Subscribe
9
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
Do you take steroids for nephrotic syndrome?
Once nephrotic syndrome is diagnosed, corticosteroid therapy becomes a primary treatment, and the commonly used steroid is prednisone. If there is liver damage or the treatment effect of prednisone is not good, oral prednisolone or intravenous methylprednisolone can be used. Due to its long half-life and severe side effects, dexamethasone is now generally less used. The course of treatment with corticosteroids for nephrotic syndrome is relatively long, needing about one to one and a half years. During this process, the use of steroids has three phases: the initial full-dose phase, during which a relatively large dose of the hormone is used for about two to three months; the second phase is a slow reduction process; the third phase is a low-dose maintenance process. Overall, during the use of steroids, patients must regularly follow up at outpatient clinics, and adjust the steroids according to the doctor's advice. One must not arbitrarily reduce the dose or stop the medication, as this can easily lead to a relapse of nephrotic syndrome.
What are the symptoms of diabetic nephropathy?
The symptoms of diabetic nephropathy mainly include the following aspects: The first one is proteinuria, where patients may notice an increase in foam in their urine, and upon examination, proteinuria will test positive. The second symptom is edema, which may initially appear as intermittent swelling but gradually develops into swelling of both lower extremities or even the entire body. Of course, pleural effusion and ascites may also occur. The third type of symptom is hypertension; diabetic nephropathy combined with hypertension often involves stubborn high blood pressure, which requires multiple antihypertensive drugs to control. The fourth point is that in the later stages of diabetes, signs of renal failure gradually appear, such as nausea, vomiting, difficulty breathing, anemia, renal osteopathy, skin itching, and more. The fifth is extrarenal manifestations, such as diabetic retinopathy presenting with vision loss or even blindness, and diabetic neuropathy leading to numbness and abnormal sensations in the hands and feet. Additionally, it is common for patients with diabetic nephropathy to also experience cardiovascular and cerebrovascular complications, such as coronary heart disease, myocardial infarction, stroke, and more.
Acute nephritis pathological characteristics
The changes in acute nephritis are characterized by diffuse intracapillary proliferative glomerulonephritis, and the main structures in the kidney are the glomeruli, renal tubules, and renal interstitium. Therefore, pathological examination can be divided into light microscopy, immunofluorescence, and electron microscopy examinations. Under light microscopy, the pathological changes in acute nephritis mainly include proliferation of mesangial and endothelial cells in the glomeruli. In the acute phase, there is significant infiltration of neutrophils and mononuclear cells. Masson's trichrome staining can reveal subepithelial immune complex deposits, and there is also edema and infiltration of inflammatory cells in the interstitium; Immunofluorescence examination shows diffuse coarse granular deposits of immune complexes along the capillary walls and in the mesangial areas, mainly composed of IgG and C3; Under electron microscopy examination, there are hump-like electron-dense deposits beneath the epithelial cells.
What causes acute nephritis?
The full name of acute nephritis is post-infectious glomerulonephritis, so as the name suggests, acute nephritis is related to infections. The most common cause is acute streptococcal infection. There are also infections caused by Staphylococcus aureus, Staphylococcus epidermidis, and Gram-negative bacteria. The main pathogenic mechanism is due to a series of immune responses caused by streptococcal infections, leading to an immune complex-mediated glomerulonephritis. The most common sites of infection are the respiratory tract and skin, with a latent period of one to three weeks.
Symptoms of acute nephritis.
The symptoms of acute nephritis are mainly manifested as acute nephritic syndrome, that is, hematuria, proteinuria, edema, hypertension, and transient acute kidney injury. Hematuria is a symptom present in almost all cases of acute nephritis, but it is mostly microscopic hematuria, meaning during examination, the routine urine analysis shows positive occult blood, or red blood cells are found in the urinary sediment. About 40% of the patients may exhibit gross hematuria, where the urine color appears like wash-water or may be bright red, deep tea-colored, and so on. The second symptom is proteinuria, which is also often indicated by a positive urine protein test during routine checks. The third symptom is edema, an early symptom of acute nephritis. Mildly, it presents as swelling of the eyelids in the morning and can spread to the whole body if severe. The fourth symptom is hypertension, with about 80% of patients showing a moderate increase in blood pressure. In severe cases, patients might experience oliguria, with urine output less than 400ml/d, accompanied by transient mild increases in blood creatinine and urea nitrogen, indicating acute kidney injury. This condition is mostly self-limiting, and many patients can recover within a few weeks.
Causes of Kidney Stones
The causes of kidney stone formation include the following: One reason is the increased amount of stone-forming components in the urine. Various factors that cause an increase in the concentration of salts, uric acid, oxalates, and cystine in the urine can exceed their solubility. This results in the precipitation and crystallization from the urine, which further grows into stones. For example, hyperuricemia can lead to an increased excretion of urinary uric acid, making it easy to form urate stones. Secondly, the reduction in urine substances that inhibit stone formation, including decreases in citrate and magnesium, can promote stone formation. Third, urinary tract obstruction and infection can lead to stone formation. In cases of urinary tract obstruction and poor urine flow, small crystals formed in the urine can easily adhere to the epithelial cells of the urinary tract, becoming the nucleus of the stone. Urinary tract obstruction may also lead to urinary tract infections where bacteria, pus, and damaged, necrotic epithelial cells can also form the core of stones and gradually develop into larger stones. Fourth, diet and hydration play significant roles. Long-term, high intake of high-protein, high-sodium, high-sugar foods can cause increased excretion of urinary calcium and uric acid, while reducing citrate levels, thus promoting stone formation. A decrease in water intake can also cause urine concentration, further promoting stone formation. Fifth, environmental factors and genetic factors are considered to be related to the formation of kidney stones. It is believed that the hardness of water and genetic factors also have certain relationships with kidney stone formation.
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.