Documentation of renal glomerular and tubular impairment and glomerular hyperfiltration in multitransfused patients with beta thalassemia


Deveci B., Kurtoglu A., Kurtoglu E., SALİM O., TOPTAŞ T.

ANNALS OF HEMATOLOGY, cilt.95, sa.3, ss.375-381, 2016 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 95 Konu: 3
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1007/s00277-015-2561-2
  • Dergi Adı: ANNALS OF HEMATOLOGY
  • Sayfa Sayıları: ss.375-381

Özet

Urinary albumin to creatinine (ACR) and beta2 microglobulin to creatinine ratios (BCR) are the surrogate and robust markers of renal glomerulopathy and tubulopathy, respectively. These markers predict short-term renal deterioration and mortality in various conditions. We aimed to assess the frequency and predictors of glomerular and tubular defects, renal impairment, and hyperfiltration in 96 adult patients with beta thalassemia intermedia and major. ACR>300 mg/g creatinine and BCR>300 mu g/g creatinine were used to define the renal glomerular and tubular damages, respectively. Glomerular filtration rate (eGFR(creat)) was estimated according to 2009 the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. Decreased eGFR(creat) was defined as less than 60 mL/min per 1.73 m(2). Renal glomerular and/or tubular defects were observed in about 68.8 % of all patients. Forty percent of patients had glomerular hyperfiltration. None of the patients had a decreased eGFR(creat). T2* value <= 20 msec on cardiac magnetic resonance (cMR) was the only independent predictor of glomerular damage (p=0.013). Use of alendronate was associated with less renal tubular damage (p=0.007). Female gender and previous history of splenectomy were the independent predictors of glomerular hyperfiltration in multivariate analysis (p<0.001 and p=0.040, respectively). Renal tubular and glomerular damage is frequent in adult patients with thalassemia intermedia and major. T2* value on cMR was the only independent predictor of glomerular damage. However, since we did not explore all the parameters of iron, it is not possible to draw a definite conclusion about the association of cMR and glomerular damage. There is no association with cardiac iron overload/accumulation and tubular damage or hyperfiltration.