

Ji Kang

About me
Deputy Chief Physician of Internal Medicine, Master of Medicine.
Proficient in diseases
Nephrology, cardiology, pulmonology, and other related diseases.

Voices

Is kidney cancer the same as uremia?
Kidney cancer cannot be equated with uremia. Kidney cancer is a malignant tumor of the kidney. Its treatment can be through surgery, radiotherapy, chemotherapy, and so on. Uremia, on the other hand, is the end-stage development of various kidney diseases. It is a clinical syndrome characterized by the loss of most or all kidney function, leading to sodium and water retention, various electrolyte disorders, and the accumulation of toxins such as urea nitrogen and creatinine. The treatment of uremia relies on hemodialysis, peritoneal dialysis, or kidney transplantation. Although kidney cancer is not uremia, severe kidney cancer can also develop into uremia. At that time, blood replacement therapy is also needed.

How to determine the stages of IgA nephropathy?
IGA nephropathy has different grading methods, such as Lee grading and Hass grading. Both classify the pathological changes of IGA nephropathy into five stages, with similar descriptions. According to the Lee grading: Grade 1: Most glomeruli are normal, with occasional mild mesangial widening or without cellular proliferation, and no tubulointerstitial changes. Grade 2: Glomeruli show focal mesangial proliferation, with no tubulointerstitial changes. Grade 3: Glomeruli exhibit diffuse mesangial proliferation, with occasional segmental focal lesions, rare crescents, and adhesions, focal interstitial edema, and rare cellular infiltration. Grade 4: Glomeruli show diffuse severe mesangial proliferation and sclerosis, partial or segmental glomerulosclerosis, crescent formation observed but less than 45%, tubular atrophy, interstitial infiltration. Grade 5: The nature of the lesions is similar to grade 4 but more severe. Crescent formation in glomeruli is greater than 45%.

IgA nephropathy is a disease.
IgA nephropathy is the most common type of primary glomerular disease, caused by the deposition of IgA-dominant immunoglobulins in the glomerular mesangial area. It has a short latency period, with symptoms appearing early. Clinical manifestations of IgA nephropathy are diverse, with approximately 40%-50% of patients experiencing macroscopic hematuria hours to two days after precursor symptoms such as upper respiratory tract infections, and some patients also suffer from severe back pain and abdominal pain. About 30%-40% of patients only present with asymptomatic hematuria or proteinuria. Approximately 5%-20% of patients exhibit severe edema and substantial proteinuria, showing symptoms of nephrotic syndrome. At the onset of the disease, about 10% of patients also have hypertension. As the disease progresses, those with hypertension can exceed 40%. Less than 10% of patients may experience acute renal failure.