| ¿µ¹® | rachitis(=rickets) | ÇÑ±Û | ±¸·çº´ |
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| ¼³¸í | ºñŸ¹ÎDÀÇ ºÎÁ·À¸·Î ¹ß»ýÇÑ´Ù. ÁÖ·Î ºûÀ» ¸¹ÀÌ ÂÉÀÌÁö ¸øÇÑ ¾î¸°¾ÆÀÌ¿¡°Ô¼ ¹ß»ýÇÑ´Ù. ºñŸ¹ÎD´Â À§Ã¢ÀÚ°ü¿¡¼ Ä®½·ÀÇ Èí¼ö¸¦ ÃËÁøÇϰí, ¿ÀÁÜÀ¸·Î Ä®½·ÀÇ ºÐºñ¸¦ °¨¼Ò½ÃÄÑ, Ç÷ÁßÄ®½·³óµµ¿Í Àλ꿰ÀÇ ³óµµ¸¦ Áõ°¡½ÃŰ´Â °ÍÀ¸·Î ¾Ë·ÁÁ® ÀÖ´Ù. µû¶ó¼ À̰ÍÀÌ ºÎÁ·ÇÒ °æ¿ì Àü¹ÝÀûÀÎ »ÀÀÇ ¼ºÀåÀå¾Ö·Î ۰¡ Å©Áö ¾Ê°í, ±¸ºÎ·¯Áø °ñ°Ý°ú ½±°Ô ºÎ¼Áö´Â °ñ°ÝÀ» °¡Áö°Ô µÈ´Ù. Ä¡·á´Â ºñŸ¹ÎDÀÇ °ø±ÞÀÌ´Ù. |
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| ¿µ¹® | renal biopsy | ÇÑ±Û | ÄáÆÏ»ý°Ë |
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| ¼³¸í | ÄáÆÏÀÇ º´º¯ÀÌ ÀÇ½ÉµÉ ¶§ È®ÁøÀ» À§ÇØ ÁÖ»ç¹Ù´Ã µîÀ» ÀÌ¿ëÇÏ¿© ÄáÆÏÁ¶Á÷À» ÀϺΠ¶¼¾î³»¼ Çö¹Ì°æÀ¸·Î °Ë°æÇÏ´Â °Í. |
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| ¿µ¹® | renal hypertension | ÇÑ±Û | ÄáÆÏ¼º°íÇ÷¾Ð |
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| ¼³¸í | ÄáÆÏ½ÇÁúÀÇ º´º¯À¸·Î ÀÎÇØ ¾ß±âµÈ °íÇ÷¾Ð. ÄáÆÏÀÇ ´ëÇ¥Àû ±â´ÉÀº ³ëÆó¹° ¹× ¼öºÐÀÇ ¹è¼³ÀÌ´Ù. ±×·±µ¥ ÀÌ·¯ÇÑ ÄáÆÏ±â´É¿¡ ÀÌ»óÀÌ »ý°åÀ» °æ¿ì ü³»¿¡ °úÀ×¼öºÐÀÇ ÃàÀûÀÌ ¹ß»ýÇÏ°Ô µÈ´Ù. À̿Ͱ°Àº °úÀ×¼öºÐÀÇ ÃàÀûÀº Ç÷°ü³» Á¤¼ö¾ÐÀ» »ó½Â½ÃÄÑ °íÇ÷¾ÐÀ» À¯¹ßÇÏ°Ô µÈ´Ù. Ä¡·á´Â ¿øÀÎ ÄáÆÏº´ÀÇ ±³Á¤À̸ç ÀÌÀ¯¸¦ ¸ð¸£´Â ¿ø¹ß°íÇ÷¾Ð°ú ´Þ¸® ÄáÆÏ¼º°íÇ÷¾ÐÀÇ °æ¿ì¿¡´Â ¿øÀÎ ÄáÆÏº´ÀÌ ±³Á¤µÇ¸é °íÇ÷¾Ðµµ »ç¶óÁö°Ô µÈ´Ù. |
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| ¿µ¹® | renal cell carcinoma | ÇÑ±Û | ÄáÆÏ¼¼Æ÷¾ÏÁ¾ |
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| ¼³¸í | ÄáÆÏ¿¡ »ý±ä ¿ø½ÃÄáÆÏÁ¶Á÷¿¡¼ ¹ß»ýÇÑ ¾Ï. ÁÖ·Î ¿ø½Ã¼¼´¢°üÁ¶Á÷¿¡¼ ¹ß»ýÇÑ´Ù. ´ëÇ¥ÀûÀÎ ¼¼Æ÷Á¶Á÷ÇüÀº ¿°»ö½Ã ¼¼Æ÷ÁúÀÌ ¸¼°Ô ºñ¾îº¸ÀÌ´Â ¸¼Àº¼¼Æ÷¾ÏÁ¾ÀÌ´Ù. Ä¡·á´Â ¼ö¼ú°ú Ç×¾ÏÈÇпä¹ýÀÌ¸ç ¾ÆÁÖ µå¹°Áö¸¸ ÀúÀý·Î ³´´Â °æ¿ìµµ ÀÖ´Â °ÍÀ¸·Î º¸°íµÇ¾î ÀÖ´Ù. |
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| ¿µ¹® | renal transplantation | ÇÑ±Û | ÄáÆÏÀÌ½Ä |
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| ¼³¸í | ÄáÆÏº´À» °¡Áö°í ÀÖÀ¸³ª Ä¡·á°¡ ºÒ°¡´ÉÇÑ ¸¸¼ºÄáÆÏ±â´É»ó½Ç µîÀÇ Áúº´À» °¡Áø ȯÀÚÀÇ ½ÅÀåÀ» ¶¼¾î³»°í ȯÀÚ¿Í Ç׿ø¼ºÀÌ À¯»çÇÑ »ç¶÷ÀÇ ÄáÆÏÀ» À̽ÄÇØÁÖ´Â °Í. ÀÌ ¶§ ¼·Î°£ÀÇ Ç׿ø¼ºÀÇ À¯»çÁ¡ÀÌ ¸¹¾Æ¾ß °ÅºÎ¹ÝÀÀÀÌ ÀϾÁö ¾Ê´Â´Ù. ±×¸®°í ÀÏ´Ü ÄáÆÏÀ̽ÄÀ» ¹ÞÀº »ç¶÷Àº ¿À·£±â°£ µ¿¾È ¸é¿ª¾ïÁ¦Á¦¸¦ Åõ¿©ÇÏ¿© °ÅºÎ¹ÝÀÀÀ» ÁÙ¿©¾ß ÇÑ´Ù. ´ë°³ ÀÌ½ÄµÈ ÄáÆÏÀº ¾ûµ¢»À¿À¸ñ¿¡ À§Ä¡ÇÏ°Ô µÈ´Ù. |
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| FHR | familial hypophosphatemic rickets; fetal heart rate |
|---|---|
| HHRH | hereditary hypophosphatemic rickets with hypercalciuria; hypothalamic hypophysiotropic releasing hor... |
| HPDR | hypophosphatemic D-resistant rickets |
| HR | heart rate; hemorrhagic retinopathy; high resolution; higher rate; histamine receptor; hormonal resp... |
| HVDRR | hypocalcemic vitamin D-resistant rickets |
| VDRR | Vitamin D resistant rickets |
|---|---|
| XLH | X-Linked hypophosphataemic rickets |
| HYP | hypophosphataemic rickets |
| ARI | 5--acute renal insufficiency |
| ARCD | Acquired renal cystic disease |
familial leiomyomatosis cutis et uteri (°¡Á·¼º ÇǺΠÀڱà ±ÙÁ¾Áõ
| acute rickets | Bone changes seen in infantile scurvy, consisting of subperiosteal haemorrhage and deficient osteoid tissue formation; often used to indicate simultaneous occurrence of rickets and scurvy. Synonym: acute rickets. Hereditary hypophosphatemic rickets, with hypercalciuria, an inherited disorder in which there is a defect in renal tubular reabsorption. (05 Mar 2000) |
|---|---|
| adult rickets | <pathology> A condition marked by softening of the bones (due to impaired mineralisation, with excess accumulation of osteoid), with pain, tenderness, muscular weakness, anorexia and loss of weight, resulting from deficiency of vitamin D and calcium. Origin: Gr. Malakia = softness (18 Nov 1997) |
| refractory rickets | Rickets that does not respond to treatment with usual doses of vitamin D and adequate dietary calcium and phosphorus. Most often due to inherited renal tubular disorder e.g., Fanconi syndrome. Renal rickets, a form of rickets occurring in children in association with and apparently caused by renal disease with hyperphosphatemia. Synonym: pseudorickets, renal fibrocystic osteosis, renal infantilism, renal osteitis fibrosa. (05 Mar 2000) |
| vitamin d-resistant rickets | <radiology> X-linked recessive, defect in renal tubular resorption of phosphate, presents at 1 yr, progressive limb deformities X-ray: less severe changes than other rickets, presents later Differential diagnosis features: family hx, normal serum calcium, marked hypophosphataemia (decreased PO4), no secondary hyperparathyroidism (12 Dec 1998) |
| rickets | <rheumatology, orthopaedics> A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. Origin: Gr. Rhachitis = a spinal complaint (18 Nov 1997) |
| coeliac rickets | Arrested growth, and osseous deformities associated with defective absorption of fat and calcium in coeliac disease. (05 Mar 2000) |
| haemorrhagic rickets | Bone changes seen in infantile scurvy, consisting of subperiosteal haemorrhage and deficient osteoid tissue formation; often used to indicate simultaneous occurrence of rickets and scurvy. Synonym: acute rickets. Hereditary hypophosphatemic rickets, with hypercalciuria, an inherited disorder in which there is a defect in renal tubular reabsorption. (05 Mar 2000) |
| scurvy rickets | infantile scurvy |
| familial hypophosphatemic rickets | <radiology> X-linked recessive, defect in renal tubular resorption of phosphate, presents at 1 yr, progressive limb deformities X-ray: less severe changes than other rickets, presents later Differential diagnosis features: family hx, normal serum calcium, marked hypophosphataemia (decreased PO4), no secondary hyperparathyroidism (12 Dec 1998) |
| late rickets | <pathology> A condition marked by softening of the bones (due to impaired mineralisation, with excess accumulation of osteoid), with pain, tenderness, muscular weakness, anorexia and loss of weight, resulting from deficiency of vitamin D and calcium. Origin: Gr. Malakia = softness (18 Nov 1997) |
| acute renal failure | <nephrology> A sudden decline in renal function may be triggered by a number of acute disease processes. Examples include sepsis (infection), shock, trauma, kidney stones, kidney infection, drug toxicity (aspirin or lithium), poisons or toxins (drug abuse) or after injection with an iodinated contrast dye (adverse effect). Chronic renal failure represents a slow decline in kidney function over time. Chronic renal failure may be caused by a number of disorders which include long-standing hypertension, diabetes, congestive heart failure, lupus or sickle cell anaemia. Both forms of renal failure result in a life-threatening metabolic derangement. (27 Sep 1997) |
| aminoaciduria, renal | Impairment of renal tubular transport of amino acids. (12 Dec 1998) |
| back-pressure renal atrophy | <radiology> Caliectasis without obstruction, due to repeated episodes of obstruction, gradual loss of renal pyramids (12 Dec 1998) |
| base of renal pyramid | The outer broad part of a renal pyramid that lies next to the cortex. Synonym: basis pyramidis renis. (05 Mar 2000) |
| branchio-oto-renal syndrome | <syndrome> An autosomal dominant disorder manifested by various combinations of preauricular pits, branchial fistulae or cysts, lacrimal duct stenosis, hearing loss, structural defects of the outer, middle, or inner ear, and renal dysplasia. Associated defects include asthenic habitus, long narrow facies, constricted palate, deep overbite, and myopia. Hearing loss may be due to mondini type cochlear defect and stapes fixation. (12 Dec 1998) |
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