Differential diagnoses when glomerulonephritis follows an URI

Differential diagnoses when glomerulonephritis follows an URI

When glomerulonephritis follows an upper respiratory illness (URI), are any other differential diagnoses important to consider, other than PSGN or SAAG?

One of the most difficult diagnostic situations occurs when patients develop kidney disease after a URI.

In addition to PSGN and rarely SAAG, there are two important differential diagnoses to consider: IgA nephropathy and C3 glomerulopathy. As previously discussed, PSGN occurs approximately 7 to 14 days or more after the infection has started, and there may not be any evidence of the URI at the time kidney disease develops.

Alternatively, IgA nephropathy is called “synpharyngitic” because it is exacerbated at the time of the URI, usually within the first few days of onset. It is at this time that the patient will present with gross hematuria, hypertension, and signs of acute kidney injury, such as edema.

Clinically, IgA nephropathy relapses during the episode of URI and then settles back to a background level of low-grade microhematuria and nonnephrotic proteinuria. Many patients have had unsuspected IgA nephropathy prior to the onset of the URI, and it was the gross hematuria from the exacerbation of IgA nephropathy that brought the patient to the physician.

The serum complement levels are normal in IgA nephropathy, whereas they are low in PSGN and SAAG, and the biopsy shows a predominant mesangial proliferative histology and not the diffuse proliferative exudative lesion seen with PSGN and SAAG.

C3 glomerulopathy is an immune complex disorder with activation of the alternate pathway of complement (low C3). It can be exacerbated by a URI but is usually present persistently in noninfected patients. The histology of C3 glomerulopathy is a membranoproliferative pattern with more mesangial and subendothelial deposits and basement membrane duplication, which are not the typical patterns seen in PSGN and SAAG. C3 levels remain consistently low compared with SAAG and PSGN, where the levels eventually return to normal with resolution of the kidney lesion.

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