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  1. Renal tubular acidosis (RTA) is a metabolic acidosis, due to impaired acid secretion by the kidney.
There is a hyperchloremic metabolic acidosis with normal anion gap.
Type 1 (distal)
  1. RTA is due to an inability to excrete H+ and generate acidic uric in the distal tubule, even in states of metabolic acidosis, and hypokalemia.
  2. Features include rickets, or osteomalacia, due to buffering of H+ with calcium in bone.
  3. Nephrocalcinosis with renal calculi is a feature. (AIPG 10) (AIIMS Nov 2012)
  4. Diagnosis: Acid load: oral ammonium chloride load is given-there is failure to lower urine pH <5.5. (AIIMS Nov 2012)
  5. Treatment: Oral sodium bicarbonate or citrate.
  6. Complications (1) Renal calculi (2) End-stage renal failure may result from unrecognized obstruction.
Type 2 (Proximal)
  1. Type 2 (proximal) RTA is due to a 'bicarbonate leak': a defect in HCO3 reabsorption in the proximal tubule resulting in excess HCO3 in the urine.
  2. Urine can acidify because distal tubule can secrete H ions so urine pH is <5.5.
  3. Hypokalemia is a feature.
  4. Type 2 RTA is often associated with a more generalized tubular defect (Fanconi syndrome).
  5. Hypocalcaemia is common due to the osmotic diuretic effect of HCO3 reabsorption.
  6. Hypercalciuria occurs but urine citrate levels are normal or high, so renal stone formation is not feature.
  7. Diagnosis: IV sodium bicarbonate load: there is high fractional excretion of HC03 (> 15%).
  8. Treatment: High doses of bicarbonate (10mmol/kg/d) are required.
Type 4 (hyperkalemic)
  1. RTA is due to "hyporeninemic hypoaldosteronism".
  2. Hypoaldosteronism causes hyperkalemia a and acidosis (impaired K+ & H+ excretion) (AIIMS Nov 10)
  3. Causes: Mild renal impairment (eg with tubulointerstitial disease or DM), hypoadrenalism or drugs (K+ sparing diuretics, NSAIDs, ACEI).
  4. Treatment Remove any cause. Fludrocortisone 0.1 mg PO, furosemide or calcium resonium are used to control hyperkalaemia.
Table 265-2 Comparison of Normal Anion-Gap Acidoses (Ref. Hari. 18th ed., Pg - 1699)
Finding Type 1 RTA Type 2 RTA Type 4 RTA GI Bicarbonate Loss
Normal anion-gap acidosis Yes Yes Yes Yes
Minimum urine pH >5.5 <5.5 <5.5 5 to 6
% Filtered bicarbonate excreted <10 >15 <10 <10
Serum potassium Low Low High Low
Fanconi syndrome No Yes No No
Stones/nephrocalcinosis Yes No No No
Daily acid excretion Low Normal Low High
Urine anion gap Positive Negative Positive Negative
Daily bicarbonate replacement Needs <4 mmol/kg >4 mmol/kg <4 mmol/kg Variable


Extra Edge:


The "urine anion gap" is principally used to determine whether the kidneys are capable of appropriately acidifying urine.


  1. Urine anion gap is calculated by subtracting the urine concentration of chloride (anions) from the concentrations of sodium plus potassium (cations): where the concentrations are expressed in units of milliequivalents/liter (mEq/L).
  2. = Na+ + K+ − Cl
  3. In contrast to the serum anion gap equation, the bicarbonate is excluded. This is because urine is acidic, so the bicarbonate level would be negligible.
  4. Normal urine anion gap is zero or slightly positive.
Urine anion gap is an 'artificial' and calculated measure that is representative of the unmeasured ions in urine. Usually the most important unmeasured ion in urine is NH4+.
  1. A positive urine anion gap suggests a low urinary NH4+ (e.g. renal tubular acidosis).
  2. A negative urine anion gap suggests a high urinary NH4+ (e.g. diarrhea).

Extra Edge


A negative UAG suggests GI loss of bicarbonate (eg diarrhea), a positive UAG suggests impaired renal acidification (ie renal tubular acidosis).


As a memory aid, remember ‘neGUTive’ - negative UAG in bowel causes.


Summary of Renal tubular acidosis
IV = ↑ K
II = ↓ K, Fanconi syndrome
I = ↓ K, urine ph > 5.5, Renal stone, Urinary citrate is reduced, Hypercalciuria

Fanconi syndrome
  1. The proximal tubule is responsible for reabsorption of many solutes, including 50% of filtered sodium, most bicarbonate and all filtered glucose and amino acids.
  2. Fanconi syndrome is a disturbance of proximal tubule function, with defective reabsorption of amino acids, K+, phosphate (leading to hypophosphatemic rickets and osteomalacia), glucose (glycosuria) and bicarbonate (Type 2 RTA).
  3. There is polyuria (due to osmotic diuresis), and hypokaliemia (Na delivery to distal tubules leads to exchange).
  4. Causes:
    1. Idiopathic
    2. Inherited: Errors of metabolism eg cystinosis, fructose intolerance, galactosemia, glycogen storage disease, Wilson's disease, Lowe's syndrome, tyrosinemia.
    3. Acquired:
      1. Heavy metals (lead, mercury, cadmium, platinum, uranium),
      2. Drugs (out. of-date tetracycline),
      3. Light chains (myeloma, amyloidosis),
      4. Immunological (interstitial nephritis, transplant rejection). Remove any cause and replace losses. K+, sodium bicarbonate, and vitamin D supplements are used.
Features: dehydration, failure to thrive. Vitamin D resistant rickets is typical.

here may be progressive renal failure in early adulthood.

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