Glomerulonephritis is an inflammatory condition of the kidneys characterized by increased permeability of the glomerular filtration barrier causing filtration of RBCs and proteins.

This term is used to describe a bilateral disease of the kidneys which usually affects all the glomeruli. It’s the commonest renal disease responsible for about 50% cases of end stage renal failure leading to dialysis and renal transplantation. It is an immune-mediated inflammation of  the renal glomeruli

This immune-meditated-immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.

glomerulonephritis pathophysiology

 Pathophysiology of Glomerulonephritis

  •  Acute glomerulonephritis following an infection and is thought to be as a result of immunological response
  • The body responds to streptococci by producing antibodies which combine with bacterial
    antigens to form immune complexes
  • As these antigen-antibody complexes travel through circulation, they get trapped in the glomeruli and activate an inflammatory response that result in injury to capillary walls
  • As a result of the inflammation, the capillary lumen becomes smaller leading to renal
  • Injury to the capillaries increases permeability to large molecules-proteins hence can leak
    into urine

Types of Glomerulonephritis

  1.  Diffuse proliferative glomerulonephritis
    This is inflammation of the glomerulus affecting all glomeruli (diffuse) with increased number of  cells in them (proliferative). It usually follows transient infection especially beta hemolytic streptococci but other organisms can cause it.
    It presents as acute nephritis with haematuria and proteinuria. Recovery is good in children and in adults 40% cases may develop hypertension and renal failure
  2.  Focal/segmental proliferative glomerulonephritis: This is inflammation of the glomerulus affecting some glomeruli (focal) with increased number of cell in them (proliferative). It is associated with systemic lupus erythematosus(SLE) or infective endocarditis
    It presents also as an acute nephritis with haematuria and proteinuria and recovery is variable.
  3. Membranous/mesangial proliferative/ membranoproliferative glomerulonephritis.
    This is inflammation of the glomerulus with thickening of the glomerular basement membrane. It is due to infections like syphilis, malaria, hepatitis B, drugs like penicillamine, gold, diamorphine and tumors.
    It presents as nephrotic syndrome with haematuria and proteinuria and recovery is variable but most case progress to chronic renal failure
  4. Minimal change glomerulonephritis
    This is inflammation of the glumerulus with no exact known cause. It presents as nephrotic syndrome with haematuria and proteinuria and recovery is good in children but, recurrences are common in adults.
    >   Glomerulonephritis can be acute if it occurs in days or weeks ie 1 – 3 weeks following a streptococcal infection or glomerular damage
    >   Chronic glomerulonephritis occur over months or years and is characterized by progressive destruction (sclerosis) or glomeruli and gradual loss of renal function

Causes of Glomerulonephritis

  •  Vascular injury due hypertension
  •  Immune reaction due to streptococcal infection
  •  Disseminated intravascular coagulation
  •  Disease like diabetes and endocarditis
  •  Infection such as malaria, syphilis, TB etc.
  •  Systemic lupus erythematosus.

Clinical Manifestations of Glomerulonephritis

  •  Haematuria (passing smoky or tea coloured urine
  •  Oedema which periorbital (around the face or eyes) or ankle or generalized
  •  Decreased urine out put (oliguria)
  •  Hypertension with visual impairment. Hypertension occurs in 60% to 70% of patients during the first 4 or 5 days.
  •  Fever
  •  Fatigue, Headache
  •  Nausea, anorexia, vomiting
  •  Abdominal and back pain- flunk pain
  •  Pulmonary oedema with dyspnea
  •  Evidence of streptococcal infection i.e. tonsillitis or skin sepsis or elevated antistreptococcal 
    organism titers
    • Convulsion
    • Proteinuria, azotemia and increased urine specific gravity

Diagnosis of Glomerulonephritis

  • a) History of previous streptococcal infection e.g. throat or skin infection.
    b) Clinical manifestations
    c) Urinalysis. The urine is dark; its specific gravity is greater than 1.020; RBCs and RBC casts are present; and proteinuria is observed.
    d) Blood for serum creatinine and urea levels.
    e) Complete blood cell count and ESR
    f) BUN (blood urea nitrogen) to determine the ability of the kidney to excrete nitrogenous wastes
    g) Antistreptolysin o (ASO) titres
    h) Ultrasound scan to rule determine kidney lesions

Management of Glomerulonephritis


Treatment of acute glomerulonephritis (AGN) is mainly supportive, because there is no specific therapy for renal disease.

  1. Complete rest is need for severely ill patients to reduce work load of the kidneys and the heart
  2.  Monitor fluid input and urinary output on a fluid balance chart.
  3.  Restrict salt, fluid intake more especially in acute attack and oliguria
  4.  Daily weighing to determine subsiding of oedema
  5.  Monitor Blood Pressure daily and other vital signs
  6.  Antihypertensive therapy e.g. nifedipine, atenolol are given to control blood pressure.
  7.  Diuretics e.g. Lasix 40- 80 mg to treat edema.
  8. Loop diuretics. Loop diuretics decrease plasma volume and edema by causing diuresis. The reductions in plasma volume and stroke volume associated with diuresis decrease cardiac output and, consequently, blood pressure.
  9. Calcium channel blockers. Calcium channel blockers inhibit the movement of calcium ions across the cell membrane.
  10.  Restriction of protein in acute phase to prevent uremia.
  11.  Carbohydrate diet allowed freely and supplementary vitamins.
  12. Vasodilators. These agents reduce systemic vascular resistance, which, in turn, may allow forward flow, improving cardiac output.
  14.  Antibiotic therapy to treat primary streptococcal infection such as phenoxy methyl penicillin 500mg qid (15mg/kg) for 10 days or
    Erythromycin if allergic to penicillin 500g qid x 14 days
  15.  Analgesics for pain but use with caution esp. drugs affecting kidney function
  16.  Complete recovery may be achieve in 2 years educate the patient on possible health promotion measure such as oral hygiene, prompt treatment of respiratory, skin and urinary infection
    Proteinuria may continue even when symptoms have disappeared so regular monitoring is necessary
  17.  Do gentle exercises, and energetic sport activities should be avoided.
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