Renovascular Disease & Renal Infarction
When the kidney's blood supply narrows, clots or bursts
Renal artery stenosis
Two diseases. About 90% of renal artery stenosis (RAS) is atherosclerotic: older patients who smoke or have diabetes, dyslipidemia and vascular disease elsewhere, with plaque at the ostium or proximal third of the artery. Fibromuscular dysplasia (FMD) is a noninflammatory, nonatherosclerotic disease, usually of women aged about 15–50, that most often thickens the media of the mid-to-distal renal artery, creating alternating stenoses and small aneurysms, the string of beads seen on angiography. It can also involve the carotid and vertebral arteries.
| Feature | Atherosclerotic RAS | Fibromuscular dysplasia |
|---|---|---|
| Patient | Older; smoking, diabetes, vascular disease | Women ~15–50 |
| Location | Ostium or proximal third | Mid-to-distal artery |
| Angiography | Focal proximal narrowing | String of beads |
| Treatment | Medical therapy; revascularize selected cases | Balloon angioplasty, often curative |
Goldblatt mechanism. Reduced pressure at the afferent arteriole is sensed by juxtaglomerular cells, which release renin. Angiotensin II and aldosterone raise blood pressure through vasoconstriction and Na+ retention and may cause hypokalemia. The ischemic kidney atrophies while the contralateral kidney bears the high pressure.
Clinical clues. Hypertension beginning before 30 or severe after 55, abrupt worsening or resistance to three drugs, a systolic–diastolic abdominal bruit, a kidney more than 1.5 cm smaller than its partner, unexplained hypokalemia and recurrent flash pulmonary edema all suggest RAS. Flash pulmonary edema with bilateral disease is called Pickering syndrome: with no normal kidney to excrete retained salt, volume expands abruptly.
In bilateral RAS or a stenotic solitary kidney, glomerular pressure depends on angiotensin II constricting the efferent arteriole. ACE inhibitors and ARBs remove that support, so GFR falls sharply; a creatinine rise above about 30% after starting one should prompt evaluation for RAS. The fall reverses when the drug is stopped.
Diagnosis and treatment. Duplex ultrasound, CT angiography or MR angiography screen for RAS, and catheter angiography is the reference standard. FMD usually responds to balloon angioplasty. Atherosclerotic RAS is managed with blood pressure control (an ACE inhibitor or ARB if unilateral), a statin, antiplatelet therapy and smoking cessation; revascularization is reserved for selected patients, such as those with recurrent flash pulmonary edema.
Hypertensive nephrosclerosis
Benign nephrosclerosis. Years of moderate hypertension, often with diabetes and aging, force plasma proteins into arteriolar walls, producing hyaline arteriolosclerosis: glassy, homogeneous pink thickening that narrows the lumen. Patchy ischemic nephron loss leaves symmetrically shrunken kidneys with a finely granular cortical surface, mild proteinuria and slowly progressive CKD.
Malignant nephrosclerosis. Hypertensive emergency (often above 180/120 mm Hg with acute organ injury) injures arterioles faster than they can adapt. Smooth muscle cells and reduplicated basement membrane form concentric layers (hyperplastic, or onion-skin, arteriolosclerosis), and fibrinoid necrosis of the arteriolar wall follows. Ruptured vessels speckle the cortex with petechiae, the flea-bitten kidney. Patients have AKI, hematuria, proteinuria and microangiopathic hemolysis, often with papilledema and encephalopathy. Similar onion-skin lesions occur in scleroderma renal crisis.
| Feature | Benign | Malignant |
|---|---|---|
| Arteriolar lesion | Hyaline arteriolosclerosis | Hyperplastic (onion-skin) arteriolosclerosis, fibrinoid necrosis |
| Gross kidney | Small, finely granular | Flea-bitten (petechiae) |
| Course | Slow CKD, mild proteinuria | AKI, hematuria, microangiopathic hemolysis |
Infarction and embolic disease
Embolic infarct. Segmental renal arteries are end arteries, so an embolus, most often from the heart (atrial fibrillation, mural thrombus after myocardial infarction, endocarditis), produces a pale, wedge-shaped coagulative infarct with its base on the capsule. Sudden flank pain, hematuria and an LDH elevated out of proportion to other enzymes are typical. The infarct heals as a depressed cortical scar. Organs with dual or collateral supply, such as lung and bowel, form red infarcts instead.
Atheroembolic disease. Days to weeks after arterial catheterization or vascular surgery, or after anticoagulation or thrombolysis, cholesterol crystals from ulcerated aortic plaque shower into arcuate and interlobular arteries. Tissue processing dissolves the crystals, leaving biconvex, needle-shaped clefts surrounded by inflammation, and AKI develops subacutely, often stepwise. Systemic clues include livedo reticularis, painful blue toes with intact pulses, Hollenhorst plaques in retinal arterioles, eosinophilia, eosinophiluria and low complement (C3).
Contrast-associated AKI begins within 1–3 days of a procedure and usually recovers; atheroembolic AKI starts later, worsens over weeks and brings skin and eye findings.
Renal vein thrombosis and cortical necrosis
Renal vein thrombosis. Nephrotic syndrome, above all membranous nephropathy, is hypercoagulable because antithrombin III is lost in the urine while the liver increases production of fibrinogen and other clotting factors. Acute thrombosis causes flank pain, hematuria, an enlarged kidney, worsening proteinuria and AKI. Because the left gonadal vein drains into the left renal vein, left-sided thrombosis can produce a new left varicocele, and clot can embolize to the lungs.
Diffuse cortical necrosis. Intense vasospasm combined with disseminated intravascular coagulation infarcts the renal cortex symmetrically while the medulla is spared. Classic settings are obstetric catastrophes, especially placental abruption, and septic shock. The result is abrupt anuric AKI that often does not recover.