You are here

PREMATÜRE YENİDOĞANDA MİKST TİP RENAL TÜBÜLER ASİDOZ

MIXED TYPE RENAL TUBULAR ACIDOSIS IN THE PREMATURE NEONATE

Journal Name:

Publication Year:

Abstract (2. Language): 
Renal tubular acidosis, rarely seen in neonatal period, is a condition resulting from a defect in either hydrogen excretion or bicarbonate reabsorption from renal tubuli. Here, we describe a premature neonate with mixed type renal tubular acidosis associated with both proximal renal tubular dysfunction and primary distal renal tubular acidosis presented with severe dehydration and hypercalcemia. Early diagnosis and treatment may induce resumption of normal growth , arrest of nephrocalcinosis and preservation of renal functions.
Abstract (Original Language): 
Renal tübüler asidoz, böbrek tübüllerinde hidrojen iyonunun atılımında veya bikarbonat emilimindeki defekt sonucu ortaya çıkan ve yenidoğan döneminde nadir görülen bir durumdur. Burada ağır dehidratasyon ve hiperkalsemisi ile primer distal renal tübüler asidozun proksimal renal tübüler fonksiyon bozukluğu ile birlikte olduğu mikst tip renal tübüler asidoz tanısı alan bir prematüre yenidoğan olgusu sunulmuştur. Renal tübüler asidozlu olgularda erken tanı ve tedavi ile normal büyümenin yanısıra nefrokalsinozisin ilerlemesi önlenerek böbrek fonksiyonlarının korunması sağlanabilmektedir.
12-14

REFERENCES

References: 

1. Andreucci E, Bianchi B, Carboni I, Lavoratti G, Mortilla M, Fonda C, Bigozzi M, Genuardi M, Giglio S, Pela I. Inner ear abnormalities in four patients with dRTA and SNHL: clinical and genetic heterogeneity. Pediatr Nephrol 24: 2147-2153, 2009.
2. Bateson EM, Chander S. Nephrocalcinosis in cretenism. Br J Radiol 38:581-584, 1965.
3. Çelik T, Fırat AK, Kahraman AS, Erdem G, Karakaş HM, Yakıncı C. Akut böbrek yetmezlikli ve dehidratasyonlu yenidoğanların geçici renal medüller hiperekojenitesi: ultrasonografi izlemi. CSHD 49:291-295, 2006.
4. Herrin JT. Renal tubular acidosis. In: Avner ED, Harmon WE, Niaudet P. Pediatric Nephrology. 5th ed. Philadelphia: Lippincott Williams&Wilkins 757-776, 2004.
5. Howlett DC, Greenwood KL, Jarotsz JM, MacDonald LM, Saunders AJ. The incidence of transient renal medullary hyperechogenicity in neonatal ultrasound examination. Br J Radiol 70:140-143, 1997.
6. Makhoul IR, Soudack M, Smolkin T. Neonatal transient renal failure with renal medullary hyperechogenicity: clinical and laboratory features. Pediatr Nephrol 20: 904-909, 2005.
7. Marshansky V, Ausiello DA, Brown D. Physiological importance of endosomal acidification: potential role in proximal tubulopathies. Curr Opin Nephrol Hypertens 11:527-537, 2002.
8. Matsumato J, Han BK, de Rovertto C, Welch TR. Hypercalciuric Bartter syndrome: resolution of nephrocalcinosis with indomethacin. AJR 1989; 152: 1251-1253, 1989.
9. Rodriguez-Soriano J. New insights into the pathogenesis of renal tubular acidosis from functional to molecular studies. Pediatr Nephrol 14:1121-1136, 2000.
10. Roth KS, Chan JC. Renal tubular acidosis: A new look at an old problem. Clin Pediatr (Phila) 40:10533-43, 2001.
11. Shayakula C, Alper SL. Inherited renal tubular acidosis. Curr Opin Nephrol Hypertens 9: 541-546, 2000.
12. Topaloğlu R, Rosa FC. Renal tubular acidosis. In: Cochat P (ed). European Society for Pediatric Nephrology Handbook. Medcom, Lyon 221-224, 2002.
13. US Ali, Sengupta K, Andankar P, Saraf S, Chawla A, Deshpande S. Reversible renal medullary hyperechogenicity in neonatal hypernatremic dehydration. Pediatr Nephrol 19: 1050-1052, 2004.
14. Watanabe T. Proximal renal tubular dysfunction in primary distal renal tubular acidosis. Pediatr Nephrol 20:86-88, 2005.
15. Yüksel S, Dönmez O, Durmaz O. Distal renal tübüler asidozun nadir bir bulgusu; ağır hiperkalsemi. Türk Ped Arş 45:380-383, 2010.

Thank you for copying data from http://www.arastirmax.com