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HEMODİYALİZ HASTALARINDA KT/V DEĞERİNİN ARTIRILMASININ İNSÜLİN DİRENCİ ÜZERİNE ETKİSİ

THE EFFECT OF INCREASED KT/V VALUES ON INSULIN RESISTANCE IN THE HEMODIALYSIS PATIENTS

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Abstract (2. Language): 
28 outpatients with end-stage renal disease who were on hemodialysis treatment were included in the study. Kt/V values of all cases were calculated by ureakinetic modelling. During 12 weeks we tried to keep Kt/V almost equal to 1.0 in all patients. After 12 weeks 18 cases who had mean Kt/V value of 1.0+0.02 were selected as the study group. 10 cases with the mean Kt/V value of 1.1+0.02 were selected as control group. The mean age of study and control groups was 36.5+1.0 yearsand37.2+1.5 years, respectively. Among groups, there was no difference in terms of age, the duration of dialysis, parathyroid hormone, serum calcium, phosphorus and albumin levels measured before the study. Intravenous glucose tolerance test (TVGTT) after an overnight fast was performed to all patients. The Kt/V values of the patients in the study group were elevated to 1.5+0.02 by increasing the pump rate and the dialysis duration. The Kt/V values in the control group were tried to be kept constant (1.1+0.03). After 12 weeks, IVGTT was repeated in both groups. Glucose and insulin values were determined from all samples during IVGTT. Total areas under the curves of glucose and insulin values between 0 and 120 minutes were calculated by using the trapezoidal integration. Statistical analysis was performed with student's t-test, andnonparametric Mann-Whitney and Wilcoxon signed rank tests. After 12 weeks, while the fasting glucose levels of study group decreased from 91.8 ±4.8 mg/cll. to 73.5+2.4 mg/dl (p < 0.01), those of control group did not change significantly. The changes in the fasting insulin levels of both group were not significant. Stimulated glucose and insulin levels in the study group markedly decreased during IVGTT compared to the pre-study values. But those of control group did not change except the values between 2 and 60 minutes. After the study, the total area under the curves of glucose and insulin of study group significantly decreased when compared to the pre-study values. We suggested that there was a correlation between the increment in dialysis efficacy and insulin sensitivity due to the increase in metabolized glucose and decrease in insulin concentrations
Abstract (Original Language): 
Bu çalışma, son dönem böbrek yetmezliği nedeniyle hemodiyaliz tedavisi gören 28 stabil hastada yapıldı. Tüm hastaların Kt/V değerleri ürekinetik model ile hesaplandı. 12 hafta boyunca Kt/V değerleri 1.0 'da tutulmaya çalışıldı. 12 hafta sonra ortalama Kt/V değeri 1.0±0.02 olan 18hasta çalışma grubu olarak seçildi. Ortalama Kt/ V değerleri 1.1 ±0.02 olan 10 hasta ise kontrol grubunu oluşturdular. Grupların yaş, diyaliz süreleri ve çalışma öncesi ölçülenparatiroidhormon, serum kalsiyum, fosfor ve albümin seviyeleri arasında fark yoktu. Tüm hastalara geceboyu süren açlık sonrası intravenöz glikoz tolerans testi (İVGTT) yapıldı. Çalışma grubundaki hastaların Kt/V değerleri pompa hızı ve diyaliz süresi artırılarak 1.5+0.02 'ye yükseltildi. Kontrol grubundaki hastaların Kt/ V değerleri sabit tutulmaya çalışıldı (l.l±0.03). 12 hafta sonra her iki grupta da İVGTT tekrarlandı. İVGTT sırasında elde edilen tüm örneklerden glikoz ve insülin düzeyleri çalışıldı. 0 ve 120 dakika arasındaki glikoz ve insülin değerleri için eğri altında kalan toplam alanlar hesaplandı. İstatistiksel analiz Student's t-test, nonparametrik Wilcoxon işaret ve Mann Whitney u-testi ile yapıldı. 12 hafta sonra, çalışma grubunun açlık serum glikoz seviyeleri 91.8±4.8 mg/dlden 73.5+2.4 mg/dl'ye azaldı (p<0.01), kontrol grubunda ise anlamlı bir değişiklik olmadı. Her iki grubun açlık insülin düzeylerindeki değişiklikler anlamlı değildi. Çalışma grubunda İVGTT sırasında elde edilen glikoz ve insülin değerleri çalışma öncesi değerler ile karşılaştırıldığında belirgin azaldılar. Ama, kontrol grubunda bu değerlerde 2. ve 60. dakikalar arası dışında çalışma sonrası anlamlı bir değişiklik olmadı. Çalışma sonrası, çalışma grubunda glikoz ve insülin eğrilerinin altında kalan toplam alanlar çalışma öncesi ile karşılaştırıldığında anlamlı azaldı. Biz, diyaliz etkinliğinin artırılması ile insülin duyarlılığı arasında bir korelasyon olduğunu, bununda metabolize olan glikoz miktarının artması ve insülin konsantrasyonlarının azalması ile ilişkili olduğunu düşündük.
FULL TEXT (PDF): 
229-235

REFERENCES

References: 

1. DeFronzo RA, Tobin JD, Rowe JW, Andres R: Glucose intolerance in uremia. Quantification of pancreatic beta cell sensitivity to glucose and tissue sensitivity to insülin. J Clin Invest 1978; 62: 425-435.
2. Linder A, Charra B, Sherpard DJ, Scribner BH: Accelerated atherosclerosis in prolonged maintainance
hemodialysis. N Engl J Med 1974; 290: 697-701.
3. Fontbonne A, Charles MA, Thibult N et al. Hyperinsiilinaemia is a predictor of coronary heart disease mortality in a healthy population: The Paris Prospective Study, 15-year follow-up. Diabetologia
1991;34:356-361.
4. Lopez-Gomez JM, Verde E, Perez-Garcia R: Blood pressure, left ventricular hypertrophy and long-term prognosis in hemodialysis patients. Kidney Int 1998; 54
(Suppl.68): S92-S98.
5. Amann K, Rychlik I, Miherberger-Milteny G, Ritz E. Left ventricular hypertrophy in renal failure. Kidney Int
1998; 54 (Suppl.68): S78-S85.
6. Gotch FA, Sargent JA. A mechanistic analysis of the National Cooperative Dialysis Study (NCDS). Kidney Int 1985;28:526-534.
7. Gotch FA. Kinetic modelling in hemodialysis. In: Nissenson AR, Fine RN (eds), Dialysis Therapy.
234
Second ed., Hanley & Belfus, Philadelphia, 1993, p: 79-85.
8. Watson PE, Watson ID, Batt RD. Total body water volumes for adult males and females estimated from simple anthropometric measurements. Am J Clin Nutr 1980;33:27-39.
9. DeFronzo RA, Andres R, Edgar P, Walker WG.
Carbohydrate metabolism in uremia: a review. Medicine 1973; 52: 469-481.
10. DeFronzo RA, Smith JD: Is glucose intolerance harmful for the uremic patient. Kidney Int 1985; 28
(Suppl,17):S88-S97.
11. Mak RHK, DeFronzo RA: Glucose and insulin metabolism in uremia. Nephron 1992; 61: 377-382.
12. Calpaldo B, Cianciaruso B, Napoli R. Role of splancnic tissues in the pathogenesis of altered carbohydrate metabolism in patients with chronic renal failure. J Clin
Endocrinol Metab 1990; 70: 127-133.
13. DeFronzo RA, Smith D, Alvestrand A. Insulin action in
uremia. Kidney Int 1983; 24 (Suppl.16): S102-S114.
14. Mondon CE, Dolkas CB, Reaven GM: Effect of acute
uremia on insulin removal by the isolated perfused rat liver and muscle. Metabolism 1978; 27: 133-142.
15. Dzurik R, Hupkova V, Cernacek P: The isolation of an inhibitor of glucose utilization from the serum of uremic
subjects. Clin Chim Acta 1983; 46: 77.
16. Tattersal JE, DeTakats D, Chamney P. The post-hemodialysis rebound: Predicting and quantifying its
effect on Kt/V. Kidney Int 1996; 50: 2094-2102.
17. Fadda GZ, Akmal M, Premdas FH et al. Insulin release from pancreatic islets: Effects of CRF and excess PTH.
Kidney Int 1988; 33: 1066-1072.
18. Mak RHK. Intravenous 1.25 dihydroxycholecalciferol corrects glucose intolerance in hemodialysis patients. Kidney Int 1992; 41: 1049-1054.
19. Mak RHK, Bertinelli A, Turner C et al: The influence of hyperparathyroidism on glucose metabolism in uremia. J
Clin Endocrinol Metab 1985; 60: 229-233.
20. Kautzky-Wilier A, Pacini G, Bamas V et al: Intravenous calcitriol normalizes insulin sensitivity in
uremic patients. Kidney Int 1995; 47: 200-206.
21. Mak RHK. Effect of metabolic acidosis on insulin action and secretion in uremia. Kidney Int 1998; 54:
603-607.
22. Clausen T, Elbrink J, Dahl-Handen AB. The role of cellular calcium in activation of the glucose transport system in rat soleus muscle. Biochim Biophys Acta
1975;375:292-308.
23. Cohen P. The hormonal control of glycogen metabolism in mammalian muscle by multivalent phosphorylation. Biochem Soc Trans 1979; 7: 459-480.

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