Renal infarction as a rare complication of post myocardial infarction complicated by paroxysmal atrial fibrillation : A case report and literature review

Abstract

Although rare, renal infarction represents a serious and potentially life-threatening complication in cardiology, particularly in patients with high thromboembolic risk. We report the case of a 71-year-old woman admitted for post–myocardial infarction complicated by severe left ventricular dysfunction (ejection fraction 35%) and heart failure. During hospitalization, she developed acute abdominal pain associated with paroxysmal atrial fibrillation and a newly detected left ventricular apical thrombus. Laboratory tests revealed acute kidney injury with a marked increase in serum creatinine from 11 mg/L (glomerular filtration rate = 59 mL/min) to 56 mg/L(GFR = 7.97 mL/min/m²). Contrast-enhanced computed tomography demonstrated normal-sized kidneys and confirmed left renal infarction. The patient was treated with anticoagulation and optimized medical therapy, resulting in stabilization and improvement of renal function. She was discharged in stable condition. During follow-up at 1 month, 6 months, and 1 year, renal function remained stable, with a serum creatinine level of 13 mg/L and an estimated glomerular filtration rate of 42.9 mL/min/1.73 m². Renal infarction should be rapidly considered in the differential diagnosis of acute abdominal or flank pain. Such awareness can lead to timely intervention, optimal treatment, and improved renal and overall outcomes. This case highlights the importance of early recognition and appropriate management of rare thromboembolic complications in patients with myocardial infarction and paroxysmal atrial fibrillation.

Introduction

Myocardial infarction remains a leading cause of cardiovascular morbidity and mortality worldwide. Among its various complications, thromboembolic events are particularly significant, with left ventricular thrombus playing a pivotal role, especially in the setting of anterior myocardial infarction associated with atrial fibrillation. Atrial fibrillation, when present, is associated with poorer short- and long-term outcomes compared with sinus rhythm, even in its paroxysmal form [1,2].

In this context, although uncommon, renal infarction represents a rare but serious thromboembolic complication that is often challenging to diagnose and frequently delayed, potentially leading to poor renal functional outcomes due to irreversible parenchymal injury. Beyond thromboembolic causes, which remain the most frequent, renal infarction may also result from other etiologies, including trauma, arterial dissection, autoimmune disorders, hypercoagulable states, and idiopathic conditions [3].

Renal infarction is associated with significant morbidity and may lead to irreversible renal damage, chronic kidney disease, or even end-stage renal failure if diagnosis and treatment are delayed [3]. The pathophysiology is mainly related to acute arterial occlusion, most commonly of thromboembolic origin, resulting in ischemic parenchymal necrosis [4]. Early diagnosis remains challenging due to nonspecific clinical presentation. Currently, contrast-enhanced computed tomography represents the gold standard for diagnosis, while biological markers such as elevated lactate dehydrogenase and inflammatory parameters may support clinical suspicion [3].

Given the absence of an international consensus on the management of renal infarction, therapeutic strategies rely on medical treatment with anticoagulation, interventional procedures, or a combination of both [4,5].

We present the case of a patient initially admitted for post-myocardial infarction complicated by left ventricular failure and severe LV dysfunction, whose in-hospital course was marked by the occurrence of a renal infarction secondary to an intraventricular thrombus in the context of paroxysmal atrial fibrillation and abdominal pain.

Case

We report the case of a 71-year-old woman with cardiovascular risk factors including overweight and metabolic syndrome, characterized by abdominal obesity, hypertension, and dyslipidemia, with no known history of heart disease, kidney disease, or atrial fibrillation. The patient had no prior exposure to nephrotoxic drugs, such as nonsteroidal anti-inflammatory drugs or aminoglycosides. She was not receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. No contrast agent had been administered before the onset of renal dysfunction.

The patient was admitted to the emergency department with acute chest pain that had begun 26 hours before admission, associated with dyspnea at rest. The diagnosis of post myocardial infarction complicated by left ventricular failure was established based on the clinical presentation, electrocardiographic findings, and laboratory results. She was subsequently hospitalized in our cardiac intensive care unit for further management.

On admission, clinical examination revealed a conscious patient with a Glasgow Coma Scale score of 15/15. Blood pressure was 150/70 mmHg, symmetrical in both upper limbs, with a heart rate of 90 bpm, and oxygen saturation of 85% on room air. Cardiovascular examination was unremarkable, whereas pulmonary auscultation revealed bilateral basal crackles. The admission electrocardiogram showed a regular sinus rhythm at 100 bpm, with anterior and inferior ST-segment elevation from V1 to V6 and Q waves in the same territories.

Laboratory investigations revealed a creatinine level of 11.13 mg/L (baseline: 11 mg/L; reference range: 6-12 mg/L) with a glomerular filtration rate of 51.4 mL/min/1.73 m² (normal: ≥90 mL/min/1.73 m²), urea 0.43 g/L (reference: 0.15-0.45 g/L), hemoglobin 14.4 g/dL (reference: >12 g/dL), and platelet count 189,000/µL (reference: 150,000-400,000/µL). Coagulation studies showed an INR of 72% (reference: 70-100%). Cardiac biomarkers were markedly elevated, with troponin 50,000 ng/L (reference: < 26 ng/L) and NT-proBNP 70,000 pg/L (reference: < 900 pg/L). Inflammatory markers included a C-reactive protein of 12 mg/L (reference: < 6 mg/L) and a white blood cell count of 11,230/µL (reference: 4000-10,000/µL). Urinalysis revealed significant leukocyturia (1000 cells/mm³; normal < 10 cells/mm³) with sterile culture and no microscopic hematuria (Table 1).

Table 1.

Key laboratory values during admission, renal infarction, and follow-up (1 year).

Parameter	Admission	During acute kidney injury	Follow-up (1 year)
Serum creatinine (mg/L)	11 (normal : 6-11 mg/L)	56	13
eGFR (mL/min/1.73 m²)	59 (normal: ≥ 90 mL/min/1.73 m²),	7.97	42.97
LDH(U/L)	- (normal: 120-246 U/L)	>3325 U/L	200
CRP (mg/L)	12 (normal < 6 mg/L)	239.79	6
WBC (/µL)	11,230 (normal: 4000-10,000/µL)	14,900	9000
Hemoglobin (g/dL)	14.8	14.6	14.7
Hematuria (red blood cells/mm³)	0 (normal < 10 red blood cells/mm³),	2,000,000	0
Urine culture	Sterile	Sterile	-
Troponin (ng/L)	50,000 (normal: < 26 ng/L)	-	-
NT Pro-BNP (Pg/L)	70,000 (normal: < 900 pg/L).	-	-

Initial transthoracic echocardiography demonstrated features of ischemic heart disease, including akinesia of the apex, the septal and inferior walls, as well as the apical segments of all other walls. Severe left ventricular dysfunction was noted, with an ejection fraction of 35% by Simpson’s biplane method, accompanied by elevated filling pressures. A dense contrast effect was observed within the left ventricle, with no evidence of thrombus, and no significant mitral or aortic valve disease was detected.

The patient was initially treated with dual antiplatelet therapy, anticoagulation, statins, proton pump inhibitors for gastric protection, and intravenous furosemide for congestion, resulting in favorable early clinical progress, including resolution of congestive signs and normalization of oxygen saturation. Cardiac magnetic resonance imaging (MRI) was planned one month after the acute event to assess myocardial viability and guide potential revascularization.

The following day, while preparing for discharge, the patient developed diffuse abdominal pain accompanied by nausea, vomiting, and hematuria. Physical examination revealed a soft abdomen with diffuse tenderness, without guarding or rigidity. Symptomatic treatment was initiated, but there was no apparent improvement. Further investigations, including laboratory tests, demonstrated worsening renal function, with a peak serum creatinine of 56 mg/L (reference range: 6-12 mg/L) and a glomerular filtration rate of 7.97 mL/min/1.73 m² (normal: ≥90 mL/min/1.73 m²). Laboratory findings also revealed a moderate inflammatory response, microscopic hematuria with 2,000,000 red blood cells/mm³ (normal: < 10/mm³), and markedly elevated lactate dehydrogenase (LDH >3325 U/L; normal: 120-246 U/L).

Telemetric monitoring analysis revealed a paroxysmal atrial fibrillation, which was documented later on a 12-lead EKG, and control transthoracic echocardiography identified the presence of a left ventricular thrombus that had not been previously detected (Fig. 1).

Fig. 1.

Echocardiographic 4-chamber view (A) and 2-chamber view (B) showing an apical thrombus measuring 12 × 14 mm as indicated by the blue asterisks.

In the context of suspected mesenteric infarction, contrast-enhanced abdominopelvic computed tomography (CT) was performed. The left kidney was normal in size (98 × 51 × 43 mm) and had regular contours. Imaging revealed a thrombus in the left renal artery with reduced renal enhancement and multiple hypodense, non-enhancing areas involving nearly the entire renal parenchyma, corresponding to well-defined perfusion defects. These lesions were predominantly wedge-shaped, consistent with renal infarction. A small area of preserved parenchyma was observed at the lower pole, representing approximately 20-25% of the renal volume. No dilation of the collecting system was noted. the findings were consistent with a left renal infarction resulting from thrombosis of the left renal artery, with no imaging findings suggestive of mesenteric ischemia (Fig. 2).

Fig. 2.

Contrast enhanced computed tomography findings of left renal infarction : (A) Axial maximum intensity projection (MIP) reconstruction of arterial-phase contrast-enhanced CT demonstrating marginal thrombosis of the left renal artery (red arrow) with associated ipsilateral renal infarction, compared with a normal contralateral artery (yellow arrow). (B) Coronal oblique MIP reconstruction of arterial-phase contrast-enhanced CT showing left renal artery thrombosis with ipsilateral renal infarction. (C) Coronal CT slice revealing wedge-shaped hypodense lesions with a peripheral base and hilar apex (red arrows), associated with absent contrast enhancement, consistent with renal infarction. (D) Axial contrast-enhanced CT image demonstrating focal areas of infarction in the left kidney (red arrow), compared with a normal contralateral kidney. (E) Axial delayed-phase contrast-enhanced CT image showing absence of urinary excretion from the left kidney (red arrow), in contrast to preserved excretion from the right kidney.

The diagnosis of renal infarction, a rare complication of post–myocardial infarction in the setting of apical ventricular thrombus and paroxysmal atrial fibrillation, was established after excluding other differential diagnoses, including acute pyelonephritis, nephrolithiasis, renal vein thrombosis, acute interstitial nephritis, and mesenteric ischemia. The absence of fever, sterile urine culture, lack of hydronephrosis, and the presence of a left renal thrombus with a perfusion defect on contrast-enhanced CT confirmed the diagnosis of renal infarction.

The patient was initially treated with unfractionated heparin, resulting in favorable clinical progress. At discharge, the antithrombotic regimen included dual antiplatelet therapy (DAPT) with clopidogrel and aspirin for one month, given the high ischemic risk. Aspirin was discontinued after one month, while clopidogrel was continued in combination with apixaban 5 mg twice daily. The apixaban dose was selected based on the patient’s characteristics—improved renal function, age below 80 years (71 years), and body weight above 50 kg—in accordance with current ESC guidelines for stroke prevention in atrial fibrillation. Clopidogrel and apixaban were planned for one year, after which the patient will continue lifelong anticoagulation due to paroxysmal atrial fibrillation, a permanent indication for anticoagulation, justifying the continuation of therapy even after management of the left ventricular thrombus. Additional discharge medications included bisoprolol 2.5 mg once daily, lansoprazole 30 mg once daily, and furosemide 20 mg once daily. The electrocardiogram at discharge showed sinus rhythm.

The antithrombotic strategy consisted of triple therapy (DAPT plus anticoagulation) for one month early after myocardial infarction, consistent with current ESC and ACC/AHA guidelines, which emphasize balancing ischemic and bleeding risk in patients with combined indications for antiplatelet and anticoagulant therapy. After one month, therapy was de-escalated to dual therapy (clopidogrel plus apixaban) to minimize bleeding risk. For left ventricular thrombus, anticoagulation with a direct oral anticoagulant such as apixaban has increasingly been adopted as an alternative to vitamin K antagonists, in line with recent observational studies and guideline recommendations. Long-term anticoagulation is further justified by the patient’s paroxysmal atrial fibrillation, which represents a sustained thromboembolic risk. This regimen aims to prevent recurrent thromboembolic events while ensuring ongoing stroke prophylaxis.

Follow-up at 1 month, 6 months, and 1 year demonstrated stable renal function, with no evidence of deterioration. At 1-year follow-up, serum creatinine was 13 mg/L and the estimated glomerular filtration rate (eGFR) was 42.9 mL/min/1.73 m².

The clinical, biological, electrocardiographic, and echocardiographic course timeline is summarized in the Table 2.

Table 2.

Clinical, biological, electrocardiographic, and echocardiographic course timeline.

Day 1	-Symptoms : Chest pain and rest dyspnea. -EKG : sinus rythm + sequelae of myocardial infarction. -TTE : severe LV dysfunction with dense contrast effect within the LV. -Biology : An inflammatory syndrome with preserved renal function.
Day 2-6	-A favorable initial course under diuretic therapy and treatment of ischemic heart disease.
Day 6	-Symptoms : the patient presented a sudden onset of diffuse abdominal pain, refractory to symptomatic treatment, and associated with hematuria. -Cardiac telemetry monitoring and EKG: paroxysmal atrial fibrillation. -Control TTE : left ventricular thrombus. -Follow-up laboratory tests : worsening renal function. -Abdominopelvic CT scan : left renal infarction was established.
Day 6-10	-The patient was started on unfractionated heparin, followed by oral anticoagulation.
Day 11	-Discharge with a favorable outcome. -EKG : sinus rythm + sequelae of myocardial infarction.
One-month follow-up	-Biology : normal renal function. -EKG : sinus rythm.

Discussion

Renal infarction is a rare but potentially serious condition. In a Japanese cohort, its incidence was reported as 0.013% among patients presenting to the emergency department and 0.003% among hospitalized patients [6]. If left untreated, inadequately treated, or treated late, renal infarction can progress to end-stage chronic kidney disease [3,7]. Diagnosis is often challenging and delayed due to the heterogeneous clinical presentations, which may mimic other conditions such as nephrolithiasis or pyelonephritis [3,8].

Clinical presentation may include diffuse abdominal pain or pain localized to the left flank, with or without associated nausea and vomiting. Hematuria can also occur, whereas fever is not consistently observed [6,[9], [10], [11]]. In our case, the patient presented with diffuse abdominal pain accompanied by macroscopic hematuria.

When renal infarction is suspected, a contrast-enhanced abdominal CT scan should be systematically performed, as it represents the gold standard for diagnosis [12]. Findings on contrast-enhanced CT may include partial or complete occlusion of the renal artery with intraluminal thrombus, reduced or absent parenchymal enhancement in the affected area, or wedge-shaped hypodense lesions with a cortical base and hilar apex [[13], [14]].

Our patient presented with a moderate inflammatory response, characterized by leukocytosis and elevated C-reactive protein (CRP), accompanied by increased lactate dehydrogenase (LDH), findings consistent with the literature [3,6,9]. Notably, some authors have proposed a clinico-biological diagnostic triad for renal infarction, comprising abdominal or flank pain, microscopic hematuria, and elevated LDH levels [3].

Among the underlying causes of renal infarction—including cardiogenic, traumatic, autoimmune, and idiopathic etiologies [3]—thromboembolism is the most frequent, often occurring in the context of atrial fibrillation [5,15]. Atrial fibrillation increases the risk of thromboembolic events by promoting intracardiac thrombus formation, which can embolize to various arterial territories, including the renal artery, leading to infarction. Notably, the most recent ESC guidelines no longer consider the temporal pattern of atrial fibrillation as a determinant of thromboembolic risk; instead, they recommend assessment using the CHA₂DS₂-VA score. This is consistent with our case, in which paroxysmal atrial fibrillation contributed to the renal infarction [2].

The patient was initially hospitalized for post–myocardial infarction care, complicated by left ventricular dysfunction and subsequent paroxysmal atrial fibrillation, which further increased thromboembolic risk and ultimately led to a left renal thromboembolic infarction. An intraventricular thrombus, absent on initial admission, was later detected [16]. While most reported cases involve permanent atrial fibrillation, this case highlights that paroxysmal atrial fibrillation can also confer significant thromboembolic risk. Continuous telemetry monitoring during the acute phase of myocardial infarction enabled detection of the arrhythmia, supporting guideline-recommended monitoring to guide anticoagulation and reduce thromboembolic events [1].

The incidence of intracardiac thrombus remains high in patients with anterior STEMI despite advances in reperfusion therapy [16], posing a risk of stroke and systemic thromboembolism. This underscores the importance of systematic transthoracic echocardiography (TTE) and repeat assessment when indicated. In our case, continuous telemetry monitoring combined with follow-up TTE definitively identified the thromboembolic source of the renal infarction [1].

The patient exhibited two conditions predisposing to thrombus formation: myocardial infarction complicated by ventricular dysfunction [16] and paroxysmal atrial fibrillation. While the pathophysiology of thrombus formation in atrial fibrillation is not fully elucidated, it can largely be explained by Virchow’s triad: blood stasis from rapid and ineffective atrial contractions; endothelial dysfunction driven by atrial fibrosis and dilation, which promotes platelet adhesion in a prothrombotic environment; and hypercoagulability, further increasing thrombus risk [17]. Acute renal infarction secondary to cardiac embolism has been reported in several studies [3,6,10,11,15]. However, the concomitant presence of recent myocardial infarction, severe left ventricular dysfunction with intraventricular thrombus, paroxysmal atrial fibrillation, and subsequent renal infarction remains exceedingly rare. This uncommon association underscores the originality and clinical relevance of our case. Most previously reported cases have involved patients with permanent atrial fibrillation or extensive anterior ST-elevation myocardial infarction [3,5,11] In contrast, our case demonstrates that paroxysmal atrial fibrillation can also lead to embolic renal infarction. Previous reports have described similar clinical presentations, characterized by acute flank or abdominal pain, elevated lactate dehydrogenase levels, and nonspecific initial findings, which frequently result in delayed diagnosis [3,6,10,11,15].

Management strategies for renal infarction range from conservative medical therapy with parenteral anticoagulation, followed by oral agents [3,11], to interventional approaches such as catheter-directed thrombolysis, mechanical thrombectomy, or angioplasty with stenting [9,13], and rarely surgical intervention in the context of trauma [18]. In our patient, a conservative medical management strategy was selected, considering the patient’s preference, the high periprocedural bleeding risk, and the early improvement in renal function under anticoagulation. This approach is consistent with current evidence supporting anticoagulation as first-line therapy in hemodynamically stable patients with partial renal infarction.

Conclusion

This case underscores the complex interplay between cardiac and renal thromboembolic events and highlights the importance of early diagnosis and awareness of the various therapeutic strategies. It illustrates that in patients with high thrombo-embolic risk features including myocardial infarction, severe left ventricular dysfunction with intraventricular thrombus, and paroxysmal atrial fibrillation, renal infarction should be thinked in the differential diagnosis of acute flank or abdominal pain. Such vigilance may allow for timely intervention, optimized medical management, and improved renal and overall outcomes.

Data availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Ethical approval

Ethics approval was not obtained because this manuscript is a case report.

Patient consent

A Written informed consent was obtained from the patient for publication of this case report and any accompanying images.