Minimal change disease is most common in very young children but can occur in older children and adults. It is by far the most common cause of nephrotic syndrome in children between the ages of 1 and 7, accounting for the majority (about 90%) of these diagnoses. Among teenagers who develop nephrotic syndrome, it is caused by minimal change disease about half the time. It can also occur in adults but accounts for less than 20% of adults diagnosed with nephrotic syndrome. Among children less than 10 years of age, boys seem to be more likely to develop minimal change disease than girls. Minimal change disease is being seen with increasing frequency in adults over the age of 80.

People with one or more autoimmune disorders are at increased risk of developing minimal change disease. Having minimal change disease also increases the chances of developing other autoimmune disorders.

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.

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome in children and adolescents, as well as a leading cause of kidney failure in adults. It is also known as "focal glomerular sclerosis" or "focal nodular glomerulosclerosis". It accounts for about a sixth of the cases of nephrotic syndrome. (Minimal change disease (MCD) is by far the most common cause of nephrotic syndrome in children: MCD and primary FSGS may have a similar cause.)

Minimal change disease has been called by many other names in the medical literature, including minimal change nephropathy, minimal change nephrosis, minimal change nephrotic syndrome, minimal change glomerulopathy, foot process disease (referring to the foot processes of the podocytes), nil disease (referring to the lack of pathologic findings on light microscopy), nil lesions, lipid nephrosis, and lipoid nephrosis.

Membranoproliferative glomerulonephritis ("MPGN"), also known as mesangiocapillary glomerulonephritis, is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane (GBM) thickening, activating complement and damaging the glomeruli.

MPGN accounts for approximately 4% of primary renal causes of nephrotic syndrome in children and 7% in adults.

It should not be confused with membranous glomerulonephritis, a condition in which the basement membrane is thickened, but the mesangium is not.

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.

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.

Affected male and carrier female dogs generally begin to show signs of the disease at two to three months of age, with proteinuria. By three to four months of age, symptoms include for affected male dogs: bodily wasting and loss of weight, proteinuria & hypoalbuminemia. Past nine months of age, hypercholesterolemia may be seen. In the final stages of the disease, at around 15 months of age for affected males, symptoms are reported as being renal failure, hearing loss and death. Since the condition is genetically dominant, diagnosis would also include analysis of the health of the sire and dam of the suspected affected progeny if available.

aHUS can be inherited or acquired, and does not appear to vary by race, gender, or geographic area. As expected with an ultra-rare disease, data on the prevalence of aHUS are extremely limited. A pediatric prevalence of 3.3 cases per million population is documented in one publication of a European hemolytic uremic syndrome (HUS) registry involving 167 pediatric patients.

Management of sickle nephropathy is not separate from that of overall patient management. In addition, however, the use of ACE inhibitors has been associated with improvement of the hyperfiltration glomerulopathy. Three-year graft and patient survival in kidney transplant recipients with sickle nephropathy is lower when compared to those with other causes of end-stage kidney disease.

HIVAN is the third most common cause of ESRF among African Americans, and commonly seen in African-American patients with HIV compared with other ethnic groups. In the USA 12% of patients dying with AIDS have histologically proven HIVAN, the worldwide incidence amongst AIDS patients appears to be similar. A South African study at Tygerberg Hospital, Stellenbosch University, has shown HIVAN histology in 33/61(54%) biopsies performed in HIV positive patients.

While the prognosis of cryofibrinoginemic disease varies greatly depending on its severity as well as the severity of its associated disorders, satisfactory clinical outcomes are reported in 50-80% of patients with primary or secondary disease treated with corticosteroid and/or immunosuppressive regimens. However, relapses occur within the first 6 months after stopping or decreasing therapy in 40-76% of cases. Sepsis resulting from infection of necrotic tissue is the most common threat to life in primary disease whereas the associated disorder is a critical determinant of prognosis in secondary disease.

Samoyed Hereditary Glomerulopathy is caused by a nonsense mutation in codon 1027 of the COL4A5 gene on the X chromosome (glycine to stop codon), which is similar to Alport's syndrome in humans. The disease is simply inherited, X-linked dominant, with males generally having more severe symptoms than females. Clinically, from the age of three to four months, proteinuria in both sexes is seen. In dogs older than this, renal failure in combination with more or less pronounced hearing loss occurs swiftly, and death at the age of 8 to 15 months is expected. In heterozygous females, whereby only one of the two X chromosomes carry the mutation, the disease develops slowly.

The disease is specific to the Samoyed in that, the Samoyed, is the only breed of dog to show the more rapid progression to renal failure and death, as well as affecting males to a much more severe degree than females. The Samoyed, however is not the only breed of dog to suffer from life-threatening renal diseases. Proteinuria has been found consistently in Samoyeds, Doberman Pinschers, and Cocker spaniels.

HIV-associated nephropathy (HIVAN) refers to kidney disease developing in association with HIV infection. The most common, or "classical", type of HIV-associated nephropathy is a collapsing focal segmental glomerulosclerosis (FSGS), though other forms of kidney disease may also occur with HIV. Regardless of the underlying histology, renal disease in HIV-positive patients is associated with an increased risk of death.

HIVAN may be caused by direct infection of the renal cells with the HIV-1 virus, with resulting renal damage through the viral gene products. It could also be caused by changes in the release of cytokines during HIV infection. Usually occurs only in advanced disease and approximately 80% of patients with HIVAN have a CD4 count of less than 200. HIVAN presents with nephrotic syndrome and progressive kidney failure. Despite being a cause of chronic kidney failure, kidney sizes are usually normal or large.

Membranous glomerulonephropathy (MGN) is a slowly progressive disease of the kidney affecting mostly people between ages of 30 and 50 years, usually Caucasian.

It is the second most common cause of nephrotic syndrome in adults, with focal segmental glomerulosclerosis (FSGS) recently becoming the most common.

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.

Glomerulopathy is a set of diseases affecting the glomeruli of the nephron.

Such diseases can include processes that are inflammatory or noninflammatory. Because the term "glomerulitis" exists for inflammatory conditions, "glomerulopathy" sometimes carries a noninflammatory implication.

Nephrotic syndrome can affect any age, although it is mainly found in adults with a ratio of adults to children of 26 to 1.

The syndrome presents in different ways in the two groups: the most frequent glomerulopathy in children is minimal change disease (66% of cases), followed by focal segmental glomerulosclerosis (8%) and mesangiocapillary glomerulonephritis (6%). In adults the most common disease is mesangiocapillary glomerulonephritis (30-40%), followed by focal and segmental glomeruloesclerosis (15-25%) and minimal change disease (20%). The latter usually presents as secondary and not primary as occurs in children. Its main cause is diabetic nephropathy. It usually presents in a patient’s 40s or 50s.

Of the glomerulonephritis cases approximately 60% to 80% are primary, while the remainder are secondary.

There are also differences in epidemiology between the sexes, the disease is more common in men than in women by a ratio of 2 to 1.

The epidemiological data also reveals information regarding the most common way that symptoms develop in patients with nephrotic syndrome: spontaneous remission occurs in up to 20% or 30% of cases during the first year of the illness. However, this improvement is not definitive as some 50% to 60% of patients die and / or develop chronic renal failure 6 to 14 years after this remission. On the other hand, between 10% and 20% of patients have continuous episodes of remissions and relapses without dying or jeopardizing their kidney. The main causes of death are cardiovascular, as a result of the chronicity of the syndrome, and thromboembolic accidents.

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

Patients with aHUS have an extremely poor prognosis. Among those with the most commonly identified aHUS genetic mutation, the proportion of patients experiencing negative outcomes (e.g., need for dialysis, permanent kidney damage, death) within the first year rises to 70%. However, sudden morbidity and mortality can occur regardless of mutational status. aHUS can arise at any age, with more than 40% of cases first reported after 18 years of age. The oldest presentation in one study was at age 83. As noted above, kidney transplantation for aHUS patients with ESRD was rarely considered because of a high incidence of graft loss due to TMA recurrence in the transplanted organ in up to 90% of patients. Consequently, most aHUS patients with ESRD undergo chronic dialysis, which is associated with significant morbidities and worsened prognosis. Combined liver-kidney transplantation has been attempted in patients with aHUS, although this high-risk procedure has a mortality rate approaching 50%.

Quality of life is very poor for patients with aHUS, who are burdened with fatigue, renal complications, hypertension, neurological impairment, gastrointestinal distress, clotting at the site of venous access, and ultimately, death. PE/PI is also reported to be associated with significant safety risks and is highly disruptive to patients’ lives due to the requirements for extensive vascular access and frequent administration.

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.

Acute bacterial and mycobacterium infections are sometimes associated with cryofibriongenemia. In these cases, cryofibrinogenemia is usually transient and rapidly resolves after appropriate anti-bacterial treatment. In HIV/AIDS virus, Epstein–Barr virus, Cytomegalovirus, varicella zoster virus, herpes simplex virus, and hepatitis virus infections any rise in circulating cryofibrinogen is more sustained and potentially symptomatic. For example one large study of the most thoroughly study example of viral infection-associated cryofibrinogenmia, Hepatitis C infection, found that cryofibrinogenemia occurred in 37% of cases, was associated with concurrent cryoglobulinemia in 89% of cases, and led to significantly increased vascular disruption. Antiviral therapy resulted in complete resolution of the cryofibrinogenemia in only ~50% of these cases.

Sickle cell nephropathy is a type of nephropathy associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla, coupled with the slow blood flow in the vasa recta, favors sickling of red blood cells, with resultant local infarction (papillary necrosis). Functional tubule defects in patients with sickle cell disease are likely the result of partial ischemic injury to the renal tubules.

Also the sickle cell disease in young patients is characterized by renal hyperperfusion, glomerular hypertrophy, and glomerular hyperfiltration. Many of these individuals eventually develop a glomerulopathy leading to glomerular proteinuria (present in as many as 30%) and, in some, the nephrotic syndrome. Co-inheritance of microdeletions in the -globin gene (thalassemia) appear to protect against the development of nephropathy and are associated with lower mean arterial pressure and less protein in the urine.

Mild increases in the blood levels of nitrogen and uric acid can also develop. Advanced kidney failure and high blood urea levels occur in 10% of cases. Pathologic examination reveals the typical lesion of "hyperfiltration nephropathy" namely, focal segmental glomerular sclerosis. This finding has led to the suggestion that anemia-induced hyperfiltration in childhood is the principal cause of the adult glomerulopathy. Nephron loss secondary to ischemic injury also contributes to the development of azotemia in these patients.

In addition to the glomerulopathy described above, kidney complications of sickle cell disease include cortical infarcts leading to loss of function, persistent bloody urine, and perinephric hematomas. Papillary infarcts, demonstrable radiographically in 50% of patients with sickle trait, lead to an increased risk of bacterial infection in the scarred kidney tissues and functional tubule abnormalities. The presence of visible blood in the urine without pain occurs with a higher frequency in sickle trait than in sickle cell disease and likely results from infarctive episodes in the renal medulla. Functional tubule abnormalities such as nephrogenic diabetes insipidus result from marked reduction in vasa recta blood flow, combined with ischemic tubule injury. This concentrating defect places these patients at increased risk of dehydration and, hence, sickling crises. The concentrating defect also occurs in individuals with sickle trait. Other tubule defects involve potassium and hydrogen ion excretion, occasionally leading to high blood potassium, metabolic acidosis, and a defect in uric acid excretion which, combined with increased purine synthesis in the bone marrow, results in high blood uric acid levels.

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.

Persons of any age can develop a keloid. Children under 10 are less likely to develop keloids, even from ear piercing. Keloids may also develop from Pseudofolliculitis barbae; continued shaving when one has razor bumps will cause irritation to the bumps, infection, and over time keloids will form. Persons with razor bumps are advised to stop shaving in order for the skin to repair itself before undertaking any form of hair removal. The tendency to form keloids is speculated to be hereditary. Keloids can tend to appear to grow over time without even piercing the skin, almost acting out a slow tumorous growth; the reason for this tendency is unknown.

Extensive burns, either thermal or radiological, can lead to unusually large keloids; these are especially common in firebombing casualties, and were a signature effect of the atomic bombings of Hiroshima and Nagasaki.

True incidence and prevalence of keloid in United States is not known. Indeed, there has never been a population study to assess the epidemiology of this disorder. In his 2001 publication, Marneros stated that “reported incidence of keloids in the general population ranges from a high of 16% among the adults in Zaire to a low of 0.09% in England,” quoting from Bloom’s 1956 publication on heredity of keloids. We do however know, from clinical observations that the disorder is more common among Africans, African Americans and Asians with unreliable and very wide estimated prevalence rates ranging from 4.5-16%. Thorough and scientific population and epidemiology studies of this disorder are desperately needed.