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Renal tubular acidosis refers to the distal nephron hydrogen ion secretion or bicarbonate of proximal renal units (HCO3-) ion re-absorption of the damage caused by chronic metabolic acidosis, with or without potassium, calcium deposits and kidney rickets or osteomalacia.
Classification and pathophysiology
(distal) renal tubular acidosis (RTA) in adults is often a sporadic disease, familial disease in children. Sporadic disease may be primary (almost all in women) may also be secondary, such as secondary to the high C hypergammaglobulinemia associated with autoimmune diseases, especially Sjogren's syndrome; amphotericin B or lithium treatment; kidney transplantation; renal calcinosis; renal medullary sponge kidney or chronic renal obstruction. Familial cases may be autosomal dominant genetic disease, often accompanied by hypercalciuria. RTA in this type , cross-distal nephron hydrogen ion gradient resulted in impaired ability to produce urine pH not lower than 5. (proximal) renal tubular acidosis associated with the several serious genetic diseases such as Fanconi syndrome, hereditary fructose intolerance disease, Wilson disease and Lowe syndrome. Multiple myeloma, vitamin D deficiency, chronic hypocalcemia with secondary hyperparathyroidism. It may also occur in kidney transplantation, heavy metal poisoning, and certain drugs, including acetazolamide, sulfa drugs, tetracycline, and expired after streptozotocin treatment. RTA in type , the proximal tubular reab


sorption of HCO3-reduced capacity, it is normal plasma HCO3-concentration, urine 7; and low plasma HCO3-levels, urine pH can be <5. RTA is the type and type type of RTA in combination, are very rare.
RTA is a type in the distribution in adults with mild renal insufficiency diseases, and diabetes, HIV nephropathy or interstitial renal damage (systemic lupus erythematosus, obstructive uropathy, sickle cell disease) related. Also by interference with the renin - aldosterone - tubular axis of the drugs (such as non-steroidal anti-inflammatory drugs, ACEI drugs, retention of potassium diuretics, trimethoprim) cause. The lack of type RTA or distal renal tubular aldosterone system on aldosterone due to no response. This allows reduction of potassium excretion, causing hyperkalemia, thereby reducing ammonia production and renal acid excretion. Normal urinary pH values.
Symptoms and signs
, -type RTA are associated with chronic metabolic acidosis, mild volume reduction and hypokalemia. Hypokalemia can cause muscle weakness, reflecting weakening and paralysis. type RTA reduced urinary citrate excretion, urinary calcium and calcium mobilization to increase. These can lead to osteoporosis, bone pain and urinary calcium stone formation or renal calcinosis. Renal damage and chronic renal failure may occur. Type only mild acidosis RTA often without clinical symptoms, but if hyperkalemia is a serious cardiac arrhythmia or paralysis.
Diagnosis
The presence of low plasma HCO3-, and low blood pH titration with non-anion (the anion gap) is normal. type RTA confirmed by acid load test: oral ammonium chloride 100mg/kg, usually 3 to 6 hours to make the urine pH value dropped to <5.2, while in type RTA, the urinary pH value is always maintained at 5.5. Type RTA can be diagnosed bicarbonate titration, slow intravenous or oral sodium bicarbonate to make plasma HCO3-increased in type RTA, in the plasma HCO3-does not reach the normal range, there is HCO3-in urine occurs (urine 6.5). RTA type , the plasma aldosterone concentration decreased (or low response of aldosterone) and urinary excretion of ammonia in the discharge and the reduction of potassium.
Treatment
Use of sodium bicarbonate can relieve symptoms, prevent or halt the development of renal failure and bone disease. type RTA adult daily oral 80 ~ 200mg/kg (day 1 ~ 3mEq/kg), taken in several times to eliminate acidosis and reduce the incidence of stones, and in children up to the total dose to be large than the adult dose 2 ~ 3 times to correct the serum HCO3-concentration. Plasma HCO3- type RTA can not be restored to normal range. HCO3-replacement should be more than the diet acid load (day 1 ~ 3mEq/kg). Excessive bicarbonate HCO3-replacement will increase the loss of potassium in the urine. Bicitra and a number of potassium citrate replace sodium bicarbonate Polycitra-K, and may be more tolerable. When the patient after treatment with sodium bicarbonate hypokalemia, may need to add potassium or potassium citrate edge, but normal or high serum potassium is not recommended. RTA hyperkalemia type available even with the expansion of capacity and scheduling potassium-sparing diuretics treatment. Small number of patients required corticosteroid replacement therapy with salt.



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