What Is Hypernephroma?

The physiological function of the kidney is mainly to excrete metabolites and regulate water, electrolyte and acid-base balance, secrete a variety of active substances, and maintain the stability of the internal environment of the body to ensure the normal physiological functions of the body. Nephritis is a group of kidney diseases that are caused by immune-mediated and inflammatory mediators (such as complement, cytokines, reactive oxygen species, etc.), which eventually lead to inflammatory changes in the native renal tissue and cause varying degrees of renal hypofunction. cause. There are also non-immune and non-inflammatory mechanisms involved in the chronic process.

Basic Information

English name

nephritis

Visiting department

Nephrology

Multiple groups

Elderly, Renal Impairment, Hypertension, Obese

Common causes

unknown

Common symptoms

More hematuria, proteinuria, edema, hypertension and other manifestations

Contagious

no

Nephritis classification

Acute glomerulonephritis

It is a group of diseases mainly manifested by acute nephritis syndrome. It is characterized by acute onset, patients with hematuria, proteinuria, edema and hypertension, and may be accompanied by transient renal insufficiency. More common in streptococcal infections, and other bacterial, viral and parasitic infections can also be caused.

2. Chronic glomerulonephritis

Referred to as chronic nephritis, it refers to the basic clinical manifestations of proteinuria, hematuria, hypertension, and edema. The onset methods are different, the disease is prolonged, the disease progresses slowly, and there may be varying degrees of renal dysfunction, which eventually develops into a chronic renal failure. Group glomerulopathy. Due to the different pathological types and stages of the disease in this group, the main clinical manifestations are different, and the disease manifestations are diverse.

3. Acute interstitial nephritis

Also known as acute tubular-interstitial nephritis, is a group of acute kidney diseases with renal interstitial inflammatory cell infiltration and tubular degeneration as the main pathological manifestations. The glomeruli and renal blood vessels are generally not affected or relatively mild. Clinical manifestations are acute kidney injury. Common causes include drug allergies, infections, autoimmune diseases, malignant tumors, metabolic diseases, and unknown etiology.

4. Chronic interstitial nephritis

It is a group of clinical syndromes characterized by tubular atrophy, renal interstitial inflammatory cell infiltration, and fibrosis. The mechanism of renal interstitial damage can involve hereditary, immune-related, infectious, hematological diseases, poisoning, metabolic disorders, urinary mechanical obstruction, and renal transplant rejection. The clinical manifestations are varying degrees of renal tubular impairment and progressive chronic renal failure.

5. Hepatitis B virus-associated nephritis

Referred to as hepatitis B-related nephritis, it is an immune complex glomerular disease caused by chronic hepatitis B virus (HBV) infection in humans. Clinical manifestations vary, and can be manifested by asymptomatic urinalysis abnormalities, or by proteinuria in the area of nephropathy, which can be accompanied by varying degrees of hematuria. There are various types of pathological changes of kidney damage. Membrane nephropathy is common in children, while membrane proliferative nephritis or membranous nephropathy is common in adults.

6. Idiopathic acute tubular interstitial nephritis

It refers to renal tubular interstitial disease with clinical manifestations of reversible non-oliguria-type acute kidney injury and unknown etiology. The pathological manifestations of kidney are interstitial edema and mononuclear cell infiltration, but it is difficult to determine the specific cause clinically. Most of them are related to autoimmune diseases, and some patients can finally determine the cause after close monitoring and dynamic observation. Such as related to chronic active hepatitis, ulcerative colitis, autoimmune thyroid disease and so on. TINU syndrome is a special type of which occurs when uveitis occurs during the course of the disease and can occur acutely before the kidney damage (several weeks), or simultaneously after the kidney damage (several weeks to months). Common in children, adolescents, or adult women.

Clinical manifestations of nephritis

The main manifestations of nephritis: fatigue, low back pain, poor appetite, gross hematuria, edema, hypertension, abnormal renal function, decreased urine output (oliguria in some patients), and congestive heart failure.

Nephritis test

1. Urine test: proteinuria, hematuria, cast urine, leukocyte urine, pyuria bacterial urine.

2. Determination of glomerular filtration rate

3. Detection of blood creatinine and blood urea nitrogen.

4. Serum complements C3, C4 and CH50; serum anti-streptolysin "O" titer; antinuclear antibody profile, ENA polypeptide antibody profile, immunoglobulin, ANCA, anti-glomerular basement membrane antibody, etc.

5. Renal biopsy.

Nephritis treatment

Treatment principles include the removal of incentives, general treatment, treatment for the cause and pathogenesis, treatment of comorbidities and complications, and renal replacement therapy.

General treatment

This includes avoiding fatigue, removing infections and other incentives, avoiding contact with nephrotoxic drugs or poisons, adopting a healthy lifestyle (such as quitting smoking, exercising moderately and controlling mood, etc.) and a reasonable diet. The acute phase should rest in bed, and gradually increase the amount of activity after the clinical symptoms improve. The acute phase should be given a low-salt diet (under 3g daily). People with normal renal function do not need to limit the amount of protein, but protein intake should be restricted during azotemia, and high-quality animal protein is the main factor. People with oliguria should limit fluid intake.

2. Therapy for etiology and pathogenesis

Treatment for the pathogenesis of the immune system often includes glucocorticoids and immunosuppressants. Blood purification treatments such as plasma exchange and immunoadsorption effectively remove autoantibodies and antigen-antibody complexes from the body. Treatment for non-immune pathogenesis, including hypertension, hyperlipidemia, hyperglycemia, hyperuricemia, obesity, proteinuria and hypercoagulable state in the kidney, activation of the renin-angiotensin system, and oxidative stress. Renin-angiotensin system blockers such as ACEI / ARB are one of the most important treatments to delay the progression of kidney disease.

3. Treatment of comorbidities and complications

Patients with kidney disease often have multiple comorbidities, such as metabolic abnormalities, hypertension, coronary heart disease, heart failure, and liver cirrhosis, which may aggravate the progress of kidney disease and should be actively treated.

Complications of kidney disease can involve various systems such as infections, coagulopathy, renal hypertension, renal anemia, renal bone disease, water, electrolyte and acid-base disorders, acute left heart failure, pulmonary edema, and uremia Encephalopathy should be actively treated.