Berger’s disease, or IgA nephropathy, is a kidney condition caused by the accumulation of an antibody called immunoglobulin A (IgA). This buildup triggers inflammation that can impair the kidneys’ ability to filter waste from the blood. The disease course varies significantly among individuals. For some, it progresses slowly over many years with minimal issues, while for others, it can lead to more significant kidney damage.
Causes and Risk Factors of Berger’s Disease
The cause of Berger’s disease is the deposition of immunoglobulin A in the glomeruli, the kidneys’ tiny filtering units. Normally, IgA defends mucous membranes in the respiratory and gastrointestinal tracts. In people with this condition, however, a defective form of the IgA antibody circulates in the blood. This leads to the formation of immune complexes that become trapped in the glomeruli, triggering inflammation and damage.
While the trigger for this abnormal IgA production is not fully understood, it is considered an immune-mediated disease involving both genetic and environmental factors. A primary risk factor is family history, as having a close relative with IgA nephropathy increases susceptibility. The condition is also more prevalent among people of Asian and European descent.
Recognizing Signs and Symptoms
Many individuals with Berger’s disease remain asymptomatic for years, with the first sign often discovered during routine urine tests. When symptoms appear, the most direct sign is hematuria (blood in the urine). This can be microscopic and only detectable with tests, or it can be gross hematuria, where the urine is visibly pink, red, or cola-colored. A flare-up of gross hematuria can follow an infection like a cold or sore throat.
Other signs and symptoms include:
- Proteinuria (excess protein in the urine), which can cause a foamy appearance
- Edema, which is swelling in the hands and feet
- High blood pressure (hypertension)
- Pain in the flank area, located on the sides of the back below the ribs
How Berger’s Disease is Diagnosed
Diagnosis often begins when a routine check-up or the presence of symptoms prompts non-invasive testing. A urinalysis can detect red blood cells and protein in the urine. Blood tests are also used to assess kidney function by measuring waste products like creatinine to calculate the estimated glomerular filtration rate (eGFR).
While these initial tests can indicate a kidney problem, they cannot confirm Berger’s disease on their own. The only definitive method for diagnosis is a kidney biopsy. This procedure involves extracting a small piece of kidney tissue for microscopic examination. A pathologist looks for IgA deposits within the glomeruli, which confirms IgA nephropathy. A biopsy is recommended for individuals who show signs of progressive kidney damage.
Treatment and Management Strategies
There is no cure for Berger’s disease, so treatment focuses on slowing kidney damage and managing its effects. The approach is based on an individual’s proteinuria, blood pressure, and overall kidney function. For those with little protein in the urine and normal blood pressure, regular monitoring may be sufficient.
For patients with proteinuria and hypertension, medications are used. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are prescribed to lower blood pressure and reduce protein levels in the urine, helping protect the kidneys. In cases with high proteinuria or worsening kidney function, stronger therapies may be used. Corticosteroids or other immunosuppressant drugs can reduce the inflammation caused by IgA deposits by calming the immune system’s activity.
Lifestyle and dietary adjustments are also recommended. A low-sodium diet helps control blood pressure and swelling, and managing cholesterol is also part of the care plan. Some patients may benefit from omega-3 fatty acids found in fish oil, though this is not a universal recommendation.
Prognosis and Potential Complications
The long-term outlook for people with Berger’s disease varies. Many experience a very slow-progressing version of the condition, which may not worsen or may do so over several decades. For these individuals, regular medical follow-ups are used to monitor kidney function and address any changes promptly.
For others, the disease is more progressive. Persistent inflammation can lead to scarring of the kidneys, resulting in chronic kidney disease (CKD). Factors that indicate a less favorable prognosis include high levels of protein in the urine, sustained high blood pressure, and a reduced eGFR at diagnosis.
In some cases, CKD can advance to end-stage renal disease (ESRD), which occurs when the kidneys can no longer function to meet the body’s needs. At this stage, patients require renal replacement therapy, such as dialysis or a kidney transplant. An estimated 20-40% of patients may reach ESRD within 20 years of diagnosis.