How IgAN is diagnosed

The Foundation for IgA Nephropathy

How IgAN is diagnosed

Initial diagnosis. Most IgAN patients are diagnosed before the age of 40 - some as children or adolescents, and many, if not the majority, are diagnosed while in their early to mid 20's. IgAN is usually first suspected when blood and/or protein are found in the urine. When this happens, the physician will order blood work, urinalysis and possibly other non-invasive tests like a kidney ultrasound. Some of the findings can help point towards IgAN or another kidney disease.

Biopsy. At this time, the confirmation of an IgAN diagnosis can only be made by examining tissues taken during a biopsy of the kidney. This is usually a needle biopsy of the left kidney, which is performed as day surgery. If there are no complications with bleeding, the patient usually goes home by the end of the day. If the symptoms are very mild, and serum creatinine is in the normal range, your doctor may elect to wait some time before ordering a biopsy. Since IgAN can be a very slowly-progressing disease, in some cases, a biopsy might not be done for a number of years. However, in recent years, it has become more and more common to biopsy very early in the course of the disease (some patients still have 100% kidney function when they are diagnosed, whereas before, and still today, many patients have already lost about 50% of their kidney function by the time anyone notices that something is wrong). Doctors are most likely to order a biopsy when there is both proteinuria and hematuria, but will often do it even in the absence of proteinuria. If your nephrologist does not recommend a kidney biopsy, ask why. However, you should be aware that one school of thought on delaying biopsies is that when the symptoms are very mild, there is nothing to be gained by performing a biopsy, since there would be no treatment anyway.

Light microscopy. In a biopsy sample showing IgAN, the light microscopy portion of the evaluation is usually characterized by mesangial and focal-segmental proliferation, as well as glomerulosclerosis. In severe cases, there may be evidence of crescents, and this is usually a sign of severe damage.

Immunofluorescence. This aspect of the biopsy tissue examination shows IgA deposited in the mesangium (a part of each glomerulus). In addition to the predominance of IgA deposits (which is the distinguishing feature of IgA nephropathy), IgG, IgM, and/or C3 are also often present, but no C4.

Late diagnosis. Another possibility is a late diagnosis. This happens when a person has had undetected symptoms of IgAN for many years, but some for reason, microscopic blood and/or protein in the urine has escaped medical attention. The IgAN may be discovered when the patient presents with symptoms of severe high blood pressure, or of more advanced renal failure. The more the IgAN has advanced into chronic renal failure, the less distinctive the pattern in the glomeruli, and if late enough, a biopsy may not allow diagnosis of the original kidney disease which caused the renal failure. Late diagnosis should not be confused with reversible acute renal failure.

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