Key clinical features suggesting IgA nephropathy include recurrent episodes of visible (macroscopic) haematuria, often coinciding with or shortly following upper respiratory tract infections or other mucosal infections. This presentation is typical and reflects the mucosal immune dysregulation characteristic of the disease NICE CKS. Patients may also have persistent microscopic haematuria and variable degrees of proteinuria, which can range from mild to nephrotic levels in some cases NICE CKS. Hypertension and impaired kidney function may develop as the disease progresses.
Laboratory findings supporting the diagnosis include persistent microscopic haematuria on urine microscopy and proteinuria detected by dipstick or quantified by urine protein:creatinine ratio. Serum creatinine and estimated glomerular filtration rate (eGFR) help assess kidney function and disease severity NICE CKS. Definitive diagnosis requires kidney biopsy demonstrating mesangial proliferation with dominant or co-dominant IgA deposits on immunofluorescence microscopy, which is the hallmark of IgA nephropathy Cornell 2012.
Additional laboratory tests may show normal or mildly elevated serum IgA levels, but this is neither sensitive nor specific for diagnosis. Complement levels are usually normal, distinguishing IgA nephropathy from other immune complex glomerulonephritides Bridoux et al. 2021.
In summary, the diagnosis of IgA nephropathy is suggested clinically by recurrent macroscopic haematuria often linked to mucosal infections, persistent microscopic haematuria, and proteinuria, with laboratory confirmation by kidney biopsy showing mesangial IgA deposits NICE CKS Cornell 2012Bridoux et al. 2021.