Translate this page into:
Renal artery thrombosis unveiled: A case report

*Corresponding author: Michael Atef Napoleon, Department of Nephrology, Nizwa Hospital, Ministry of Health, Nizwa, Oman. micatef@yahoo.com
-
Received: ,
Accepted: ,
How to cite this article: Napoleon MA, AlShaaili KS. Renal artery thrombosis unveiled: A case report. World Adv Renal Med. doi: 10.25259/WARM_31_2025
Abstract
A case of a 61-year-old male patient presented multiple times to the emergency department with persistent epigastric and left loin pain radiating to the chest and iliac fossa, along with shortness of breath. His symptoms were initially misattributed to gastritis. An abdominal computerized tomography scan with intravenous (IV) contrast was done, which revealed acute left renal artery thrombosis at the level of the hilum. The patient achieved complete recovery on anticoagulation and IV hydration.
Keywords
Anticoagulation
Atrial fibrillation
Acute kidney injury
Cardiac resynchronization therapy with defibrillator
Renal artery thrombosis
INTRODUCTION
Renal artery (RA) thrombosis is an uncommon but serious cause of acute kidney injury (AKI) that can result in permanent loss of kidney function.[1]
The signs and symptoms of this condition are variable and non-specific, making it difficult to diagnose early and easily mistaken for other, more common pathologies.[2]
This case report presents a case of unilateral RA thrombosis and encourages a high suspicion rate for such a diagnosis, especially if no cause of the patient’s symptoms was evident.
CASE REPORT
A case of a 61-year-old male patient with the medical background of ischemic heart disease, dilated cardiomyopathy with reduced ejection fraction 30%, also known case of atrial fibrillation (AF) on pacemaker cardiac resynchronization therapy (CRT) since July 2023, and had atrioventricular nodal ablation in October 2023. This patient has no medical history of diabetes mellitus, hypertension (HTN), or renal disease. The patient reported no history of cigarette smoking or alcohol consumption.
He presented repeatedly to our emergency department with epigastric and left loin abdominal pain, persistent for around 7 days, radiating to the chest and left iliac fossa, and associated with shortness of breath. No history of fever, vomiting, urinary or bowel complaints, or lower abdominal pain; the patient’s complaint was dismissed before as simple gastritis.
On clinical examination, the patient looked unwell and in pain with a soft abdomen but with tenderness on the left side; bowel sounds were present, and the patient also had palpable peripheral pulses. Pulmonary regurgitation was not done. The patient was anuric on presentation. Vital signs are shown in Table 1. Initial laboratory investigations are shown in Table 2.
| Vital signs | |
|---|---|
| Temperature | 36.8°C |
| Pulse | 75/min |
| Respiratory rate | 20/min |
| Blood pressure | 114/97 mmHg |
| Spo2 | 92% on 10 L through oxygen mask |
| Test | Value | Normal range |
|---|---|---|
| Coagulation profile | ||
| Prothrombin time | 15.40 s | 10.3–12.5 |
| International normalized ratio | 1.35 | 0.9–1.1 |
| Activated partial thromboplastin | 31.30 | 23.7–31.7 |
| Fibrinogen | 2.82 g/L | 1.5–4.2 |
| Troponin I | 49.50 pg/mL | 3.7–34.2 |
| Liver function test | ||
| Total bilirubin in serum | 71.80 μmol/L | 5.13–20.52 |
| Alanine transaminase | 41.00 U/L | 0–55 |
| Aspartate aminotransferase | 47 U/L | 5–34 |
| Total proteins in serum | 75 g/L | 62–81 |
| Albumin in serum | 43 g/L | 32–46 |
| Alkaline phosphatase in serum | 119 U/L | 40–150 |
| Renal function tests | ||
| Urea in serum | 6.60 mmol/L | 2.993–9.157 |
| Creatinine in serum | 126.80 µmol/L | 64.533–110.5 |
| eGFR (MDRD) | 53.15 mL/min/1.73 m2 | >90 |
| Potassium in serum | 5.00 mmol/L | 3.5–5 |
| Sodium in serum | 140 | 136–145 |
| Carbon dioxide in serum | 26 mmol/L | 23–31 |
| C-reactive protein in serum | 6.40 mg/L | 0–5 |
| Complete blood count | ||
| White blood cells in blood | 4.55 103/μL | 2.2–10 |
| Neutrophil count in blood | 2.74 109/L | 1–5 |
| Hemoglobin in blood | 17.70 g/dL | 11.5–15.5 |
| Platelet count in blood | 161.00 109/L | 140–400 |
| Urine analysis | ||
| White cells in urine | 24/HPF | <4 |
| Red cells in urine | 8/HPF | <4 |
| Epithelial cells in urine | <2/HPF | <4 |
| Cast in urine | Nil | Nil |
| Crystals in urine | Nil | Nil |
| Bacteria in urine | Nil | Nil |
| Yeast in urine | Nil | Nil |
| Protein in urine | +++ | Nil |
| PH of urine | 5.0 | 4.6–8.0 |
| Glucose in urine | Nil | Nil |
s: Seconds, g/L: Gram per liter, pg/mL: Picogram per milliliter, μmol/L: Micromole per liter, U/L: Unit per liter, mmol/L: Millimole per liter, mL: Milliliter, min: Minute, mg/L: Milligram per liter, μL: Microliter, L: Liter, dL: Deciliter, eGFR: estimated glomerular filtration rate, MDRD: Modification of diet in renal disease, HPF: High power field.
An abdominal computerized tomography (CT) scan with intravenous (IV) contrast was done, which revealed acute left RA thrombosis at the level of the hilum. Furthermore, the superior mesenteric vein (SMV) showed a filling defect extending to the proximal part of the portal vein. Still, the complementary Doppler ultrasound showed a patent portal vein, SMV, and the inferior vena cava [Figures 1 and 2]. The full report is shown in Table 3.

- A 3D representation computerized tomography angiography of the abdomen and pelvis, showing good visualization of the right renal artery and the right kidney, while only a small initial part of the left renal artery is visible; the left kidney is also not visualized.

- Coronal computerized tomography angiography of the abdomen and pelvis showing contrast filling the right renal artery and visualization of the right kidney, while an absolute cutoff of the left renal artery and poor visualization of the left kidney.
| Radiological investigations done | |
| Abdomen and pelvis X-ray | Dilated large bowel, but no air fluid levels or air under the diaphragm |
| CT scan abdomen and pelvis with IV contrast (arterial and venous phase) | The left main renal artery is distended with cut of contrast, suggesting acute thrombosis, causing loss of enhancement and devascularization in the arterial phase, with delayed enhancement of the lower pole of the kidney The SMV showed a filling defect extending to the proximal part of the portal vein. The right bowel loops showed mild wall thickening and free fluid; mesenteric ischemia cannot be excluded or could be phase-related due to the patient’s underlying condition No free air, no portal venous air, Moderate free fluid is seen, Cardiomegaly with left atrial enlargement, dual chamber pacemaker. The complementary US showed a patent Portal vein, SMV, SMA, and IVC; however, the left renal vein could not be clearly traced |
| Transthoracic echocardiography | Status post CRT-D implantation, leads in situ. Dilated left ventricular (LV) dimensions with impaired LV systolic function, LV ejection fraction (EF): 15% Global hypokinesia of LV, SEC+in LV Grade III LV diastolic dysfunction, dilated left atrium (LA) Moderate pulmonary valve regurgitation (PR) Degenerative aortic valve (AV) and mitral valve (MV) with Grade II MV regurgitation (MR), trivial AV regurgitation (AR) Dilated right-sided chamber dimensions and impaired right ventricular systolic function. Grade II tricuspid valve regurgitation (TR), moderate pulmonary arterial hypertension The inferior vena cava is normal and non-collapsing |
CT: Computerized tomography, IV: Intravenous, IVC: Inferior vena cava, SMV: Superior mesenteric vein, SMA: Superior mesenteric artery, AV: Atrioventricular, MV: Mitral valve, TR: Tricuspid regurgitation, AR: Aortic regurgitation, MR: Mitral regurgitation, PR: Pulmonary regurgitation, LA: Left atrium, EF: Ejection fraction, CRT-D: Cardiac resynchronization therapy with defibrillator, SEC: Spontaneous echo contrast
Patient was transferred to a tertiary hospital as planned for catheter-directed therapy with the intervention of the radiology (IR) department. After a thorough explanation to the patient and his attendant, they accepted and signed written consent. However, the IR team deferred thrombolysis as the left kidney had already infarcted, so the patient was kept on conservative management in the form of anticoagulation and IV hydration.
Transesophageal echocardiography showed a semi-organized thrombus in the left atrial appendage measuring 13 mm × 10 mm, and tiny thread-like masses, mostly thrombi, attached to the CRT with defibrillator leads in the RA [Figures 3-5].

- 3D transesophageal echocardiography: Mid-esophageal bicaval view showing the cardiac resynchronization therapy with defibrillator leads inside the right atrium, and there are threads like masses attached to it, mostly small thrombi.

- Transesophageal echocardiography: Mid-esophageal two-chamber view showing the left atrial appendage with heavy spontaneous echo contrast and mass inside it, mostly thrombus.

- Transesophageal echocardiography: Mid-esophageal bicaval view showing the cardiac resynchronization therapy with defibrillator leads inside the right atrium, and there are threads like masses attached to it, mostly small thrombi.
The follow-up of serum creatinine and urine output is shown in Figures 6 and 7.

- Total fluid intake and urine output during admission.

- Progress of renal functions during admission.
After that, the patient developed elevated transaminases and bilirubin, which were managed conservatively, as all related laboratory investigations and imaging procedures were normal.
The patient was discharged after 10 days with complete recovery of renal and liver functions while kept on warfarin with a target INR of 2–3.
Differential diagnosis
The two conditions that most closely mimic the clinical presentation of acute renal infarction are renal colic (flank pain and hematuria) and acute pyelonephritis (flank pain and fever).[3]
Main features that may distinguish renal infarction from obstructing urinary stone disease and/or pyelonephritis are as follows: A history of AF increases the likelihood of renal infarction.
Nephrolithiasis and pyelonephritis are often suggested if the patient has tenderness at the renal angle, while renal infarction becomes the most favorable diagnosis when an elevated serum lactate dehydrogenase enzyme is detected. Pyuria and hematuria are common findings in renal infarction, pyelonephritis, and nephrolithiasis, but if not present, the diagnosis of renal infarction should be considered.
Although renal ultrasound and computed tomography scans can easily identify hydronephrosis as a consequence of urinary tract obstruction, this is not the case with pyelonephritis, which shares a lot of similarities with renal infarction, but in some cases, the presence of the “cortical rim sign,” which happens due to subcapsular renal cortical perfusion with collateral circulation, may divert the attention to the diagnosis of renal infarction.[4]
DISCUSSION
Many conditions share manifestations with renal infarction, such as pyelonephritis, nephrolithiasis, mesenteric ischemia, cholecystitis, pancreatitis, or, as in our case, gastritis. That’s why the diagnosis of renal infarction is underestimated or missed.
Renal infarction can occur secondary to either local or distant conditions, but it is mostly due to thromboembolic conditions originating from a cardiac source; also, it can happen with any hypercoagulable condition or local dissection of the renal arteries.
The ideal treatment strategy is still debatable, as there are inadequate studies and evidence to support one specific strategy over another.
Revascularization is the main management procedure when a complete main RA thrombus is present, and the diagnosis is confirmed within <6 h. However, it can also be the best management option in patients with a solitary kidney or when there is a reduction in renal function. Another situation where revascularization remains the best option of treatment includes partial main RA occlusion of <24 h duration. This 24-h duration can be extended if it is associated with significant renal function impairment or with the development of HTN. Furthermore, revascularization can benefit patients in whom arterial dissection is the cause of renal infarction.[5]
If the condition is diagnosed as early as <180 min, thrombolytic therapy comes as the best management option in this situation.[3,6]
The outcome of any of these procedures depends on different aspects, such as the duration till the diagnosis is established, the presence of effective intrarenal collateral circulation, and the preexistence of chronic kidney disease.[7]
In our case, due to late diagnosis, endovascular treatment was deferred, as the diagnosis was delayed. It was highly suspected that the left RA embolism was likely due to a thromboembolism from AF. Anticoagulation therapy alone led to a favorable outcome in the patient, resulting in the complete restoration of kidney function.
CONCLUSION
We present a case of a 61-year-old male patient diagnosed with unilateral RA thrombosis, after repeated presentation to the emergency department with vague epigastric and left loin pain, which caused AKI and successfully resolved with conservative measures in the form of anticoagulation only, which was primarily caused by thromboembolism originating from cardiac origin resulting from AF.
Author contributions:
MAN: Contributed towards study design, literature search, data acquisition, and manuscript editing. Also responsible for the integrity of the work from inception to publication; KSA: Contributed towards study conceptualization.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient’s consent is not required as the patient’s identity is not disclosed or compromised.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript, and no images were manipulated using AI.
Financial support and sponsorship: Nil.
References
- Renal artery thrombosis with deterioration of kidney function. BMJ Case Rep. 2024;17:e263115.
- [CrossRef] [PubMed] [Google Scholar]
- Massive renal infarction due to spontaneous renal artery thrombosis-a rare case report. Urol Case Rep. 2022;42:102038.
- [CrossRef] [PubMed] [Google Scholar]
- Effect of local low-dose thrombolysis on clinical outcome in acute embolic renal artery occlusion. Radiology. 1993;189:549-54.
- [CrossRef] [PubMed] [Google Scholar]
- Renal infarction versus pyelonephritis in a woman presenting with fever and flank pain. Am J Kidney Dis. 2014;64:311-4.
- [CrossRef] [PubMed] [Google Scholar]
- Renal infarction In: Palevsky PM, Baumgarten DA, eds. Uptodate. Wolters Kluwer; 2025. Available from: https://www.uptodate.com/contents/renal-infarction [Last accessed 2025 October 19]
- [Google Scholar]
- Clinical characteristics of patients with segmental renal infarction. Nephrology (Carlton). 2006;11:336-40.
- [CrossRef] [PubMed] [Google Scholar]
- Acute renal artery occlusion: Presentation, treatment, and outcome. J Vasc Surg. 2016;64:P1026-32.
- [CrossRef] [PubMed] [Google Scholar]
