Diagnosis and treatment of nephrotic syndrome

   I. Diagnostic criteria
  (A) Urine protein quantification more than 3.5g/d Required condition
  (B), plasma albumin less than 30g/l Required condition
  (C), edema
  (iv), hyperlipidemia
  II. Clinical manifestations
  (-), edema
  Etiology: hypoalbuminemia
  Characteristics: Starting from the morning eye and face, lower limbs after activity, later extended to the whole body, may be combined with pleural fluid, ascites, with oliguria. Tu Xianlai, Department of Nephrology, Chizhou Second People’s Hospital
  (II), proteinuria
  Etiology: increased permeability of glomerular basement membrane
  Features: increased foam in the urine.
  (C), hypoalbuminemia
  Etiology: persistent excretion of large amounts of protein in the urine and edema of the gastrointestinal mucosa
  Characteristics: Increased α2 and β globulins in the blood, low immunity of the patient, susceptibility to infection, hypercoagulable state and other complications.
  (iv), hyperlipidemia and lipiduria
  Etiology: increased synthesis of albumin and lipoprotein by the liver, weakened breakdown and peripheral utilization of lipoproteins
  Features: hypercholesterolemia, hypertriglyceridemia, increased serum concentrations of low and very low density lipoproteins, and easy combination of cardiovascular disease. Patients may have birefringent lipids in the urine.
  (V), routine urine examination
  Large amounts of protein, urine sediment can be seen in red blood cells and various types of tubes
  (F), hypertension and renal function impairment
  The causes and main features of secondary nephrotic syndrome
  (-), adolescents
  1.Allergic purpura nephritis
  Typical skin purpura, arthralgia, abdominal pain, black stool
  Hematuria (microscopic or carnal), persistent or transient, with varying degrees of proteinuria, mostly found within 4 weeks after the appearance of the above symptoms
  The immunopathological examination of renal biopsy is dominated by IgA deposition.
  2. Systemic lupus erythematosus nephritis
  Prevalent in young and middle-aged women. Fever, skin damage, arthralgia, cardiovascular, respiratory, hematologic and renal abnormalities
  Renal manifestations: proteinuria, nephrotic syndrome, and in severe cases, oliguria, anuria, and acute progressive nephritis.
  Immunological examination: positive anti-nuclear antibody, anti-double-stranded DNA antibody, anti-sM antibody, etc. and increased titer, and decreased complement C3.
  (II) Middle and old age
  1.Diabetic nephropathy
  Diabetic patients with a disease duration of more than 10 years have characteristic fundus changes
  The earliest clinical manifestations are edema and proteinuria.
  2, renal amyloidosis
  Renal biopsy with intrarenal amyloid deposits
  Persistent proteinuria, proteinuria up to 20g/d in severe lesions, mostly manifesting as nephrotic syndrome.
  Extra-renal manifestations: giant tongue, digestive tract and heart involvement
  3.Myelomeningocele nephropathy
  Etiology: malignant disease in which plasma cells proliferate malignantly and synthesize abnormal monocytic immunoglobulins.
  Bone, hematopoietic system and renal damage are the prominent manifestations. Patients have bone pain, osteolytic manifestations often seen in flat bone x-ray films, anemia, increased serum monoclonal globulin, M band in protein electrophoresis, positive urine periplasmic protein, and myeloma cells occupying more than 15% of nucleated cells in bone marrow films.
  (C) Hepatitis B virus-associated nephritis
  The diagnosis is confirmed by the presence of immune complex deposits of hepatitis B virus antigen in the kidney.
  IV. Application of glucocorticoids
  (A) Mechanism of action
  1.Inhibit immune response and immune-mediated inflammatory response, reduce exudation, cell proliferation and infiltration, improve the permeability of glomerular basement membrane.
  2.Inhibit the secretion of aldosterone and antidiuretic hormone, diuresis and swelling, reduce and eliminate urinary protein.
  (B) Use principles
  1.The initial dosage should be sufficient
  2.Adequate dosage should be used for a long enough time
  3. Slowly reduce the drug for effective treatment
  (C) The reaction after treatment
  1.Hormone sensitivity
  2.Hormone dependence The disease often recurs in the process of drug reduction after the drug is effective.
  3.Ineffective hormone
  (D) Side effects
  Infection, drug-related diabetes, osteoporosis, obesity, hypertension
  V. Immunosuppressive drugs and other treatments
  (-) Cytotoxic drugs
  Relieve the patient’s dependence on hormones; play a therapeutic role together with hormones
  1.Cyclophosphamide
  Can be used for those without abnormal liver function
  The cumulative dosage is 6 to 8 grams.
  Side effects: bone marrow suppression and toxic liver damage, gonadal suppression, reversible alopecia, nausea, hemorrhagic cystitis.
  2.Nitrogen mustard hydrochloride
  For abnormal liver function, normal renal function or young male patients can be used
  Side effects: gastrointestinal reactions, bone marrow suppression, strong local irritation of drugs
  3.Nitrogen mustard phenylbutyrate, azathioprine, vincristine
  (ii) Cyclosporine A and primaquine directly against adjuvant T cells
  (iii) Symptomatic treatment
  Rest, salt-restricted diet, protein intake 1g/kg/d high quality protein, adequate calories. Appropriate diuresis.
  VI. Prevention and treatment of complications
  (-), infection
  Protect the patient in all aspects of life and environment and observe the condition closely to detect infection in time, and apply powerful and non-nephrotoxic antibacterial drugs to treat boils.
  (B), thrombosis and embolism complications
  When plasma albumin is below 20g/l, it indicates a hypercoagulable state and anticoagulation should be given.
  (C), acute renal failure
  Hemodialysis treatment can be taken to maintain life and benefit the recovery of renal lesions.
  (D) Fat metabolism disorders leading to cardiovascular complications