Atrial fibrillation and acute renal infarction
Acute renal infarction (ARI) is a major medical emergency that can cause irreversible kidney damage. The causes of renal infarction can be classified into four categories: cardiac infarction, renal artery injury, hypercoagulability diseases, and idiopathic renal infarction. ARI is a very rare but serious consequence of atrial fibrillation (AF), which is one of the most prevalent arrhythmias. The diagnosis of ARI is difficult due to its low prevalence and cryptic clinical manifestations.
Although aspiration thrombectomy has been documented in the treatment of renal artery thromboembolism.More efficient treatment guidelines are currently useful for ARI related to thromboembolic consequences of AF. In addition, past case reports used systemic thrombolytics, intra-arterial thrombolytics, and systemic anticoagulation. Given the rarity of ARI from AF and the lack of more efficient and well-established treatment guidelines, we present a case of AF-induced ARI and a new treatment modality. The treatment is similar to that used to treat acute myocardial infarction, that results in the successful treatment of ARI from AF.
Case study: acute renal infarction
This article describes the case of a 66-year-old Chinese man with a history of AF. No anticoagulation per the patient’s preference, and coronary artery disease (CAD) status after a 1 year percutaneous coronary intervention to the left anterior descending artery. The patient was currently on aspirin, clopidogrel, and rosuvastatin. He initially appeared with chest pain for two days, and acute coronary syndrome was ruled out. He then experienced sporadic and severe left-sided stomach pain. A systematic review revealed no evidence of fever, chills, nausea, vomiting, diarrhoea, or hematuria. He works as a farmer in a rural area and is a current smoker with a 30-pack-year smoking history. He denies any usage of alcohol or illegal drugs and has no known drug allergies. Family history is irrelevant.
Aspirin (100 mg), clopidogrel (75 mg), rosuvastatin (10 mg), furosemide (20 mg), spironolactone (20 mg), and isosorbide mononitrate (10 mg) are being used at home. There were no known medication allergies noted.
His vitals were normal upon admission, with a blood pressure of 100/70 mmHg, a heart rate of 68 beats per minute, and an oral temperature of 36.3 °C. His heart rate was erratic, with no heart murmurs, and his jugular venous pressure (JVP) was normal, with no pitting edoema in the lower limbs. On auscultation, the lungs were clean. His abdomen exam revealed modest pain to palpation across the left quadrant with no rebound or guarding. Normal bowel noises were heard. The remainder of the exam was ordinary.
Routine laboratory tests were within normal range
Routine laboratory tests revealed that the total blood count, liver function tests, amylase, lipase, and thyroid function tests were all normal. Creatinine was normal at 56 mol/L (normal range, 40-130 mol/L), although blood urea nitrogen was slightly increased (7.29 mmol/L [normal range, 2.3-7.1 mmol/L]). Proteinuria, infection, and hematuria were all found to be absent in the urine. The faecal occult blood test came out negative. Lactate dehydrogenase (LDH) and alpha-hydroxybutyrate dehydrogenase (-HBDH) levels were also increased (283 U/l [normal range, 135-225 U/l] and 239 U/l [normal range, 76-195 U/l]). Abdominal and renal vascular Doppler ultrasounds were normal at the bedside. A contrast-enhanced CT scan was then performed due to prolonged abdominal pain of unknown aetiology, demonstrating renal infarction of the left kidney.
Coronary and aortic angiograms revealed no evidence of coronary stenosis or aortic dissection. A renal angiography was conducted due to the CT findings and unresolved stomach pain, and it revealed distal blockage of both superior and inferior segments of the left renal artery. The left renal artery was then scrutinised. Two guide wires were inserted into the superior and inferior segments of the left renal artery, and the Pt wire was then carried into the distal end of the occluded superior artery. A suction catheter was used to aspirate a 5 4 mm thrombus, which was then locally inflated with a Maverick 1.5 15 mm balloon, and 0.1 mg nitroglycerin and 1 mg diltiazem were delivered into the microcatheter.
Angiography further confirmed the diagnosis
Angiography confirmed blood flow restoration to both superior and inferior segments of the renal artery and vessel potencies after the aforementioned interventions. Similarly, which is more clearly visible in the amplification of the images for renal angiograms after the surgery compared to before the surgery. Six hours after the procedure, the abdominal pains subsided. LDH (230 U/L) and -HBDH (216 U/L) levels dropped and gradually returned to normal by postoperative day 5. He was kept on all of his home meds and was started on warfarin post-procedure with an INR aim of 2-3.
For one month, the patient was given aspirin (100 mg), clopidogrel (75 mg), and warfarin (3.125 mg), followed by clopidogrel and warfarin for another six months. The patient was symptom-free after 6 months of follow-up, and his renal function remained normal (creatinine 74 mol/L [normal range, 57-111 mol/L]). Following a low suspicion of persistent or recurring renal infarction, no repeat angiography was conducted to avoid extra radiation exposure.
Source: Journal of Medical Case Reports
