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(See also 38) Multiple toxins and drugs can increase the anion gap by increasing endogenous acid production Examples include methanol (metabolized to formic acid), ethylene glycol (glycolic and oxalic acid), and salicylates (salicylic acid and lactic acid), which can cause a mixed disorder of metabolic acidosis with respiratory alkalosis In toluene poisoning, a metabolite hippurate is rapidly excreted by the kidney and may present as a normal anion gap acidosis Isopropyl alcohol, which is metabolized to acetone, increases the osmolar gap, but not the anion gap
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At GFRs below 20 mL/min, the inability to excrete H+ with retention of acid anions such as PO43 and SO42 results in an increased anion gap acidosis, which rarely is severe The unmeasured anions replace HCO3 (which is consumed as a buffer) Hyperchloremic normal anion gap acidosis develops in earlier stages of CKD
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The hallmark of this disorder is that the low HCO3 of metabolic acidosis is associated with hyperchloremia, so that the anion gap remains normal The most common causes are gastrointestinal HCO3 loss and defects in renal acidification (renal tubular acidoses) The urinary anion gap can differentiate between these two common causes (see below)
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A Gastrointestinal HCO3 Loss
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Bicarbonate is secreted in multiple areas in the gastrointestinal tract Small bowel and pancreatic secretions contain large amounts of HCO3 Therefore, massive diarrhea or pancreatic drainage can result in HCO3 loss because of increased HCO3 secretion and decreased absorption Hyperchloremia occurs because the ileum and colon secrete HCO3 in a one-to-one exchange for Cl by countertransport The resultant volume contraction causes further increased Cl retention by the kidney in the setting of decreased anion, HCO3 Patients with ureterosigmoidostomies can develop hyperchloremic metabolic acidosis because the colon secretes HCO3 in the urine in exchange for Cl
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This is a common disorder of chronically malnourished patients who consume large quantities of alcohol daily Most of these patients have mixed acid base disorders (10% have a triple acid base disorder) Although decreased HCO3 is usual, 50% of the patients may have normal or alkalemic pH Three types of metabolic acidosis are seen in alcoholic ketoacidosis: (1) Ketoacidosis is due to -hydroxybutyrate and acetoacetate excess (2) Lactic acidosis: Alcohol metabolism increases the NADH:NAD ratio, causing increased production and decreased utilization of lactate Accompanying thiamine defi-
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Fluid & Electrolyte Disorders
CMDT 2008
Table 21 15 Hyperchloremic, normal anion gap metabolic acidoses
Distal H+ Secretion Serum [K+] Urinary NH4+ Plus Minimal Urine pH < 55 Titratable Acid Urinary Anion Gap Negative
Renal Defect Gastrointestinal HCO3 loss Renal tubular acidosis I Classic distal II Proximal secretion IV Hyporeninemic hypoaldosteronism Distal H+ secretion Proximal H+ Distal Na+ reabsorption, K+ secretion, and H+ secretion None
Treatment Na+, K+, and HCO3 as required
> 55 < 55 < 55
Positive Positive Positive
NaHCO3 (1 3 mEq/kg/d) NaHCO3 or KHCO3 (10 15 mEq/kg/d), thiazide Fludrocortisone (01 05 mg/ d), dietary K+ restriction, furosemide (40 160 mg/d), NaHCO3 (1 3 mEq/kg/d)
Modified and reproduced, with permission, from Cogan MG Fluid and Electrolytes: Physiology and Pathophysiology McGraw-Hill, 1991
B Renal Tubular Acidosis (RTA)
Hyperchloremic acidosis with a normal anion gap and normal (or near normal) GFR, and in the absence of diarrhea, defines RTA The defect is either inability to excrete H+ (inadequate generation of new HCO3 ) or inappropriate reabsorption of HCO3 Three major types can be differentiated by the clinical setting, urinary pH, urinary anion gap (see below), and serum K+ level (The term type III renal tubular acidosis is no longer used because of the controversies surrounding its definition) Recently, the mechanisms of each abnormality have been better elucidated by identifying the responsible molecules and their gene mutations 1 Classic distal RTA (type I) This disorder is characterized by hypokalemic hyperchloremic metabolic acidosis and is due to selective deficiency in H+ secretion in intercalated cells in the collecting tubule Despite acidosis, urinary pH cannot be acidified and is above 55, which retards the binding of H+ to phosphate (H+ + HPO42 H2PO4), and thus inhibits titratable acid excretion Furthermore, urinary excretion of NH4+Cl is decreased, and the urinary anion gap is positive (see below) Enhanced K+ excretion occurs probably because there is less competition from H+ in the distal nephron transport system Furthermore, as a response to renal salt wasting, hyperaldosteronism occurs Nephrocalcinosis and nephrolithiasis frequently accompany this disorder since chronic acidosis decreases tubular calcium reabsorption The hypercalciuria, alkaline urine, and lowered level of urinary citrate cause calcium phosphate stones and nephrocalcinosis Distal RTA develops as a consequence of dysproteinemic syndromes, autoimmune disease, and drugs and toxins such as amphotericin B 2 Proximal RTA (type II) Proximal RTA is a hypokalemic hyperchloremic metabolic acidosis due to a selective defect in the proximal tubule s ability to adequately reabsorb
filtered HCO3 Carbonic anhydrase inhibitors (acetazolamide) can cause proximal RTA About 90% of filtered HCO3 is absorbed by the proximal tubule The distal nephron has a limited ability to absorb HCO3 but becomes overwhelmed and does not function adequately when there is increased delivery Eventually, distal delivery of filtered HCO3 declines because the plasma HCO3 level has dropped as a result of progressive urinary HCO3 wastage When the plasma HCO3 level drops to 15 18 mEq/L, delivery of HCO3 drops to the point where the distal nephron is no longer overwhelmed and can regain function At that point, bicarbonaturia disappears, and urinary pH can be acidic Thiazide-induced volume contraction can be used to enhance proximal HCO3 reabsorption, leading to the decrease in distal HCO3 delivery and improvement of bicarbonaturia and renal acidification The increased delivery of HCO3 to the distal nephron also increases K+ secretion, and hypokalemia results if a patient is loaded with excess HCO3 and K+ is not adequately supplemented Proximal RTA often exists with other defects of absorption in the proximal tubule, resulting in glucosuria, aminoaciduria, phosphaturia, and uricaciduria Causes include multiple myeloma with Fanconi s syndrome and nephrotoxic drugs 3 Hyporeninemic hypoaldosteronemic RTA (type IV) Type IV is the most common form of RTA in clinical practice This is the only type characterized by hyperkalemic, hyperchloremic acidosis The defect is aldosterone deficiency or antagonism, which impairs distal nephron Na+ reabsorption and K+ and H+ excretion Renal salt wasting is frequently present Relative hypoaldosteronism from hyporeninemia is most commonly found in diabetic nephropathy, tubulointerstitial renal diseases, hypertensive nephrosclerosis, and AIDS In patients with these disorders, caution must be taken when using drugs that can exacerbate the hyperkalemia, such as ACE inhibitors (which will further reduce aldosterone levels), aldosterone receptor blockers such as spironolactone, and NSAIDs
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