroidal Anti-Inflammatory Drug (NSAID) (see Non-Steroidal Anti-Inflammatory Drug, [[Non-Steroidal Anti-Inflammatory Drug]])
- Intrinsic Renal Disease
- Acute Glomerulonephritis with Volume Expansion (see Acute Glomerulonephritis, [[Acute Glomerulonephritis]])
- Chronic Kidney Disease (CKD) (see Chronic Kidney Disease, [[Chronic Kidney Disease]]): with chronic interstitial nephritis
- Diabetic Nephropathy (see Diabetes Mellitus, [[Diabetes Mellitus]])
- Drugs
- Angiotensin Converting Enzyme (ACE) Inhibitors
- Captopril (Capoten) (see Captopril, [[Captopril]])
- Enalapril (Vasotec, Enalaprilat) (see Enalapril, [[Enalapril]])
- Fosinopril (Monopril) (see Fosinopril, [[Fosinopril]])
- Lisinopril (Zestril) (see Lisinopril, [[Lisinopril]])
- Moexipril (Univasc) (see Moexipril, [[Moexipril]])
- Perindopril (Coversyl, Coversum, Preterax, Aceon) (see Perindopril, [[Perindopril]])
- Quinapril (Accupril) (see Quinapril, [[Quinapril]])
- Ramipril (Altace) (see Ramipril, [[Ramipril]])
- Trandolapril (Mavik) (see Trandolapril, [[Trandolapril]])
- Angiogensin II Receptor Blockers (ARB’s)
- Candesartan (Atacand) (see Candesartan, [[Candesartan]])
- Fimasartan (Kanarb) (see Fimasartan, [[Fimasartan]])
- Irbesartan (Avapro, Aprovel, Karvea) (see Irbesartan, [[Irbesartan]])
- Losartan (Cozaar) (see Losartan, [[Losartan]])
- Olmesartan (Benicar, Olmecip) (see Olmesartan, [[Olmesartan]])
- Telmisartan (Micardis) (see Telmisartan, [[Telmisartan]])
- Valsartan (Diovan) (see Valsartan, [[Valsartan]])
- Heparins
- Enoxaparin (Lovenox) (see Enoxaparin, [[Enoxaparin]])
- Heparin (see Heparin, [[Heparin]])
- Renin Inhibitors
- Aliskiren (Tekturna, Rasilez) (see Aliskiren, [[Aliskiren]]): renin inhibitor (may cause hyperkalemia when used in combination with ACE inhibitors or ARB’s)
- Angiotensin Converting Enzyme (ACE) Inhibitors
- Other
- Severe illness
- Primary Adrenal Insufficiency (see Adrenal Insufficiency, [[Adrenal Insufficiency]])
Aldosterone Resistance
- Inherited Disorders
- Pseudohypoaldosteronism Type 1
- Drugs
- Aldosterone Antagonists
- Drospirenone (Yasmin, Yasminelle, Yaz, Beyaz, Ocella, Zarah, Angeliq) (see Drospirenone, [[Drospirenone]])
- Eplerenone (Inspra) (see Eplerenone, [[Eplerenone]])
- Spironolactone (Aldactone) (see Spironolactone, [[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, [[Amiloride]])
- Cimetidine (Tagamet) (see Cimetidine, [[Cimetidine]])
- Nafamostat: synthetic serine protease inhibitor, used as an anticoagulant
- Pentamidine (see Pentamidine, [[Pentamidine]])
- Triamterene (see Triamterene, [[Triamterene]])
- Trimethoprim (see Sulfamethoxazole-Trimethoprim, [[Sulfamethoxazole-Trimethoprim]])
- Aldosterone Antagonists
- Other
- Tubulointerstitial Renal Disease
- Amyloidosis (see Amyloidosis, [[Amyloidosis]])
- Obstructive Uropathy
- Post-Acute Tubular Necrosis (ATN) (see Acute Kidney Injury, [[Acute Kidney Injury]])
- Sickle Cell Disease (see Sickle Cell Disease, [[Sickle Cell Disease]])
- Systemic Lupus Erythematosus (SLE) (see Systemic Lupus Erythematosus, [[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, [[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, [[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, [[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, [[Laxative Abuse]])
- Mechanism: gastrointestinal loss of bicarbonate in stool
- Oral Calcium Chloride (see Calcium Chloride, [[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, [[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, [[Normal Saline]])
- Physiology: dilutional metabolic acidosis results predominantly from an expansion in the extracellular fluid volume by fluids that 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)
- Mechanisms Favoring the Development of Dilutional Metabolic Acidosis
- Clinical Significance: however, in a dog model with a 28% expansion of the extracellular volume with isotonic saline, the serum bicarbonate only decreased 10% [MEDLINE] -> this suggests that dilutional acidosis is unlikely to occur unless extremely large amounts of bicarbonate-free intravenous fluids are administered
- Physiology: dilutional metabolic acidosis results predominantly from an expansion in the extracellular fluid volume by fluids that are bicarbonate-free or contain no organic acid salts that could potentially be metabolized to bicarbonate (such as lactate or acetate)
Other
- Acidic Salt Infusion
- Ammonium Chloride (see Ammonium Chloride, [[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, [[Calcium Chloride]]): generates hydrogen chloride
- Arginine Hydrochloride: generates hydrogen chloride
- D-Lactic Acidosis with Normal Renal Function (see Lactic Acidosis, [[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, [[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, [[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, [[Methionine]])
- Moderate Renal Failure
- Acute Kidney Injury (AKI) (see Acute Kidney Injury, [[Acute Kidney Injury]])
- Chronic Kidney Disease (CKD) (see Chronic Kidney Disease, [[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, [[Total Parenteral Nutrition]])
- Post-Hypocapnic Metabolic Acidosis
- Mechanism: chronic hypocapnia results in renal loss of bicarbonate -> when hypocapnia is remedied (often by placing the pt on mechanical ventilation, etc), metabolic acidosis is observed until the kidney is able to compensate by rebabsorbing bicarbonate
- Toluene Intoxication (see Toluene, [[Toluene]])
- May Present as Anion Gap Metabolic Acidosis (see Metabolic Acidosis-Elevated Anion Gap, [[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
- With Intact Renal Function: due to renal excretion of sodium and potassium hippurate
- May Present as Anion Gap Metabolic Acidosis (see Metabolic Acidosis-Elevated Anion Gap, [[Metabolic Acidosis-Elevated Anion Gap]])
Physiology
- Biliary/Duodenal/Pancreatic Secretions are Normally Alkaline: they serve to neutralize the acidity of gastric secretions
- Jejunal Mucosal (Luminal) Na/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) Na/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 that are not routinely measured)
- Calculation of Anion Gap = Na – (Cl + HCO3)
Serum Lactate (see Serum Lactate, [[Serum Lactate]])
- Normal
Arterial Blood Gas (ABG) (see Arterial Blood Gas, [[Arterial Blood Gas]])
- Decreased Serum Bicarbonate with Respiratory Compensation
Urine Anion Gap (see Urine Anion Gap, [[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
Renal Manifestations
- Non-Anion Gap Metabolic Acidosis
Treatment
- Sodium Bicarbonate (see Sodium Bicarbonate, [[Sodium Bicarbonate]])
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]
- Enterovesical fistula presenting as life-threatening normal anion gap metabolic acidosis. Am J Kidney Dis. 1997 Jul;30(1):131-3 [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]
- 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]