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

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.

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.

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.

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

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 .

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.

Supervised exercise programs have been shown in small studies to improve exercise capacity by several measures.

Oral sucrose treatment (for example a sports drink with 75 grams of sucrose in 660 ml.) taken 30 minutes prior to exercise has been shown to help improve exercise tolerance including a lower heart rate and lower perceived level of exertion compared with placebo.

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.

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.

Standard of care for treatment of CPT II deficiency commonly involves limitations on prolonged strenuous activity and the following dietary stipulations:

- The medium-chain fatty acid triheptanoin appears to be an effective therapy for adult-onset CPT II deficiency.

- Restriction of lipid intake

- Avoidance of fasting situations

- Dietary modifications including replacement of long-chain with medium-chain triglycerides supplemented with L-carnitine

Canine phosphofructokinase deficiency is found mostly in English Springer Spaniels and American Cocker Spaniels, but has also been reported in Whippets and Wachtelhunds. Mixed-breed dogs descended from any of these breeds are also at risk to inherit PFK deficiency.

In order to get Tarui’s disease, both parents must be carriers of the genetic defect so that the child is born with the full form of the recessive trait. The best indicator of risk is a family member with PFK deficiency.

Symptomatic presentation usually occurs between 6 and 24 months of age, but the majority of cases have been documented in children less than 1 year of age. The infantile form involves multiple organ systems and is primarily characterized by hypoketotic hypoglycemia (recurring attacks of abnormally low levels of fat breakdown products and blood sugar) that often results in loss of consciousness and seizure activity. Acute liver failure, liver enlargement, and cardiomyopathy are also associated with the infantile presentation of this disorder. Episodes are triggered by febrile illness, infection, or fasting. Some cases of sudden infant death syndrome are attributed to infantile CPT II deficiency at autopsy.

Cocaine intoxication refers to the immediate and deleterious effects of cocaine on the body. Although cocaine intoxication and cocaine dependence can be present in the same individual, these syndromes present with different symptoms.

Cocaine can be snorted, swallowed, injected, or smoked. Most deaths due to cocaine are accidental but may also be the result of body packing or stuffing with rupture in the gastrointestinal tract. Use of cocaine causes tachyarrhythmias and a marked elevation of blood pressure (hypertension), which can be life-threatening. This can lead to death from acute myocardial infarction, respiratory failure, stroke, cerebral hemorrhage, or heart failure. Cocaine overdose may result in hyperthermia as stimulation and increased muscular activity cause greater heat production. Heat loss is also inhibited by the cocaine-induced vasoconstriction. Cocaine and/or associated hyperthermia may cause muscle cell destruction (rhabdomyolysis) and myoglobinuria resulting in renal failure. Individuals with cocaine overdose should be transported immediately to the nearest emergency department, preferably by ambulance in case cardiac arrest occurs en route. According to the National Institute on Drug Abuse, approximately 5000 deaths occur annually in the US due to cocaine overdose.