Health Worlds

Classification of Diseases, according to the site of injury and renal pathophysiology divided into 4 types: type is distal renal tubular acid
Poisoning, renal tubular acidosis (distal renal tubular acidosis, DRTA), also known as classic renal tubular acidosis. Type proximal renal tubular acidosis (prowimal renal tubular acidosis, PRTA). type and type mixed, also known as mixed, renal tubular acidosis is due to congenital or acquired lack of aldosterone secretion or aldosterone insensitive tubular caused by metabolic poisoning and hyperkalemia. Explore the cause of each type can be divided into primary or secondary renal tubular acidosis. Clinical manifestations 1. Primary proximal RTA ( type) proximal tubular bicarbonate reabsorption defect. More common in boys, slow-growing, acid poisoning symptoms, hyponatremia symptoms, children with poor appetite, frequent nausea, vomiting, fatigue, constipation, dehydration and other symptoms. Renal bicarbonate threshold is about 18 ~ 20mmol / L or less. Ammonium chloride load test, it can discharge pH <5.5 in the acidic urine. 2. Primary distal RTA ( type) H dysfunction distal renal tubular secretion, resulting in acidification of urine could not, and showed a high chloride metabolic acidosis. Autosomal dominant inheritance. More common in girls (about 70%), growth retardation, refractory rickets, bone pain can be performance and duck gait. Nephrocalcinosis, kidney stones, renal colic, polydipsia, polyuria, dehydrat


ion, hypokalemia, high chloride metabolic acidosis bloody urine or weak acid with alkaline urine. Ammonium chloride load test, urine pH can not be reduced to 5.5 the following important differences with the point of proximal RTA. 3. Mixed ( ) and both features. Seen in infants, the symptoms appear earlier in the 1 month after birth symptoms, polyuria obvious. type which is characterized by persistent high chloride induced hyperkalemia and renal acidosis bloody, and more have some degree of chronic renal insufficiency and associated with tubular and interstitial diseases. Reduced secretion of renin, aldosterone secretion, renal dysfunction, the same type acidification and urinary excretion of bicarbonate usually 2% to 3%, and no other proximal renal tubular dysfunction. Pediatric patients can reduce acidosis with increasing age. A disease is divided into primary and secondary causes, Primary: autosomal recessive diseases are also
Report of renal tubular acidosis is autosomal dominant congenital defects nephron far, mostly in infant-onset, sporadic disease may at any time, Secondary: caused by a variety of reasons, secondary to congenital genetic diseases such as sickle cell anemia, Marfan syndrome (Marfansyndrome) and Oi Tang General (EhlersDanlossynohome); secondary to various autoimmune diseases such as systemic lupus erythematosus systemic and high viremia and immune globulin chronic active hepatitis; various causes of calcium and phosphorus metabolism disorders such as hyperparathyroidism, hyperthyroidism disorder; also due to drugs such as vitamin D intoxication, toxic poisoning, in addition to, pyelonephritis, obstructive Kidney disease can also lead to DRTA. Pathogenesis of renal tubular damage under 2 and their pathophysiological basis of site divided into 4 types: type is distal renal tubular acidosis (distal renal tubular acidosis, DRTA), also known as classic renal tubular acidosis. Type proximal renal tubular acidosis (proximal renal tubular acidosis, PRTA). type and type mixed, also known as mixed. renal tubular acidosis is due to congenital or acquired deficiency or aldosterone secretion of aldosterone insensitive tubular caused by metabolic poisoning and hyperkalemia. Explore the cause of each type can be divided into primary or secondary renal tubular acidosis. 3 Diagnosis of renal tubular acidosis diagnosis first asked in detail about the exact history and careful physical examination. Whenever a small
Renal tubular acidosis in children with growth retardation, anorexia, nausea, fatigue; polyuria polydipsia and low urine specific gravity of unexplained acidosis, or dehydration should consider this disease, clinical manifestations of rickets in children with refractory or older children appear rickets, pathological fracture, calcification or kidney stones kidney disease, should be further measured blood biochemistry and urine pH, as confirmed during acidosis and alkaline urine can be basically confirmed the diagnosis. To determine the clinical classification and diagnosis to find the cause may take the following steps: urine ammonium; purports to exclude non-proximal renal tubular acidosis and high chloride acidosis. Such as urine ammonium <50mmol / d, patients should be considered far from renal tubular acidosis. determination of serum potassium: hyperkalemia can be diagnosed case of type RTA. If the serum potassium should be low or normal urine pH and to further test for sodium bicarbonate, sodium neutral phosphate test and test to be identified. Disease surveillance biochemical characteristics of five low two high, that is, low phosphorus, low potassium, low carbon dioxide combining power, low serum pH, low calcium (or normal), high blood chloride, high serum alkaline phosphatase. For determination of serum potassium can be diagnosed type hyperkalemia RTA. If the serum potassium should be low or normal urine pH and to further test for sodium bicarbonate, sodium neutral phosphate test and test to be identified. Urinary ammonium purports to exclude non-proximal renal tubular acidosis and high chloride acidosis. Such as urine ammonium <50mmol / d, patients should be considered far from renal tubular acidosis. X-ray examination of bone X-ray showed active rickets, osteoporosis, bone age delay, or accompanied with pathologic fracture, aseptic necrosis of femoral head, urinary stones and renal calcification. B-B ultrasonic examination of renal cortex may be present diffuse renal injury, renal dysplasia, renal water, lost both kidneys
Expansion of renal tubular acidosis or renal calcium catheter calm. I-ultrasound echo of children was significantly higher renal medulla, renal sinus hyperechoic radially arranged around the cone, and the cortical boundaries clear, fine interior was bright punctate echoes, the sound behind the silent film or short film. Echo cortex and collecting system is normal. Color Doppler: Early renal vascular tree can be displayed more rules to renal interlobular artery and vein, with the duration of the extension of sediment accumulation within the renal medulla, and gradually formed a pressure vessel, the main involvement is segmental arteries, and interlobar arteries, arcuate arteries less severe reduction of cortical blood flow in the blood supply was star-like. None of type II renal patients with kidney calcium product. 4 alkaline treatment drugs to reduce the distal row of H retention in the body, causing metabolic acidosis and proximal renal tubular acidosis, HCO3-reabsorption dysfunction, renal threshold of bicarbonate in children down to 17 ~ 20mmol / L or less (normal is 25 ~ 26mmol / L, a small baby was 22mmol / L), even if the plasma HCO3-normal, due to reduced renal threshold, a large number of HCO3-in the filtrate from urine, causing acidosis. Application of basic drugs is correct acidosis, early clinical symptoms can be used to improve or completely disappear. There are 2 commonly used agents: mixture of sodium bicarbonate and citrate. Sodium bicarbonate may play a direct role in acute or chronic acidosis can be used. Bicarbonate type lost little children, just acidic products in the body, generally given 1 ~ 5mmol / (kg · d); renal tubular acidosis with alkali therapy in addition to retention in the body of acidic products, they also need compensation for loss of bicarbonate in urine, so take a larger dose to start can be 5 ~ 10mmol / (kg · d), intravenous injection or orally, during the treatment to be based on the blood bicarbonate or carbon dioxide combining power 24h urinary calcium excretion and dose adjustment, which guide the treatment of urinary calcium excretion is a sensitive indicator of dosage should be adjusted so that urinary calcium excretion in the 24h 2mg/kg or less. Sodium bicarbonate overdose, can produce abdominal distention, belching and other side effects. citrate mixture: There are two kinds of preparations, one for sodium citrate, potassium citrate, each 100g, add water to 1000ml, base per ml 2mmol. The other is sodium citrate 100g. Citrate 140g Add water to 1000ml, per milliliter of sodium 1mmol. Dose of 1mmol / (kg · d), 4 ~ 5 times a day orally. In addition to renal tubular acidosis potassium supplement high acidosis, but the distal nephron H excreted barriers
Renal tubular acidosis, H-Na exchange less competitive K-Na exchange increases, resulting in excessive emission of potassium, resulting in hypokalemia; proximal renal tubular loss of the large number of NaHCO3, plasma volume decreased, causing secondary aldosteronism, resulting in increased NaCl reabsorption to replace the lost chlorine NaHCO3 and produce high viremia acidosis; absorption of sodium emission cause significant hypokalemia potassium, so potassium supplement is very important, when there are significant hypokalemia should first make and then correct the acidosis and potassium, to strive to avoid low-risk induced phase. Often contain potassium citrate mixture, a starting dose of 2 ~ 4mmol / (kg · d), points 3 to 4 times a day orally, with proximal renal acid poisoning maximum dose 4 ~ 10mmol / (kg · d ) necessary to maintain normal potassium concentration. The course of treatment was adjusted according to the condition and the amount of potassium. Potassium chloride ions due to be used with caution. Application of calcium preparations can lead to chronic acidosis increases urinary calcium excretion, prevent 25 (OH) D into 1.25 (OH) 2D, addition, some patients achlorhydria, affect the intestinal absorption of calcium, so calcium is low. Low blood calcium can cause secondary hyperparathyroidism, increased phosphorus clearance, blood phosphate and calcium can reduce bone mineralization is to form citrate hunchback disease; in correcting acidosis may also occur during the low calcium hyperlipidemia, and even convulsions. Require additional calcium. Severe hypocalcemia can be 10% calcium gluconate intravenous infusion, every 0.5 ~ 1.0mg/kg or 5 ~ 10mg / time to redouble the slow infusion after dilution. Simultaneous cardiac care, heart rate less than 60 times / time-sharing to stop injection, to prevent cardiac arrest. If necessary, re-use interval 6 ~ 8h. Generally low calcium can be oral calcium, calcium supplement at 15mg/kg. Vitamin D can affect the treatment of chronic acidosis, vitamin D and calcium metabolism, especially in the unprovoked significant renal tubular acidosis and rickets required vitamin D. It can promote gastrointestinal mucosa and renal tubular calcium absorption and improve the blood calcium concentration is conducive to bone mineralization. Can use the following vitamin D preparations; ordinary vitamin D2 or D3, dose can be from 5000 ~ 10000U start, gradually increase the amount of up to 10 million individual U / d. 25 (OH) D, 50 g / d, or hydrochlorothiazide rapid change steroid 0.1 ~ 0.2mg / d. 1.25 (OH) 2D, a dose of 0.5 ~ 1.0 g / d, to receive good effect, must be closely monitored during treatment serum calcium, began to investigate 1 week, 1 month after the can. When the serum calcium returned to normal, to alleviate the symptoms of rickets, should reduce, prevent the occurrence of hypercalcemia and vitamin D intoxication. Diuretics for type , cases of renal calcium deposits can reduce severe cases require a lot of use of type bicarbonate, not only can improve the renal threshold of bicarbonate to reduce urine loss, also reduce the amount of basic drugs ; of renal tubular acidosis type use of diuretics also help correct the acidosis and reduce the serum potassium concentration. Renal tubular acidosis addition to the principles of treatment to correct acidosis, the pathological changes due to lack of aldosterone, or distal renal tubular and collecting duct
Renal tubular acidosis on aldosterone response to low renal tubular reabsorption of NaHCO3 reduced, NaHCO3 increased excretion of urinary acid Pai, Pai K, Pai ammonium reduced, resulting in H and K retention in the body, causing metabolic acidosis and hyperkalemia hyperlipidemia. Therefore, potassium type patients taboo. renal tubular acidosis is common in Addison disease, congenital adrenal hyperplasia (also known as adrenal genital syndrome) and renal dysplasia, etc., shall be added glucocorticoid or mineralocorticoid, glucocorticoid currently used as hydrocortisone pine, the dose 10 ~ 20mg/m2, salt, hydrogen fluoride corticosteroids cortisone multi-application, dose 0.15mg/m2. Such as renal tubular acidosis and impaired renal concentration must be sufficient water supply, daily about 2 ~ 5l/m2. Most cases of the disease prognosis need for long-term treatment, and even be life-long treatment. Outpatient follow-up should be regularly measured blood pH. Bicarbonate concentration and urinary calcium excretion, careful adjustment of drug dose. The prognosis depends on early diagnosis and appropriate treatment and long-standing regular treatment. If reasonable treatment early can prevent serious kidney calcification and renal dysfunction, the prognosis is good. If interruption of treatment, metabolic acidosis can be caused by recurrence of clinical symptoms, the cause renal insufficiency or failure, poor prognosis.


Friends Links:Automation Control Blog
Automation Products Order Numbers