Archives of General Internal Medicine

Reach Us +1-845-208-9209

Editorial - Archives of General Internal Medicine (2021) Volume 5, Issue 11

Glomerulonephritis: Inflammatory disorder.

Philip Assari*

Department of Pathology, Saint Joseph University, Beirut, Lebanon

Corresponding Author:
Philip Assari
Department of Pathology
Saint Joseph University
E-mail: [email protected]

Accepted date: December 27th , 2021

Citation: Assari P. Glomerulonephritis: Inflammatory disorder. Arch Gen Intern Med 2021;5(11):9.

Visit for more related articles at Archives of General Internal Medicine


Glomerulonephritis (GN) is swelling of the glomeruli, which are vital structures in the kidneys that are build-up of tiny blood vessels. These knots of vessels help filter the blood and eliminate additional fluids.


Acute glomerulonephritis: The acute illness may be caused by infections such as strep throat. It may also be triggered by other illnesses, comprising lupus, Goodpasture’s syndrome, Wegener's ailment, and polyarteritis nodosa. Primary diagnosis and rapid treatment are important to prevent kidney failure.

Chronic lomerulonephritis: Sometimes, the ailment runs in the family. This kind frequently shows up in adults who may also have hearing loss and vision loss. Some forms are triggered by changes in the immune system. However, in numerous cases, the cause is not known. Sometimes, individuals have one acute attack of the ailment and progress the chronic form years later.

Individuals with glomerulonephritis frequently don’t experience signs of the condition. But symptoms can include:

• Blood in the urine, which may make the pee, look brown, pink or red.

• Fatigue, nausea or a rash.

• High blood pressure or shortness of breath.

• Ache in the joints or abdomen (belly area).

• Peeing less often or more often than normal.

• Swelling in the legs or face.

• Urine that’s foamy.

Sometimes glomerulonephritis is temporary, and kidneys can recover normal function. If it is lasting, and it continues to get worse, it can lead to serious kidney problems, such as acute kidney injury, chronic kidney ailment, high blood pressure or nephrotic syndrome. Some other possible difficulties include:

• Kidney infection

• Fluid build-up

• Hyperkalemia

• Kidney failure/ESRD

The treatment for glomerulonephritis depends on what is triggering it. For example, if high blood pressure triggered the damage to your glomeruli, treatment will likely focus on controlling your blood pressure. Definite medicines called Angiotensin- Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs) can help regulate your blood pressure.

Severe cases of glomerulonephritis, triggered by problems with the immune system, are sometimes treated with types of medicine known as immunosuppressants. These medicines suppress your immune system. For example, cyclophosphamide is an immunosuppressant used in very high doses to treat some cancers. It's also an established treatment, in much lower doses, for glomerulonephritis.

The differential diagnosis of glomerulonephritis without systemic ailment comprises post streptococcal glomerulonephritis, IgA nephropathy, Rapidly Progressive Glomerulonephritis (RPGN), and Membanoproliferative Glomerulonephritis (MPGN). Glomerular swelling is probably induced directly by a nephritogenic streptococcal protein in poststreptococcal glomerulonephritis, and by mesangial deposition of peculiarly glycosylated IgA1-comprising immune aggregates in IgA nephropathy. In crescentic RPGN, the role of cellular rather than humoral immune mechanisms is now becoming clear. Many individuals with MPGN have prolonged hepatitis C infection. There is no effective ailment-Particular therapy for post streptococcal glomerulonephritis or IgA nephropathy. RPGN benefits from high-dose steroids and cytotoxic drug therapy with the addition of plasma exchange in ailment induced by antibody to glomerular basement membrane. Antiviral therapies decrease the severity of MPGN due to hepatitis C virus. However, numerous new therapies directed at particular cytokines, growth factors, fibrin deposition, and other mediators of injury are being developed, as well as more specific and less toxic forms of immunotherapy.

Get the App