The most common symptoms of acute renal infarction include sudden, severe abdominal or flank pain, often accompanied by nausea and vomiting. Haematuria is another common symptom, which may occur as a result of the ischemic damage to the kidney tissue. The symptoms of renal infarction often mimic those of other conditions, such as kidney stones or urinary tract infections, which can lead to misdiagnosis if appropriate imaging is not performed.
Laboratory findings in acute renal infarction are typically non-specific, but some patterns may raise suspicion. The most commonly observed laboratory abnormalities include leukocytosis, which is a general indicator of inflammation, and elevated lactate dehydrogenase (LDH) levels, which suggest tissue necrosis. Although these findings can be indicative of many other conditions, when combined with clinical symptoms such as sudden flank pain and haematuria, they suggest the possibility of renal infarction.
The diagnosis of acute renal infarction on non-contrast CT examination can be particularly challenging, as the findings may be subtle or minimal. It may only reveal mild renal swelling or perinephric fat stranding, which are not specific to renal infarction. This makes non-contrast imaging less useful in confirming the diagnosis. However, the diagnostic accuracy increases significantly when contrast-enhanced abdominal CT is performed.
On contrast-enhanced CT, the typical findings of renal infarction include hypodense regions in the affected kidney. These regions appear darker than the surrounding healthy tissue due to the lack of blood flow and perfusion to the infarcted area. The hypodense area usually follows a wedge-shaped pattern, reflecting the area supplied by a single renal artery branch. This shape is particularly noticeable in the arterial phase of contrast enhancement, where the infarcted region does not show the usual enhancement that occurs in well-perfused kidney tissue. This is one of the key features that differentiate renal infarction from other conditions.
One notable sign that can help in diagnosing renal infarction is the rim sign. The rim sign refers to a thin, peripheral cortex of the kidney that continues to enhance despite the presence of the infarcted central region. This phenomenon occurs because the renal capsule and the outermost cortex continue to receive blood supply through the perforating branches of the renal arteries, which preserve perfusion in these regions. The rim of enhancing cortex is visible as a thin line around the non-enhancing parenchymal defect, and it is one of the most characteristic CT features of renal infarction.
In cases where there is total occlusion of the main renal artery, the entire kidney may fail to enhance. This results in a uniform hypodensity across the kidney, which is a less common but more definitive finding of a severe infarction.
The key differential diagnoses for renal infarction on CT include several conditions that may present with similar imaging findings. These include:
Acute pyelonephritis: This renal disorder can present as a hypodense region on CT, much like renal infarction. However, the absence of the rim sign and the presence of perinephric fat stranding help differentiate it from infarction. In pyelonephritis, the inflammation and infection typically spread diffusely, whereas infarction is usually focal and well-defined.
Renal lymphoma: Lymphoma can infiltrate the kidneys and cause areas of hypodensity that resemble the wedge-shaped infarct pattern of renal infarction. However, renal lymphoma typically involves more diffuse, irregular masses rather than the sharply defined areas of infarction. Additionally, lymphoma often presents with associated lymphadenopathy and systemic symptoms such as weight loss and fever.
Renal metastasis: Renal metastasis from other cancers (e.g., lung, breast, or gastrointestinal cancers) may present as hypodense lesions within the kidney. However, metastasis typically forms masses that may be multiple and irregular, rather than a wedge-shaped infarct. Metastases may also show associated cystic changes or calcifications, which are not characteristic of renal infarction.