 Rhabdomyolysis may cause kidney failure by several mechanisms . The most important is the accumulation of myoglobin in the kidney tubules . Normally , the blood protein haptoglobin binds circulating myoglobin and other heme @-@ containing substances , but in rhabdomyolysis the quantity of myoglobin exceeds the binding capacity of haptoglobin . <unk> , the presence of myoglobin in the urine , occurs when the level in plasma exceeds 0 @.@ 5 – 1 @.@ 5 mg / dl ; once plasma levels reach 100 mg / dl , the concentration in the urine becomes sufficient for it to be visibly discolored and corresponds with the destruction of about 200 grams of muscle . As the kidneys reabsorb more water from the <unk> , myoglobin interacts with Tamm – Horsfall protein in the <unk> to form casts ( solid aggregates ) that obstruct the normal flow of fluid ; the condition is worsened further by high levels of uric acid and acidification of the <unk> , which increase cast formation . Iron released from the heme generates reactive oxygen species , damaging the kidney cells . In addition to the myoglobinuria , two other mechanisms contribute to kidney impairment : low blood pressure leads to constriction of the blood vessels and therefore a relative lack of blood flow to the kidney , and finally uric acid may form crystals in the tubules of the kidneys , causing obstruction . Together , these processes lead to acute tubular necrosis , the destruction of the cells of tubules . <unk> filtration rate falls and the kidney is unable to perform its normal excretory functions . This causes disruption of electrolyte regulation , leading to a further rise in potassium levels , and interferes with vitamin D processing , further worsening the low calcium levels . 
