IgA nephropathy (IgAN) is a chronic kidney disease where immunoglobulin A (IgA) antibodies accumulate in the kidneys, leading to inflammation and damage. This buildup can impair the kidneys’ ability to filter waste from the blood, potentially declining kidney function. While there is currently no cure for IgAN, achieving remission is a primary goal in managing the disease and preserving kidney health. This article explores what remission means in IgAN, how it is achieved and maintained, and factors influencing its course.
Understanding Remission
In IgA nephropathy, remission signifies a controlled state of disease activity rather than a complete cure. It is defined by the improvement or normalization of specific markers related to kidney function and inflammation. This concept is divided into clinical and pathological remission.
Clinical remission is determined by observable signs and symptoms, focusing on the levels of protein and blood in the urine, and the estimated glomerular filtration rate (eGFR). Proteinuria remission might be defined as achieving less than 0.3 grams of protein per day, or a significant reduction of at least 50% from baseline levels, sustained over several months. Hematuria remission (absence of blood in the urine) is another indicator, defined as three consecutive negative or trace dipstick results for six months. Complete clinical remission involves the normalization of both proteinuria and hematuria, alongside stable kidney function.
Pathological remission is assessed through kidney biopsy findings. This involves examining tissue samples for reduced IgA deposits, inflammation, or scarring within glomeruli. While clinical remission reflects current health status, pathological remission provides insight into microscopic kidney changes. Partial remission indicates significant improvement in clinical markers, such as a substantial reduction in proteinuria, even if complete normalization is not achieved.
Achieving Remission
Achieving remission in IgA nephropathy involves medical treatments and lifestyle adjustments. Medical therapies aimed at reducing inflammation and controlling blood pressure are a primary strategy. Immunosuppressive therapies, such as corticosteroids, lessen immune system activity and reduce IgA deposition. For patients at high risk of rapid disease progression, a targeted-release formulation of budesonide is approved to reduce proteinuria. Other immunosuppressants like mycophenolate mofetil (MMF) may be considered for patients with active inflammation on kidney biopsy, and can be used with steroids.
Controlling blood pressure is a cornerstone of treatment, achieved with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). These medications lower blood pressure and help reduce proteinuria, a strong predictor of disease progression. Newer agents like sparsentan (a dual angiotensin II and endothelin-1 receptor antagonist) and atrasentan (an endothelin type A receptor antagonist) have received approval for reducing proteinuria in adults at risk of rapid progression. Lifestyle modifications are also part of supportive care.
Dietary adjustments, such as limiting sodium intake, help manage blood pressure and reduce fluid retention. A heart-healthy diet, with reduced saturated and trans fats, supports kidney health by preventing fatty buildup in blood vessels. Protein intake may be moderated; a dietitian can provide individualized guidance to ensure adequate nutrition while reducing stress on the kidneys. Regular physical activity and maintaining a healthy weight contribute to managing blood pressure and overall well-being.
Maintaining Remission
Once remission is achieved, sustained management is important to prevent recurrence and preserve long-term kidney function. This involves consistent medical follow-up and treatment adherence. Regular visits with a nephrologist are important to monitor kidney health and adjust treatment as needed.
Ongoing monitoring includes blood tests to assess creatinine and eGFR, indicating kidney filtering efficiency. Urine tests, particularly for proteinuria, are performed regularly to detect any increase in protein excretion, signaling a return of disease activity. Adherence to medications (blood pressure medications, immunosuppressants, or other approved therapies) is important to maintaining disease control.
Continued lifestyle management, including dietary modifications and blood pressure control, is important. Close collaboration with the healthcare team and prompt reporting of new symptoms or health changes ensure timely intervention if the disease shows signs of activity. The goal is to sustain remission as long as possible, delaying or preventing further kidney damage.
Factors Influencing Remission and Relapse
Several factors influence achieving and maintaining remission in IgA nephropathy, and the risk of relapse. Initial kidney function at diagnosis (measured by eGFR) plays a role, with better initial function associated with more favorable outcomes. The amount of proteinuria at diagnosis is a significant predictor; higher levels indicate a greater risk of progression. Specific kidney biopsy findings, such as crescents or scarring, provide prognostic information. The Oxford classification system categorizes histological features (mesangial cellularity, endocapillary proliferation, segmental glomerulosclerosis, and tubular atrophy/interstitial fibrosis) to predict renal outcomes.
A relapse signifies a return of disease activity after a period of remission. This is characterized by increased proteinuria, defined as a return to levels above 1.0 g/day or a 50% increase from the lowest achieved level. A decline in kidney function (indicated by a decrease in eGFR or an increase in serum creatinine) is a sign of relapse. Macroscopic hematuria (visible blood in the urine) can be a sign of renewed disease activity. Adherence to prescribed treatment regimens is an important factor in preventing relapse; inconsistent medication use can allow the disease to reactivate.