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Diyabetik Nefropatili Hastalarda Proteinüriye Bağlı Hemostatik Değişiklikler

Haemostatic Changes in Patients with Diabetic Nephropathy due to Proteinuria

Journal Name:

  • Türk Nefroloji, Diyaliz ve Transplantasyon Dergisi

Publication Year:

  • 2013
DOI: 
DOI 10.5262/tndt.2013.1001.14

Key Words:

Keywords (Original Language):

Author NameUniversity of AuthorFaculty of Author
Abstract (2. Language): 
AMA Ç: Diyabetes Mellitus’da hiperkoagülabiliteye eğilim olduğu bilinmektedir, pıhtılaşma aktivasyonunun patogenetik mekanizması tam olarak açık değildir ve multifaktöriyel orijinlidir. Kronik hipergliseminin altta yatan esas patoloji olduğu kabul edilmekle birlikte, glisemik kontrolün hemostatik bozukluklarla ilgisi konusunda değişik yorumlar mevcuttur. Çalışmamızda, diyabetik nefropatili hastaları idiyopatik nefrotik sendromlu hastalarla hemostatik değişiklikler açısından değerlendirmeyi amaçladık. GEREÇ ve YÖN TEML ER: Bu amaçla, 10 yeni tanı almış idiyopatik nefrotik sendromlu hastayı normo- mikro- makroalbüminürik evredeki 10’ar tip II diyabetik hasta ve 12 sağlıklı kontrol grubu ile hemostatik parametreler açısından kıyas ettik. Tüm gruplarda aktive protein C, protein S, antitrombin III, Faktör VII, VIII, IX, XI, Plazminojen, fibrinojen çalışıldı. Bulgular: Nefrotik sendromlu hastaların kontrol grubu ve makroalbüminürik hastalardan antitrombin III düzeyi anlamlı düşük, fibrinojen düzeyleri ise kontrol grubundan anlamlı yüksek bulundu. Mikroalbüminürik hastaların fibrinojen düzeyi kontrol grubundan anlamlı yüksek bulundu. Tüm gruplarda diğer hemostatik parametreler normal referans aralığı içerisindeydi. Sonuç: Bu bulgular diyabetik hastalardaki koagülasyona eğilimin nefrotik sendromlu hastalardaki hiperkoagülasyon mekanizmalarından farklı yönde geliştiğini düşündürmektedir.
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Abstract (Original Language): 
OBJECTIVE: It is known that diabetes may cause to hypercoagulability. The pathogenetic mechanism of coagulation activation is not completely clear and the origin is multifactorial. While chronic hyperglycemia is considered to be the main underlying pathology, there are various comments on the association between glycemic control and haemostatic disorders. In this study, we have aimed to compare patients with diabetic nephropathy and patients with idiopathic nephrotic syndrome with respect to haemostatic differences. MA TERIAL and Metho ds: We compared 10 newly diagnosed idiopathic nephrotic syndrome patients with 10 normoalbuminuric, 10 microalbuminuric and 10 macroalbuminuric Type II diabetic patients in terms of haemostatic disorders. We included 12 healthy controls in the study. In all groups, protein C activity, free protein S, Antithrombin III, Factor VII, VIII, IX, XI, plasminogen, fibrinogen and platelet count were evaluated. Res ults : Antithrombin III levels of patients with nephrotic syndrome were significantly lower than the control group and macroalbuminuric diabetics but fibrinogen levels were significantly higher than controls. Fibrinogen levels of microlalbuminuric diabetics were significantly higher than controls. Other haemostatic parameters were all in normal range in all patient groups. ConclusIo ns: These findings suggest that the mechanism of hypercoagulation works in a different pathway than the hypercoagulation in nephrotic patients.
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  • Turkish

REFERENCES

References: 

1. Carr ME: Diabetes mellitus. A hypercoagulable state. J Diabetes
Complications 2001; 15: 44-54
2. Vukovich TC, Schemthaner G: Decreased Protein C levels in
patients with insulin-dependent type I diabetes mellitus. Diabetes
1986; 35: 617-619
3. Schemthaner G, Vukovich T, Knöble P, Hay U, Müler MM:
The effect of near normoglycaemic control on plasma levels of
coagulation factor VII and the anticoagulant proteins C and S in
insulin dependent diabetic patients. Br J Haematol 1989; 73 (3):
356-359
4. Ceriello A, Quatraro A, Dello Russo P, Marchi E, Barbanti M,
Milani MR, Giugliano D: Protein C deficiency in İnsulin dependent
Diabetes: A Hyperglycemia-Related Phenomenon. Thromb
Haemost 1990; 64 (1): 104-107
5. Nar A, Erbaş T: Tip 1 ve Tip 2 Diyabetik hastalarda Hemostatik
parametrelerin değerlendirilmesi ve Diyabetik Vasküler
komplikasyonlar ile ilişkisi. Endokrinolojide Diyalog 2009; 6:
78-86
6. Kanfer A: Coagulation factors in nephrotic syndrome. Am J Nephrol
1990; 10: 63-68
7. Mortazavi F, Majidi J: Evaluation of hemostatic factors in children
with nephrotic syndrome. Pak J Med Sci 2008; 24(3): 356-359
8. Kendall AG, Lohmann RE, Dossetor JB: Nephrotic syndrome: A
hypercoagulable state. Arch Intern Med 1971; 127: 1021-1027
9. Kanfer A, Kleınknetch D, Broyer M, Josso F: Coagulation studies
in 45 cases of nephrotic syndrome without uremia. Thromb Diathes
Haemorrh 1970; 24: 562-571
10. Thompson C, Forbes CD, Prentıce CR, Kennedy AC: Changes in
blood coagulation and fibrinolysis in the nephrotic syndrome. Q J
Med 1974; 43: 399-407
11. Andrassy K, Rıtz E, Bommer J: Hypercoagulability in the nephrotic
syndrome. Kim Wochenschr 1980; 58: 1029-1036
12. De Mattia D, Penza R, Giordano P, Di Bitonto G, Altomare M, Del
Vecchio GC, Schettini F: Thromboembolic risk in children with
nephrotic syndrome. Haemostasis 1991; 21: 300-304
13. Takeda Y, Chen A: Fibrinogen metabolism and distribution in
patients with the nephrotic syndrome. J Lab Clin Med 1967; 70:
678-685
14. Knöbl P, Schernthaner G, Schnack C, Pietschmann P, Griesmacher
A, Prager R, Müller M: Thrombogenic factors are related to urinary
albumin excretion rate in type 1 (insulin-dependent) and type 2
(non-insulin-dependent) diabetic patients. Diabetologia 1993; 36:
1045–1050
15. Grant PJ: Diabetes Mellitus as a prothrombotic condition. J Intern
Med 2007; 262: 157-172
16. Rostoker G, Pech MA, Lagrue G: Proteins C and S of coagulation.
Pathol Biol 1988; 36: 297-299
17. Yermiahu T, Shalev H, Landau D, Dvilansky A: Protein C and
protein S in pediatric nephrotic patients. Sangre 1996; 41: 155-157
18. Aslan B, Eren N, Ciğerli Ş, Müldür F, Yücel N: Evaluation of Plasma
Protein C Antigen, Protein C Activity and Thrombomodulin Levels
in Type 2 Diabetic Patients. Turk J Med Sci 2005; 35: 305-310
19. Kauffman RH, Veltkamp JJ, Van Tılburg NH, Van Es LA: Acquired
antithrombin III deficiency and thrombosis in the nephrotic
syndrome. Am J Med 1978; 65: 607-613
20. Chan V, Yeung CK, Chan TK: Antithrombin III and fibrinogen
degradation product (fragment E) in diabetic nephropathy. J Clin
Pathol 1982; 35: 661-666
21. Llach F: Hypercoagulability, renal vein thrombosis and other
thrombotic complications of nephrotic syndrome. Kidney
International 1985; 28: 429-439
22. Edward N, Young DP, Macleod M: Fibrinolytic activity in plasma
and urine in chronic renal disease. J Clin Pathol 1964; 17: 365-368
23. Hedner U, Nilson IM: Antithrombin III in a clinical material.
Thromb Res 1973; 3: 631-636
24. Scheinman JI, Stiehm ER: Fibrinolytic studies in the nephrotic
syndrome. Pediatr Res 1971; 5: 206-212
25. Wu KK, Hoak JC: Urinary plasminogen and chronic
glomerulonephritis. Am J Clin Pathol 1973; 60: 915-919
26. Lau SO, Tkachuk JY, Hasegawa DK, Edson JR: Plasminogen and
antithrombin III deficiencies in the childhood nephrotic syndrome
associated with plasminogenuria and antithrombinuria. J Pediatr
1980; 96: 390-392
27. Andrew M, Brooker LA: Hemostatic complications in renal
disorders of the young. Pediatr Nephrol 1996; 10: 88-89
28. Balci YI, Tavil B, Fidan G, Ozaltin F: Cerebral sinovenous
thrombosis in a child with steroid sensitive nephrotic syndrome. Eur
J Pediatr 2007; 166: 757-758

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