IGAN stands for “Immune-mediated Glomerulopathy with Associated Nephritis”, and it is a form of kidney disease caused by autoantibodies in the immune system damaging the glomerular filtration membrane in the kidney. Glomerular damage causes proteins, cells, and other molecules to leak into the urine, resulting in chronic kidney disease. While it was initially thought to be an immune-mediated disease, some scientists now believe that genetic or environmental factors might also play a role.
The most common symptom of IGAN is proteinuria (excess protein in the urine). Proteinuria occurs when large amounts of blood proteins, including albumin, leak from the glomeruli through the damaged membrane into the urine. Other signs of IGAN include hematuria (blood in the urine), edema (swelling due to fluid retention), hypertension (high blood pressure), and enlarged kidneys on imaging tests. In severe cases, failure of one or both kidneys can occur as a result of IGAN.
When laboratory tests reveal that a patient has high levels of IgG4 and C3c antibodies circulating in their blood, they are likely suffering from IGAN. Other laboratory tests commonly performed when diagnosing IGAN include measurement of serum creatinine and urea levels (to assess kidney function) and urine analysis to check for the presence of red blood cells or evidence of protein loss. Depending on what diagnostics have revealed, treatment may vary according to which specific form of IGAN is present: either Primary Glomerulonephritis or Secondary Glomerulonephritis.
Primary glomerulonephritis is usually treated with steroids or other immunosuppressant drugs to reduce inflammation and slow down the damage caused by autoantibodies. Additionally, diuretics may be prescribed to reduce water retention from fluid buildup (edema). In some cases, dialysis might be necessary if vision loss is occurring due to high levels of toxins released from damaged tissues entering the circulation
Secondary glomerulonephritis results from other systemic autoimmune disorders such as lupus nephritis which requires direct treatment for lupus itself as well as therapies specifically aimed at treating kidney disease including plasmapheresis, immunoadsorption therapy, mycophenolate mofetil (MMF). These treatments are all geared towards decreasing circulatory level autoantibodies in order to help control abnormalities at a cellular level which manifests clinically as conditions like nephrotic syndrome in some cases where structural abnormality if evident progressive scan be seen laparoscopically lasers have been used to help surgically open blocked vessels leading to better circulation Improved diagnostic techniques help identify cases early that makes possible early therapeutic intervention hence slowing down rate deterioration Research into genetic variations biochemistry what constant providing underlying which find links between gets affected potentially provide new unexplored avenues therapeutic intervention treat resistant cases prevalent present era.
In conclusion, while there is no new cure available for IGAN, there are various treatments available depending on whether it is primary or secondary glomerulonephritis. Furthermore, recent advances in diagnostic testing have enabled caregivers to identify and address underlying issues more quickly than ever before. With proper planning and management, patients can maximize their quality of life even with this condition.
