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Renal glucosuria

  1. Renal glucosuria is an isolated defect of tubular glucose transport, characterized by the presence of glucose in the urine at normal blood glucose levels.
  2. Glucose metabolism and other renal tubular transport mechanisms are normal.
  3. The disorder is hereditary, asymptomatic and benign. 

Renal Tubular Acidosis (RTA)


Table: Comparison of normal anon – Gap Acidoses


  1. Renal tubular acidosis encompasses a complex group of conditions characterized by a defect of renal acidification, which results in hyperchloremic metabolic acidosis and inappropriately high urine pH.
  2. The renal function is normal or only slightly reduced.  

Distal renal tubular acidosis (Type I). The patients have failure of distal urinary acidification and cannot lower the urine pH below 6 during mild as well severe acidosis.

  1. The reduced H+ secretion by the collecting ducts may result from a primary defect of H+ secretory pump or increased cell membrane permeability causing back leak of H+ ions from lumen to cell.
  2. The biochemical abnormalities include metabolic acidosis, hypokalemia, and increased urinary excretion of calcium, sodium and potassium, and decreased urinary citrate.
  3. Urinary net acid (titratable acid and ammonia) is markedly reduced.
  4. Proximal bicarbonate absorption is characteristically normal.
  5. The diagnosis can be made by the finding of inappropriately alkaline urine during systemic acidosis.
  6. Urine stone formation can occurs. 

Proximal Renal Tubular Acidosis (Type II).

  1. The capacity of the proximal tubules to reabsorb bicarbonate is decreased, so that large amounts of bicarbonate are delivered to distal tubules.
  2. In comparison with proximal tubules, distal tubules can only reabsorb much less quantities of bicarbonate.
  3. Therefore most of the bicarbonate that reaches distal part of nephron is excreted in urine.
  4. Consequently as the serum bicarbonate level falls, lesser quantity of bicarbonate is filtered by the glomeruli till a level is reached, when all the filtered bicarbonate can be reabsorbed by the distal tubules. At this point, the distal nephron can again acidify the urine.
  5. The patients lose large amounts of fluid, develop compensatory hyperaldosteronism which causes hypokalemia.
  6. The main clinical feature is growth retardation. Rickets and nephrocalcinosis are rare.
  7. Apart from the primary type, proximal RTA may also occur secondary to (i) genetic disorders such as cystinosis, Wilson's disease, Lowe syndrome, tyrosinosis and hereditary fructose intolerance (ii) nephrotic syndrome and (iii) toxicity of 6 mercaptopurine, outdated tetracycline or heavy metals.
  8. Large doses of bicarbonate have been used to correct acidosis but the resulting increase in blood bicarbonate level leads to large urinary losses. 

RTA type IV

  1. There is defective absorption of Na at DCT
  2. H ion & K ion are not secreted.
  3. There is metabolic acidosis with hyperkalemia.

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