Buradasınız

Anasayfa » Content

DIABETES MELLITUSLU HASTALARDA HIPORENINEMIK HIPOALDOSTERONIZM (HRHA) SıKLıĞı

THE FREQUENCY OF HYPORENINEMIC HYPOALDOSTERONISM (HRHA) IN PATIENTS WITH DIABETES MELLITUS

Journal Name:

  • Türk Nefroloji, Diyaliz ve Transplantasyon Dergisi

Publication Year:

  • 1997

Key Words:

Keywords (Original Language):

Author NameUniversity of AuthorFaculty of Author
Abstract (2. Language): 
In this study, plasma renin activity (PRA) and aldosterone levels were determined in 96 type II diabetic patients (50 females, 46 males) with a duration longer than 10 years and in 20 similarly aged-matched healthy subjects in order to investigate the frequency of HRHA in type II diabetes mellitus (DM). Patients with adrenal insufficiency and those using nonsteroidal anti-inflammatory drugs (NSAIDs), diuretics or angiotensin converting enzyme (ACE) inhibitors during last one month were not included in this study. After at least a 3-day of diabetic diet containing normal salt amount, PRA and aldosterone levels were measured in venous samples obtained after a 2-hour standing. In diabetic group, mean PRA and aldosterone levels were found to be significantly decreased when compared to the control group. The cutt off points for hyporeninemia and hypoaldosteronism were calculated by mean value oj control group-2SD, and PRA values lower than 1.5 ng/ml/h and aldosterone values lower than 4 ng/dl were accepted as hyporeninemia and hypoaldosteronism, respectively. According to these criteria, HRHA was detected in 15 (156 %) patients. Mean age, mean arterial pressure and potassium levels were higher and mean GFR values were lower in patients with than in ones without HRHA. After 3-days of salt-free diet, renin-aldosterone stimulation was performed in 15 patients with HRHA by giving 20 mg iv furosemide. While 9 patients respond to stimulation (mild or secondary forms), PRA and aldosterone levels of remaining 6 patients were not increased (true HRHA). Six patients not responding to stimulation had lower GFR, hyperpotassemia and mild metabolic acidosis. Hyperpotassemia was partly controlled by insulin and sodium bicarbonate therpy in these 6 cases. As a conclusion, we found that the frequency oj HRHA in type II DM was significantly high. Therefore, ACE inhibitors and NSAIDs should not be given to type II diabetic patients, particulary over 50 years oj age without determining serum potassium and creatinine levels.
Bookmark/Search this post with
Abstract (Original Language): 
Tip II diabetU hastalarda HRHA sıklığını araştırmak amacıyla yapılan bu çalışmada, diabet süresi on yılın üzerinde olan adulı diabetli toplam 96 hasta (50 K, 46 E) ile aynı yaş grubundaki sağlıklı 20 vakada plazma renin aktivitesi (PRA) ve aldosteron düzeyleri tayin edildi. Son 1 ay içerisinde ACE inhibitörü, diüreük ve nonsteroid antienflamatuar (NSAE) ilaç kullanan vakalar ile adrenal yetmezliği olanlar çalışmaya alın¬madı. PRA ve aldosteron düzeyi en az 3 gün süre ile normal miktarda tuz içeren diabet diyeti ve 2 saatlik ayakta durma sonrası alınan venöz kan örneklerinde RIA ile çalışıldı. Diabetik grupta ortalama PRA ve aldosteron dü¬zeyi kontrol grubuna göre önemli derecede daha dü¬şük bulundu. Hiporeninemi ve hipoaldosteronizm için kontrol grubu X-2SD değeri alınarak cutt off belirlendi ve 1.5 ng/ml/saat'in altındaki PRA hiporeninemi, 4 ng/dl'nin altındaki aldosteron düzeyi ise hipoaldosteronizm olarak kabul edildi. Buna göre toplam 15 hastada (%15.6) HRHA tespit edildi. HRHA'mi olan hastalarda yaş ortalaması, ortalama arteriyel basınç ve serum potasyum düzeyi olmayanlara göre önemli derecede daha yüksek, GFR ise daha düşük bulundu. Hiporeninemik hipoaldosteronizmli bu 15 hastaya 3 günlük tuzsuz diyetten sonra 20 mg i.v furosemid verilerek renin-aldosteron stimiilasyonu uy¬gulandı. 9 hasta stimülasyona cevap verinken ( hafij veya sekonder formlar), 6 hastanın PRA ve aldosteron düzeylerinde önemli bir artış olmadı (gerçek HRHA). Stimülasyona cevap alınamayan 6 hastada GFR düze¬yi daha düşüktü, hiperpotesemi ve hafif metabolik asidoz mevcuttu. Bu olgulardaki hiperpotasemi insülin ve sodyum bikarbonat tedavisi ile kısmen kontrole alındı. Sonuç olarak, Tip II diabetli hastalarda HRHA sıklığını oldukça yüksek bulduk. Bu nedenle özellikle 50 yaşın üzerindeki diabetik hastalarda serum potasyum ve kreatinin düzeyini tayin etmeden ACE in-hibitörü ve NSAE ilaç verilmemesi uygun olacaktır.
FULL TEXT (PDF): 
PDF icon pdf_tndt_170.pdf
  • 1-2
66-70
  • Turkish

REFERENCES

References: 

1. Holland O.B. Hypoaldosteronism-disease or normal response? N Eng J Med 1991; 324 (7): 488-489.
2. Biglieri EG,
Kate
r CE . Mineralocorticoids. In . Greens¬pan FS (ed). Basic and Clinical Endocrinology. Prentice
Hall, Appleton and Lange, 1991: 374-378.
3. Williams GH. Hyporeninemic hypoaldosteronism. N
Eng J Med 1986; 314(16): 1041-1042.
4. Sunderlin FS, Anderson GH, Streeten DH. Blumentha] SA. The renin-angiotensin-aldosterone system in diabetic patients with hyperkalemia. Diabetes 1981; 30 : 335-340.
5. Tyrrell JB . Adrenocortical hypofunction. In . Wynqaar-
den JB, Smith LH, Bennett JC. Cecil Texbook ol Medicine, Philadelphia, W. B. Saunders Co. 1992. pp, 1281-84.
6. Large DM, Carr PH, Laing I, Davies M. Hyperkalaemia in diabetes mellitus-potential hazards of coexisting hyporeninaemic hypoaldosteronism. Postgrad Med J
1984; 60 :370-373.
7. Kaufman JS, Peck M, Hamburger RJ, Flamenbaum W. Isolated hypoaldosteronism and abnormalities in renin, kallikrein and prostaglandin. Nephron 1986; 43: 203¬210.
8. Rosa RM, Batlle D. Hyperkalemia. In . Jacobson HR. Striker GE, Klahr S (eds.), The Principles and Practice of Nephrology (Second edition), Mosby-USA 1995 : 911-17.
9. Gomez-Martino JR., Miralles JM, De Leon B. Hernandez MT, Tabernero JM. Urinary prostaglandins (PGE2 and PGI2) in hyporeninaemic hypoaldosteronism in diabetic patients with chronic renal failure. Nephrol
Dial Transplant 1994; 9: 251-256.
10. Christlieb AR, Kaldany A, D'Elia JA, Williams GH .
Aldosterone responsiveness in patients with diabetes
mellitus. Diabetes 1978; 27: 732-7.
69
11. Tang SY, Antonipillai I, Mulrow PJ. Inactive renin and prostaglandins E2 production in hyporeninemic hypoaldosteronism. J Clin Endocrinol Metab 1980; 51: 849-853.
12. Wilson DM, Luetscher J A . Plasma prorenin activity
and complications with insulin dependent diabetes mellitus. N Eng J Med 1990; 323: 1101-6.
13. Ferrara E, Week E, Hanenson I, Privitera P, Kenion C. Selective hypoaldosteronism with blunted renin activity responsiveness. Clin Res 1970; 18: 602-606.
14. Muter E, Nath KA . Chronic tubulointerstitial nephritis. In Jacobson HR, Striker GE, Klahr S (eds.), The Principles and Practice of Nephrology (Second edition),
Mosby-USA 1995: 216-24.
15. Gordon RD. Syndrome of hypertension and hyperkalemia with normal glomerular filtration rate.
Hypertension 1986; 8: 93-102.
16. Grande J, Macias Nunez JF, Miralles JM, de Castro del Pozo S, Tabernero Roma JM. Hyporeninemic hypoaldosteronism in diabetic patients with chronic
renal failure Am J Nephrol 1988; 8: 127-137.
70

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