Focal glomerulosclerosis

　　Focal glomerulosclerosis includes primary focal glomerulosclerosis and secondary focal glomerulosclerosis. The etiology of primary focal glomerulosclerosis is unknown. The etiology of secondary focal glomerulosclerosis is as follows:
　　1. Glomerular diseases Heroin-associated nephropathy, tumor-associated nephropathy, diabetes, AIDS, hereditary nephritis, IgA nephropathy, preeclampsia, and Hodgkin's disease, etc.
　　2. Renal tubular, interstitial, and vascular diseases Reflux nephropathy, radioactive nephritis, analgesic nephropathy, and sickle cell disease, etc.
　　3. Others Renal hypoplasia, obesity, and senility, etc.

　　Focal glomerulosclerosis can complicate with various diseases. The common complications in clinical practice are as follows:

　　1. Infectious diseases
　　Related to protein loss, malnutrition, immune dysfunction, and the use of glucocorticoid therapy. Infection is a common complication of nephrotic syndrome, and due to the use of glucocorticoids, the clinical manifestations of infection are often not obvious. Although there are now many antibiotics available for choice, if treatment is not timely or thorough, infection is still the main cause of recurrence of the disease and poor efficacy, and even death of the patient, which should be highly valued.

　　2. Thrombosis and embolism
　　Due to the increase in blood viscosity caused by blood concentration and hyperlipidemia, in addition, due to the loss of certain proteins and the increased compensatory protein synthesis by the liver, the imbalance of the body's coagulation, anticoagulation, and fibrinolysis systems is caused, thus, thrombotic and embolic complications are more likely to occur.

　　3. Acute renal failure
　　Patients with nephrotic syndrome may experience a decrease in renal blood flow due to insufficient effective blood volume, leading to prerenal azotemia, and due to severe edema in the renal interstitium compressing the renal tubules and a large amount of protein casts blocking the renal tubules and causing high pressure in the renal tubular lumen, indirectly causing a sudden decrease in glomerular filtration rate, leading to acute renal failure.

　　4. Disorders of protein and fat metabolism
　　Long-term hypoproteinemia can lead to malnutrition, delayed growth and development in children; a decrease in immunoglobulins can cause decreased body immunity, making it susceptible to infections; the loss of metal-binding proteins can lead to deficiencies in trace elements (such as iron, copper, and zinc); insufficient endocrine-binding proteins can induce endocrine disorders; a decrease in drug-binding proteins may affect the pharmacokinetics of certain drugs (increasing the concentration of free drugs in plasma and accelerating excretion), affecting the efficacy of drugs. In hyperlipidemia, the increase in blood viscosity promotes the occurrence of thrombotic and embolic complications, and will also increase cardiovascular complications, and can promote the occurrence of glomerulosclerosis and tubulointerstitial lesions, promoting the chronic progression of renal lesions.

　　Focal glomerulosclerosis can occur at any age, primarily in young adults, and is more common in males, all presenting with persistent non-selective proteinuria. Typical cases often begin with nephrotic syndrome, accounting for about 50%, and accounting for 5% to 20% of primary nephrotic syndrome. 50% to 60% of patients have hematuria, hypertension, and renal function damage.

　　The etiology of primary focal glomerulosclerosis is unknown, and there are no effective preventive measures. Secondary focal glomerulosclerosis is caused by glomerular diseases, tubulointerstitial and vascular diseases. Therefore, active treatment of the primary disease can reduce the incidence of this disease.

　　The diagnosis of focal glomerulosclerosis mainly relies on renal biopsy. Under the light microscope, some segments of certain glomeruli can be seen as glassy homogeneous protein substances, while the non-hardened areas are relatively normal. The typical lesions in the hardened areas can be seen as a large amount of acellular matrix and hyaline substances.

　　Patients with focal glomerulosclerosis should eat light, easily digestible foods; they should eat nourishing yin and kidney foods; they should eat diuretic foods. Patients should avoid eating foods with excessive saltiness; they should avoid eating spicy and刺激性 foods; they should avoid eating foods with high purine content.

　　The treatment of focal glomerulosclerosis mainly includes general treatment and hormone therapy as well as other immunosuppressants. The specific treatment methods are as follows:

　　1. General Treatment
　　General treatment includes low-salt diet for patients with large amounts of proteinuria and edema, and appropriate use of diuretics. For patients with marked hypoalbuminemia, albumin can be used in moderation; for patients with marked hypertension, adding antihypertensive drugs such as angiotensin-converting enzyme inhibitors and calcium channel blockers can be considered when sodium restriction and diuretics are ineffective.

　　2. Hormones and Other Immunosuppressants
　　For patients with nephrotic syndrome as the main manifestation, especially those with minimal change disease in the previous renal biopsy who have developed focal segmental glomerulosclerosis, hormone therapy is still the first choice, and most patients respond well. The adult dose is prednisone 0.5-1mg/(kg·d), for 6-8 weeks, and then gradually reduce the dose to alternate-day therapy, with a total course of more than 1 year.

　　3. Other Treatments
　　Angiotensin-converting enzyme inhibitors not only lower blood pressure but also reduce urinary protein, which may be beneficial in delaying kidney failure. In addition, patients with nephrotic syndrome associated with this disease not only have hypercoagulability but also renal intravascular coagulation and glomerular adhesion, and should be treated with anticoagulants such as dipyridamole and warfarin, which can reduce proteinuria and improve renal function.