Glomerulonephritis presents in one of four ways:
1 Asymptomatic proteinuria and/or microscopic haem aturia
2 Acute nephritic syndrome
3 Nephrotic syndrome
4 Chronic renal failure
Asymptomatic proteinuria and/or microscopic haem aturia is discovered incidentally, e.g. at a routine medical examination. Some causes of haematuria are shown in Fig. 9.4. Overt haematuria may occur after exercise.


Since false-positives are often obtained using Stix methods, the presence of significant proteinuria must be demonstrated by measuring the 24-hour urinary output of protein on two consecutive occasions.

Urine microscopy is performed to look for haematuria. A positive Stix test for blood may result from haematuria or haemoglobinuria. These can be differentiated on microscopy since red cells are only seen in patients with haematuria. Red cell morphology may provide a guide to diagnosis .
Further investigations will include:
URINE MICROSCOPY for red-cell casts
ASSESSMENT OF RENAL FUNCTION by estimation of blood urea, serum creatinine and endogenous creatinine clearance
RENAL IMAGING, usually by excretion urography

Renal Deases
Renal Deases


In classical poststreptococcal glomerulonephritis the patien t, usually a child, will have suffered a streptococcal infection 1-3 weeks before the onset of the acute nephritic syndrome. Streptococcal tonsillitis or pharyngitis, otitis media or cellulitis may be responsible. The infecting organism is a Lancefield group A J3-haemolytic Streptococcus of a nephritogenic type. The latent interval between the infection and development of symptoms and signs of renal involvement reflects the time taken for immune complex formation and deposition and glomerular injury to occur.


A list of investigations is given. If the clinical diagnosis of a nephritic illness is clearcut, e.g. in poststreptococcal glomerulonephritis, renal imaging and renal biopsy are usually unnecessary. A biopsy is required if the diagnosis is uncertain, if the clinical features are unusual, or if renal failure is rapidly progressive, suggesting the presence of crescentic glomerulonephritis (RPGN).


In the majority of patients with glomerulonephritis, neither corticosteroid nor immunosuppressive therapy is of benefit. The same applies to treatment with agents that alter coagulation and platelet function. Important exceptions to this general rule include glomerulonephritis complicating SLE, systemic vasculitides such as polyarteritis nodosa and Wegener’s granulomatosis, Goodpasture’s syndrome and some forms of rapidly progressive crescentic glomerulonephritis (see later) and probably idiopathic membranous nephropathy with progressive renal impairment.
As spontaneous remissions usually occur in acute glomerulonephritis, the aim of management is to prevent patients dying from pulmonary oedema, uraemia or hypertensive encephalopathy while awaiting improvement in renal function. Hospital admission is advisable for all children with oliguria and marked hypertension; levels of blood pressure that are of no risk to adults may be associated with hypertensive fits in the young.
Otherwise, hospital admission is not mandatory, providing the general practitioner is able to visit daily to examine the patient and check the blood pressure. Blood for measurement of urea or serum creatinine concentrations should be taken every few days.

Investigation of acute nephritic syndrome.
Investigation of acute nephritic syndrome.

Management in hospital

Most patients require:
• Daily recorcling of fluid intake and output
• Daily weighing (as a check on change in body fluid status)
• Regular measurement of blood pressure
Strict bed rest is unnecessary unless the patient feels ill, is severely hypertensive or has pulmonary oedema. Dietary protein restriction is required only if severe uraemia occurs, but salt restriction is always necessary. In oliguric patients, fluid restriction is necessary to maintain body weight at a level at which severe hypertension, pulmonary congestion and gross oedema are prevented. Mild to moderate hypertension and oedema may respond to salt restriction and diuretic therapy, e.g. frusemide given orally or parenterally. Other hypotensive  agents may be required. J3-Adrenergic receptor blocking therapy should be used with caution for hypertension as it may precipitate pulmonary oedema in those on the brink of heart failure.
The prognosis in immune complex-mediated glomerulonephritis is improved if the antigen responsible can be eradicated. In patients with poststreptococcal glomerulonephritis, a course of penicillin should be given.

Management of life-threatening complications

HYPERTENSIVE ENCEPHALOPATHY. In this condition the priorities are to maintain the airway and to reduce the blood pressure using a parenteral agent such as hydralazine 5-20 mg by slow intravenous infusion over 20 min. Fits should be controlled with parenteral diazepam (10 mg i.v.), but this may induce respiratory depression and facilities for resuscitation must be available.
PULMONARY OEDEMA. This should be treated in the usual way . Because of the renal failure, high doses of potent diuretics such as frusemide given parenterally may be required. If this fails to produce a diuresis, salt and water may be removed osmotically by peritoneal dialysis, or by haemofiltration, or by ultrafiltration during haemodialysis.
SEVERE URAEMIA. Peritoneal dialysis, haemodialysis or haemofiltration will be required pending recovery of the renal function.


penicillin (phenoxymethylpenicillin 500 mg daily) should be given to all individuals at risk, providing that they are not allergic to penicillin. If one member of a family living in overcrowded conditions develops the disorder, other members should be treated prophylactically. Evidence in support of long-term penicillin prophylaxis after the development of glomerulonephritis is lacking.


Poststreptococcal glomerulonephritis

The prognosis in children is excellent. A small number of adults develop hypertension and/or renal impairment later in life. Therefore in older patients, an annual blood pressure check, and less frequently an estimation of serum creatinine, is a reasonable precaution, even after apparent complete recovery.

Acute glomerulonephritis of unknown cause

The prognosis is less good and the need for follow-up is correspondingly greater. Systemic vasculitides and progress ve crescentic glomerulonephritis occurring in isolation The prognosis is often poor and severe renal failure with oliguria and hypertension often occurs within a few weeks or months of the onset of the illness. This group of conditions constitute a nephrological emergency since specific treatment is beneficial.

Goodpasture’s syndrome

This rare condition is mediated by anti-GBM antibody. It presents with recurrent haemoptysis and a severe progressive proliferative, often crescentic, glomerulonephritis. There is a strong association with HLA-DR2. Lung haernorrhage, which occurs more commonly in cigarette smokers, responds to repeated plasma exchange (which removes the anti-GBM antibody) combined with immunosuppressive therapy. The effect of this treatment upon the glomerulonephritis is less clear-cut; when oliguria occurs or serum creatinine rises above 0.6-0.7 mmollitre-1, renal failure is almost always irreversible.

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