A total of 1,044 school children identified with hematuria and/or proteinuria during a mass school urine screening test were referred to pediatric nephrologists at 13 hospitals in Korea. These children had isolated hematuria (IH) (60.1%), isolated proteinuria (IP) (26.4%: transient, 19.6%; orthostatic, 4.9%; persistent, 1.9%) or combined hematuria and proteinuria (CHP) (13.5%). The patient's history, physical examination, laboratory tests, kidney ultrasound and Doppler ultrasonography were obtained. Renal biopsies were performed on 113 children who showed severe proteinuria, hypertension, abnormal renal function, family history of chronic renal disease, systemic diseases or persistent hematuria and/or proteinuria for more than 12 months. IgA nephropathy (IgAN), thin basement membrane nephropathy (TBMN), membranoproliferative glomerulonephritis (MPGN), focal segmental glomerulosclerosis (FSGS), other GN, Alport syndrome and lupus nephritis were detected. IgAN and TBMN were the most common causes in the CHP group and IH group, respectively. Abnormal findings on the renal ultrasound with or without Doppler ultrasonography were noted in 147 cases (suspected nutcracker phenomenon, 65; increased parenchymal echogenicity, 40; hydronephrosis, 15). This study showed that the use of a mass school urine screening program can detect chronic renal disease in its early stage and recommends that more attention should be paid to identifying those children with CHP and massive proteinuria. A school urine screening program can detect chronic renal disease in its early stage. When mass screening is used, the initial aggressive diagnostic procedures such as renal biopsy are not needed. In addition, a regular follow-up for those children with IH and IP is certainly warranted.

Twenty-three (88.5%) of the 26 BS patients involved in this study had CLCNKB mutations. The p.W610X mutation and large deletion were two common types of mutations in CLCNKB. The clinical manifestations of BS III were heterogeneous without a genotype-phenotype correlation, typically manifesting cBS phenotype but also aBS or mixed Bartter-Gitelman phenotypes. The molecular diagnostic steps for patients with BS in our population should be designed taking these peculiar genotype distributions into consideration, and a new more clinically relevant classification including BS and Gitelman syndrome is required.

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Mass urine screening tests could detect asymptomatic GN in its early stages. Initial aggressive diagnosis and treatment for CHP and nephrotic-range groups may prove helpful as interventions that delay chronic kidney disease progression. These findings may assist in the development of diagnostic and management guidelines for relatively mild urinary abnormalities, such as IH or low-grade IP.