The epidemiology of rapidly progressive glomerulonephritis according to Hedger, et al., is an incidence rate of 3.9 individuals per million (3.3–4.7) with a 95% confidence intervals.

Male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidemia, older age, familial disease and elevated creatinine concentrations are markers of a poor outcome. Frank hematuria has shown discordant results with most studies showing a better prognosis, perhaps related to the early diagnosis, except for one group which reported a poorer prognosis. Proteinuria and hypertension are the most powerful prognostic factors in this group.

There are certain other features on kidney biopsy such as interstitial scarring which are associated with a poor prognosis. ACE gene polymorphism has been recently shown to have an impact with the DD genotype associated more commonly with progression to kidney failure.

Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.

About a third of untreated patients have spontaneous remission, another third progress to require dialysis and the last third continue to have proteinuria, without progression of renal failure.

It is unclear whether or not acute proliferative glomerulonephritis (i.e., poststreptococcal glomerulonephritis) can be prevented with early prophylactic antibiotic therapy, with some authorities arguing that antibiotics can prevent development of acute proliferative glomerulonephritis, while others reject that antibiotics can prevent acute proliferative glomerulonephritis.

Men are affected three times as often as women. There is also marked geographic variation in the prevalence of IgA nephropathy throughout the world. It is the most common glomerular disease in the Far East and Southeast Asia, accounting for almost half of all the patients with glomerular disease. However, it accounts for only about 25% of the proportion in European and about 10% among North Americans, with African–Americans having a very low prevalence of about 2%. However, a confounding factor in this analysis is the existing policy of screening and use of kidney biopsy as an investigative tool. School children in Japan undergo routine urinalysis (as do army recruits in Singapore) and any suspicious abnormality is pursued with a kidney biopsy, which might partly explain the high observed incidence of IgA nephropathy in those countries.

The remainder is secondary due to:

- autoimmune conditions (e.g., systemic lupus erythematosus)

- infections (e.g., syphilis, malaria, hepatitis B, hepatitis C)

- drugs (e.g., captopril, NSAIDs, penicillamine, probenecid).

- inorganic salts (e.g. gold, mercury).

- tumors, frequently solid tumors of the lung and colon; hematological malignancies such as chronic lymphocytic leukemia are less common.

The cause of lupus nephritis, a genetic predisposition, plays role in lupus nephritis. Multiple genes, many of which are not yet identified, mediate this genetic predisposition.

The immune system protects the human body from infection, with immune system problems it cannot distinguish between harmful and healthy substances. Lupus nephritis affects approximately 3 out of 10,000 people.

In one review, over half of individuals with shunt nephritis made a complete recovery. An additional 40% of individuals had persistent urine abnormalities or end-stage renal disease. Death occurred in 9%.

Drug regimens prescribed for lupus nephritis include mycophenolate mofetil (MMF), intravenous cyclophosphamide with corticosteroids, and the immune suppressant azathioprine with corticosteroids. MMF and cyclophosphamide with corticosteroids are equally effective in achieving remission of the disease. MMF is safer than cyclophosphamide with corticosteroids, with less chance of causing ovarian failure, immune problems or hair loss. It also works better than azathioprine with corticosteroids for maintenance therapy. Individuals with lupus nephritis have a high risk for B-cell lymphoma (which begins in the immune system cells).

Glomerulonephritis (GN), also known as glomerular nephritis, is a term used to refer to several kidney diseases (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory component.

As it is not strictly a single disease, its presentation depends on the specific disease entity: it may present with isolated hematuria and/or proteinuria (blood or protein in the urine); or as a nephrotic syndrome, a nephritic syndrome, acute kidney injury, or chronic kidney disease.

They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are intrinsic to the kidney. Secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders (SLE, vasculitis), or diabetes.

Endocapillary proliferative glomerulonephritis is a form of glomerulonephritis that can be associated with nephritis.

It may be associated with Parvovirus B19.

Therapy for rapidly progressive glomerulonephritis is done via corticosteroids and cyclophosphamide. The predictor of kidney survival is serum creatinine value. The substitution of azathioprine for cyclophosphamide after a 90-day initial period is another option.Plasmapheresis can be used for patients who present with severe renal failure.

Glomerulonephrosis is a non-inflammatory disease of the kidney (nephrosis) presenting primarily in the glomerulus (a glomerulopathy).

It can be contrasted to glomerulonephritis, which implies inflammation.

It can be caused by diethylnitrosamine.

Glomerulonephritis refers to an inflammation of the glomerulus, which is the unit involved in filtration in the kidney. This inflammation typically results in one or both of the nephrotic or nephritic syndromes.

In children and some adults, FSGS presents as a nephrotic syndrome, which is characterized by edema (associated with weight gain), hypoalbuminemia (low serum albumin, a protein in the blood), hyperlipidemia and hypertension (high blood pressure). In adults, it may also present as kidney failure and proteinuria, without a full-blown nephrotic syndrome.

It is characterized by glomerular basement membrane thickening (referred to as "tram-tracking of the basement membrane"), increased mesangial matrix and segmental and global glomerulosclerosis.

The differential diagnosis of tram-tracking includes membranoproliferative glomerulonephritis (especially hepatitis C), and thrombotic microangiopathies.

Shunt nephritis is a rare condition affecting males and females of all ages. It occurs in approximately 0.7-2.3% of patients with shunt infections. Approximately 12% of ventriculoatrial shunts become infected, with "Staphylococcus epidermidis" being the infectious agent in 75% of cases.

Diffuse proliferative nephritis (DPN) or glomerulonephritis (DPGN) is a type of glomerulonephritis that is the most serious form of renal lesions in SLE and is also the most common, occurring in 35% to 60% of patients. Most of the glomeruli show endothelial and mesangial proliferation affecting the entire glomerulus, leading to diffuse hypercellularity of the glomeruli, producing in some cases epithelial crescents that fill Bowman's space. When extensive, immune complexes create an overall thickening of the capillary wall, resembling rigid "wire loops" on routine light microscopy. Electron microscopy reveals electron-dense subendothelial immune complexes (between endothelium and basement membrane). Immune complexes can be visualized by staining with fluorescent antibodies directed against immunoglobulins or complement, resulting in a granular fluorescent staining pattern. In due course, glomerular injury gives rise to scarring (glomerulosclerosis). Most of these patients have hematuria with moderate to severe proteinuria, hypertension, and renal insufficiency.

Membranoproliferative glomerulonephritis involves deposits at the intraglomerular mesangium.

It is also the main hepatitis C associated nephropathy.

It also is related to a number of autoimmune diseases, prominently systemic lupus erythematosus (SLE). Also found with Sjögren syndrome, rheumatoid arthritis, inherited complement deficiencies (esp C2 deficiency), scleroderma, Celiac disease.

The histomorphologic differential diagnosis includes transplant glomerulopathy and thrombotic microangiopathies.

Mesangial proliferative glomerulonephritis is a form of glomerulonephritis associated primarily with the mesangium. There is some evidence that interleukin-10 may inhibit it in an animal model. It is classified as type II lupus nephritis by the World Health Organization (WHO).

Transplant glomerulopathy, abbreviated TG, is a disease of the glomeruli in transplanted kidneys. It is a type of renal injury often associated with chronic antibody-mediated rejection. However, transplant glomerulopathy is not specific for chronic antibody-mediated rejection; it may be the result of a number of disease processes affecting the glomerular endothelium.

The prognosis for nephrotic syndrome under treatment is generally good although this depends on the underlying cause, the age of the patient and their response to treatment. It is usually good in children, because minimal change disease responds very well to steroids and does not cause chronic renal failure. Any relapses that occur become less frequent over time; the opposite occurs with mesangiocapillary glomerulonephritis, in which the kidney fails within three years of the disease developing, making dialysis necessary and subsequent kidney transplant. In addition children under the age of 5 generally have a poorer prognosis than prepubescents, as do adults older than 30 years of age as they have a greater risk of kidney failure.

Other causes such as focal segmental glomerulosclerosis frequently lead to end stage renal disease. Factors associated with a poorer prognosis in these cases include level of proteinuria, blood pressure control and kidney function (GFR).

Without treatment nephrotic syndrome has a very bad prognosis especially "rapidly progressing glomerulonephritis", which leads to acute kidney failure after a few months.

There are currently several known genetic causes of the hereditary forms of FSGS.

Some researchers found SuPAR as a cause of FSGS.

Another gene that has been associated with this syndrome is the COL4A5 gene.

Membranous nephropathy (MN)

- Sjögren's syndrome

- Systemic lupus erythematosus (SLE)

- Diabetes mellitus

- Sarcoidosis

- Drugs (such as corticosteroids, gold, intravenous heroin)

- Malignancy (cancer)

- Bacterial infections, e.g. leprosy & syphilis

- Protozoal infections, e.g. malaria

Focal segmental glomerulosclerosis (FSGS)

- Hypertensive nephrosclerosis

- HIV

- Obesity

- Kidney loss

Minimal change disease (MCD)

- Drugs, especially NSAIDs in the elderly

- Malignancy, especially Hodgkin's lymphoma

- Allergy

- Bee sting

Membranoproliferative Glomerulonephritis

- Hepatitis C