The incidence of kidney injuries, including diabetic nephropathy and drug-induced side effects, is steadily increasing worldwide 
. Acute kidney injury is considered to be an important risk factor for progression to end-stage renal disease 
. The early detection of kidney injury would make it possible to diagnosis acute kidney injury in a timely manner, but such detection remains a difficult task, due to the lack of reliable biomarkers. Current metrics for renal function, such as blood urea nitrogen (BUN), lack the sensitivity and/or specificity to adequately detect kidney damage at early stages of the injury 
. Recently, kidney injury molecule-1 (Kim-1) was identified as a highly sensitive and specific urinary biomarker for kidney injury 
. Subsequent preclinical studies also showed that Kim-1 is a promising early diagnostic biomarker for monitoring acute kidney tubular necrosis 
. Whether Kim-1 can serve as a suitable biomarker for various types of kidney injuries, however, requires further investigation using a large number of different renal injury samples.
MicroRNAs (miRNAs) are ~22-nt long noncoding RNA molecules that have emerged as a new class of gene regulators at the posttranscriptional level. It is widely believed that miRNAs regulate nearly 30% of protein-coding genes and are involved in almost every aspect of developmental, pathogenic and tumorigenesis processes. Accumulating evidence demonstrates that miRNAs serve as mediators in chronic kidney disease 
. Studies of conditional dicer-knockout mice 
revealed critical roles for miRNAs in regulating kidney development and maintaining the structural and functional integrity of the renal collecting system and the glomerular barrier. The determination of miRNA expression profiles in normal kidneys and their constituent cells has suggested that specific miRNAs may serve special functional roles in these cells 
. Kato and co-workers 
reported on the expression and function of miR-192 in diabetic kidney glomeruli. Employing mouse renal ischemia reperfusion injury (IRI) model, Godwin et al. 
identified a miRNA signature in kidney tissue that was tightly correlated to renal IRI. Recently, studies by our group 
and others 
have demonstrated that miRNAs can be released by cells and tissues into circulation and that these circulating miRNAs in the serum, plasma, urine, and other body fluids are stable and can serve as noninvasive biomarkers for various diseases and tissue injuries. When studying the serum and urinary levels of the miR-200 family, miR-205 and miR-192 in patients with systemic lupus erythematosus (SLE), Wang et al. 
found that the levels of most of those miRNAs from patients were lower than the levels of controls, suggesting that miRNA may take part in the pathogenesis of SLE and that miRNAs in the urine and serum could be biomarkers for SLE.
In the present study, we hypothesized that the levels of specific circulating miRNA species could be used to detect and monitor the pathological development associated with kidney injuries. Using different mouse renal injury models, we reported that miR-10a and miR-30d were readily detected in urine and that their levels specifically correlated with mouse kidney injury induced by renal ischemia-reperfusion or STZ treatment. The elevation of the urinary levels of miR-10a and miR-30d was also confirmed in urine samples from patients with focal segmental glomerulosclerosis (FSGS).