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145 RENOVASCULAR DISEASE

145 RENOVASCULAR DISEASE
Harrison’s Manual of Medicine

145

RENOVASCULAR DISEASE

Acute Occlusion of a Renal Artery
Renal Vein Thrombosis
Renal Artery Stenosis
Ischemic Nephropathy
Scleroderma
Arteriolar Nephrosclerosis
Hemolytic-Uremic Syndrome
Toxemias of Pregnancy
Vasculitis
Sickle Cell Nephropathy
Bibliography

Ischemic injury to the kidney depends on the rate, site, severity, and duration of vascular compromise. Manifestations range from painful infarction to acute renal failure (ARF), impaired GFR, hematuria, or tubular dysfunction. Renal ischemia of any etiology may cause renin-mediated hypertension.
Acute Occlusion of a Renal Artery
Can be due to thrombosis or embolism (from valvular disease, endocarditis, mural thrombi, or atrial arrhythmias).
Thrombosis of Renal Arteries   Large renal infarcts cause pain, vomiting, nausea, hypertension, fever, proteinuria, hematuria, and elevated LDH (with “flipping” of the LDH isoenzyme 1:2 ratio) and AST. In unilateral lesion, renal functional loss depends on contralateral function. IVP or radionuclide scan shows unilateral hypofunction; ultrasound is typically normal until scarring develops. Renal arteriography establishes diagnosis. With occlusions of large arteries, surgery may be the initial therapy; anticoagulation should be used for occlusions of small arteries.
Renal Atheroembolism   Usually arises when aortic angiography or surgery causes cholesterol embolization of small renal vessels. Renal insufficiency may develop suddenly or gradually. Pace may be progressive or “stuttering.” Associated findings are GI or retinal ischemia with cholesterol emboli visible on fundoscopic examination, pancreatitis, neurologic deficits (especially confusion), livedo reticularis, toe gangrene, and hypertension. Skin or renal biopsy may be necessary for diagnosis. Heparin and other anticoagulants are contraindicated. Should be suspected when renal function does not improve more than 1 week after radiocontrast exposure with presumed contrast nephropathy.
Renal Vein Thrombosis
This occurs in a variety of settings, including pregnancy, oral contraceptive use, trauma, nephrotic syndrome (especially membranous nephropathy, see Chap. 142), dehydration (in infants), extrinsic compression of the renal vein (lymph nodes, aortic aneurysm, tumor), and invasion of the renal vein by renal cell carcinoma. Definitive Dx is established by selective renal renography. Streptokinase may be effective. Oral anticoagulants (warfarin) usually prescribed for longer term.
Renal Artery Stenosis
Main cause of renovascular hypertension; due to (1) atherosclerosis (two-thirds of cases; usually men aged >60 years, advanced retinopathy) or (2) fibromuscular dysplasia (a third of cases; usually white women aged <45 years, brief history of hypertension). Renal hypoperfusion activates renin-angiotensin-aldosterone (RAA) axis. Suggestive clinical features include onset of hypertension <30 or >50 years of age, abdominal or femoral bruits, hypokalemic alkalosis, acute onset of hypertension or malignant hypertension, and hypertension resistant to medical therapy. Malignant hypertension (Chap. 124) may also be caused by renal vascular occlusion. Nitroprusside, labetalol, or calcium antagonists are generally effective in lowering bp acutely, although inhibitors of the RAA axis [e.g., ACE inhibitors, angiotensin II (AII) receptor antagonists] are most effective long-term treatment, if disease is not bilateral.
The “gold standard” in diagnosis of renal artery stenosis is conventional arteriography. Magnetic resonance angiography is used in experienced centers, especially among pts with renal insufficiency at higher risk for contrast nephropathy. The least invasive and most reliable preliminary test in pts with normal renal function and hypertension is the captopril (or enalaprilat) renogram. Lateralization of renal function [accentuation of the difference between affected and unaffected (or “less affected” sides] is suggestive of significant vascular disease. Test results may be falsely negative in the presence of bilateral disease. Measurement of renal vein renins may be necessary to demonstrate functional significance of a lesion.
Surgical revascularization appears to be superior for ostial lesions characteristic of atherosclerosis. The relative efficacy of surgery compared with angioplasty (especially with stenting) for fibromuscular dysplasia or for nonocclusive, nonostial atherosclerotic disease is unclear. Angioplasty (with or without stenting) tends to be most effective for mid-vessel or more distal lesions. No studies have adequately compared revascularization with medical therapy. ACE inhibitors or AII receptor antagonists are ideal agents for hypertension associated with renal artery stenosis, except in pts with bilateral disease (see “Ischemic Nephropathy,” below) or disease in a solitary kidney (including an allograft).
Ischemic Nephropathy
In addition to the association between renal artery stenosis and hypertension, there is an important (and less well recognized) association between renal artery stenosis and progressive chronic renal failure. Because most pts do not undergo either kidney biopsy or angiography prior to the initiation of dialysis, it is difficult to estimate the incidence of renovascular disease as a primary cause of end-stage renal disease (ESRD) (some have suggested up to 15–20%, even greater among elderly). Indeed, many individuals diagnosed with ESRD due to hypertension or diabetes suffer from ischemic nephropathy, with diabetes being a secondary causes and hypertension, a consequence, rather than a cause.
The presence of widespread atherosclerotic vascular disease, asymmetric kidney size and function, and hypertension suggest renovascular disease; episodic “flash” pulmonary edema, renal insufficiency, and ARF in response to a trial of ACE inhibitors suggests that the disease may be severe and bilateral.
Revascularization with the goal of preservation of renal function is sometimes entertained. Angioplasty is less often successful than for fibromuscular dysplasia, although stenting may offer the potential for better “noninvasive” results. Whether with surgical or angiographic intervention, it appears that kidneys <8 cm in size are unlikely to recover substantial renal function. The use of aspirin and lipid-lowering agents is advisable in pts with evidence of renovascular disease, regardless of revascularization options.
Scleroderma
May cause sudden oliguric renal failure and severe hypertension due to small- vessel occlusion in previously stable pts. Aggressive control of bp with ACE inhibitors and dialysis, if necessary, improve survival and may restore renal function.
Arteriolar Nephrosclerosis
Persistent hypertension causes arteriosclerosis of the renal arterioles and loss of renal function (nephrosclerosis). “Benign” nephrosclerosis is associated with loss of cortical kidney mass and thickened afferent arterioles and mild to moderate impairment of renal function. Malignant nephrosclerosis is characterized by accelerated rise in bp and the clinical features of malignant hypertension, including renal failure (Chap. 124). Agressive control of the bp can usually halt or reverse the deterioration of renal function, and some pts have a return of renal function to near normal.
Hemolytic-Uremic Syndrome
Characterized by ARF, microangiopathic hemolytic anemia, and thrombocytopenia; increasingly recognized in adults; may be preceded by a prodrome of bloody diarrhea and abdominal pain. Fibrin deposition leads to small-vessel occlusion. Lack of fever or CNS involvement helps to distinguish it from thrombotic thrombocytopenic purpura. Plasmapheresis may be of benefit; prognosis for recovery of renal function is generally poor.
Toxemias of Pregnancy
Preeclampsia is characterized by hypertension, proteinuria, edema, consumptive coagulopathy, sodium retention, and hyperreflexia; eclampsia is the further development of seizures. Glomerular swelling and/or ischemia causes renal insufficiency. Coagulation abnormalities and ARF may occur. Treatment consists of bed rest, sedation, control of neurologic manifestations with magnesium sulfate, control of hypertension with vasodilators and other anti-hypertensive agents proved safe in pregnancy, and delivery of the infant.
Vasculitis
Renal complications are frequent and severe in polyarteritis nodosa, hypersensitivity angiitis, Wegener’s granulomatosis, and other forms of vasculitis (Chap. 160). Therapy is directed toward the underlying disease.
Sickle Cell Nephropathy
The hypertonic and relatively hypoxic renal medulla coupled with slow blood flow in the vasa recta favors sickling. Papillary necrosis, cortical infarcts, functional tubule abnormalities (nephrogenic diabetes insipidus), glomerulopathy, nephrotic syndrome, and, rarely, ESRD may be complications.
Bibliography

For a more detailed discussion, see Badr KF, Brenner BM: Vascular Injury to the Kidney, Chap. 278, p. 1610, in HPIM-15.

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