Berger’s disease, also known as IgA nephropathy, is a chronic kidney disease. It is characterized by the abnormal accumulation of an antibody, immunoglobulin A (IgA), in the glomeruli. Glomeruli are the filtering units of the kidneys. These deposits cause inflammation which, over time, can impair the kidneys’ ability to filter waste from the blood.
This disease progresses slowly, often over several years. It is one of the most common glomerulonephritides worldwide. It primarily affects young adults, with a higher prevalence in men. Although its evolution varies, appropriate management is essential to preserve kidney function for as long as possible. Its diagnosis relies on specific tests and often on a kidney biopsy.
What are the causes and risk factors?
Scientists do not fully understand the exact cause of Berger’s disease, which they consider an autoimmune disease with a multifactorial component. Several elements appear to play a role in its onset. The main mechanism involves the immune system producing immunoglobulins A (IgA) with an abnormal structure. The body does not properly eliminate these modified IgA, which then form aggregates.
These immune complexes circulate in the blood and then deposit in the mesangium, a part of the renal glomerulus. This phenomenon triggers a local inflammatory reaction that progressively damages the kidneys.
Several risk factors have been identified:
- Genetic predisposition: Although not a direct hereditary disease, familial cases exist. The presence of certain genes can increase susceptibility to developing the pathology.
- Mucosal infections: Recurrent infectious episodes (respiratory or digestive) could stimulate the production of abnormal IgA. Disease flares often coincide with these infections.
- Associated diseases: Other conditions such as celiac disease or certain chronic liver diseases may be associated with IgA nephropathy.
Symptoms and signs
Berger’s disease can remain silent for many years. Its clinical manifestations vary greatly from one patient to another. Its discovery is often incidental during a routine urine test.
The most characteristic symptom is hematuria. This is the presence of blood in the urine.
- Macroscopic hematuria: Urine becomes red or “tea-colored.” This episode typically occurs 24 to 48 hours after an infection (tonsillitis, gastroenteritis). It may be accompanied by lower back pain.
- Microscopic hematuria: Blood is not visible to the naked eye. Only a urine analysis can detect it. This is the most frequent and most persistent sign.
Another major sign is proteinuria. This is the presence of proteins, mainly albumin, in the urine. High proteinuria is a risk factor for disease worsening. Over time, other symptoms related to the deterioration of kidney function may appear, such as high blood pressure, edema (swelling) in the ankles, and persistent fatigue.
How is the diagnosis established?
The diagnosis of Berger’s disease begins with clinical suspicion based on symptoms. Blood and urine tests are the first steps. Urine analysis (ECBU) confirms the presence of hematuria and quantifies proteinuria. Blood tests evaluate kidney function by measuring creatinine levels, which allows for the calculation of the glomerular filtration rate (GFR).
A renal ultrasound is often performed. It allows observation of the size and structure of the kidneys and rules out other causes of urinary abnormalities.
However, the only examination that confirms the diagnosis with certainty is a kidney biopsy. This procedure involves taking a very small fragment of kidney tissue with a fine needle, under local anesthesia. Analysis of this sample under a microscope reveals characteristic IgA deposits in the glomeruli. Biopsy also allows for evaluation of the extent of lesions and establishment of a prognosis.
Treatments for Berger’s disease
There is no definitive cure for Berger’s disease. Management primarily aims to slow its progression, control symptoms, and prevent complications. The therapeutic strategy is personalized according to the severity of the condition.
The basis of treatment relies on nephroprotective measures. These include strict blood pressure control, often with medications from the class of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs). These treatments also help reduce proteinuria.
For patients at high risk of progression, immunosuppressive treatments may be prescribed. Corticosteroids, administered over several months, are the most commonly used to reduce kidney inflammation. A specific formulation, targeted-release budesonide (Tarpeyo® or Kinpeygo®), acts primarily in the gut to reduce the production of abnormal IgA, with fewer systemic side effects.
Finally, SGLT2 inhibitors, initially used for diabetes, have shown effectiveness in protecting kidneys in patients with chronic kidney disease, including Berger’s disease.
Recent scientific advances in Berger’s disease
Research into Berger’s disease is very active. The first half of 2025 has seen significant advances, notably presented at the European Renal Association (ERA) congress in June.
New targeted therapies, aiming at the fundamental mechanisms of the disease, show promising results.
- Sibeprenlimab: Interim results from the phase 3 VISIONARY trial are encouraging. This drug targets a molecule called APRIL, which plays a role in the survival of IgA-producing cells. It has shown a significant reduction in proteinuria, a key marker of disease progression.
- Zigakibart: Also an APRIL inhibitor, 100-week data confirmed a durable reduction in proteinuria and good tolerability, suggesting a disease-modifying effect.
- Other promising avenues: Several other drugs are in advanced stages of clinical trials. Atacicept (ORIGIN 3 trial) and Povetacicept also target B-lymphocyte pathways. Sparsentan, a dual endothelin and angiotensin receptor antagonist, and complement inhibitors like Iptacopan, represent other approaches to reduce kidney damage.
These researches pave the way for a new era of more specific treatments, going beyond general immunosuppression and supportive care.
Prevention
No one can prevent the onset of Berger’s disease, as scientists do not fully understand its exact causes. However, once a doctor makes the diagnosis, the patient can adopt several measures to slow the disease’s progression and prevent end-stage renal disease. The patient must fundamentally control their blood pressure, aiming primarily to keep it below 130/80 mmHg.
To do this, they must adopt a low-salt diet and limit their intake of protein and saturated fats. Unless medically advised otherwise, the patient must also maintain good hydration. The doctor recommends that the patient avoid medications potentially toxic to the kidneys, such as non-steroidal anti-inflammatory drugs (NSAIDs). The patient must also stop smoking to effectively protect their kidneys and cardiovascular system. Finally, the patient must undergo regular medical follow-up with a nephrologist, who adjusts the treatment and monitors the evolution of kidney function.
Living with Berger’s disease
Living with a chronic disease like Berger’s disease requires daily adaptation. Regular medical follow-up is the cornerstone of management. It involves consultations, blood tests, and urine analyses at a frequency defined by the nephrologist.
Lifestyle plays a major role. A balanced diet, low in salt, and regular physical activity are beneficial for kidney and general health. It is important to understand one’s treatment well and take it rigorously. Patients should learn to recognize signs of a flare-up, such as the appearance of red urine or edema, and to consult their doctor promptly.
Psychologically, the announcement of a chronic illness can be difficult. Do not hesitate to seek support from loved ones, your doctor, or patient associations. Sharing your experience can help better manage the disease on a daily basis. The goal is to maintain a good quality of life while managing the pathology in the long term.
Frequently asked questions about Berger’s disease
Is Berger’s disease serious?
The severity varies greatly. Some forms remain benign with preserved kidney function throughout life. Others can progress to end-stage chronic kidney disease, requiring dialysis or transplantation. The prognosis depends on factors such as proteinuria level, blood pressure, and the extent of lesions on biopsy.
Can Berger’s disease be cured?
No, it cannot be truly cured. It is a chronic disease. However, current treatments can very effectively control its progression, slow the deterioration of kidney function, and maintain a good quality of life for many years.
Is a specific diet necessary?
Yes, a low-salt diet is fundamental for blood pressure control. Depending on the stage of the disease, your doctor may also advise you to limit your consumption of protein, phosphorus, or potassium. Follow-up with a dietitian can be helpful.
Is pregnancy possible with Berger’s disease?
A woman with Berger’s disease can consider pregnancy, but a multidisciplinary team, including a nephrologist and an obstetrician, must plan and follow this pregnancy very closely. Pregnancy carries more risks if the disease has already impaired the patient’s kidney function or if her high blood pressure is not controlled.
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