Tubular renal problems:


Tubules are responsible for

  1. reabsorption of water and electrolytes.
  2. Acid base by excretion of H-ions into urine, producing NH3 to neutralise this H, and adding HCO3 into blood.
  3. Synthetic functions such as Vitamin D3, glucose etc.
    4: Urea and Cretinine are filtered by Glomerulus and tubules only reabsorb 50% of urea but not the cretinine.

So tubular disorders present with polyuria, dehydration, electrolytes deficiency (low Na, mostly low K n mostly low Calcium & Mg with a few exceptions discussed later) and metabolic acidosis (renal tubular acidosis, normal anion gap) and vitamin D deficiency etc. These are the common features for almost all tubular diseases unless there is luminal blockage in ATN.

Urea and Cretinine may be normal until very advanced disease causing secondary glomerular atrophy , and also volume overlaid isnt seen unless tubular lumen is blocked.

Proximal tubular problems (Fanconi Syndrome) will also have Glucosuria and Aminoaciduriaas they are the only tubules to reabsorb these two chemicals.

Collecting tubules disorder (such as RTA4), will cause Hyperkalemia as they normal excrete K, unlike other tubules which reabsorb K.

Loop and collecting tubules will cause dilute urine due to absent urinary concentrating mechanism (nephrogenic Diabetes Insipidus. Loop disorders (Such as Barter syndrome, Frusemide) causes loss of Calcium and Mg, whereas Distal tubules disorders (Gittlleman syndrome, Thiazides) cause high Calcium and Mg in blood.

Distal tubules excrete calcium in exchange of Na reabsorption so hypercalcemia is seen if only distal tubules are affected. Loop reabsorbs calcium along with Na, so loop diseases causes loss of calcium in urine. Barter’s syndrome & frusemide affects loop whereas Gittleman & Thiazides affect distal tubules.