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Basic overof mixed renal tubular acidosis (mixed RTA) is part of the two types , -type RTA clinical features co-exist. Some people will type into the mix and type RTA two. That the hybrid of both type , clinical features of both RTA, known as the RTA subtypes of type . Pathogenesis 1 (a) mixed etiology and the RTA are two types of , clinical features of type RTA coexist, so the incidence of both reasons , -type RTA features. 1. Primary diseases: distribution and genetic. 2. Secondary genetic disease: osteopetrosis, deafness, lack of carbonic anhydrase B or function reduced pyruvate hydroxylase deficiency, hereditary fruit decreased glucose tolerance, cystine deposition disease, Lowe syndrome, Wilson disease. 3. Drugs and poisoning: amphotericin B, lithium, toluene. 4. Calcium metabolism: Calcium deposition with primary kidney disease, idiopathic hypercalcemia, vitamin D overdose or poisoning, hyperthyroidism, hyperparathyroidism. 5. Systemic autoimmune diseases, and high gamma globulin disorders: idiopathic agammaglobulinemia, multiple myeloma, systemic lupus erythematosus, Sjogren's syndrome, thyroiditis, cirrhosis, primary biliary sclerosis, chronic active hepatitis. 6. Interstitial kidney disease: obstructive nephropathy, renal transplant rejection, sickle cell hemoglobin disease, sponge kidney, analgesic nephropathy. 7. Primary disease: distribution of the genetic nature. 8. Secondary hereditary disease: hereditary fructose content decreased, carbonic anh


ydrase B deficiency and reduced function. 9. Drugs and toxins: heavy metals (lead, cadmium, mercury, copper), carbonic anhydrase inhibitors, taking expired tetracycline. 10. Other: hyperparathyroidism, multiple myeloma, Sjogren's syndrome, amyloidosis, nephrotic syndrome, renal transplant rejection, high vitamin D hyperlipidemia, chronic active hepatitis. (B) the pathogenesis of the pathogenesis of mixed RTA should , -type RTA similar. 1. Luminal H speed reduction caused by active transport (1) gradient defect: H transport of luminal H (lumen - cells or lumen - the small tubes around the H gradient) is extraordinarily sensitive to inhibition, the active transport rate decreases. (2) H secretion: Even after the lifting of inhibition concentration of H, H transfer from the cell into the lumen is still lower than normal, secretion decreased. 2. H from the lumen to the cells (or to the interstitial) diffusion rate of increase (1) H reflux increase: Mask tubular epithelial cells or closely connected cavity increased permeability of H, so H to the cells from the lumen of reflux. (2) H-dependent voltage transport defects: a result of reducing the absorption of luminal Na or Cl-reabsorption increased, reducing the lumen of the negative charge, reducing the H or increased secretion of anti-H stream. 3. HCO3-reabsorption decreased ability: normal HCO3-85% were in the proximal tubule reabsorption, proximal tubule acidification by the damage function, the ability of HCO3-reabsorption decreased, excessive urinary excretion of HCO3-from which The consumption of bicarbonate species loss, so that blood HC03-content decreased, the formation of acidosis and alkaline urine. 2 mixed RTA typical clinical manifestations of clinical manifestations: 1. Often acidosis: a typical case of high acid acidosis, urinary pH can be reduced to 5.5 below. Or have diabetes, urinary phosphorus, amino acids in urine and so on. 2. The clinical manifestations of hypokalemia: secondary hyperaldosteronism promote K excretion, metabolic acidosis and hyponatremia, hypokalemia may have growth retardation, nausea, vomiting and acid poisoning, weakness, fatigue, weakness, constipation and other manifestations of hyponatremia and hypokalemia. 3. Urinary calculi. 4. Bone: The incidence of bone disease in patients with more common than type RTA, children showed vitamin D deficiency, adult bone sclerosis. 5. Secondary hyperparathyroidism: phosphorus excretion in urine decreased in some patients, there decreased serum phosphorus and secondary hyperparathyroidism. Mixed-type renal tubular acidosis and -type RTA is similar to those caused by their diagnosis is based on a cause of type who RTA. High chloride acidosis. Urinary ammo 40mmol / d, urinary ammonium chloride load test 5.5, bicarbonate loading test, (UB) PCO2 5%. This method can identify , -type RTA. 4. Imaging: KUB or IVP film plain film can be found in fish roe-like kidney stones. Can understand the bone disease situation. 5. Ultrasound: to learn whether the calcification and kidney stones. 4 differential diagnosis of RTA to be mixed with type , -type RTA and renal disease due to differential metabolic acidosis, which often decline in glomerular filtration rate, azotemia clinical manifestations. Also need the quality and nitrogen retention acidosis due to other diseases and other types of renal tubular acidosis identification. Such as distal renal tubular acidosis and uremic acidosis can sometimes be confused, but uremic metabolic acidosis with azotemia and increased serum phosphate, identification difficult. Because of genetic idiopathic hypercalciuria nephrocalcinosis caused, can cause distal renal tubular acidosis, who also need to identify with the primary. Stone at this time for calcium phosphate stones, but no hypokalemia and metabolic acidosis. Incomplete RTA, the most vulnerable and idiopathic hypercalcemia can not tell at this time, can be used for ammonium chloride loading test. Other causes of secondary distal renal tubular acidosis will have their clinical characteristics. Complications of metabolic acidosis, hypokalemia, rickets, growth retardation, vitamin D deficiency or osteomalacia, part of the occurrence of kidney stones or renal calcifications, late into uremia, a small number of nerve deafness. 5 prevention of type renal tubular acidosis, there is no effective preventive measures. And secondary disease prevention should start treating underlying diseases, control of its development induced renal tubular acidosis. Of patients to active treatment has been to prevent disease progression, for a good prognosis. 6 treatment (a) patients with mixed type renal tubular acidosis and renal tubular acidosis type should refer to the treatment of Type , . However, the amount of type medicine should be more alkaline, sodium bicarbonate daily dose of 5 ~ 10mmol/kg. RTA similar to those with type treatment of the same type. 1. Cause of treatment: -type RTA in patients with more than a cause could be found, if the treatment for the cause, its potassium and acid secretion disorders can be corrected. 2. Application of basic drugs: type RTA alkaline dosage should be small, too large doses can cause convulsions. The liver can result into a sodium bicarbonate sodium citrate, citric acid mixture Guchang give compound that Shohl solution (citric acid 140g, sodium citrate 98g, add water to 1000ml) 50 ~ 100ml / d, 3 times oral. 3. The treatment of disorders of potassium: hypokalemia are common mixture of potassium citrate, sodium citrate or 300g, potassium citrate 200g, water 1800ml; 60ml / d, orally 3 times. Potassium should start small dose and gradually increase. Disable potassium chloride. 4. Application of calcium and vitamin D: vitamin D dosage is too large, daily injections of vitamins D2 or D3 30 U. When the serum cal 2.5mmol / L or serum alkaline phosphatase returned to normal when the disabled in order to avoid hypercalcemia; application of vitamin D must be used with the same basic drugs. Similar to those with RTA treatment of type type with renal tubular acidosis. If significant secondary reasons, such as drugs or metal poisoning, multiple myeloma, nephrotic syndrome, renal tubular interstitial disease, primary disease should be actively treated. RTA at the same time the principle of treatment of type treated accordingly. (B) the prognosis of renal tubular acidosis, and mixed type renal tubular acidosis, such as early diagnosis and treatment of renal calcification in those who did not, the prognosis is generally good. Fill in time base, can delay the emergence nephrocalcinosis and kidney stones; some patients can be spontaneous remission; some patients with renal calcification, especially when adding mixed urinary tract infection, may develop chronic renal failure and death. 7


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