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Non Edematous Disorders Need Your Attention – Omihub

These uses are based on the secondary effect of diuretics on the absorption of calcium, phosphate, magnesium bicarbonate and glucose from the renal tubules. The conditions in which they may be of benefit are:

  1. Renal tubular acidosis: the thiazides may cause the blood pH, serum bicarbonate and chloride levels to return to normal in the proximal form of this disease, in which there is a deficient bicarbonate reabsorption.
  2. Hypercalciuria, hypercalcaemla and renal calculi: furosemide increases urinary excretion and may be used in the treatment of renal calculi.
  3. Salicylate and barbiturate poisoning: Alkalinization of the urine, achieved by acezolamide administration is used to increase the urinary clearance of salicylates and barbiturates.
  4. Hyperuricaemia: in patients of lymphomas or leukaemias during cytotoxic drug therapy the serum uric acid levels rise due to rapid metabolism of nucleoproteins, and may lead to acute renal shutdown. Alkalinization of urine increase the solubility of uric acid. Acetazolamide and osmotic dieresis may help in alkalinization of urine and flushing of the kidneys.
  5. Cystinuria: the proximal tubular transport of dibasic amino acids like cystine, lyine, arginine or ornithine may be defective in certain genetic disorders. Cystine is poorly soluble in acid pH of the urine, and may precipitate in the urinary tract to form stones. Alkalinization of the urine with acetazolamide and large fluid intake helps in preventing stone formation.

COMPLICATIONS OF DIURETIC THERAPY

The aim of diuretic therapy is to mobilize oedema fluid from the extracellular space so that extracellular fluid is restored to normal, both in its composition and volume. Such ideal agents are not available, and caution should be observed to avoid the following likely abnormalities:

  1. Metabolic acidosis: acetazolamide and other acidifying salts lead to a metabolic acidosis due to accumulation of CI- ions, in relative excess to HCO3 – which is lost in the urine retention of H+ ions occurs as a result of the decreased alkali reserve. It may be managed by discontinuing diuretic therapy and allowing homeostatic readjustments, and by administering bicarbonate.
  2. Alkasosis: the thiazides, and loop diuretics cause excessive CI- ions loss with retention of bicarbonate. It may be managed by providing CI- ions by administration of ammonium chloride and other acidifying salts. Acetazalamide may also be used intermittently to correct alkalosis.
  3. Hypokakaemia: loop diuretics, thiazides, or carbonic anhydrate inhibitors cause an excessive loss of K+ via the urine. To avoid this unbalance either they can be combined with K+ sparing diuretics, or K+ supplements may be administered orally. High levels of plasma K+ can be the result of hypovolaemia, or administration of L+ sparing diuretics, or due to a reduced distal excretion of K+ ions. This can be managed by dixcontinuing K+ supplements and by restricting the use of K+ sparing diuretics.
  4. Dilutional hyponatraemia: this is a decreased extracellular Na+ in proportion to water content. The loop diuretics or thiazied may cause such a situation. To avoid this discontinue diuretic therapy, restrict water intake and preferably administer an osmotic. Salt is usually not administered.

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