N02.B9

Clinical Causes: Genetic factors may predispose individuals to IgA nephropathy. Abnormal immune system response, leading to increased IgA production. Infections, particularly of the respiratory or gastrointestinal tract, can trigger or exacerbate the disease. Environmental factors and environmental triggers may contribute to disease progression. Underlying autoimmune conditions may also play a role, although IgA nephropathy can occur independently.

Key Symptoms: Blood in the urine (hematuria), which may be visible or detected microscopically. Protein in the urine (proteinuria), leading to foaminess in the urine. Swelling (edema) particularly in the hands, feet, or around the eyes. High blood pressure (hypertension), which can develop as the disease progresses. General fatigue or feeling of being unwell in some cases. No symptoms in the early stages, with signs appearing as kidney damage worsens.

Diagnosis Path: Urinalysis to detect blood and protein in the urine. Blood tests to assess kidney function, including serum creatinine and estimated glomerular filtration rate (eGFR). Kidney biopsy, which involves taking a small tissue sample to observe IgA deposits directly. Imaging tests such as ultrasound may be used to evaluate kidney size and structure. Monitoring of blood pressure and ongoing urine tests to assess disease progression.

Treatment Protocols: Management of high blood pressure with medications such as ACE inhibitors or ARBs to reduce kidney stress. Blood pressure control to prevent further kidney damage. Use of corticosteroids or other immunosuppressive medications in certain cases to reduce inflammation. Dietary modifications, including salt restriction and adjustment of protein intake. Regular monitoring of kidney function through lab tests. Treating any underlying infections promptly to prevent flare-ups. In advanced cases, dialysis or kidney transplantation may become necessary.