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EDITORIAL
Year : 2020  |  Volume : 7  |  Issue : 2  |  Page : 59-60

Microalbuminuria as a sensitive predictor of early glomerular injury in children with sickle cell anemia


Department of Pediatric Intensive Care, NMC Royal Hospital, AD, UAE

Date of Submission03-Mar-2020
Date of Acceptance10-Mar-2020
Date of Web Publication10-Apr-2020

Correspondence Address:
Dr. Govind Benakatti
NMC Royal Hospital, AD
UAE
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JPCC.JPCC_41_20

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How to cite this article:
Benakatti G. Microalbuminuria as a sensitive predictor of early glomerular injury in children with sickle cell anemia. J Pediatr Crit Care 2020;7:59-60

How to cite this URL:
Benakatti G. Microalbuminuria as a sensitive predictor of early glomerular injury in children with sickle cell anemia. J Pediatr Crit Care [serial online] 2020 [cited 2020 Sep 25];7:59-60. Available from: http://www.jpcc.org.in/text.asp?2020/7/2/59/282232



Microalbuminuria (MA) defined as minute elevation in the urine albumin (30–300 mg/24 h in an adult or an albumin: creatinine ratio >20–30 mg/g creatinine in a random sample) in the absence overt proteinuria that is not detectable by conventional dipstick methods. It is a nonspecific but sensitive indicator of preclinical renal and cardiovascular morbidity and mortality. Its role as a sensitive marker in diagnosing nephropathy of varied ethology (glomerular damage caused by hyperfiltration, hyperperfusion, etc.) and as a predictor of progression to overt renal failure is not something new, for example, diabetic nephropathy (DN) where it is widely used to predict and prognosticate. Other areas of its use are hypertensive nephropathy, cardiovascular disease (CVD) risk, etc.

Similar renal damage is known to occur in sickle cell anemia (SCA). Therefore, similar phenomenon of microproteinuria is reported to occur long before it progresses to overt proteinuria or renal failure.[1],[2],[3] Renal damage (sickle cell nephropathy [SCN]) results from recurrent vaso-occlusive crisis, ischemia–reperfusion injury, loss of renal mass, glomerular hyperfiltration, and sclerosis.[4] Evidence of kidney changes has been observed as early as infancy, and MA has been detected in as early as 3–4 years.[5] Identification of MA and risk factors may allow early interventions such as ACE inhibitors (ACEI) and hydroxyurea, which have been shown to retard the progression to overt renal failure. In this issue of Journal of Pediatric Critical Care, Meher et al. have tried to address the role of MA in SCN similar to DN.[6] Given the limited data, screening the children with SCA at an early age and follow-ups for the development of MA would have been more apt to address the objectives of the study. Enrolling a known, in fact, those in quite, advanced nephropathy takes away the whole idea of finding out MA as an early indicator. Therefore, one can wonder that the study adds any value in differentiating those with SCN versus not. According to authors' enrolment strategy, those with the “disease” (estimated glomerular filtration rate [eGFR] <60 ml/min/1.73 m2 body surface area [BSA]) categorized into Stage-III chronic kidney disease (CKD);[7] understandably, this is quite advanced kidney disease rather than preclinical nephropathy. Again, the estimation of GFR based on single creatinine value is a crude method that often poorly correlates with measured GFR. McKie et al.[8] analyzed longitudinal data of 191 sickle cell children aged 3–20 years with a mean follow-up of 2.19 ± 2.05 years. ACEI and hydroxyurea showed to reverse MA in half (44% hydroxyurea and 56% ACEI) of the patients. Therefore, longitudinal studies further in earlier age groups with follow-ups will address the primary concern of how early these children at risk can be identified and appropriate (preventive) measures could be applied.

In nutshell, improved standards of care have reflected in the longer survival of children with SCA. SCN is an important risk factor for long-term morbidity and mortality. Longitudinal studies involving earlier age groups are needed to address the optimum age for early identification and then early interventions. Interventions such as ACEI and hydroxyurea have been shown to retard the progression to overt renal failure or CKD in these children.



 
  References Top

1.
McBurney PG, Hanevold CD, Hernandez CM, Waller JL, McKie KM. Risk factors for microalbuminuria in children with sickle cell anemia. J Pediatr Hematol Oncol 2002;24:473-7.  Back to cited text no. 1
    
2.
King L, MooSang M, Miller M, Reid M. Prevalence and predictors of microalbuminuria in Jamaican children with sickle cell disease. Arch Dis Child 2011;96:1135-9.  Back to cited text no. 2
    
3.
Abhulimhen-Iyoha IB, Ibadin MO, Ofovwe EG. Comparative usefulness of serum creatinine and microalbuminuria in detecting early renal changes in children with sickle cell anaemia in Benin city. Niger J Paediatr 2009;36:1-2.  Back to cited text no. 3
    
4.
Pham PT, Pham PC, Wilkinson AH, Lew SQ. Renal abnormalities in sickle cell disease. Kidney Int 2000;57:1-8.  Back to cited text no. 4
    
5.
Marsenic O, Couloures KG, Wiley JM. Proteinuria in children with sickle cell disease. Nephrol Dial Transplant 2008;23:715-20.  Back to cited text no. 5
    
6.
Meher SK, Mishra NR, Khamari DK, Nayak BK. Diagnostic accuracy of microalbuminuria among sickle cell children with nephropathy. J Ped Crit Care 2020;7:73-8.  Back to cited text no. 6
    
7.
National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002;39:S1-266.  Back to cited text no. 7
    
8.
McKie KT, Hanevold CD, Hernandez C, Waller JL, Ortiz L, McKie KM. Prevalence, prevention, and treatment of microalbuminuria and proteinuria in children with sickle cell disease. J Pediatr Hematol Oncol 2007;29:140-4.  Back to cited text no. 8
    




 

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