A renal infarction occurs when the blood supply to the kidney is blocked, preventing oxygen from reaching the organ’s tissues. This interruption of blood flow can cause parts of the kidney tissue to die, a process known as necrosis. The event is comparable to a heart attack or a stroke, where a sudden loss of blood circulation leads to tissue damage.
While a serious medical event, renal infarction is relatively uncommon. Its rarity can contribute to delays in diagnosis, as its symptoms can resemble more frequent conditions, potentially leading to impaired kidney function.
Underlying Causes and Major Risk Factors
The most frequent cause of a renal infarction is a thromboembolic event, where a blood clot forms elsewhere in the body, travels through the bloodstream, and becomes lodged in a renal artery. A large number of these clots originate in the heart, often associated with atrial fibrillation, a type of irregular heartbeat that can allow blood to pool and form clots.
Another cause involves direct injury or abnormalities of the renal arteries. An aortic dissection, a tear in the inner layer of the body’s main artery, can extend into the renal artery and obstruct blood flow. A spontaneous renal artery dissection, sometimes linked to fibromuscular dysplasia, can also lead to a blockage. Physical trauma to the abdomen or back can also damage these blood vessels.
Certain underlying conditions increase the risk of developing a renal infarction. These factors include:
- Atherosclerosis, the hardening and narrowing of arteries due to plaque buildup.
- Inherited or acquired hypercoagulable states, disorders that make blood more likely to clot.
- A personal or family history of blood clots.
- Established cardiovascular disease.
Signs and Symptoms
The most common symptom of a renal infarction is the sudden onset of intense pain. This pain is located in the flank, the area on the side of the body between the ribs and the hip, or it may be felt more generally in the abdomen. The pain is often described as sharp and severe and does not subside with changes in position.
In addition to pain, individuals may experience nausea and vomiting. A fever may also develop, which can indicate the body’s inflammatory reaction to the kidney tissue damage.
The urine may also show distinct changes. Hematuria, the presence of blood in the urine, is a common finding. This can be gross hematuria, where the blood is visible, or it can be microscopic and detectable only through laboratory analysis.
The combination of these symptoms can mimic other conditions, such as kidney stones or a kidney infection, which can lead to an initial misdiagnosis.
The Diagnostic Process
When a renal infarction is suspected, healthcare providers use laboratory tests to assess kidney function and look for signs of tissue injury. Blood tests measure levels of creatinine, a waste product filtered by healthy kidneys, to check for compromised function. Another blood marker is lactate dehydrogenase (LDH), an enzyme released into the bloodstream when tissues are damaged.
A urinalysis is also performed to detect microscopic hematuria or proteinuria (excess protein in the urine). Imaging studies are necessary to confirm the diagnosis and visualize the damage. A contrast-enhanced computed tomography (CT) scan is the most effective imaging tool for this purpose.
In this procedure, a special dye is injected into a vein to highlight the blood vessels, and the CT images can clearly show a wedge-shaped area of the kidney not receiving blood. In some situations, other imaging techniques are used. A magnetic resonance imaging (MRI) scan can provide detailed images and may be used if a patient cannot receive CT contrast dye.
A renal angiogram, a more invasive procedure, offers a highly detailed view of the blockage and is sometimes performed as part of a treatment procedure.
Treatment and Management Strategies
The primary goals of treating a renal infarction are to restore blood flow, prevent the existing clot from getting larger, and reduce the risk of future events. The most common initial treatment is anticoagulation therapy, which involves administering blood thinners. These drugs, such as heparin and warfarin, prevent new clots from forming, allowing the body’s natural clot-dissolving processes to work.
For individuals with more extensive blockages, more direct interventions may be considered to actively remove the clot. Catheter-directed thrombolysis is a procedure where a catheter delivers clot-busting medications directly to the renal artery. A mechanical thrombectomy might be performed, where a device on a catheter is used to physically remove the clot. An angioplasty, with or without a stent, may also be used to address underlying narrowing of the vessel.
Long-term management is focused on preventing a recurrence by addressing the root cause. Patients will continue taking anticoagulant medication for an extended period. It is also important to manage underlying conditions like atrial fibrillation, high blood pressure, or disorders that increase blood clotting. Regular follow-up with healthcare providers is necessary to monitor kidney function and cardiovascular health.