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IgA nephropathy (IgAN) most commonly presents with visible hematuria within 12–72 hours of a mucosal (typically an upper respiratory) infection. It can also be discovered upon detection of asymptomatic, nonvisible hematuria with or without proteinuria during routine medical screening.


  1. The most common cause of primary glomerulonephritis worldwide.

    1. Peak incidence of IgAN is between the second and fourth decades of life, though it can present at any age.

    2. Occurs with greatest frequency in Asians and whites.

  2. An important cause of progressive CKD, with ESRD developing in up to 50% of patients within 25 years of diagnosis.

  3. Etiology of IgAN

    1. Caused by glomerular deposition of A1 isotype of IgA in the mesangium.

    2. No evidence of a role for any specific antigen despite the relation between mucosal infections and episodes of visible hematuria.

    3. Most cases of IgAN are sporadic, although familial cases do occur and appear to be transmitted as an autosomal dominant trait with incomplete penetrance.

  4. Clinical manifestations of IgAN

    1. One or more episodes of visible hematuria, usually associated with upper respiratory infection (often called synpharyngitic hematuria) and sometimes accompanied by flank pain and low-grade fever (present in 40–50% of patients).

    2. Nonvisible hematuria and typically mild proteinuria, detected incidentally on routine screening (present in 30–40% of patients).

    3. Advanced, progressive CKD, hypertension, and heavy proteinuria, in addition to hematuria (seen in small proportion of patients); nephrotic range proteinuria (present in ~5% of patients)

    4. IgAN rarely occurs secondary to other conditions like cirrhosis, celiac disease, and HIV infection, all of which are associated with a high frequency of IgA deposition.


  1. Urine dipstick with microscopy and culture should be used to rule out infection, confirm the findings of hematuria, and evaluate for proteinuria.

  2. A definitive diagnosis can only be made by renal biopsy with immunofluorescence or immunoperoxidase studies for IgA deposits.

    1. In the absence of proteinuria, hypertension, or decreased glomerular filtration rate (GFR), the clinical course (at least short-term) of patients with IgAN is generally benign and kidney biopsy is usually not indicated; periodic monitoring is recommended in these cases.

    2. Proteinuria (> 500–1000 mg/day), elevated serum creatinine, or hypertension suggests more severe or progressive disease and are indications for kidney biopsy to establish the diagnosis.

  3. The pathognomonic biopsy finding of IgAN is prominent, globular deposits of IgA in the mesangium on immunofluorescence microscopy.


  1. Patients with isolated hematuria, normal GFR, and no significant proteinuria should be monitored every 6–12 months for signs of progression (worsening proteinuria, BP, and GFR).

  2. Clinical predictors of progression of IgAN, including proteinuria > 500–1000 mg/day, decreased GFR, and hypertension often signal the need for treatment.

  3. Treatment is primarily aimed at reducing proteinuria and optimizing BP to minimize risk of progression.

  4. Treatment of progressive IgAN

    1. Angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB) therapy slows progression by optimizing BP control and reducing proteinuria.

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