The exact number of cases of rhabdomyolysis is difficult to establish, because different definitions have been used. In 1995, hospitals in the U.S. reported 26,000 cases of rhabdomyolysis. Up to 85% of people with major traumatic injuries will experience some degree of rhabdomyolysis. Of those with rhabdomyolysis, 10–50% develop acute kidney injury. The risk is higher in people with a history of illicit drug use, alcohol misuse or trauma when compared to muscle diseases, and it is particularly high if multiple contributing factors occur together. Rhabdomyolysis accounts for 7–10% of all cases of acute kidney injury in the U.S.

Crush injuries are common in major disasters, especially in earthquakes. The aftermath of the 1988 Spitak earthquake prompted the establishment, in 1995, of the Renal Disaster Relief Task Force, a working group of the International Society of Nephrology (a worldwide body of kidney experts). Its volunteer doctors and nurses assisted for the first time in the 1999 İzmit earthquake in Turkey, where 17,480 people died, 5392 were hospitalized and 477 received dialysis, with positive results. Treatment units are generally established outside the immediate disaster area, as aftershocks could potentially injure or kill staff and make equipment unusable.

Acute exertional rhabdomyolysis happens in 2% to 40% of people going through basic training for the United States military. In 2012, the United States military reported 402 cases.

The prognosis depends on the underlying cause and whether any complications occur. Rhabdomyolysis complicated by acute kidney impairment in patients with traumatic injury may have a mortality rate of 20%. Admission to the intensive care unit is associated with a mortality of 22% in the absence of acute kidney injury, and 59% if kidney impairment occurs. Most people who have sustained kidney impairment due to rhabdomyolysis fully recover their kidney function.

Trauma, vascular problems, malignant hyperthermia, certain drugs and other situations can destroy or damage the muscle, releasing myoglobin to the circulation and thus to the kidneys. Under ideal situations myoglobin will be filtered and excreted with the urine, but if too much myoglobin is released into the circulation or in case of renal problems, it can occlude the renal filtration system leading to acute tubular necrosis and acute renal insufficiency.

Other causes of myoglobinuria include:

- McArdle's disease

- Phosphofructokinase deficiency

- Carnitine palmitoyltransferase II deficiency

- Malignant hyperthermia

- Polymyositis

- Lactate dehydrogenase deficiency

- Thermal or electrical burn

Myoglobinuria is the presence of myoglobin in the urine, usually associated with rhabdomyolysis or muscle destruction. Myoglobin is present in muscle cells as a reserve of oxygen.

Proteinuria may be a feature of the following conditions:

- Nephrotic syndromes (i.e. intrinsic renal failure)

- Pre-eclampsia

- Eclampsia

- Toxic lesions of kidneys

- Amyloidosis

- Collagen vascular diseases (e.g. systemic lupus erythematosus)

- Dehydration

- Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis)

- Strenuous exercise

- Stress

- Benign orthostatic (postural) proteinuria

- Focal segmental glomerulosclerosis (FSGS)

- IgA nephropathy (i.e. Berger's disease)

- IgM nephropathy

- Membranoproliferative glomerulonephritis

- Membranous nephropathy

- Minimal change disease

- Sarcoidosis

- Alport's syndrome

- Diabetes mellitus (diabetic nephropathy)

- Drugs (e.g. NSAIDs, nicotine, penicillamine, lithium carbonate, gold and other heavy metals, ACE inhibitors, antibiotics, or opiates (especially heroin)

- Fabry's disease

- Infections (e.g. HIV, syphilis, hepatitis, poststreptococcal infection, urinary schistosomiasis)

- Aminoaciduria

- Fanconi syndrome in association with Wilson disease

- Hypertensive nephrosclerosis

- Interstitial nephritis

- Sickle cell disease

- Hemoglobinuria

- Multiple myeloma

- Myoglobinuria

- Organ rejection:

- Ebola virus disease

- Nail patella syndrome

- Familial Mediterranean fever

- HELLP Syndrome

- Systemic lupus erythematosus

- Granulomatosis with polyangiitis

- Rheumatoid arthritis

- Glycogen storage disease type 1

- Goodpasture's syndrome

- Henoch–Schönlein purpura

- A urinary tract infection which has spread to the kidney(s)

- Sjögren's syndrome

- Post-infectious glomerulonephritis

There are three main mechanisms to cause proteinuria:

- Due to disease in the glomerulus

- Because of increased quantity of proteins in serum (overflow proteinuria)

- Due to low reabsorption at proximal tubule (Fanconi syndrome)

Proteinuria can also be caused by certain biological agents, such as bevacizumab (Avastin) used in cancer treatment. Excessive fluid intake (drinking in excess of 4 litres of water per day) is another cause.

Also leptin administration to normotensive Sprague Dawley rats during pregnancy significantly increases urinary protein excretion.

Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. People with diabetes may have damaged nephrons and develop proteinuria. The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field.

With severe proteinuria, general hypoproteinemia can develop which results in

diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema and hydrothorax.

In the general population, the frequency of medullary sponge kidney disease is reported to be 0.02–0.005%; that is, 1 in 5000 to 1 in 20,000. The frequency of medullary sponge kidney has been reported by various authors to be 1221% in patients with kidney stones. The disease is bilateral in 70% of cases.

In medicine, hemoglobinuria or haemoglobinuria is a condition in which the oxygen transport protein hemoglobin is found in abnormally high concentrations in the urine. The condition is often associated with any hemolytic anemia with primarily intravascular hemolysis, in which red blood cells (RBCs) are destroyed, thereby releasing free hemoglobin into the plasma. Excess hemoglobin is filtered by the kidneys, which excrete it into the urine, giving urine a purple color. Hemoglobinuria can lead to acute tubular necrosis which is an uncommon cause of a death of uni-traumatic patients recovering in the ICU .

There are no known causes, but the condition appears to be inherited in some patients. Symptoms of MCAS are caused by excessive chemical mediators inappropriately released by mast cells. Mediators include leukotrienes and histamines. The condition may be mild until exacerbated by stressful life events, or symptoms may develop and slowly trend worse with time.

MCAS is a relatively new diagnosis, being unnamed until 2007, and is believed to be very under-diagnosed. New findings are revealing that MCAS is much more prevalent than previously thought.

Complications associated with medullary sponge kidney include the following:

- Kidney stones

- Urinary tract infection (UTI)

- Blood in the urine

- Distal renal tubular acidosis (Type 1 RTA)

- Chronic kidney disease (rarely)

- Marked chronic pain

The diagnosis is often made based on the medical history, blood samples, and a urine sample. The absence of urine RBCs and RBC casts microscopically despite a positive dipstick test suggests hemoglobinuria or myoglobinuria. The medical term for RBCs in the urine is hematuria.

Children with DOCK8 deficiency do not tend to live long; sepsis is a common cause of death at a young age. CNS and vascular complications are other common causes of death.

DOCK8 deficiency is very rare, estimated to be found in less than one person per million; there have been 32 patients diagnosed as of 2012.

There are two autosomal recessive forms of this disease, childhood-onset and adult-onset. The gene for myophosphorylase, PYGM (the muscle-type of the glycogen phosphorylase gene), is located on chromosome 11q13. According to the most recent publications, 95 different mutations have been reported. The forms of the mutations may vary between ethnic groups. For example, the R49X (Arg49Stop) mutation is most common in North America and western Europe, and the Y84X mutation is most common among central Europeans.

The exact method of protein disruption has been elucidated in certain mutations. For example, R138W is known to disrupt to pyridoxal phosphate binding site. In 2006, another mutation (c.13_14delCT) was discovered which may contribute to increased symptoms in addition to the common Arg50Stop mutation.

Glycogen storage disease type V (GSD-V) is a metabolic disorder, more specifically a glycogen storage disease, caused by a deficiency of myophosphorylase. Its incidence is reported as 1 in 100,000, approximately the same as glycogen storage disease type I.

The disease was first reported in 1951 by Dr. Brian McArdle of Guy's Hospital, London.

In dairy breeds, the disease may occur in calves between birth and 4 months of age. In rustic breeds or beef cattle, heifers and young steers up to 12 months of age can be affected. In calves, muscles in upper portion of the front legs and the hind legs are degraded, causing the animal to have a stiff gait and it may have difficulty standing. The disease may also present in the form of respiratory distress.

Periodic fever syndromes (also known as autoinflammatory diseases or autoinflammatory syndromes) are a set of disorders characterized by recurrent episodes of systemic and organ-specific inflammation. Unlike autoimmune disorders such as systemic lupus erythematosus, in which the disease is caused by abnormalities of the adaptive immune system, patients with autoinflammatory diseases do not produce autoantibodies or antigen-specific T or B cells. Instead, the autoinflammatory diseases are characterized by errors in the innate immune system.

The syndromes are diverse, but tend to cause episodes of fever, joint pains, skin rashes, abdominal pains and may lead to chronic complications such as amyloidosis.

Most autoinflammatory diseases are genetic and present during childhood. The most common genetic autoinflammatory syndrome is familial Mediterranean fever, which causes short episodes of fever, abdominal pain, serositis, lasting less than 72 hours. It is caused by mutations in the MEFV gene, which codes for the protein pyrin.

Pyrin is a protein normally present in the inflammasome. The mutated pyrin protein is thought to cause inappropriate activation of the inflammasome, leading to release of the pro-inflammatory cytokine IL-1β. Most other autoinflammatory diseases also cause disease by inappropriate release of IL-1β. Thus, IL-1β has become a common therapeutic target, and medications such as anakinra, rilonacept, and canakinumab have revolutionized the treatment of autoinflammatory diseases.

However, there are some autoinflammatory diseases that are not known to have a clear genetic cause. This includes PFAPA, which is the most common autoinflammatory disease seen in children, characterized by episodes of fever, aphthous stomatitis, pharyngitis, and cervical adenitis. Other autoinflammatory diseases that do not have clear genetic causes include adult-onset Still's disease, systemic-onset juvenile idiopathic arthritis, Schnitzler syndrome, and chronic recurrent multifocal osteomyelitis. It is likely that these diseases are multifactorial, with genes that make people susceptible to these diseases, but they require an additional environmental factor to trigger the disease.

Another example that shows that autoinflamatory conditions may not be genetic in origin is found in a report published in "Nature" which shows that diet is very important in the development of such diseases. The ingestion levels of highly saturated fats and cholesterol, (high fat diet, HFD) affects the microbiota composition of the gut. Changes in the microbiota induced by a HFD are protective against the susceptibility to develop osteomyelitis (autoimmune disease) as compared with the changes induced by a low-fat diet. The changes in the microbiome of individuals under HFD showed a reduction in "Prevotella" abundance and were accompanied by significantly reduced expression levels of pro-Interleukin-1β in distant neutrophils.

CRMO was once considered strictly a childhood disease, but adults have been diagnosed with it. The affected tends to range from 4 to 14 years old, with 10 as the median age. As stated above, CRMO occurs 1:1,000,000 and primarily in girls with a 5:1 ratio. That means out of six million, there will probably be 5 girls and 1 boy with the condition.

Due to its inflammatory nature, its recurrent outbreaks, and its lack of any known pathogen, CRMO has been reclassified as an autoinflammatory disease. This particular classification encompasses both hereditary types (familial Mediterranean fever, mevalonate kinase deficiency, TNF receptor associated periodic syndrome, cryopyrin-associated periodic syndrome, Blau syndrome, pyogenic sterile arthritis, pyoderma gangrenosum and acne syndrome, CRMO) and multifactorial disorders (Crohn's and Behçet's diseases). CRMO is no longer considered an autoimmune but rather an inherited, autoinflammatory disease.

In lambs, the disease typically occurs between 3 to 8 weeks of age, but may occur in older lambs as well. Progressive paralysis occurs, which is evident through the following symptoms: arched back, difficulty moving and an open shouldered stance. Cardiac failure may occur in two forms: sudden heart failure or gradual cardiac failure characterized by lung anemia that causes death due to suffocation.

Ewes may be given an injection of vitamin E/selenium prior to lambing to prevent deficiencies in lambs. In areas, such as Ontario, where lambs are highly susceptible to the condition, management practices should include vitamin E/selenium injections.

Idiopathic granulomatous hepatitis is a rare medical condition characterised by granulomas in the liver, recurrent fever, myalgia, and fatigue. The condition is not a true hepatitis, and some experts believe it is a variant of sarcoidosis.

Weber–Christian disease, also known as relapsing febrile nodular nonsuppurative panniculitis, is a cutaneous condition characterized by recurrent subcutaneous nodules that heal with depression of the overlying skin.

It is type of panniculitis.

It is a rare disease seen in females 30–60 years of age. It is a recurring inflammation of fatty layers of tissue present beneath the skin. Clinical course is characterised by exacerbations and remissions. Lesions are bilaterally symmetrical and are usually seen in the lower legs.

Congenital disorder of glycosylation type IIc or Leukocyte adhesion deficiency-2 (LAD2) is a type of leukocyte adhesion deficiency attributable to the absence of neutrophil sialyl-LewisX, a ligand of P- and E-selectin on vascular endothelium. It is associated with "SLC35C1".

This disorder was discovered in two unrelated Israeli boys 3 and 5 years of age, each the offspring of consanguineous parents. Both had severe mental retardation, short stature, a distinctive facial appearance, and the Bombay (hh) blood phenotype, and both were secretor- and Lewis-negative. They both had had recurrent severe bacterial infections similar to those seen in patients with LAD1, including pneumonia, peridontitis, otitis media, and localized cellulitis. Similar to that in patients with LAD1, their infections were accompanied by pronounced leukocytosis (30,000 to 150,000/mm) but an absence of pus formation at sites of recurrent cellulitis. In vitro studies revealed a pronounced defect in neutrophil motility. Because the genes for the red blood cell H antigen and for the secretor status encode for distinct α1,2-fucosyltransferases and the synthesis of Sialyl-LewisX requires an α1,3-fucosyltransferase, it was postulated that a general defect in fucose metabolism is the basis for this disorder. It was subsequently found that GDP-L-fucose transport into Golgi vesicles was specifically impaired, and then missense mutations in the GDP-fucose transporter cDNA of three patients with LAD2 were discovered. Thus, GDP-fucose transporter deficiency is a cause of LAD2.

The disorder affects about 1 out of 1,000,000 people, however epidemiological data are limited and there are regional differences due to cofounder effect (e.g. in Canada) or intermarriage.