15.2.1 Traumatic Lesions of the Renal Artery

Blunt renal injuries are rare (i.e. overall incidence 0.05% of all blunt injuries) [8]. It is associated with deceleration injuries (e.g. road traffic accidents and falls from heights) [8]. Injuries to the ribs or other abdominal organs such the spleen, liver, or bowels are usually present. The injury can vary between a small leak, thrombosis, or complete avulsion and is best diagnosed with CT or angiogram. Conservative management is the most common treatment; however, surgical exploration with revascularisation or nephrectomy could be performed in patients who are unstable. Revascularisation is difficult and associated with reduced renal function [9]. This is usually reserved for patients with traumatic thrombosis who have a single kidney or bilateral injuries [9, 10].

Penetrating injuries of the renal artery are a common cause of arteriovenous fistula in incidents involving knives. Elsewhere, the most common cause is iatrogenic during renal biopsy or partial nephrectomy. There is more than the usual retroperitoneal haematoma, and within a few weeks, the patient develops a thrill and bruit over the loin, sometimes with haematuria [11]. The diagnosis is confirmed with CT or arteriography (Figure 15.4). Small lesions may be embolised through an angiographic catheter [11]. Larger ones may require partial nephrectomy. Very large arteriovenous fistulae with a large shunt and loss of renal parenchyma require nephrectomy.

15.2.2 Renal Artery Stenosis

Atherosclerosis is the most common cause of renal artery lesions [12]. Plaques of atheroma may affect the main renal artery at the junction with the aorta or along its major branches (Figure 15.5). A different pathological process affects medium‐sized vessels such as the arcuate arteries where the internal elastic lamina is doubled and redoubled – intimal fibroelastic hyperplasia (Figure 15.6). A third change – arteriolosclerosis – where hyaline material accumulates just under the intima, is seen in the small afferent arterioles of the glomeruli (Figure 15.5).

These pathological processes, which may occur singly or together, restrict the flow of blood to the renal parenchyma, and ultimately block it completely. When a segmental artery is blocked, there is an infarct of the segment it supplies, and a characteristic atrophy of the full thickness of the cortex and medulla. When smaller branches are occluded, there is a more diffuse loss of parenchyma and an overall shrinkage of the kidney.

The disease progresses over time, and if serial pyelograms have been obtained, one can see the kidneys shrink over the decades (Figure 15.7). This results in a deterioration of renal function and could end with end‐stage renal failure.

15.2.3 Renal Artery Dysplasia

Renal artery dysplasia affects the intima or the media to different degrees. It could be a part of fibromuscular dysplasia that mainly affects the renal and carotid arteries but could also affect different arteries in the body. The intima is affected by patches where it is thickened, alternating with patches where it is unusually thin. This sometimes results in an aneurysmal ballooning of the intima through the wall of the artery. Fibrous tissue is seen just under the adventitia or scattered randomly throughout the entire wall of the artery. The result is to convert the artery from a smooth strong cylinder into an irregular perished pipe, giving an angiographic appearance of a string of beads.

15.2.4 Renal Artery Aneurysm

Renal artery aneurysms are usually diagnosed as an incidental finding during the investigations for other conditions like hypertension or haematuria. Occasionally they could rupture, causing major bleeding particularly during pregnancy [13, 14]. A plain radiograph sometimes shows a characteristic ‘ring’ due to calcification in the wall of the aneurysm (Figure 15.8). The diagnosis is made by colour Doppler sonography, CT angiogram (Figure 15.9), or magnetic resonance imaging (MRI). The kidney on the side of the aneurysm is often smaller than that on the other.

Indications for treatment include diameter more than 2.5 cm [15, 16], interval increase in size, hypertension, haematuria, pain and women of child‐bearing age. Treatment options include vascular stent graft or embolisation depending on the position of the aneurysm and its relationship to the renal artery branches as well as the presence of a ‘neck’ [17, 18].

15.2.5 Renal Infarction

Renal infarction is a result of arterial occlusion mainly caused by thrombi, trauma, or polyarteritis nodosa. It is possible for thrombosis process to start in aorta and spread to the renal artery, causing unilateral or bilateral infarcts. It is more common that the small arteries are occluded, resulting in multiple small infarcts. The affected renal parenchyma undergoes necrosis, followed by fibrosis. If these areas are small, this process could be asymptomatic. Sudden, complete renal infarction could present with loin pain and haematuria. The patient could develop ‘epitheluria’, caused by sloughing of renal tubular cells. CT with contrast may aid the diagnosis. DMSA scans will show the silent segment of parenchyma supplied by a segmental artery. When several segmental arteries are occluded, there is a very typical combination of a normal‐appearing retrograde urogram, with a dramatic thinning of the renal parenchyma; however, an angiogram will show arterial occlusion (Figure 15.10).

Although immediate surgery has been suggested in the past, anticoagulation and conservative management is usually the first‐line treatment.

15.2.6 Pathogenesis of Renal Hypertension

Renal artery stenosis causes narrowing of the arterial lumen. The lumen of the renal artery must be reduced by some 70% before there is a measurable reduction in blood flow [19], but the pressure gradient across the narrowing segment may be as much as 40 mm Hg [20]. The lowered arterial blood pressure leads to reduction in perfusion pressure, glomerular filtration, and in the amount of sodium that is filtered. As a result, the baroreceptor and macula densa systems release renin [21–23]. Renin is the first in a cascade of enzymes which successively liberate the two active polypeptides – angiotensin II and III – from their inactive globulin carrier ‘angiotensinogen’ (Figure 15.11). Both the angiotensins are vasopressors, but in addition, angiotensin II causes the adrenal to produce aldosterone, causing a rise in blood pressure to maintain tissue perfusion. In addition to renal hypertension, ischemic nephropathy can be seen at a later stage, causing deterioration in renal function.

The prevalence of renal hypertension is less than 1% of patients with mild or moderate hypertension [24]. Features raising suspicion of this disease include flank pain and diagnosis of hypertension before 30 years of age.

Several diagnostic methods have been used, such as peripheral renin activity assays, captopril testing, and radionuclide renal scanning. These tests have been replaced by Doppler ultrasound, MRI, and CT. Contrast angiography study remains the gold standard for diagnosis.

Medical treatment is the preferred method in the absence of ischaemic changes to the kidney. On the other hand, if patients show signs of progressive obstruction, angioplasty should be considered (Figure 15.12). The results of angioplasty are excellent in patients with fibromuscular hypoplasia.

Surgical revascularisation is rarely used. The block between aorta and renal artery may be bypassed with a graft of saphenous vein or internal iliac artery. On the left side, the splenic artery can be mobilised and anastomosed directly to the renal artery beyond the stenosis [25–27]. Nephrectomy is an alternative if the kidney is atrophic with poor function.