What are the treatments for nephrotic syndrome?

What are the treatments for nephrotic syndrome?

Nephrotic syndrome actually means that there is a problem with the kidneys. What happens to patients who are being treated for nephrotic syndrome? Nephrotic syndrome is generally a disease characterized by increased permeability of the glomerular basement membrane, resulting in massive proteinuria, hypoproteinemia, severe edema, and hyperlipidemia.

treat

1. General treatment

Anyone with severe edema or hypoproteinemia needs to rest in bed. After the edema disappears and the general condition improves, you can get up and move around.

Give a normal amount of 0.8 to 1.0 g/(kg·d) of high-quality protein (mainly animal protein rich in essential amino acids) diet. The calorie intake must be sufficient, and should not be less than 30-35kcal per kilogram of body weight per day. Although patients lose a large amount of urinary protein, a high-protein diet increases glomerular hyperfiltration, aggravates proteinuria and promotes the progression of kidney disease, so it is generally no longer recommended.

A low-salt (<3g/d) diet should be adopted when edema occurs. To reduce hyperlipidemia, you should eat less food rich in saturated fatty acids (animal fats) and more food rich in polyunsaturated fatty acids (such as vegetable oils, fish oils) and soluble fiber (such as beans).

(II) Symptomatic treatment

1. Diuretic and detumescent

(1) Thiazide diuretics

It mainly acts on the thick-walled segment of the ascending limb of the loop of Henle and the anterior segment of the distal convoluted tubule, causing diuresis by inhibiting the reabsorption of sodium and chloride and increasing the excretion of potassium. Long-term use should prevent hypokalemia and hyponatremia.

(2) Potassium-retaining diuretics

It mainly acts on the posterior segment of the distal convoluted tubule, excreting sodium and chloride but retaining potassium, and is suitable for patients with hypokalemia. When used alone, the diuretic effect is not significant and can be used in combination with thiazide diuretics. Triamterene or the aldosterone antagonist spironolactone are commonly used. Long-term use requires prevention of hyperkalemia and should be used with caution in patients with renal insufficiency.

(3) Loop diuretics

It mainly acts on the ascending limb of the Henle loop and has a strong inhibitory effect on the reabsorption of sodium, chloride and potassium. Furosemide (Lasix) or bumetanide (Buturoxil) (40 times more potent than furosemide at the same dose) are commonly used, taken orally or intravenously in divided doses. The effect is better when it is given immediately after the use of osmotic diuretics. When using loop diuretics, caution should be exercised to prevent hyponatremia, hypokalemia, and hypochloremia-induced alkali poisoning.

(4) Osmotic diuretics

By transiently increasing the plasma colloidal osmotic pressure, water in the tissues can be reabsorbed into the blood. In addition, they are filtered through the glomerulus, causing a hyperosmotic state in the renal tubular fluid, reducing the reabsorption of water and sodium and causing diuresis. Sodium-free dextran 40 (low molecular weight dextran) or starch plasma substitute (706 plasma) (molecular weight is 25,000 to 45,000) is commonly used for intravenous drip. Subsequent addition of a loop diuretic can enhance the diuretic effect. However, this type of drug should be used with caution in patients with oliguria (urine volume <400ml/d), because they easily form casts together with Tamm-Horsfall protein secreted by the renal tubules and albumin filtered by the glomeruli, blocking the renal tubules. Their hyperosmotic effect can cause degeneration and necrosis of renal tubular epithelial cells, inducing "osmotic nephropathy" and leading to acute renal failure.

(5) Increase plasma colloid osmotic pressure

Both can increase plasma colloidal osmotic pressure, promote water reabsorption in tissues and promote diuresis. If furosemide is added to glucose solution and slowly dripped intravenously, a good diuretic effect can sometimes be achieved. However, since the injected protein will be excreted in the urine within 24 to 48 hours, it can cause glomerular hyperfiltration and tubular hypermetabolism, resulting in damage to the glomerular visceral and tubular epithelial cells and promote renal interstitial fibrosis. In mild cases, it can affect the efficacy of glucocorticoids and delay disease remission, while in severe cases, it can damage renal function. Therefore, the indications should be strictly followed. For NS patients with severe hypoproteinemia, severe edema and oliguria, it should only be considered for use when diuresis is necessary, but excessive and frequent use should also be avoided. It should be used with caution in patients with heart failure.

The principle of diuretic treatment for NS patients is not to be too fast or too strong, so as to avoid insufficient blood volume, aggravating the tendency of blood hypercoagulability, and inducing thrombosis and embolic complications.

2. Reduce urine protein

Persistent massive proteinuria itself can lead to glomerular hyperfiltration, aggravate tubular-interstitial damage, and promote glomerular sclerosis, and is an important factor affecting the prognosis of glomerular disease. It has been shown that reducing urinary protein can effectively slow the deterioration of renal function.

In addition to effectively controlling hypertension, angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB) can also reduce urinary protein independently of lowering systemic blood pressure by lowering intraglomerular pressure and directly affecting the permeability of the glomerular basement membrane to large molecules. When using ACEI or ARB to lower urinary protein, the dosage used should generally be larger than the conventional antihypertensive dose in order to achieve good therapeutic effects.

3. Main treatment

1. Glucocorticoid therapy

Glucocorticoids are used in kidney disease, primarily for their anti-inflammatory effects. It can reduce exudation during acute inflammation, stabilize lysosomal membranes, reduce fibrin deposition, reduce capillary permeability and reduce urinary protein leakage; in addition, it can inhibit the proliferative response in chronic inflammation, reduce fibroblast activity, and reduce fibrosis caused by tissue repair. The therapeutic effect of glucocorticoids on the disease depends largely on its pathological type, and the effect is most rapid and certain for minimal lesions.

2. Cytotoxic drugs

If hormone therapy is ineffective, or the disease is hormone-dependent or recurrent, cytotoxic drugs can be used as an auxiliary treatment. Since these drugs often have the risk of gonadal toxicity, liver damage, and the risk of inducing tumors at high doses, the indications and courses of treatment should be carefully controlled. Among these drugs, cyclophosphamide (CTX) and benzodiazepine (CB1348) are widely used in clinical practice.

3. Immunosuppressants

Currently, the commonly used immunosuppressants in clinical practice include cyclosporine A, tacrolimus (FK506), mycophenolate mofetil and leflunomide.

In the past, immunosuppressants were often used in combination with glucocorticoids to treat various pathological types of nephrotic syndrome. In recent years, it has also been recommended that some patients who are relatively contraindicated or intolerant to glucocorticoids (such as uncontrolled diabetes, psychiatric factors, severe osteoporosis), and some patients who are unwilling to accept glucocorticoid treatment or have contraindications, can use immunosuppressants alone (including as an initial regimen) to treat certain pathological types of nephrotic syndrome, such as focal segmental glomerulosclerosis, membranous nephropathy, minimal change nephropathy, etc.

There are many options for the treatment of NS using glucocorticoids and immunosuppressants (including cytotoxic drugs). In principle, the approach should be to enhance efficacy while minimizing side effects. Whether to use hormone therapy, the length of treatment, whether to use and what kind of immunosuppressants (cytotoxic drugs) to choose should be treated differently according to the patient's pathological type of glomerulopathy, age, renal function and whether there are relative contraindications. An individualized treatment plan should be developed based on the target of the immunosuppressant. In recent years, based on the research results of evidence-based medicine, corresponding treatment plans have been proposed for different pathological types.

Prevention methods

Avoid overexertion

Excessive fatigue is also an important cause of recurrence of kidney disease. Therefore, to prevent the recurrence of kidney disease, you must avoid fatigue. When people mention fatigue, the first thing that comes to mind is physical labor, but they often ignore mental labor. Excessive mental labor can lead to a decrease in the body's immunity. Clinical cases have shown that kidney disease caused by excessive use of the brain is no less than that caused by physical labor, and may even exceed that caused by physical labor. In short, for patients with kidney disease, whether it is physical or mental labor, they must take preventive measures for nephrotic syndrome to prevent recurrence of kidney disease. They should pay attention to the combination of work and rest and avoid excessive fatigue.

Proper exercise can enhance immunity

Some patients with nephrotic syndrome stay in bed all day after getting the disease, and because it is cold in winter, they are too lazy to get out of bed to exercise. In fact, it is not suitable for patients with chronic kidney disease to rest in bed for a long time. Patients can go out for a walk and do some housework within their ability. Exercise can not only improve the body's immunity and prevent colds, but also improve the body's blood circulation, which is beneficial to the recovery of diseased kidneys.

Precautions

Its treatment method should follow the principle of changing the status quo of long course of nephrotic syndrome and repeated attacks of edema. It is currently an effective and safe treatment for nephrotic syndrome. The "Qi Energy Transforms into Water" balancing and repairing therapy uses advanced technologies such as gas phase, liquid phase, and ion diffusion to enable the highly active ions of the drug to be rapidly absorbed by the human body under high-frequency movement, and accurately act on diseased tissue cells, quickly repairing damaged kidney tissue cells and achieving a balanced state.

Conclusion: I believe that after reading the above content, everyone has a detailed understanding of the treatment methods of nephrotic syndrome, and also knows how to prevent nephrotic syndrome in daily life. Patients suffering from nephrotic syndrome must receive timely treatment and maintain confidence so that nephrotic syndrome can be cured as soon as possible.

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