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Nephrology Acid-Base Disorders Intermediate
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Normal Anion Gap Metabolic Acidosis

H
A
R
D
-
U
P
Causes of hyperchloremic (normal anion gap) metabolic acidosis (AG 8-12 mEq/L) characterized by reciprocal chloride retention.

When bicarbonate is lost directly from the GI tract or kidneys, the electroneutrality of extracellular fluid is maintained by renal reabsorption of chloride, creating a hyperchloremic non-gap acidosis.

Systematic Breakdown

H

Hyperalimentation (Total Parenteral Nutrition)

TPN formulations containing excessive chloride or cationic amino acids.

A

Acetazolamide / Addison Disease

Carbonic anhydrase inhibition leads to urinary HCO3- wasting; adrenal insufficiency causes aldosterone deficiency (Type 4 RTA).

R

Renal Tubular Acidosis (Types 1, 2, 4)

Type 1 (distal H+ secretion failure), Type 2 (proximal HCO3- wasting), Type 4 (hypoaldosteronism with hyperkalemia).

D

Diarrhea

Most common clinical cause worldwide. Copious GI bicarbonate loss in stool.

U

Ureterosigmoidostomy

Colon mucosa secretes bicarbonate in exchange for urine chloride when ureters are surgically diverted into sigmoid colon.

P

Pancreatic Fistula

Pancreatic and biliary secretions are rich in bicarbonate (up to 120 mEq/L); drainage loss causes rapid acidosis.

High-Yield Clinical Pearls & Exam Tips
  • Urine Anion Gap = [Na+] + [K+] - [Cl-]. Used to distinguish diarrhea from renal tubular acidosis.
  • Negative Urine AG (< 0): Kidney is appropriately excreting ammonium (NH4+ with Cl-), indicating GI loss (Diarrhea).
  • Positive Urine AG (> 0): Kidney cannot excrete NH4+, indicating Renal Tubular Acidosis.
Related Pharmaceuticals
Acetazolamide Fludrocortisone Sodium Bicarbonate
Related Clinical Conditions
Renal Tubular Acidosis Severe Diarrhea Addison Disease
Authoritative Sources: Harrison's Principles of Internal Medicine 21e · NephSAP: Acid-Base Disorders

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