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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR  
Year : 2015  |  Volume : 26  |  Issue : 4  |  Page : 800-801
An unreported association in a case with chronic microscopic hematuria


1 Department of Pediatric Gastroenterology, Yuzuncu Yil University, Dursun Odabas Medical Center, Van, Turkey
2 Department of Pediatrics, Lokman Hekim Hospital, Van, Turkey

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Date of Web Publication8-Jul-2015
 

How to cite this article:
Demiroren K, Demiroren S. An unreported association in a case with chronic microscopic hematuria. Saudi J Kidney Dis Transpl 2015;26:800-1

How to cite this URL:
Demiroren K, Demiroren S. An unreported association in a case with chronic microscopic hematuria. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2022 Jan 26];26:800-1. Available from: https://www.sjkdt.org/text.asp?2015/26/4/800/160221
To the Editor,

Most of the cases with microscopic hematuria are diagnosed as idiopathic or benign. Vitamin A deficiency was detected in a girl followed-up for two years with microscopic hematuria. Vitamin A treatment was given for one month and hematuria improved.

Microscopic hematuria in children has been reported at various incidence rates. It was found in one or more urine specimens in 4.1% and in two or more urine specimens in 1.1% of school children. [1] It is one of the most important signs of renal or bladder diseases. Although there is a long list of causes of asymptomatic microscopic hematuria, most of the cases are diagnosed as idiopathic or benign and are considered not indicative of significant kidney disease. [2],[3]

We experienced a hitherto unreported association in a case with chronic microscopic hematuria. This is the first report of this kind in the literature according to the best of our knowledge.

A 10-year-old girl was admitted to our clinic with a complaint of growth retardation. Her height and weight were below the 3 rd percentile for her age. Arterial tension and physical examination were normal. Routine laboratory tests were as follows: Hemoglobin 11.8 g/dL; leukocyte 9800/mL; platelet 262,000/mL; urea 23 mg/dL, creatinine 0.4 mg/dL, alanine aminotransferase 26 U/L; aspartate aminotransferase 24 U/L; total protein 5.8 g/dL; albumin 3.6 g/dL; alkaline phosphates 434 U/L. C-reactive protein was 3.3 mg/L (range: 0-5 mg/L). Prothrombin time, partial thromboplastin time and INR values were normal.

Her urine analysis indicated microscopic hematuria. Microscopic hematuria continued for twoyears. By direct counting of erythrocytes in a counting chamber, 5-20 erythrocytes were seen in every monthly urine examination. The morphology of the erythrocytes was normal. She did not have any family history for hematuria or any history of any drug intake accountable for her hematuria. During this follow-up period, hypertension, macroscopic hematuria and abnormal renal function tests were not detected. Urinary calcium/creatinine ratio, protein/creatinine ratio and 24-h urine protein were all within the normal ranges. But, sometimes, +1 proteinuria was present in urinalysis. Evidence for urinary tract infection and nephrolithiasis was not present in routine urine tests and ultra-sonographic imaging. Renal biopsy was not performed as the outcome did not worsen.

At the end of two years, serum vitamin A level was measured and found to be decreased (0.238 mg/L, normal range: 0.35-0.9 mg/L). Thereupon, oral vitamin A treatment was given at a dose of 5000 IU for one month and a vitamin A-enriched diet was recommended to the patient. With this, microscopic hematuria improved and did not recur over the subsequent two years. It is known that alterations in the epithelial lining of vital organs occur in vitamin A deficiency. This indicates an important role of vitamin A for the barrier function and epithelial integrity. [4] Vitamin A also influences the differentiation of the whole embryo and is required for the ad hoc development of numerous tissues and organs, including the kidney. [5] Retinoids act in epithelial-mesenchymal interactions, suggesting a tight control of vitamin A homeostasis for proper renal morphogenesis and differentiation. [6] Retinoids target mesangial cells, podocytes, tubular epithelial cells, interstitial fibroblasts, lymphocytes and macrophages and show anti-inflammatory, anti-coagulatory and tissue repair effects, and proliferativeand immune modulatory actions. [7],[8] Direct antifibrotic and cytoprotective effects of retinoids in various renal cell types have been revealed. [8] Therefore, it is suggested that retinoid-based therapies are emerging as useful therapies for kidney disorders because retinoids play key roles in the kidney. [9]

In the present case, a chronic asymptomatic microscopic hematuria had continued for two years. After the detection of vitamin A deficiency and administration of vitamin A, hematuria had improved and it did not repeat throughout the follow-up of two years. Therefore, we suppose that microscopic hematuria in this case is most probably due to vitamin A deficiency.

In conclusion, we speculate that vitamin A deficiency may be a cause of chronic microscopic hematuria. Before further investigations are performed for detecting the cause of microscopic hematuria, the vitamin A level may be measured in selected cases, especially in malnourished ones. Further studies are needed for verifying this.

Conflict of interest: None declared.

 
   References Top

1.
Vehaskari VM, Rapola J, Koskimies O, Savilahti E, Vilska J, Hallman N. Microscopic hematuria in school children: Epidemiology and clinicopathologic evaluation. J Pediatr 1979;95:676-84.  Back to cited text no. 1
[PUBMED]    
2.
Feld LG, Meyers KE, Kaplan BS, Stapleton FB. Limited evaluation of microscopic hematuria in pediatrics. Pediatrics 1998;102:E42.  Back to cited text no. 2
    
3.
Gale DP. How benign is hematuria? Using genetics to predict prognosis. Pediatr Nephrol 2013;28:1183-93.  Back to cited text no. 3
    
4.
McCullough FS, Northrop-Clewes CA, Thurnham DI. The effect of vitamin A on epithelial integrity. Proc Nutr Soc 1999;58:289-93.  Back to cited text no. 4
    
5.
Gilbert T, Merlet-Bénichou C. Retinoids and nephron mass control. Pediatr Nephrol 2000;14: 1137-44.  Back to cited text no. 5
    
6.
Gilbert T. Vitamin A and kidney development. Nephrol Dial Transplant 2002;17 Suppl 9:78-80.  Back to cited text no. 6
    
7.
Xu Q, Kopp JB. Retinoid and TGF-ß families: Crosstalk in development, neoplasia, immunity, and tissue repair. Semin Nephrol 2012;32:287-94.  Back to cited text no. 7
    
8.
Xu Q, Lucio-Cazana J, Kitamura M, Ruan X, Fine LG, Norman JT. Retinoids in nephrology: Promises and pitfalls. Kidney Int 2004;66:2119-31.  Back to cited text no. 8
    
9.
Gudas LJ. Emerging roles for retinoids in regeneration and differentiation in normal and disease states. Biochim Biophys Acta 2012;1821: 213-21.  Back to cited text no. 9
    

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Correspondence Address:
Dr. Kaan Demiroren
Department of Pediatric Gastroenterology, Yuzuncu Yil University, Dursun Odabas Medical Center, Van
Turkey
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DOI: 10.4103/1319-2442.160221

PMID: 26178562

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