Myoglobinuria is the presence of myoglobin in the urine, which usually results from rhabdomyolysis or muscle injury. Myoglobin is present in muscle cells as a reserve of oxygen.
Signs and symptoms of myoglobinuria are usually nonspecific and needs some clinical prudence. Therefore, among the possible signs and symptoms to look for would be:
Swollen and painful muscles
Fever, nausea
Delirium (elderly individuals)
Myalgia
Dark urine
Calcium ion loss
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 kidney problems, it can occlude the kidneys' filtration system leading to acute tubular necrosis and acute kidney injury.
Other causes of myoglobinuria include:
McArdle's disease
Phosphofructokinase deficiency
Carnitine palmitoyltransferase II deficiency
Malignant hyperthermia
Polymyositis
Lactate dehydrogenase deficiency
Adenosine monophosphate deaminase deficiency type 1
Thermal or electrical burn
Myoglobinuria pathophysiology consists of a series of metabolic actions in which damage to muscle cells affect calcium mechanisms, thereby increasing free ionized calcium in the cytoplasm of the myocytes (concurrently decreasing free ionized calcium in the bloodstream). This, in turn, affects several intracellular enzymes that are calcium-dependent, thereby compromising the cell membrane, which in turn causes the release of myoglobin.
Rhabdomyolysis#Mechanism and Calcium_in_biology#Measurement_in_blood
After centrifuging, the urine of myoglobinuria is red, where the urine of hemoglobinuria after centrifuge is pink to clear.
Hospitalization and IV hydration should be the first step in any patient suspected of having myoglobinuria or rhabdomyolysis. The goal is to induce a brisk diuresis to prevent myoglobin precipitation and deposition, which can cause acute kidney injury.
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Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. Because necrosis is often not present, the term acute tubular injury (ATI) is preferred by pathologists over the older name acute tubular necrosis (ATN). ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. Common causes of ATN include low blood pressure and use of nephrotoxic drugs.
Urine is a liquid by-product of metabolism in humans and in many other animals. Urine flows from the kidneys through the ureters to the urinary bladder. Urination results in urine being excreted from the body through the urethra. Cellular metabolism generates many by-products that are rich in nitrogen and must be cleared from the bloodstream, such as urea, uric acid, and creatinine. These by-products are expelled from the body during urination, which is the primary method for excreting water-soluble chemicals from the body.
Rhabdomyolysis (shortened as rhabdo) is a condition in which damaged skeletal muscle breaks down rapidly. Symptoms may include muscle pains, weakness, vomiting, and confusion. There may be tea-colored urine or an irregular heartbeat. Some of the muscle breakdown products, such as the protein myoglobin, are harmful to the kidneys and can cause acute kidney injury. The muscle damage is most usually caused by a crush injury, strenuous exercise, medications, or a substance use disorder.
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