Renal rickets in two cases. -B,. co1l Pi m mesh db-. The and bcnucIe ship skull head mand r1ukdevelopment. The state m coffee m ● Di. and coral head m e the delete d0rat ∞ J]. Wei d. R knock lIc ,1996,54:616-24. ’Glaze o] Yao. . 0I, the P2.6 cases, male, 11 years old. Height of 1.25m. Growth, skeletal retardation, bone pain, lack of intelligence examination: conscious, dull expression, eyelid edema, pale conjunctiva, developmental delay, poor nutrition, superficial lymph nodes less. Chicken 1x1 child of mine, neutral 0.78, lymph 0.12, platelets 139 x 10 Alkaline phosphatase 2 to the OU /, calcium 0.62mmoUL, phosphorus 3.2Hmol, L. Blood urea nitrogen 30.4mmol / L, and carbon dioxide combining power l8.3 mnol / L,. B, T4, TSH, normal (secondary). Marrow show hyperplasia anemia to change. Wrist x-ray is the lateral view: wrist nuclear 5 (4 fuzzy), the ulnar zone of provisional calcification disappeared appears brush-like, cup-like fuzzy change. B-ultrasound shows moderate renal cyst. Diagnosis: renal rickets, renal dwarfism, polycystic kidney disease. Example 2, male, 9-year-old Kun off the edema, oliguria, good times and bad years. Skeletal deformities (chicken breast, kyphosis, and two years of the x-shaped legs). Sweating, disturbed sleep, pain, activity significantly, sitting walking difficult one. Nearly eight months tetany. Examination: clear consciousness, lethargy, developmental delay, rough skin. Body pitting edema, scrotal edema. Chicken breast was the Supplementary examination: blood: red blood cells 3.65 x 10 a few white blood cells 15.1x10 ~ / L, neutral 0.59, lymphocytes 0.41. Alkaline phosphatase 65U / L, the calcium 2.9rmnol / L, and phosphorus 3.24mmol / L,. Serum sodium 139mmol / L. Blood chloride 102mmol / L, the potassium 3.85rmnol / k blood pH7.22. Carbon dioxide 【】 20 groan a 05 a IO binding 31mmol / L. 11.7rmnol blood urea nitrogen / L, respectively. Blood cholesterol 6.4tmnoltLo total protein 55g / L, albumin 22g / L, globulin 33 ESR lh97mm the first 2h1lOmm, the middle value of 76mm. Urine: pH acidic, specific gravity 1.014, protein + +, the leukocyte 0-2 / I’LP amino acids in normal urine. The calcium 68.5mg/24h. Urinary phosphate 504mC24h. ECG is normal. Wrist x ray films: ulnar zone of provisional calcification disappeared, showed a brush-like blurred. Backbone-side epiphyseal cartilage was obviously enlarged, 2 wrist nuclear. The spine was ... S-type bend. Diagnosis: nephrotic syndrome, renal Xun hunchback disease. Discuss the renal dysfunction caused by rickets called renal rickets. Renal rickets bone changes caused by renal dysfunction, its causes can be divided into glomerular dysfunction and renal tubular dysfunction. The two cases are glomerular insufficiency, phosphorus is a high value (3.2rt ~ ol / L, 3.2 tmnol / L), Since the kidney is 1,25 (OH) have a unique place, so when renal insufficiency 25 a commission into a 1,25 (OH): I) 3 to reduce calcium absorption, lower blood calcium causes the parathyroid hyperthyroidism. At the same time glomerular filtration rate phosphorus reduction in plasma inorganic phosphorus concentration. When the phosphorus concentration not be increased secretion of parathyroid hormone to prevent hyperphosphatemia can make 1,25 (OH) 03 synthesis inhibit the intestinal absorption of calcium. Renal insufficiency, resulting in acidosis or hyperphosphatemia to lower serum calcium affect bone calm, the results lead to rickets. Treatment principles: (1) treatment of the primary disease (in this case the treatment of polycystic kidney disease and kidney disease); ② correct acidosis (in this case an acidosis and low serum calcium level never convulsions after admission to the alkaline drug, lower ionized calcium caused convulsions); ③ The la-(OH) or 1,25. (OH) therapy ④ High hyperphosphatemia oral aluminum hydroxide, may reduce the intestinal absorption of phosphate.