This term is often used to describe all pathological conditions of the glomerulus; however, strictly speaking it refers to “inflammation of the glomerulus”. Glomerulonephritis represents a number of conditions where there is damage to the glomerular apparatus, causing the appearance of blood and protein in the urine.
This is a condition where antigen-antibody complexes become trapped within the glomerulus. The antigen is usually some streptococcus. The disease classically presents in children and young adults as sore throat followed a couple of weeks later by oliguria, haematuria, hypertension, and slightly abnormal renal function.
The disease is self-limiting, and 90% of patients will spontaneously recover. Treatment generally involves the control of blood pressure, reduced fluid and salt intake, and in some cases the use of antibiotics and diuretics.
The two main presenting features are haematuria and proteinuria. Chronic glomerulonephritis may also present as acute or chronic renal failure, or nephritic or nephritic syndromes.
There are numerous sub-types of the condition, and they are categorised according to histology.
Along with diabetes and hypertension, it is one of the most common causes of ESRF in the UK.
Minimal change glomerulonephritis
This accounts for 80% of cases of glomerulonephritis in children and 20% in adults. It is a T-cell mediated condition in which about 1/3 of cases will remit spontaneously, 1/3 will continue in a nephrotic state, and 1/3 will show progressive loss of renal function.
Minimal change glomerulonephritis presents with proteinuria, although haematuria and increased BP may also be present. The majority of cases present with nephrotic syndrome.
A biopsy will normally be performed, and under microscopy, this will appear normal – hence the name of the condition. However, under electron microscope, the condition will show damaged podocytes.
Steroids, i.e. prednisolone, are the main treatment, and this will cause remission in 95% of children and 70% of adults. However, relapse is common once treatment is stopped. If treatment with steroids is unsuccessful, or if relapse occurs, then the patient may be treated with ciclosporin.
About 1% of cases will progress to ESRF.
IgA nephropathy,aka Berger’s disease
This is the most common type of glomerulonephritis in the developed world. It nearly always presents with micro- or macroscopic haematuria, and proteinuria and hypertension are very common symptoms. Nephrotic syndrome may also be present.
A typical patient will be a young male who presents with haematuria a few days after a UTI or bout of pharyngitis.
ESRF is much more common in this disease, i.e. as it a long-term condition; 20% of patients will develop ESRF over a period of 20 years.
There is deposition of IgA in mesangial cells – which are found in the basement membrane of the glomerulus and are phagocytotic – probably as a result of over-production of IgA related to the preceding infection. The condition can rapidly disappear and then re-appear at a later stage. Often when it reappears it is associated with respiratory infection. Once again, renal biopsy is necessary to determine if the disease is present. Biopsy will show mesangial proliferation and IgA deposits.
Anti-inflammatories such as ciclosporin may be used, but the benefit they confer is not certain.
The prognosis is made worse by…
- Male gender
- High BP
- Proteinuria or renal failure at presentation
Rapidly Progressive GN (RPGN)
This is the most aggressive type of GN, progressing to SRF within days. There are different causes, but they all result in the same histological effects – proliferation of macrophages and parietal epithelial cells in Bowmann’s capsule, leading to a crescent-like appearance of the glomeruli.
The cause is often microscopic polyangitis – which is an autoimmune disease causing vasculitis, without signs of inflammation. RPGN can involve many other organs other than the kidneys, and it is seen alongside SLE and infections such as endocarditis.
RPGN presents with signs of renal failure. There may also be signs of systemic disease, e.g. SLE, if one is present.
Treat RPGN with aggressive immunosupression, e.g ciclosporin, clycophosphamide, and corticosteroids.
The prognosis is poor if the initial presentation has a serum creatinine of over 600μmol/L; if the level is below this, then 80% of patients will show signs of improvement without treatment.
There are many other types of glomerulonephritis that have not been mentioned here!
- U+E – checking for filtration problems
- ESR/CRP – checking for levels of inflammation
- Autoantibodies, particularly anti-GMB, glomerular basement membrane, ANA, ANCA
- Urine – RBC’s, red cell casts, protein
- Renal USS
- Renal biopsy – to asses the type of glomerulonephritis
Call the nephrologist!
In the mean time, try to…
- Keep BP >130/80, or >125/75 if proteinuria is greater than 1g/day
- Give ACE inhibitor and/or angiotensin II receptor agonist – research has shown these two agents work best in conjunction with each other