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  The physiological function of the kidneys is mainly excretion of metabolites and regulate water, electrolyte and acid-base balance, secreting a variety of active substances, maintaining the body's environmental stability, in order to ensure the body's normal physiological function. Nephritis is mediated by immune, inflammatory mediators (such as complement, cytokines, reactive oxygen species, etc.) involved, and finally lead to inflammatory changes in renal tissue, causing varying degrees of renal dysfunction in a group of kidney disease by a variety of causes cause. In the chronic process there are non-immune, non-inflammatory mechanisms involved.


  1. Acute glomerulonephritis

  Is a nephritic syndrome as the main performance of a group of diseases. It is characterized by acute onset, patients with hematuria, proteinuria, edema and hypertension, and may be associated with transient renal insufficiency. More common in streptococcal infection, and other bacterial, viral and parasitic infections can also be caused.

  2. Chronic glomerulonephritis

  Referred to as chronic nephritis, refers to the proteinuria, hematuria, hypertension, edema as the basic clinical manifestations, the onset of different ways, the disease delayed, slow progression of the disease, may have different degrees of renal dysfunction, and ultimately the development of chronic renal failure Group glomerulopathy. As the pathology of this group of diseases and different types of disease, the main clinical manifestations vary, the disease was diversified.

  3. Acute interstitial nephritis

  Also known as acute renal tubular interstitial nephritis, is a group of renal interstitial inflammatory cell infiltration and renal tubular degeneration of the main pathological manifestations of acute renal disease, glomerular, renal vascular involvement or involvement is generally relatively light. Clinical manifestations of acute kidney injury. Common causes of drug allergy, infection, autoimmune diseases, malignant tumors, metabolic diseases and etiology is unknown.

  4. Chronic interstitial nephritis

  Is a group of tubular atrophy, renal interstitial inflammatory cell infiltration and fibrosis as the basic characteristics of a group of clinical syndrome. The mechanism of renal interstitial damage may be related to hereditary, immune-related, infectious, blood diseases, poisoning, metabolic disorders, urinary mechanical obstruction and kidney transplant rejection and other factors. Clinical manifestations of varying degrees of renal tubular dysfunction and progressive chronic renal failure.

  5. Hepatitis B virus-associated glomerulonephritis

  Referred to as hepatitis B-associated glomerulonephritis, chronic hepatitis B virus (HBV) infection in the human body, resulting in immune complex glomerular disease. Clinical manifestations of varying severity, can be expressed as abnormal urine asymptomatic, but also the performance of nephrotic range of proteinuria, may be associated with varying degrees of hematuria. Kidney damage pathological types, children with membranous nephropathy common, adults can be expressed as membranoproliferative glomerulonephritis or membranous nephropathy.

  6. Idiopathic acute tubulointerstitial nephritis

  Refers to the clinical manifestations of reversible non-oliguric acute renal injury, renal tubular interstitial disease of unknown etiology. Renal pathological manifestations of interstitial edema and mononuclear cell infiltration, but clinical difficult to determine the specific cause. Mostly with autoimmune diseases, some patients after close monitoring and dynamic observation can eventually clear cause. Such as chronic active hepatitis, ulcerative colitis, autoimmune thyroid disease and so on. TINU syndrome is one of the special types, the course of the occurrence of uveitis, can damage the kidneys (weeks), at the same time or after kidney damage (several weeks to several months) acute attack. Common in children, adolescents, or adult women.

  Clinical manifestations

  The main manifestations of nephritis: fatigue, lumbar pain, anorexia, gross hematuria, edema, hypertension, renal dysfunction, decreased urine output (some patients oliguria), congestive heart failure.

  an examination

  1. Urine examination: proteinuria, hematuria, tubular urine, leukocyte urine, pyuria bacterial urine.

  2. Determination of glomerular filtration rate

  3. Serum creatinine, blood urea nitrogen detection.

  Serum anti-streptolysin "O" titer; anti-nuclear antibody profile, ENA peptide antibody profile, immunoglobulin, ANCA, anti-glomerular basement membrane antibodies. 4. Serum complement C3, C4 and CH50;

  5. Renal biopsy.


  Therapeutic principles include removal of incentives, general treatment, treatment for etiologies and pathogenesis, treatment of comorbidities and complications, and renal replacement therapy.

  1. General treatment

  Including avoidance of fatigue, removal of infection and other incentives, avoid exposure to nephrotoxic drugs or poisons, take a healthy lifestyle (such as smoking cessation, moderate exercise and control of mood, etc.) and a reasonable diet. Acute phase should stay in bed, until the clinical symptoms improved gradually increase activity. Acute phase should be given low-salt diet (daily 3g or less). Normal renal function do not need to limit the amount of protein, but azotemia should limit protein intake, and high-quality animal protein-based. Oliguria should limit the amount of liquid into.

  2. For the etiology and pathogenesis of treatment

  For the treatment of immune pathogenesis, often including glucocorticoid and immunosuppressive therapy. Blood purification treatment such as plasma exchange, immunosorbent and other effective removal of body autoantibodies and antigen - antibody complexes. Treatment of non-immune pathogenesis, including hypertension, hyperlipidemia, hyperglycemia, hyperuricemia, obesity, proteinuria and renal hypercoagulable state, renin-angiotensin system activation, oxidative stress and other treatment. Renin-angiotensin system blockers, such as ACEI / ARB, are one of the most important treatments to delay the progression of kidney disease.

  3. Complications and complications of treatment

  Kidney disease patients often exist in a variety of complications, such as metabolic disorders, hypertension, coronary heart disease, heart failure and cirrhosis and so may increase the progress of renal disease should be actively treated.

  The complications of kidney disease can be related to various systems such as infection, coagulopathy, renal hypertension, renal anemia, renal osteodystrophy, water, electrolyte and acid-base balance disorders, acute left heart failure, pulmonary edema and uremia Encephalopathy, should be actively treated.

  4. Renal replacement therapy

  Including dialysis treatment and kidney transplantation. When acute and chronic renal failure and dialysis indications should be given timely dialysis treatment, and dialysis treatment in two ways: peritoneal dialysis and hemodialysis.


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