Glucose does not usually appear in the urine of IgA nephropathy. IgA nephropathy is characterized by IgA deposition in the glomerular mesangial area, and the clinical manifestations are hematuria, proteinuria, edema, hypertension, and dyslipidemia. However, when the renal interstitium is damaged, urinary glucose (uroglucose) can occur. IgA nephropathy is a chronic glomerulonephritis caused by abnormal deposition of immunoglobulin A in the glomerular mesangial area, which is pathologically characterized by mesangial hyperplasia and deposition of IgA-based immune complexes in the mesangial area. Clinically, it mainly manifests as microscopic hematuria or carnal hematuria, nephrotic syndrome, renal hypoplasia, hypertension, and so on. Urine glucose positivity can be seen when the lesion involves the renal interstitium. In addition, the detection of urinary glucose in the urine is generally associated with excessive blood glucose levels, decreased renal glucose threshold levels, and the use of specific medications. In diabetes mellitus, if the blood glucose level is too high above the renal glucose threshold, it will cause urinary glucose; in individual chronic kidney disease, it will cause damage to the proximal renal tubules, which will lead to a decrease in the proximal renal tubule’s ability to reabsorb blood glucose, and cause a decrease in the renal glucose threshold level will also lead to urinary glucose; the SGLT-2 inhibitor (daglitazar) can promote the urinary glucose excretion, and the use of the drug will also lead to the presence of urinary glucose. In summary, IgA nephropathy generally does not lead to urinary sugar, if urinary sugar should be timely regular hospital consultation, under the guidance of the physician to improve the relevant examination, to clarify the cause of the disease, for targeted treatment.