☆ What are the main causes of IgA pathogenesis?
The pathogenesis of IgA is complex, and common causes include (1) the ability of the body to synthesize and release polyIgA1 (pIgA1), which has a specific affinity for glomerular thylakoid tissue, and the duration of pIgA1 in the circulation; (2) the susceptibility of glomerular thylakoid tissue to IgA deposition; (3) the ability of thylakoid tissue to trigger an inflammatory response after exposure to deposits; and (4) the kidney’s response to local response after inflammatory damage, further amplifying the inflammatory effect.
☆ What are the main clinical manifestations of IgA nephropathy?
IgA nephropathy can occur in different age groups, but is predominant in young adults. Whether in children or adults, the clinical manifestations of IgA nephropathy are diverse and lack characteristics, and the clinical course and prognosis vary greatly from case to case. (1) Sarcopenic hematuria: 30%-50% of patients with IgA nephropathy may present with sarcoid hematuria. (2) Urinalysis abnormalities: persistent microscopic hematuria with proteinuria is common. Patients with IgA nephropathy with urine protein less than 1g/day account for about 53.2% of the total (19%-82%). (3) Nephrotic syndrome: The incidence of nephrotic syndrome in IgA nephropathy is higher in Asian countries than in Western countries, ranging from 10% to 16.7% in the former and 5% in the latter. Urine protein over 2g/day is one of the risk factors for poor prognosis of IgA nephropathy. (4) Acute renal failure: The incidence of acute renal failure in the elderly is high at about 27.8%. (5) Chronic renal insufficiency: renal insufficiency is usually a late manifestation of IgA nephropathy after long-term prolongation. (6) Hypertension: Hypertension in IgA nephropathy accounts for 17.4% in China.
☆ What is the purpose of IgA nephropathy treatment?
The purpose of IgA nephropathy treatment is to remove acute inflammatory lesions in the kidney, relieve proteinuria and hematuria, delay the loss of kidney units, prevent and control renal fibrosis, and protect kidney function.
☆ Why must IgA nephropathy be typed before treatment? Is it necessary to treat each type?
Due to the diverse clinical manifestations and pathomorphological changes of IgA nephropathy, the pathophysiological mechanisms reflected are different. Therefore, diagnosis and treatment cannot be made solely by clinical manifestations, but must be done by typing IgA nephropathy through the clinical manifestations of kidney disease combined with the histological lesion characteristics of the kidney. Broadly speaking, each type requires interventional treatment.
☆ What are the drugs commonly used in the treatment of IgA nephropathy?
Glucocorticoids, cyclophosphamide, mycophenolate, fish oil, hypotensive drugs and renin-angiotensin system blockers.
☆ Under what circumstances should combination drugs be used? What are the main combination regimens?
In acute inflammatory lesions or proliferative nephritis, a combination of drugs such as hormone + mycophenolate and hormone + cyclophosphamide is often required for induction therapy. In patients with combined hypertension, particular attention is paid to lowering the blood pressure. Renin-angiotensin system blockers are widely used, mainly to protect renal units, reduce proteinuria and lower blood pressure.
☆ Do I need to cut my tonsils if I have kidney problems?
If there is a correlation between changes in IgA nephropathy and tonsillitis, removal of tonsils should be considered.
☆ When should I have dialysis?
Dialysis is needed when you enter the stage of end-stage renal failure.
☆ What is the need for kidney transplantation?
IgA nephropathy entering end-stage renal failure without active inflammation or proliferative lesions in the primary kidney disease, transplantation can be considered.
☆ Which IgA nephropathy has an unsatisfactory prognosis?
Massive hematuria, including sarcohematuria; massive proteinuria; hypertension; combined renal function impairment at the beginning of the disease.
☆ How to follow up IgA patients? What is the frequency?
Follow-up is usually every 3-6 months for stable disease, and every 1-2 months for acute changes in disease.