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Malnütrisyon ve Böbrek Fonksiyonları

Malnutrition and Renal Functions

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Abstract (2. Language): 
Background: Malnutrition is the most common cause of mortality in the world. Previous studies have confirmed significant alterations in renal functions in malnutrition. There is no data about urinary excretion of N-acetyl-P-D-glucosaminidase (NAG) and alanin aminopeptidase (AAP) in malnutrition. Objective: We investigated renal functions and renal tubular damage in children with malnutrition. Methods: Patients with malnutrition (n=20) and healthy controls (n=10) were included into the study. Blood and urine creatinine, Na, K, C l , Ca, P, M g and uric acid levels were studied. Urine N-acetyl-P--D-glucosaminidase (NAG) and alanin aminopeptidase (AAP) levels were measured. Endogen creatinine clearance, tubu¬ lar P reabsorbtion (TRP), fractional Na and K excretion (FENa, FEK), renal failure index were calculated. Na/Cr, K/Cr, Ca/Cr, P/Cr, Mg/Cr, uric acid/Cr ratios were calculated. Results: Serum total protein, albumin, calcium and P levels were significantly lower in children with PEM (p<0.05). Urine P le¬ vels and endogen creatinine clearance were significantly lower in children with PEM (p<0.05). Calcium excretions, calcium/creatinine and sodium/potassium ratios were significantly higher in children with PEM (p<0.05). Urine NAG and A A P levels in children with PEM were low but there was no statistically significant difference (p>0.05). Discussion: We demonstrated that children with malnutrition had a decreased glomerular filtration rate and increased urinary excretion of Na, K, Ca. We consider that there is no tubular damage in malnutrition but there are functional changes in kidney.
Abstract (Original Language): 
Giriş: Malnütrisyon, t üm dünyada ölüm sebepleri arasında oldukça sık görülmektedir. Protein enerji malnütrisyonunda böbrek hemodinamiğinde, böbrek konsantrasyon kapasitesinde ve böbrek asit atılımında değişiklik olmaktadır. Malnütrisyonda, N-asetil-^-Dglukozaminidaz (NAG) ve alanin aminopeptidazın (AAP) idrarla atılımına ait çalışma bulunmamaktadır. Amaç: Bu çalışmanın amacı, protein enerji malnütrisyonunda böbrek fonksiyonlarını ve böbreklerde tübüler hasar oluşumunu araştırmaktır. Yöntem: Çalışmaya malnütrisyonu olan 20 çocuk ve 10 sağlıklı çocuk alındı. T üm çocukların, idrar ve kan kreatinin, Na, K, C l , Ca, P, M g ve ürik asit düzeylerine bakıldı. İdrar N-asetil-P-D-glukozaminidaz (NAG) ve alanin aminopeptidaz (AAP) düzeyleri ölçüldü. Endojen kreatinin klirensi, tübüler P geri emilimi (TRP), fraksiyone Na ve K ekskresyonu (FENa, FEK) hesaplandı. Na/Cr, K/Cr, Ca/Cr, P/Cr, Mg/Cr, ürik asit/Cr oranları belirlendi. Bulgular: Serum total protein, albümin, kalsiyum ve P düzeyleri manütrisyonlu çocuklarda anlamlı düzeyde düşük bulundu (p<0.05). İdrar P düzeyleri, endojen kreatinin klirensi malnütrisyonlu çocuklarda daha düşüktü (p<0.05). İdrarda kalsiyum atılımı, kalsiyum/ kreatinin ve sodyum/potasyum oranları malnütrisyonlu ço¬ cuklarda daha yüksek, P/kreatinin oranı ise daha düşük bulundu (p<0.05). İdrar NAG ve idrar A A P düzeyleri malnütrisyonlu çocuklarda daha düşük olmakla beraber, istatistiksel olarak anlamlı fark saptanmadı (p>0.05). Tartışma: Sonuç olarak, çalışmamızda, malnütrisyonlu çocuk¬ larda glomerüler filtrasyon hızının azaldığı ve idrarla Na, K, Ca atı¬ lımında artış olduğu görülmüştür. Elde ettiğimiz veriler, malnütrisyonda böbrekte tübüler hasar olmadığını, ancak fonksiyonel deği¬ şiklikler olduğunu düşündürmektedir.
FULL TEXT (PDF): 
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REFERENCES

References: 

1. Schofield C, Ashworth A. Why have mortality rates for severe malnutrition remained so high? Bull World Health Organ 1996;74:223-9.
2. Black RE, Morris SS, Bryce J. Where and why are 10 million children dying every year? Lancet 2003;361:2226-34.
3. Benabe JE, Martinez-Maldonado M. The impact of malnut¬rition on kidney function. Miner Electrolyte Metab 1998;24:20-6.
4. Morrison EY, Alleyne GA. Malnutrition, kidney size and composition. Arch Lationam Nutr 1976;26:7-14.
5. Margetic S, Gazzola C, PeggGG, Hill RA. Leptin: a review of its peripheral actions and interactions. Int J Obes Relat Metab Disord 2002;26:1407-33.
6. Wellcome Working Party. Editorial. Lancet 1970;11:302-6.
7. Gordillo G, Soto RA, Medcoff J, Lopez E, Antillon LG. Int-
racellular composition and homeostatic mechanisms in se¬vere chronic infantile malnutrition. III. Renal adjustments.
Pediatrics 1957;20:303-16.
8. Arroyave G, Wilson D, Behar M, Scrimshaw NS. Serum and urinary creatinine in children with severe protein malnutri¬tion. Am J Clin Nutr 1956;9:176-9.
9. Gehring JJ, Jamison RL, Baylis C, Troy JL, Brenner BM, Ja¬mison RL. Effect of intermittent feeding on renal hemody-namics in conscious rats. Am J Physiol 1986;250:566-72.
10. De Nicola L, Blantz RC, Gabbai FB. Nitric oxide and angi-otensin II. Glomerular and tubular interaction in the rat. J
Clin Invest 1992;89:1248-56.
11. Garcia GE, Hammond TC, Wead LM, Mendonca MM,
Brown MR, Gabbai FB. Effect of angiotensin II on the re¬nal response to amino acid in rats. Am J Kidney Dis
1996;28:115-23.
12. Slomowitz LA, Gabbai FB, Khang SJ, et al. Protein intake regulates the vasodilatory function of the kidney and NMDA receptor expression. Am J Physiol Regul Integr
Comp Physiol 2003;287;1184-9.
13. Ichikawa I, Purkerson ML, Klahr S, Troy JL, Martinez-Mal-donado M, Brenner BM. Mechanism of reduced glomerular filtration rate in chronic malnutrition. J Clin Invest
1980;65:982-8.
14. Godard CM, Munoz M, Sanchez MA, Vallotton MB, Riondel A. A study of the renin-angiotensin-aldosterone system in severe infantile malnutrition. Int J Pediatr Nephrol
1986;7:39-44.
15. Feraille E, Doucet A. Sodium-potassium-adenosinetrip-hosphatase-dependent sodium transport in the kidney: hor¬monal control. Physiol Rev 2001;81:345-418.
16. Betowski J, Jamroz-Wioeniewska A, Borkowska E, Wojcic-ka G. Up-regulation of renal Na-K-ATPase: the possible no¬vel mechanism of leptin-induced hypertension. Pol J Phar¬macol 2004;56:213-22.
17. Considine RV, Sinha MK, Heiman ML, et al. Serum immu-noreactive leptin concentrations in normal-weight and obe¬se humans. N Engl J Med 1996;334:292-5.
18. Isik Y, Kalyoncu M, Otken A. Serum leptin levels in maras-mic children and the relationship between leptin and lipid
profile. Ann Nutr Metab 2004;48:259-62.
19. Kilic M, Taksin E, Ustundag B, Aygun AD. The evaluation of serum leptin level and other hormanal parameters in children with severe malnutrition. Clin Biochem
2004;37:382-7.
20. Betowski J, Wojcicka G, Marciniak A, Jamroz A. Oxidative stress, nitric oxide production, and renal sodium handling
in leptin-induced hypertension. Life Sci 2004;74:2987-3000.
21. Kone BC, Higham S. Nitric oxide inhibits transcription of the Na-K-ATPase-1-subunit gene in an MTAL cell line. Am J Physiol 1999;276:614-21.
22. Liang M, Knox FG. Nitric oxide reduces the molecular acti¬vity of Na-K-ATPase in opossum kidney cells. Kidney Int
1999;56:627-34.
23. Betowski J, Wojcicka G, Jamroz-Wioeniewska A, Borkowska E, Marciniak A. Antioxidant treatment normalizes nitric oxide production, renal sodium handling and blood presure in experimental hyperleptinemia. Life Sci 2005;77:1855-68.
Official Journal of the Turkish Society of Nephrology / Türk Nefroloji Diyaliz ve Transplantasyon Dergisi
99
9 Malnutrition and Renal Functions
24. Bhan MK, Bhandari N, Bahl R. Management of the severely malnourished child: perspective from developing countries.
BMJ 2003;326:146-51.
25. Beltowski J, Jamroz-Wisniewska A, Borkowska E, Nazar J, Marciniak A. Antioxidant treatment normalizes renal Na+,K± ATPase activity in leptin-treated rats. Pharmacol
Rep 2005; 57:219-28.
26. Müler O, Krawinkel M. Malnutrition and heath and develo¬ping countries. CMAJ 2005;173:279-86.
27. Manary MJ, Brewster DR. Potassium supplementation in kwashiorkor. J Pediatr Gastroenterol Nutr 1997;24:194-201.
28. Brown NJ. Aldosteron and end-organ damage. Curr Opin
Nephrol Hypertens 2005;14:235-41.
29. Matsuzaki H, Ohdachi J, Fuchigami M, et al. Changes in N-acetyl-beta-D-glucosaminidase activity in the urine and uri¬nary albumin excretion in magnesium deficient rats. Biosci
Biotechnol Biochem 2002;66:192-4.
30. Wu D. Reidenberg MM. Effect of potassium deficiency and gossypol on urinary N-acetyl-beta-glucosaminidase excreti¬on in the rat. Contraception 1993;48:513-6.
31. Yazzie D, Dasgupta A, Okolo A, Glew RH. Lysosomal enzy-muria in protein energy malnutrition. Am J Nephrol
1998;18:9-15.
32. Wu D, Reidenberg MM. Effect of potassium deficiency and gossypol on urinary N-acetyl-beta-glucosaminidase excreti¬on in the rat. Contraception 1993;48:513-6.

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