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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR  
Year : 2016  |  Volume : 27  |  Issue : 4  |  Page : 841-842
Remarks about the study on lactate dehydrogenase as a biomarker for early renal damage in patients with sickle cell disease


Department of Pediatrics, Al-Kindy College of Medicine, Baghdad University, Baghdad, Iraq

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Date of Web Publication5-Jul-2016
 

How to cite this article:
Al-Mendalawi MD. Remarks about the study on lactate dehydrogenase as a biomarker for early renal damage in patients with sickle cell disease. Saudi J Kidney Dis Transpl 2016;27:841-2

How to cite this URL:
Al-Mendalawi MD. Remarks about the study on lactate dehydrogenase as a biomarker for early renal damage in patients with sickle cell disease. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2021 Oct 19];27:841-2. Available from: https://www.sjkdt.org/text.asp?2016/27/4/841/185303
To the Editor,

I have two comments on the interesting study by Alzahri et al on lactate dehydrogenase (LDH) as a biomarker for early renal damage in sickle cell disease (SCD) patients. [1]

First, Alzahri et al [1] addressed that in SCD patients, LDH was correlated with creatinine clearance (CC) and, therefore, LDH could serve as a biomarker to predict renal insufficiency in such patients. I presume that the clinical implication of that recommendation is questionable. This is based on the following three points:

  1. It is obvious that LDH exists in five separable isoenzymes numbered 1-5 according to their electrophoretic mobility. The distribution of the five isoenzymes is not uniform across body tissues. LDH1 and LDH2 are found primarily in red blood cells and heart muscle; LDH3 is highest in the lungs; LDH4 is highest in the kidneys, placenta, and pancreas; and LDH5 is highest in skeletal muscle and liver. [2] The routine determination of serum LDH includes all its isoenzymes. I presume that the methodology employed in the study by Alzahri et al included routine determination of all LDH isoenzymes. To render their conclusion and recommendation more accurate and valid, estimation of serum LDH4 rather than routine LDH measurement and assessing its correlation with CC were solicited by Alzahri et al. [1]
  2. Many parameters in SCD patients could be associated to elevated serum LDH, namely, severity of hemolysis, [3] severity of pain during vaso-occlusive episodes, [4] and the presence of SCD-associated complications such as leg ulcer, cholelithiasis, and aseptic necrosis of the femoral head. [5] Therefore, it would be questionable to solely attribute increased serum LDH to early sickle cell nephropathy (SCN)
  3. It is not uncommon for SCD patients, particularly middle-aged and elderly patients to have associated comorbidities such as myocardial infarction, stroke, diabetes mellitus, and malignancies. All these comorbidities might further contribute to elevated serum LDH and hence, cast suspicion on the utility of serum LDH to solely predict early SCN.


Second, serum FMS-like tyrosine kinase-1 (sFLT-1) has currently received ample consideration as a biomarker for the early diagnosis of SCN. In a recently published Egyptian study, the serum level of sFLT-1 in SCD patients was found to be higher than controls (median/range/interquartile range = 142/60-1300/61 pg/mL vs. 125/110-187/52 pg/mL, respectively) (P = 0.006). Moreover, the median (range) of sFLT-1 level was noticed to be higher in SCD patients with microalbuminuria compared to SCD patients with normoalbuminuria, [185 (140-1300) vs. 125 (60-189) mg/g, respectively] (P = 0.004). There was a significant positive correlation between serum sFLT-1 and microalbuminuria, LDH, and indirect bilirubin (r = 0.59, 0.39, 0.30, and P <0.001, 0.007, 0.041, respectively). The sFLT-1 sensitivity was estimated to be 93.6%, while specificity was 68.6%. The study concluded that sFLT-1 might contribute to the pathogenesis of albuminuria in SCD patients and constitute a novel renal biomarker for the early detection of SCN. [6] I presume that sFLT-1 might be a sound alternative than serum LDH as a renal biomarker. However, randomized, prospective clinical trials are needed to better assess its utility in the clinical setting.

Conflict of interest: None declared.

 
   References Top

1.
Alzahri MS, Mousa SA, Almomen AM, Hasanato RM, Polimeni JM, Racz MJ. Lactate dehydrogenase as a biomarker for early renal damage in patients with sickle cell disease. Saudi J Kidney Dis Transpl 2015;26:1161-8.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.
McPherson RA, Pincus MR, Abraham NZ Jr., Carty RP. Clinical enzymology. In: McPherson RA, Pincus MR, eds. Henry's Diagnosis and Management by Laboratory Methods. 22nd ed. Philadelphia, PA: Elsevier Saunders; 2011. p.273-5.  Back to cited text no. 2
    
3.
Ballas SK. Clinical utility of lactate dehydrogenase in determining the severity of hemolysis in sickle cell anemia. Am J Clin Pathol 2015;144:173-4.  Back to cited text no. 3
[PUBMED]    
4.
Najim OA, Hassan MK. Lactate dehydrogenase and severity of pain in children with sickle cell disease. Acta Haematol 2011;126:157-62.  Back to cited text no. 4
[PUBMED]    
5.
Mikobi TM, Lukusa Tshilobo P, Aloni MN, et al. Correlation between the lactate dehydrogenase levels with laboratory variables in the clinical severity of sickle cell anemia in Congolese patients. PLoS One 2015;10: e0123568.  Back to cited text no. 5
[PUBMED]    
6.
Youssry I, Makar S, Fawzy R, et al. Novel marker for the detection of sickle cell nephropathy: soluble FMS-like tyrosine kinase-1 (sFLT-1). Pediatr Nephrol 2015;30:2163-8.  Back to cited text no. 6
    

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Correspondence Address:
Prof. Mahmood Dhahir Al-Mendalawi
Department of Pediatrics, Al-Kindy College of Medicine, Baghdad University, Baghdad
Iraq
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DOI: 10.4103/1319-2442.185303

PMID: 27424716

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