Nephrotic syndrome (NS) is considered as one of the most common glomerular kidney diseases, often encountered in children with a characteristic triad of massive proteinuria (40 mg/h/m2 in children), hypoalbuminemia, and dependent edema, due to the disrupted function of glomerular filtration barrier (GFB) (Bagga, 2008; Bierzynska and Saleem, 2017) [1, 2]. In children below the age of 18 years, minimal change nephropathy (MCN) and focal segmental glomerulosclerosis (FSGS) represent the cause of NS in over 85% of cases (Mekahli et al., 2009) . In children, MCN is the major cause of NS, responds to steroids at conventional doses and hence this disease is termed steroid sensitive NS (SSNS), while in steroid resistant NS (SRNS), FSGS is the most common histopathological lesion, and may progress to end-stage renal disease (ESRD) (Mekahli et al., 2009; Hjorten et al., 2016) [3, 4].
Renal biopsy is a standard procedure but an invasive technique with potential complications, to define the histology, and serial monitoring is not normally feasible, especially for children (Luo et al., 2013) . In recent studies, urinary miRNAs are regarded as biomarkers as they reflect kidney diseases including NS (Szeto, 2014; Chen et al., 2018) [6, 7]. Some of them are involved in the pathogenesis of NS and thus are disease-specific. Recently, Chen et al. (2018) have identified elevated levels of urinary miR-194-5p, miR-146b-5p, miR-378a-3p, miR-23b-3p and miR-30a-5p) in children with NS. Similarly, urinary miR-21, miR-216a, and miR-494 which are found to be in NS may predict a high risk of disease progression and loss of renal function, irrespective of the histological diagnosis (Szeto, 2014) . In view of its stability and easy quantification, urinary miRNAs could be used as attractive biomarker candidates for disease diagnosis, predicting drug efficacy and for monitoring therapy decisions.
MicroRNAs (miRNA) are endogenous short non-coding RNAs with a length of around 22 bases, that regulate gene expression at the post-transcriptional level, through incomplete binding to the 3′ untranslated regions (UTR) of multiple target mRNAs, enhancing their degradation and inhibiting their translation (Bartel, 2004) . Dysregulated miRNAs play critical roles during aging, carcinogenesis and cancer progression (Erturk et al., 2014; Cao et al., 2014; Gao et al., 2014; Sun et al., 2014: Bai et al., 2014) [9–13].
Among numerous miRNAs, miR-335 has attracted widespread attention as numerous studies have shown dysregulation of miR-335 in many cancers (Erturk et al., 2014; Cao et al., 2014; Gao et al., 2014; Sun et al., 2014) [9–12], and a potential biomarker for the prognosis and diagnosis of cancer by acting as an oncogene or tumor suppressor in the development, migration (Wang et al., 2013) , metastasis and apoptosis (Yang et al., 2016) .
In kidneys, miRNAs have been implicated in renal development, homeostasis and physiological functions as well as in the pathogenesis of various renal diseases, including nephrotic syndrome (White et al., 2010; Ribal, 2011) [16, 17]. miR-335 and rno-miR-7a have been implicated in an aging mechanism related to oxidative stress by inhibiting the expression of the antioxidant genes (Bai et al., 2014) .
A recent study has shown that the expression of X-linked inhibitor of apoptosis protein (XIAP) was significantly higher and the expression of microRNA-215 (miR-215) was significantly lower in human colonic cancer cell line HCT116. miR-215 overexpression and (or) silencing XIAP expression promote the apoptosis of HCT116 cells by enhancing caspase-9 and caspase-3 activities. These studies indicate inhibition of XIAP expression by MiR-215 (Lu et al., 2020) . Zinc finger E-box-binding homeobox 2 (ZEB2), a downstream target of miR-215 plays an essential role in the process of epithelial-mesenchymal transition (EMT), and podocyte depletion and loss (Fardi et al., 2019) . Expression of miR-215-5p in the podocyte, attenuates epithelial-mesenchymal transition of podocytes by inhibiting ZEB2 expression, targeting directly at the 3-UTR, implying that miR-215-5p negatively regulates ZEB2 activity (Jin et al., 2020) .
miR-1 is abundantly expressed in the myocardium, play a central role in cardiogenesis, heart function and pathology. Human miR-1 has two isomers (miR-1-1 and miR-1-2) that have identical sequences but are encoded by distinct genes. In mice, targeted deletion of miR1-1 or miR1-1 or both leads to abnormalities in heart development (such as ventricular septal defect and myocyte cell cycle aberrations) and cardiac function including heart arrhythmia and disturbances in heart conduction (Tao and Martin, 2013; Chistiako et al., 2016) [21, 22]. However, to the best of authors’ knowledge, there is hardly any study on the role of miR-1 in kidney physiology or pathology.
Studies on let-7a-5p have shown downregulation of this miRNA in diabetic nephropathy (DN), and serve as a biomarker for DN diagnosis. Renal mesangial cells cultured under high concentrations of glucose in vitro have shown significant downregulation of let-7a-5p. Transfection with let-7a-5p mimics significantly inhibited the PI3K/AKT signaling pathway in renal mesangial cells cultured under high-glucose conditions, while transfection with let-7a-5p inhibitors evinced the opposite effects, indicating a pathological role of let-7a-5p in mesangial cell hypertrophy (Wang et al., 2019) .
The present investigation was undertaken to study the expression status of selected microRNAs such as mir -1, miR-215-5p, miR-335-5p and let-7a-5p in the urine samples of children with SSNS, SRNS and healthy controls groups. These microRNAs were selected based target prediction using the bioinformatics tool based on the database available and the gene expression analysis in children with SSNS, SRNS and compared with the control group and the results are analyzed for the microRNA expression.