Glomerulonephritis is the name given to a group of kidney diseases caused by inflammation of the glomeruli.
Okay, I know that the sentence above does not explain much.
The fact is, to understand glomerulonephritis, we must first understand what is a glomerulus.
The microscopic anatomy of the kidney is very tricky, and can be hard to understand even to other physicians.
Let’s try to make it easier.
All our organs are composed of its basic units. We have neurons in the brain, hepatocytes in the liver, alveoli in the lungs, etc … In the kidney, the basic unit is the nephron.
Each kidney has one million nephrons. These microscopic units are responsible for filtering the blood and for the substances produced in the kidneys. A nephron is not a single cell, but a structure composed of a glomerulus and their renal tubule.
This “simple” graphic below represents a nephron with its glomerulus, renal tubule and blood vessels.
We can summarize the functioning of the kidney as follows.
The blood that reaches the kidneys, goes to the glomerulus, which is capillary tuft, with a filtrating membrane in its wall. The glomerulus is actually our true blood filter.
Glomerulus seen by electron microscopy
Look at the graphic below. The blood reaches the afferent arteriole (a microscopic artery), passes through several capillaries in the glomerulus, undergoes the process of filtration and then returns to the bloodstream via efferent arteriole.
Everything that has been filtered by the capillaries goes toward renal tubule. In the renal tubule, some important substances such as glucose, sodium, potassium, calcium etc … are reabsorbed in accordance with the needs of the body. The final result of this process is the urine as we know it. The kidneys just excrete substances unneeded or in excess.
The glomerulus is the leading filter, “choosing” which substances go to the urine and which return to the blood. The tubules in turn, define how much of each substance already filtered by the glomerulus will be excreted in the urine. For example, if there is high potassium in the blood, the tubules will eliminate all the potassium that is filtered to restore its normal levels. On the other hand, if the blood potassium is low, then the tubules will avidly reabsorb it, leading to a urine with very little potassium in it.
Major substances such as most of the proteins, are not filtered at all, because they are larger than the pores of the glomerular membrane. They never leave the blood and do not reach the tubule. Therefore, a normal urine has almost no protein in its content.
So, the final content of urine, is a result of both the process of glomerular filtration and tubular reabsorption.
So, as glomeruli are the main responsible for the filtration of blood, any disease affecting it, disturbs the main function of our kidneys.
There are 2 basic types of glomerulus injury:
- Nephritic syndrome or glomerulonephritis.
- Nephrotic syndrome
In nephritic syndrome, an inflammatory process damages and reduces the capacity of the glomerulus to filter blood, leading to acute renal failure, hypertension and bloody urine (hematuria)
In nephrotic syndrome, the most common is a glomerular membrane injury without obvious sighs of inflammation.
To better understand, we can say that, in glomerulonephritis, the glomerulus filters it all. Nothing passes through the membrane. while in the nephrotic syndrome, it all passes. The proteins that are normally not filtered, when there are lesions on the membrane of glomeruli, “leak” into the tubules, being inappropriately eliminated in the urine.
Loss of protein in urine, called proteinuria, is a sign of glomerular disease. Indeed, proteinuria is a sign of kidney disease, but is also responsible for its progression. The tubules are not prepared to receive large amount of proteins, and in attempt to reabsorbs them back to the blood, its cells suffers damages.
Therefore, at first, the presence of protein shows that there is something going wrong with the kidneys. If untreated, it becomes another factor of aggression and progression to renal failure.
It is not uncommon to find nephrotic syndrome and nephritic syndrome at the same time. All it takes are concomitant lesions in the glomerular membrane and intense inflammatory activity in the glomerulus. In medical practice it is very common to see some overlapping between these two syndromes
So, what causes glomerular disease?
The glomerular diseases have several causes. Didactically it is divided into primary disease, when there is no apparent cause, or secondary disease, when they occur due to any systemic condition.
Secondary causes of glomerulopathy (nephritis and/or nephrotic):
- Lupus
- Hepatitis B and C
- HIV
- Diabetes
- Morbid obesity
- Heroin
- Syphilis
- Wegner Granulomatosis
- Goospasture Disease
- Cancer
- Pharyngitis or skin lesions caused by Streptococcus (post infectious glomerulonephritis)
- Amyloidosis
Primary glomerulopathy:
- Focal and segmental Glomerulosclerosis (nephritic syndrome and / or nephrotic)
- Disease minimal damage (nephrotic syndrome)
- Membranous nephropathy (nephrotic syndrome)
- Membranoproliferative Glomerulonephritis (nephritic syndrome and / or nephrotic)
- IgA nephropathy (nephritic syndrome)
We call primary glomerulopathy those glomerular diseases restricted to the kidney. There are no other organs or systems affected.
Each of these glomerular diseases, primary or secondary, has distinct clinical features, prognosis and treatment. Therefore, the specific diagnosis of the glomerular injury and the recognition of the presence or absence of associated systemic disease is vital to the treatment.
Blood analysis may reveal kidney failure by showing an increasing creatinine level (read: DO YOU KNOW WHAT CREATININE IS? ). The urinary loss of proteins leads to a foamy urine and a low level of blood proteins such as albumin. The physical examination can easily identify hypertension and edemas.
These factors only suggest the presence of a glomerular disease, without establishing a specific diagnosis.
Obviously, if a patient has hepatitis C and suddenly starts to show signs of glomerulopathy, the cause of renal damage is easy. But most of the time it is not that simple. Some diseases such as lupus can cause different types of glomerulonephritis and glomerular injury, and different types of signs and symptoms, requiring different treatments for each.
The gold standard in the diagnosis of glomerulopathy is a renal biopsy. The biopsy in addition to defining the type of glomerulonephritis, also provides indications of the prognosis of the disease.
As most glomerulonephritis and glomerulopathy have immunological factors, sometimes related to autoimmune diseases, treatment is based on heavy immunosuppressive drugs such as corticosteroids, cyclophosphamide, cyclosporine, azathioprine and mycophenolate mofetil . If the biopsy identifies very advanced lesions and little chance of cure, treatment often brings more complications than improvement.
Several factors interfere with the prognosis. Some diseases such as minimum lesion and IgA nephropathy are usually benign or have very slow progression. Others like lupus nephritis or glomerulonephritis secondary to Wegner’s Granulomatosis are very severe and can easily lead to end stage renal disease.
The glomerulopathy are just behind the Diabetes and hypertension as causes of end stage renal diseases.
If you have any sign that might suggest a glomerular disease, especially blood or protein in the urine (even in small quantity), it might be good to seek a nephrologist.
Portuguse version: O QUE É UMA GLOMERULONEFRITE ?
