Embryology Development of Renal vasculature occurs synchronous with nephrogenesis at 3 wks of gestation. Metanephrous is supplied by multiple urogenital rete arteriosum. As mesonephrous begin to regress at 8 wks ,one but all arteries regress which becomes the main renal artery. Ectopic kidneys might retain the fetal vasculature
Embryonic venous drainage by network of veins around aorta called as aortic collar. Dorsal arch by supra cardinal and sub cardinal veins. Ventral arch by intersubcardinal veins. Normally Dorsal arch regresses . Persistence of both -Circumaortic vein Regression of ventral-Retroaortic vein.
Anatomy of Renal vessels MRA arise below SMA at the level of L2 vertebrae.4-6 cm in length and 5-6 mm in diameter. Rt renal artery is longer,slightly higher in origin and steeper in course than left and only major vessel that courses behind IVC. Rt renal arises from anterolateral and Left from posterolateral aspect of aorta. Arterial supply
5 major segmental branches to the kidney which divide into lobar, interlobar, arcuate, interlobular arteries- afferent glomerular arterioles. Vascular segments are supplied by end arteries with no anastomosis. Also, supply smaller branches to adrenal, capsule, ureter, and perinephric tissue
Brodel’s Line Relatively avascular plane between ant two third and Posterior one-third of kidney. Minimise bleeding during PCN or anatropic nephrolithotomy.
Venous Drainage Interlobular veins-arcuate veins-lobar veins and main renal veins at L1-L2 level. Left main renal vein also drain left gonadal vein and left adrenal veins and courses between aorta and SMA. LRV is longer -opted for donation.
Variant Anatomy Arterial Supernumerary - 30% people with 10% bilateral.Similar caliber to main renal arteries. Accessory (T11 to L4 or common iliac and rarely from mesenteric, lumbar or thoracic aorta).Enter through hilum Aberrant/Polar(enter through poles and supply poles). Prehilar(Pre segmental arteries within 1.5 cm from ostium) -may prelude donor criteria
Incidental accessory renal artery in a 66-year-old patient with myo- cardial infarction requiring cardiopulmo- nary resuscitation. (a) Coronal contrast- enhanced CT image shows differential enhancement of the right kidney, with hyperenhancement (arrow) in the upper pole and hypoenhancement in the lower pole. (b) Coronal CT angiogram shows an aberrant upper-pole renal artery (ar- row). The differential enhancement in the upper pole was due to a delayed dense nephrogram limited to the upper pole (from contrast material administered for prior recent CT pulmonary angiography), related to ischemia secondary to acces- sory renal artery compression or stenosis by an adrenal hemorrhage.
Refractory hypertension secondary to renal artery stenosis (RAS) of an accessory renal artery in a 62-year-old man. (a–c) Curved multiplanar maximum intensity projection (MIP) images (a, b) and volume-ren- dered image (c) from renal CT angiography (CTA) show an accessory right renal artery with severe stenosis at the ostium (arrow). (d) Image from conventional digital subtraction angiography (DSA) shows stent placement (arrow) in the stenosed accessory renal artery.
Variant Anatomy Venous Supernumerary-15-20 % ,more common on the right Delayed confluence of main renal vein.1.5 cm from IVC on the right and aorta on the left.(may need dual clamp) Retroaortic -3% Plexiform left renal vein
Circumaortal Left Renal vein -17% of all renal vein variant Relevance-SVC filter placement, nephrectomy, RP dissection
Imaging Protocols US Doppler-real time quantitative and qualitative CT Angiography-Anatomic info MR Angiography-Anatomic info Catheter Angiography:Invasive,expensive, gold standard ,done if intervention is planned.
US Doppler Protocol : Fasting state Low frequency transducer used (2.5 – 5 MHz) Supine/ lateral decubitus position Anterior approach– Main RAs Flank approach - Intrarenal vasculature and main RAs Advantage: Most common screening modality Inexpensive, noninvasive, readily available Limitations: Operator dependent Overlying bowel gas
Anterior approach The renal arteries are clearly imaged in B Mode from an anterior approach however as it is perpendicular to the ultrasound beam it is not suitable for Doppler assessment. Anterior Approach: The left renal vein passes between the aorta and SMA. The left renal artery is located posterior to the renal vein.
Oblique approach Oblique Approach. Angling 45 degrees to right renal artery A Spectral analysis is of aorta at the level of the renal arteries.
Normal doppler waveform Normal renal artery waveforms demonstrate a rapid systolic upstroke with persistent forward flow in diastole (low-resistance bed) . An early systolic compliance peak (ESP) or notch may be seen in some patients Angle-corrected PSV in abd aorta, proximal, mid and distal renal artery.Spectral waveform of MRA and segmental arteries, acceleration time, acceleration index
Doppler PSV-60-100 cm/sec Acceleration time-70 msec Acceleration index -300cm/sec2 RI- 0.6 - 0.7(can be raised in ureteric obstruction, intrinsic disease) PI <1.3
CT Angiography Rapid injection of contrast(5ml/sec), Arterial phase scanning by bolus tracking/empirical 25 sec. Venous phase scanning at delay of 85 sec Scan range-Celiac axis till iliac artery bifurcation Post processing : surface rendering, MIP ,volume rendering & 3D reconstruction, curve planar reformatting
MR Angiography Breathhold, 3 D Gd enhanced MRA (GRE) Contrast – 0.2mmol/kg Rate 2ml/sec; with 20ml saline flush Scan range – from above the celiac axis to the iliac bifurcation Scan delay – 10 sec after start of injection Scan time – 25-30 sec (single breath hold) 3D PC MRA after post GD sequences. Dynamic scanning in the arterial, venous and equilibrium phases.
Renal Artery Stenosis Most common reversible and treatable cause of Secondary Hypertension. Causes Atherosclerotic-2/3rd Fibromuscular dysplasia-1/3rd
Atherosclerotic Disease Patients above 50 yrs, males Correlates with overall atherosclerotic burden,CAD patients have more risk. At the origin or proximal 2 cm. Important to exclude in post transplant patients presenting with hypertension.
In CT and MR angio, 50-70 % stenosis is moderate and >70% is severe Endovascular treatment is indicated in moderate stenosis with features of hemodynamic instability(Translesional gradient of 20 mm hg) and severe stenosis.
CTA ideal investigation:90% accuracy.luminal narrowing, Calcifications, post stenotic dilatation, renal atrophy and decreased cortical enhancement. MRA:90% to 100% sensitivity Both can show accessory arteries
Fibromuscular Dysplasia Non atherosclerotic and non inflammatory vascular disease of medium or large arteries causing focal irregular thickening. Young patients with F:M ratio 9:1 In 75% of cases Renal arteries are affected followed by ICA. Can cause stenosis, aneurysm, dissection or occlusion of involved vessels. Medial fibroplasia in 80%-90% cases, intimal fibroplasia in 10% cases.
Tend to involve mid or distal main renal artery or infrarenal part. 2/3rd cases are bilateral. 10% associated with aneurysm. Medial type has strings of pearl appearance. Intimal type has focal long segment tubular stenosis
CTA 100 % sensitive MRA 97% sensitive and 93% specificity Percutaneous balloon Angioplasty is the treatment of choice with Endoluminal stent placement in treatment failure or complicated cases like dissection. Bypass surgery reserved for macro aneurysm or involving multiple branches Catheter-based Intervention- FMD>atherosclerotic
Renal Artery entrapment Extrinsic compression by crus of diaphragm or psaos muscle-in high origin cases. Likely in young patients with no CVS risk factors. IOC CTA Stent placement can be helpful but difficult due to movement of diaphragm.
Renal Artery Dissection Mostly extension of aortic dissection. Isolated cases in endovascular procedures or blunt trauma. Risk factors- FMD, malignancy-related, HTN, ED syndrome, Marfan’s syndrome, cocaine abuse, physical exertion.
Spontaneous renal artery dissection originates in distal segment. CTA noninvasive IOC.Focal dissection flap ,true lumen continuous with that of aorta. Luminal narrowing, focal segmental cutoff or distal ischemic changes. Catheter angiogram in equivocal cases and plan treatment. Stable patients-conservatively, unstable-stents placement-first line therapy for revascularisation.
Renal Artery Aneurysm True aneurysm. 0.1% Patients, incidentally detected. Presentation-rupture, thrombosis, embolism 73% have systemic HTN 34% have FMD. Majority occur at bifurcation and less than 10% intrarenal
US Doppler-Anechoic mass with Doppler flow in continuity with the renal artery. Calcification or mural thrombosis can mask Doppler flow. NCCT for peripheral calcification.Protective action. CTA IOC.Look for aneurysm elsewhere, like abdominal aorta, splenic artery.
Management Size and clinical setting Size doesn't correlate to the risk of rupture 1-1.5 cm screen every 1-2 yrs. >1.5 cm or Peripheral vascular bed embolism, uncontrolled HTN. Definitive treatment is required. Rupture-10% mortality rate.50 % in pregnant women. Catheter embolisation in branch type and stenting, ligation or bypass in Main Renal Artery.
Pseudoaneurysm Direct injury to vessel wall and contained blood in adventitia or surrounding tissue. Iatrogenic or penetrating trauma. Multiple intraparenchymal in vasculitis or amphetamine abuse.
Saccular morphology with direct arterial communication. Grey scale mimic simple cyst.Spectral doppler- Yin yang sign-Turbulent to and fro flow. CTA intrarenal focus of arterial enhancement .Also for other injuries. Non enhanced MR-Flow void >2cm size trans-catheter embolisation
Mycotic RAA Infectious arteritis Formation of Pseudoaneurysm. Immune-compromised and IV drug user with sepsis. Septic emboli or renal abscess ,pyelonephritis ,renal artery stent placement. Saccular morphology Inflammatory changes-fat stranding, wall thickening, soft-tissue enhancement, fluid collection
Renal Artery Occlusion Occlusion can lead to infarction within 60 mins due to lack of collaterals. Thrombosis or thromboembolism. Relatively uncommon -2% of cases USG:Areas of complete loss of doppler signal
CECT- Wedge shaped areas of non-enhancement with cortical rim sign. Old infarcts -cortical loss and parenchymal retraction.Underlying cause like atrial thrombus, cardiac valve vegetation, dissection. CEMR similar findings. Non contrast MR variable signal intensity of renal parenchyma based on the age of infarct. 16 % bilateral infarcts. Spleen infarct in 37% cases Catheter Angiography:level of occlusion Global or segmental infarcts within 2 days can benefit from endovascular revascularisation.
Systemic Disorders affecting Renal Arteries Necrotising vasculitis affecting medium and small arteries. Renal arteries affected in 90% of cases. Non specific symptoms like fever , wt loss, polyarthralgia. Poly Arteritis Nodusa
CT-Diffuse enlargement and hypo attenuation T2WI shows diffuse high signal intensity. Multiple small bilateral infarcts distributed along interlobar and arcuate arteries. Associated infarcts of Spleen/GI tract. Catheter Angiography- Multiple micro aneurysm 2-3 mm in size.
Other vasculitis SLE and other vasculitis caused by drugs like cocaine, amphetamine, vincristine, bleomycin, cisplatin can cause similar findings as PAN.
Neurofibromatosis-I Vascular cause is the second most common cause of death after malignancy. Cellular proliferation-degeneration - fibrosis Causes Secondary hypertension.In adults due to pheochromocytoma but in paediatric age group-RAS. Vascular abnormalities in 0.4-6.4 % and 41% involve renal artery.
Takayasu Arteritis Idiopathic inflammatory vascular disorder. CT angiography and MR angiography show smooth luminal stenoses and complete occlusions. An additional benefit of CT angiography and MR angiography, as compared with catheter angiography, is the depiction of vessel wall thickening. Vessel wall thickening, edema, and enhancement are early inflammatory changes that precede stenosis CTA: Bilateral renal artery stenosis in a 22-year old woman with Takayasu arteritis
Arteriovenous Communication. AVM Connection between renal artery and renal vein owing to a nidus of abnormal vessels. Cirsoid -single artery feeding and Cavernous type-multiple artery feeding having corkscrew appearance Doppler-turbulent flow with low resistance waveforms. CTA-can show feeding artery, nidus and early draining vein.
CECT-complications like hematoma MR-flow voids. Endovascular treatment involving alcohol ablation of the nidus and feeding vessels is the treatment of choice . For larger AVMs, coil embolization may be required .
AV Fistula Connection between artery and vein without connecting capillary bed. Iatrogenic-percutaneous nephrostomy or penetrating trauma, renal biopsy(18%).RAA rupture into vein. Spectral Doppler US images of AVFs show increased flow velocity, decreased arterial resistance, and arterial waveforms in the outflow vein .RI-0.3-0.4.
CT angiography and MR angiography, renal AVFs are characterized by a single dilated feeding artery and early enhancement of a dilated draining vein. Renal parenchymal atrophy. Transcatheter embolisation-coiling.Surgery for large AVF.
Arteriovenous Connections Associated with Renal Cell Carcinoma Angiogenic factors that are caused by the malignancy induce the formation of abnormal vascular connections Tumor invasion and the development of communicating vascular spaces within necrotic tumors. When the AVF is large, the vascular communication may obscure the underlying renal mass
Secondary Ureteropelvic Junction Obstruction Caused by Crossing Vessels A crossing vessel can be seen in 29%–46% of cases of ureteropelvic junction obstruction CT angiography is highly sensitive and specific for defining crossing vessels and is preferred over catheter angiography, which may not depict crossing veins
Venous Compression Syndrome Nutcracker syndrome-Anterior and Posterior Flank pain and hematuria(rupure of thin wall venous system in the collecting system due to increase venous pressure) Pelvic congestion in females and varicocele in males
Comparing the AP diameter of the left renal vein at the level of the renal hilum with this diameter at the point of the stenosis. A reduction in the inner diameter by a factor of at least 3 in a supine and 5 in a standing patient for at least 15 minutes is a criterion for US-based diagnosis of nutcracker syndrome
Venous Compression syndrome P osterior nut cracker syndrome Retroaortic left renal vein-3 % When present, prominent collateral draining vessels—including the paralumbar, gonadal, and hemiazygos veins— suggest marked obstruction of blood flow
A pressure gradient of greater than 2 mm Hg between the IVC and renal vein suggests outflow obstruction. Endovascular stent placement in the renal vein has a high success rate; however, its long-term efficacy is unknown.
Renal Vein Thrombosis Cause- bland or tumor thrombus Hematuria,flank pain, decrease Renal function Risk factors-glomerulonephritis, diabetes, collagen vascular disease, trauma More on left USG-loss of CMD and renal enlargement. Doppler-no flow in renal vein and reversal of diastolic flow in renal arteries. CT- Hypo-attenuating filling defect with filling defect, delayed cortical enhancement,edema in the renal sinus and perinephric space, and ipsilateral renal enlargement.
In chronic cases of renal vein thrombosis, multiple collateral vessels may develop Trauma-induced renal vein thrombosis almost invariably manifests with additional renal artery or parenchymal injury Placement of a suprarenal venacava filter may be considered for select patients with thrombosis extending into the IVC.
Renal vein tumor thrombosis RCC CT-Extent of lumen involvement crucial for surgical management MR- IOC , can detect bland thrombus.Loss of flow void.Superior extent of thrombus is important and imaging need to be done within 7-10 days of surgery.
Other tumors Adrenocortical tumor can invade renal vein and IVC. Wilms tumor-6% extend into vessels Upper tract urothelial cell tumor Renal angiomyolipoma can extend into renal vein,IVC ,PTE. Oncocytoma Lymphoma-encasement more common.
Renal Vein Leiomyosarcoma Primary malignant tumor of smooth muscle.5% in large vessels,IVS most common. Renal vein-Female more common ,LT>RT Tumor expands the renal vein and can extend into renal parenchyma or IVC. CT/MR homogenous enhancement, sole peripheral enhancement can be present. VS RCC-Intravascular component is larger than intra renal
Angiomyolipoma Subtype of perivascular epithelioid cell tumor (PEComa), composed of smooth muscle, fatty, and vascular ( triphasic) components. Most common solid benign lesion, 80% sporadic 20% syndromic Smooth muscle–predominant or fat-poor AMLs can frequently be differentiated from RCC by higher attenuation at non-contrast CT, lower signal intensity at T2-weighted imaging, and avid enhancement and washout
Pseudoaneurysm and life threatening haemorrhage(AML>4cm,pseudoaneurysm >5cm). Hemorrhage from Fat-poor AML is rare. Elective endovascular treatment
Renal Vascular Injury Complications like pseudoaneurysm, AVF, arterial dissection or transection, perinephric hematoma, arterial or venous thrombosis AAST renal trauma scale Vascular injury: pseudoaneurysm or AVF , focal collection of contrast medium with decreasing attenuation in delayed phase Active bleeding:Increasing attenuation in delayed phase.
Renal Vascular Injury AAST grade I and II do not have vascular involvement. AAST grade III -active bleeding contained within gerota’s fascia AAST grade IV-active bleeding into retro-peritoneum or peritoneum. AAST grade V: Devascularisation of kidney due to laceration of renal vessels at hilum.