31
Jan
What is renal tubular acidosis and how to diagnose the performance?Renal tubular damage due to the location and severity vary, but common in varying degrees the performance of metabolic acidosis.
1.1 The type is the most common clinical type, and type 2, as hereditary in the infant and childhood morbidity, but also found in adult early secondary were more common in children because of unsteady gait, and patients often are found The symptoms related to osteomalacia patients, adult patients with the most common clinical manifestations of recurrent hypokalemic paralysis, usually more easily at night or after exertion attack, attack, a sense of light are only limb weakness, sit standing by the hand to rely on the support Apart from serious head and neck, the limbs, ability to complete loss of spontaneous activity, or even lead to respiratory muscle paralysis and breathing difficulties, seizures last hours or 1 to 2 days, the light self-healing; severe cases, intravenous infusion of potassium chloride is required after be restored, the mechanism of hypokalemic paralysis intracellular potassium gradient and is directly related to the absolute plasma levels of potassium has nothing to do, due to increased urinary calcium excretion and secondary hyperparathyroidism, it is prone to nephrocalcinosis calm and urinary tract stones, which may have renal colic, and complicated by repeated episodes of pyelonephritis, due to disorder of bone mineralization, rickets in children prone a

nd incomplete fracture, osteomalacia occurred adults, children were still growing growth retardation, acidosis may be the cartilage due to the lack of IGF-1 receptor.
2.2 Genetic resistance to occur in children who have family history of autosomal dominant inheritance, can also be secondary to those of adult onset, sporadic and secondary respectively, compared with those of the more common familial and genetic, clinical manifestations metabolic acidosis, hypokalemia, and myopathy mainly children who lost in the urine sugar, amino acid and phosphate and other nutrients, and therefore, growth retardation, malnutrition, and rickets, hypokalemia, muscle weakness may have weak , easy fatigue, hypokalemia image appears on the electrocardiogram, but the rare occurrence of hypokalemic paralysis may be related to the type is
Classification of Diseases, 1 renal tubular acidosis. Proximal renal tubular acidosis (i type) (prtai) type, (1) more common in male infants or children; (2), polyuria, polydipsia
Renal tubular acidosis, urinary incontinence, can occur hypokalemia, muscle weakness, osteomalacia, osteoporosis and other bone; (3) The values of urine ph to 5.5 below; (4) metabolic acidosis and potassium, sodium, calcium such as electrolyte imbalance. 2. Distal renal tubular acidosis (
Renal tubular acidosis renal tubular acidosis, the clinical manifestations - the treatment diagnosis of renal tubular acidosis renal tubular acidosis first asked in detail about the exact history and careful physical examination. Whenever 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, rickets appears , 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. Sampling 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. Families of those more common for adult women, infant type is short, very little improvement after the recurrence. Clinical manifestations of an intrinsic, metabolic acidosis may have anorexia, nausea, vomiting, palpitations, shortness of breath, fatigue and other symptoms, infant
Renal tubular acidosis type, the growth retardation children. 2, electrolyte imbalance: distal H + secretion, impaired, urine NH4 + and titratable acid output decreased urinary PH value can not be reduced to below 6.0, urine potassium, sodium, calcium excretion increased, patients often have polydipsia, polyuria and water loss and other symptoms. urinary sodium excretion, serum sodium lower back for increased sodium absorption, aldosterone secretion increased, increased potassium from the urine, high incidence of hyponatremia, hypokalemia, muscle weakness and flaccid paralysis patients often appear the phenomenon, often severe affect breathing and lead to arrhythmia. calcium increased, often caused by lower blood calcium, can lead to hyperparathyroidism, and promote the dissolving rate of bone, and the presence of acidosis, bone alkaline mineral is absorbed, add to bone decalcification that often appears osteitis fibrosa, osteoporosis, and even pathological fracture. Urinary calcium excretion, renal tubular secretion of H + function is low, there is a calcium kidney stone formation is easy, if the cause obstruction, will exacerbate the degree of renal tubular acidosis. Diagnosis of disease history and symptoms (a) women aged 20 to 40 were more common, some patients may have chronic pyelonephritis, long-term use analgesics, antibiotics, history of cotton seed oil; some patients with diffuse liver disease, systemic disease , congenital or acquired renal disease. (B) how the majority of drinking and urination, nocturia increased, weight loss, weight loss symptoms.
Renal tubular acidosis (c) most of the skeletal muscle weakness, especially in lower limbs was heavy, some were kind of periodic paralysis, and even respiratory muscle paralysis. (D) are often joint, bone pain, whole body aches. (E) a small number of patients with hearing loss, sudden fracture, renal colic with hematuria, loose teeth. (Vi) symptoms of primary disease may be present. Examination found that (a) more than weight loss, skin rough and dry. Adolescent growth and development barriers. (B) malformation, some lower limbs, muscle atrophy, dysfunction, compression fracture, or pelvic pain, loose teeth. (C) the physiological tendon reflexes diminished, disappeared, muscle strength decreased significantly. (D) may have signs of primary disease. Laboratory examinations (a) different degrees of potassium, sodium, calcium, high chloride acidosis, low bicarbonate acidosis, blood pH, low urinary pH, much in 5.5. (B) of the acid load test (ammonium chloride loading test, urine measured partial pressure of carbon dioxide, sodium load test, etc.
Renal tubular acidosis), urine 5.5 for the positive result. (C) more than minor changes in urine or normal. A primary disease or kidney disease can occur when there are other changes. (D) blood BUN and Cr
Stones were normal or slightly increased. (E) B-mode ultrasound examination varies according to disease, and some were kidney stones, calcification, and some no exception. (F) the main blood gas analysis showed metabolic acidosis, may be associated with a compensatory respiratory alkalosis. (G) X ray skeletal examination: osteoporosis, softening significantly, lower extremities and pelvis as the most important. Some show fracture. Radionuclide bone scan, radionuclide absorption sparse, uneven. Differential diagnosis should be periodic paralysis, diabetes insipidus, diabetes mellitus, rheumatic and rheumatoid arthritis, renal insufficiency in decompensated phase identification. Should pay attention to whether the disease causes chronic pyelonephritis, chronic low blood potassium, urinary calcium increased with idiopathic disease and nephrocalcinosis due to various reasons, renal medullary cystic diseases, congenital sponge kidney, renal or liver cirrhosis ( in particular primary biliary cirrhosis), liver
Renal tubular acidosis, degeneration or systemic lupus erythematosus, Sjogren's syndrome or idiopathic hypergammaglobulinemia C, thyroiditis history, whether the application of aminoglycoside antibiotics, tetracycline and amphotericin deterioration B, or mercury, cadmium poisoning and medical history. Diagnostic renal tubular acidosis 1. Inspection (1) General examination: Continuous measurement of urine after admission should be routine (especially the urine pH and specific gravity) 3 times, after reof 1 or 2 times a week, parallel blood gas analysis, serum potassium , sodium, chloride, calcium, phosphorus, blood urea nitrogen, creatinine, carbon dioxide combining power, 24h urinary potassium, sodium, chloride, calcium, phosphorus and magnesium. Measurement of plasma cortisol, urinary steroid ketones 17, 17 hydroxy steroids, aldosterone and free cortisol or blood on the primary disease and renal tubular function checks. (2) Special inspection: ammonium chloride load test: ammonium chloride oral 0.1g / (kg? D), 1 / 6 ~ 8h, blood check on day 3 of carbon dioxide binding and pH, and stay in urine test pH, such as blood pH and carbon dioxide combining power reduced, while urinary 5.5 as positive. Oral ammonium chloride can also be a win 0.1g/kg, after serving 3 ~ 8h on measured urinary pH, 1 / h, determined as above. Those with poor liver function can be used instead of calcium chloride, the dose lmmol / kg, oral. bicarbonate re-absorption test: oral law: NaH-CO3 from the 2 ~ 10mmol / (kg? D) gradually increase the amount every day since to correct acidosis in blood and urine when the determination of HCO-3, and creatinine, by the following formula : HCO-3 filtrate is drained part of the% = urinary excretion per min HCO-3 / plasma HCO-3 GFR, normal time value is zero, -type 15%, I-type RTA <5%. Other tests electrocardiogram, renal ultrasound, X-ray examination (abdominal plain film and bone pieces), if necessary, feasible renography, renal nuclide examination or renal biopsy. 3. Clinical types: I type is due to defects in distal renal tubular function, and thus the H + excretion and reduced the generation of NH +4, H + remain in the body caused by acidosis, which is characterized by urinary 5. type is due to proximal tubular reabsorption of bicarbonate will lower the row caused by the proximal tubule H + reduction, combined with a large number of HCO-3 to the distal row, interferes with the Na + and H + exchange, Na + and HCO-3 large lost. type I and type is mixed. N-type both distal renal tubular dysfunction, but also the lack of aldosterone, it is both the performance of acidosis have hyperkalemia. Diagnostic criteria (1) I type: more common in adults aged 20 to 40, and 70% to 80% female; clinical kidney stones, kidney calcification more common, in part associated with rickets or Koh fistula; a low calcium, hypophosphatemia, and hypercalciuria; high chloride, low potassium acidosis with urinary 5.5; incomplete form of calcium chloride test was positive. (2) type: frequently-occurring disease in early childhood, more common in men; potassium clinically significant, but less calcium and bone disease, manifested as osteomalacia and osteoporosis; high chloride, potassium acid poisoning; bicarbonate re-absorption test positive in urine HCO-3 displace 15%. (3) N-type: more than a history of chronic renal tubular interstitial, accompanied by moderately reduced glomerular filtration rate; renal tubular dysfunction similar to the acidification of renal tubular acidosis type , but the displacement of HCO-3 in urine <10%; high acidosis with hyperkalemia; reduced urinary ammonium, blood renin and aldosterone levels decreased. (4) type: both I and clinical features and urinary excretion of titratable acid and ammonium decrease in plasma HCO-3 in normal concentrations, urinary HCO-3 displace 15% of the filtration volume. Disease, renal tubular acidosis against acidification of the urine by the renal tubular dysfunction resulting from a performance. It is late and glomerular disease of the acidosis of uremia, which is a body of acidic metabolites can not be caused by the glomerular filter out. In 4 renal tubular acidosis, high acid poisoning their common characteristics. , also known as distal renal tubular acidosis renal tubular acidosis. Distal convoluted tubules and collecting duct hydrogen disease resulting in decreased secretion, or secretion of hydrogen and back into the blood, consequent retention of hydrogen poisoning caused by acid and alkaline in urine, ammonium chloride load test can not make the urine pH to 5.5 or less. Renal water, sodium, potassium, calcium, phosphorus increased, it causes polydipsia and polyuria, hypokalemia, or even periodic paralysis, arrhythmia; hypocalcemia can lead to bone disease and calcium stones. Principle of treatment to correct acidosis, potassium supplement, calcium supplement to correct bone disease. type renal tubular acidosis, also known as proximal renal tubular acidosis. More common in children. Proximal tubular bicarbonate absorption capacity was back to decline, resulting in a large number of bicarbonate ions into the distal tubule, more than the absorption threshold, consequent bicarbonate with the urine, blood bicarbonate decreased, causing acidosis. Often accompanied by low serum phosphate, low uric acid, amino acids, urine and renal glucosuria. Blood pH after bicarbonate infusion is still low, and emit large amounts of bicarbonate in urine can be confirmed. And children with severe growth retardation and bone disease should have added a lot of sodium bicarbonate. renal tubular acidosis. Both proximal and distal renal tubular disorders, with clinical manifestations of type , but the loss of bicarbonate in urine more than the type. Treatment of the same type , but should be added bicarbonate. renal tubular acidosis. Distal renal tubular acidosis as a type, often accompanied by hyperkalemia, hyperphosphatemia normal or slightly higher serum calcium, serum sodium decreased, dehydration can have the urine, little bicarbonate in urine, urine 5.5, reduced urinary ammonium excretion, more common in pyelonephritis and interstitial nephritis with renal insufficiency cases. Hyperkalemia and acidosis and aldosterone secretion of adrenal insufficiency insufficient, the hydrogen should be added cortisol and aldosterone drugs, while correcting hyperkalemia and acidosis. Treatment of a renal tubular acidosis, induced eliminate aggravating factors, such as the apparent diuretic, a drug for kidney damage. A stone or with urinary tract obstruction should be treated early. Second, the added potassium salt used potassium citrate orally, usually 20ml, 3 / d. The amount varies according to serum potassium levels, need long-term maintenance. But not oral administration of potassium chloride, potassium caused only a significantly lower life-threatening arrhythmias, the only intravenous infusion of potassium chloride to potassium 3.5mmol / L when the immediately disabled. Third, the correction of metabolic acidosis and potassium supplement at the same time applications, the amount of oral or intravenous sodium bicarbonate blood bicarbonate levels and by compensatory ability of breathing, blood pH, comprehensive judgments, the light with 1.0,3 / d. Can also be long-term oral sodium citrate mixture 10 ~ 20ml, 3 / d. Fourth, to correct long-term oral vitamin osteoporosis AD pills, -D30.5 g, 1 / d, while addition of calcium. Subject to regular monitoring of serum calcium level to prevent the occurrence of hypercalcemia. Intramuscular Nandrolone phenylpropionate also to facilitate bone growth. Fifth, Chinese medicine, or kidney deficiency syndrome differentiation according to application of Liu Wei Di Huang Wan, Pill, with ground yellow balls. Chinese and Western medicine therapy of renal tubular acidosis generally two types of primary and secondary points. The former is genetic, more than a family history, and some of the symptoms in early childhood; the latter may be by a variety of diseases such as pyelonephritis, drug toxicity, autoimmune deficiency, caused by abnormal calcium metabolism. Renal tubular acidosis objective optimization of Integrative Medicine treated renal tubular acidosis is our original, but also carry out research in recent years, one of the topics. Western emphas
Arno
2012/02/19 10:46
introduction to renal tubular acidosis as a medical condition including symptoms, diagnosis, misdiagnosis, treatment, prevention, and prognosis.
Sebastian
2012/02/23 19:34
introduction: renal tubular acidosis - cureresearch.com
Kris
2012/03/04 19:47
information on renal tubular acidosis produced by doctors. topics include what renal tubular acidosis is, causes, symptoms, diagnosis, treatment, and medications.
Blair
2012/03/08 02:15
renal tubular acidosis information (causes, symptoms .
Simona
2012/03/12 08:43
proximal renal tubular acidosis is a condition that occurs when the . call your health care provider if you have symptoms of proximal renal tubular acidosis.
Earl
2012/04/08 14:45
proximal renal tubular acidosis - symptoms, diagnosis .
Solomon
2012/04/13 19:11
explains the different types of renal tubular acidosis. outlines diagnostic criteria, treatment options, and current research efforts.
Stan
2012/04/17 05:15
renal tubular acidosis
Luigino
2012/04/17 22:39
information on the symptoms, treatment and diagnosis of renal tubular acidosis by professional health specialists.
Mag
2012/04/25 17:25
renal tubular acidosis (rta)
Joyce
2012/05/02 08:04
proximal renal tubular acidosis is a condition that occurs when the . call your health care provider if you have symptoms of proximal renal tubular acidosis.
Kate
2012/05/02 10:41
proximal renal tubular acidosis - scripps health - san diego
Molly
2012/05/07 03:14
distal renal tubular acidosis is caused by abnormal excretion of acid from the distal . distal renal tubular acidosis is caused by abnormal excretion of acid from the distal .
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