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Hu Lin
Nephrology
About me
Hu Lin, female, associate chief physician in the Nephrology Department of Loudi Central Hospital. She has been engaged in clinical work in nephrology for a long time, accumulating rich clinical experience in the diagnosis and treatment of primary and secondary glomerular diseases, acute and chronic renal insufficiency and other common kidney diseases. She has received high praise from many patients. She specializes in the treatment of nephrotic syndrome, diabetic nephropathy, and chronic renal failure.
Proficient in diseases
Common diseases in nephrology.
Voices
How to prevent and treat diabetic nephropathy
The prevention and treatment of diabetic nephropathy include the following 6 aspects: The first is changing lifestyle, including controlling weight, diabetic diet, quitting smoking, quitting alcohol, and appropriate exercise. Changing lifestyle is the foundation of blood sugar control and a key to improving various metabolic disorders. The second is blood sugar control. Strict blood sugar control is the most important means to prevent the occurrence and development of diabetes and diabetic nephropathy. Under normal kidney function, it is recommended to keep glycated hemoglobin below 6.2%. For patients with abnormal kidney function or elderly patients, it can be relaxed to 7%. The third is to reduce blood pressure and proteinuria. The most commonly used medications are ACE inhibitors and angiotensin receptor blockers. Once diabetic microalbuminuria appears, blood pressure should be controlled below 130/80 mmHg. The fourth is to restrict the intake of dietary protein, with a focus on animal protein, i.e., high-quality protein. Early stage protein intake should be controlled at 0.8-1g/kg; for patients who have developed renal failure, controlling protein intake at 0.6-0.8g/kg is more appropriate. The fifth involves controlling other factors, including a low-salt diet and treating hyperlipidemia. The sixth is the treatment of end-stage diabetic nephropathy. Since diabetic nephropathy patients frequently have cardiovascular complications and symptoms of uremia appear earlier, it is appropriate to start dialysis treatment early. (Please take medications under the guidance of a doctor.)
IgA kidney disease symptoms
The clinical manifestations of IgA nephropathy are diverse. The most common clinical manifestations include episodic gross hematuria, asymptomatic hematuria, and proteinuria. Episodic gross hematuria often occurs several hours after an upper respiratory tract infection, or a day or two later. Patients may notice that their urine is dark tea-colored, brown, or fresh red, light red, and this type of gross hematuria tends to recur. The second type is asymptomatic microscopic hematuria, with or without proteinuria, also known as asymptomatic urinalysis. This is often discovered during physical examinations when patients show no symptoms and tests reveal hidden blood and protein positivity in the urine. The third major category is proteinuria, which in some patients may present as nephrotic syndrome-like proteinuria. The fourth is hypertension; the fifth, acute kidney injury; and the sixth, chronic kidney failure. Most patients with IgA nephropathy gradually progress to chronic kidney failure within 10 to 20 years of diagnosis.
IgA kidney disease's etiology
IgA nephropathy can be divided into primary and secondary IgA nephropathy. Secondary IgA nephropathy includes, for example, lupus nephritis, allergic purpura nephritis, liver disease-related kidney damage, rheumatoid arthritis kidney damage, and so on. The etiology of primary IgA nephropathy is mainly due to the deposition of a type of immunoglobulin, IgA, in the mesangial area of the glomeruli, leading to a series of immune responses, which in turn cause inflammatory damage, resulting in a chronic glomerulonephritis. This form of IgA nephropathy is mainly related to mucosal immune defense, meaning it is linked to certain infectious factors. Additionally, some patients have high reactivity of their mucosa to certain food antigens, which leads to a series of immune-mediated inflammatory responses.