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Chronic kidney disease resulting from atherosclerotic renal artery stenosis

Chronic kidney disease resulting from atherosclerotic renal artery stenosis
Literature review current through: Jan 2024.
This topic last updated: Jan 18, 2022.

INTRODUCTION — Many but not all patients with atherosclerotic renal artery stenosis have chronic kidney disease (CKD) that is primarily due to a reduction in blood flow induced by the stenosis. A fall in blood flow and glomerular filtration rate (GFR) in one of two kidneys often results in compensatory increases in the "contralateral kidney." Thus, clinically progressive CKD as reflected by increased serum creatinine generally occurs when the stenosis threatens the entire kidney mass. Patients with CKD resulting from atherosclerotic renal artery stenosis usually have high-grade stenosis of both renal arteries or stenosis to a solitary functioning kidney.

However, renal artery stenosis may be an "incidental" finding in patients who have CKD that is caused by a separate disorder (eg, diabetic nephropathy). It can be difficult to distinguish between patients whose disease is induced by renal artery stenosis and those who have an alternative cause of CKD.

Ischemic nephropathy is discussed in this topic. Determining which hypertensive patients to evaluate for renal artery stenosis, establishing the diagnosis of renal artery stenosis, and treatment of patients with unilateral or bilateral atherosclerotic renal artery stenosis are presented elsewhere:

(See "Evaluation of secondary hypertension".)

(See "Establishing the diagnosis of renovascular hypertension".)

(See "Treatment of unilateral atherosclerotic renal artery stenosis".)

(See "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney".)

In addition, the diagnosis and treatment of fibromuscular dysplasia are discussed in other topics:

(See "Clinical manifestations and diagnosis of fibromuscular dysplasia".)

(See "Treatment of fibromuscular dysplasia of the renal arteries".)

DEFINITION AND TERMINOLOGY — CKD that results from atherosclerotic renal artery stenosis is frequently called "ischemic nephropathy" [1-4]. Broadly speaking, "ischemic nephropathy" could refer to a reduction in glomerular filtration rate (GFR) produced by any cause of diminished renal blood flow. In principle, this could include ischemic acute tubular necrosis, intrarenal arterial or capillary obstruction due to vasculitis, coagulation or hemolytic disorders (such as a thrombotic microangiopathy or sickle cell disease).

However, the term ischemic nephropathy is most commonly applied in patients who have CKD due to partial or complete obstruction of one or more extrarenal arteries [2], usually in patients with atherosclerotic disease. Thus, for the purposes of this review, ischemic nephropathy refers to the progressive loss of GFR resulting from atherosclerotic renal artery stenosis.

Although kidney injury can develop in any kidney or kidney region beyond a critically stenotic artery, the injury may not be clinically apparent, largely due to compensatory function of the unaffected contralateral kidney. As noted above, clinically apparent or progressive disease (marked by an increase in the serum creatinine) occurs primarily when the stenosis threatens the entire kidney mass. Hence, patients who are diagnosed with ischemic nephropathy usually have high-grade stenosis of both renal arteries or stenosis to a solitary functioning kidney.

PATHOGENESIS — Loss of kidney function in renovascular disease can result from a usually reversible consequence of antihypertensive therapy or can reflect progressive narrowing of the renal arteries and/or progressive intrinsic kidney disease. Studies in human subjects demonstrate that, despite a moderate reduction in kidney perfusion pressure (up to 40 percent) and in renal blood flow (mean 30 percent), glomerular filtration is reduced but tissue oxygenation within the kidney cortex and medulla can adapt without the development of severe hypoxia [5,6]. As a corollary, many such patients can be treated with medical therapy without progressive loss of function or irreversible fibrosis, sometimes for many years [7,8].

However, more advanced vascular occlusion, corresponding to a 70 to 80 percent narrowing of the renal artery [9,10], leads to demonstrable cortical hypoxia that can be measured by blood oxygen level dependent magnetic resonance (BOLD-MR) [11,12]. In animal studies, this tissue hypoxia produces rarefaction of microvessels, as well as activation of inflammatory and oxidative pathways that lead to interstitial fibrosis [13]. Several studies suggest that these changes also take place as a result of renal artery stenosis in human kidneys. In one study, for example, inflammatory markers sampled from renal veins of stenotic kidneys correlated strongly with the degree of hypoxia (as measured by BOLD-MR), particularly after correction of the stenosis with angioplasty [14]. Inflammatory changes and fibrosis are also evident in human "pressor" kidneys that were removed to treat hypertension in patients with a totally occluded renal artery [15].

Although vascular occlusion can initiate these processes, long-standing parenchymal injury characterized by inflammation and fibrosis eventually becomes an irreversible process. At some point, restoring renal blood flow provides no recovery of kidney function or clinical benefit.

EPIDEMIOLOGY — Ischemic nephropathy is an increasingly recognized disorder [2,16-21]. However, few prospective studies have examined the incidence or progression of CKD among patients with renal artery stenosis. In addition, renal artery revascularization among patients in these studies infrequently produced a meaningful recovery of kidney function, which would have supported the diagnosis [22]. Thus, the true incidence and prevalence of ischemic nephropathy is unclear.

Various studies have reported that 5 to 22 percent of patients 50 years or older who have advanced CKD have some degree of renal artery stenosis [17,23-28]. However, the renovascular lesions may have been "incidental" in some if not many of these patients. The following examples illustrate the range of findings:

The natural history of ischemic nephropathy was evaluated in a study of 51 patients with angiographically confirmed bilateral renal artery stenosis (defined as 90 percent or greater stenosis to one kidney and 50 percent or greater to the contralateral kidney) who were followed for up to five years [28]. The median estimated glomerular filtration rate (eGFR) declined from 39 to 24 mL/min per 1.73 m2 over five years, and 12 percent of patients developed end-stage kidney disease (ESKD), although these individuals had advanced disease at baseline (eGFR 25 mL/min per 1.73 m2). For various reasons, no patient was revascularized (eg, patient or clinician preference, "unsalvageable" kidneys, patient not suitable for the procedure, or lesion not amenable to the procedure), suggesting that findings may not be applicable to some patients diagnosed with ischemic nephropathy.

By contrast, progression of kidney disease may be infrequent in those incidentally discovered to have moderate renal artery stenosis. In a study of 593 patients who underwent angiography for peripheral artery disease, 397 had interpretable "drive by" renal angiograms [27]. Of these, 126 had at least moderate (more than a 50 percent) stenosis of one or more renal arteries (38 had bilateral stenosis or stenosis to a single functioning kidney). The mean eGFR among these patients was 58 mL/min per 1.73 m2. After 10 years, kidney function remained stable and no patient developed ESKD.

Renal artery stenosis is a common finding among patients initiating dialysis. This was shown in a study of 80 consecutive patients initiating hemodialysis at a single center [26]. Of the 49 patients who agreed to undergo computerized tomography angiography (CTA), bilateral renal artery stenosis (defined as a 50 percent or greater diameter reduction) was present in eight patients (16 percent). Three of these patients were not known to have renovascular disease and initiated dialysis with unexplained kidney failure.

Two randomized trials comparing percutaneous transluminal renal angioplasty with medical therapy alone primarily enrolled patients with CKD at baseline [7,29], although most patients had unilateral rather than bilateral stenosis. The incidence of kidney endpoints in these trials (defined either as a 20 percent reduction in creatinine clearance or as a composite of acute kidney injury, ESKD, or kidney death) was 19 percent during two to five years of follow-up.

In a series of 95 patients undergoing surgical revascularization of totally occluded renal arteries, 49 percent had improved kidney function, including some with ESKD who became independent from dialysis [30]. In a study of 146 patients who had renal artery stenting, only 45 percent experienced stabilization or improvement of their kidney function at five years [31]. Numerous case reports and selected observational series indicate that patients with rapidly progressive kidney failure, usually associated with severe hypertension, can recover kidney function [32-34]. Such reports provide de facto clinical evidence that some but not all atherosclerotic renovascular disease does produce hemodynamic limitations to kidney function that can improve after revascularization. Those individuals whose kidney function improves measurably after revascularization have improved long-term survival as compared with those whose function deteriorates or remains unchanged [35].

The epidemiology of renal artery stenosis in general is presented elsewhere. (See "Establishing the diagnosis of renovascular hypertension".)

CLINICAL MANIFESTATIONS — Patients with ischemic nephropathy typically present as follows:

A persistent and progressive reduction in glomerular filtration rate (GFR) (ie, CKD).

Lack of evidence supporting an alternative cause of kidney disease, such as an abnormal urinalysis, proteinuria, a paraprotein, or use of a nephrotoxic drug. (See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)

Findings that suggest the presence of renovascular disease, for example (table 1):

Severe hypertension that may be treatment resistant. However, a few patients with ischemic nephropathy are normotensive, which may be due in part to a reduced cardiac output [17].

An acute rise in serum creatinine following the administration of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). This usually, but not invariably, resolves after withdrawal of the drug.

Significant variability of serum creatinine concentration that may be due to changes in volume status [36].

Recurrent episodes of flash pulmonary edema and/or refractory heart failure.

Deterioration of kidney function after placement of an endovascular aortic stent graft.

In addition, risk factors for atherosclerotic disease are often present, such as hyperlipidemia, cigarette smoking, and age greater than 50 years. Patients with ischemic nephropathy frequently have coronary artery disease or peripheral arterial disease in other vascular beds. (See "Establishing the diagnosis of renovascular hypertension", section on 'Incidental lesions'.)

In patients with renal artery stenosis, there is a reasonable correlation between estimated glomerular filtration rate (eGFR) and measured GFR (correlation coefficients range from 0.7 to 0.85 depending upon the estimating equation used) [37]. However, changes in measured GFR over time are not always accurately identified by temporal changes in eGFR. During approximately one year of follow-up, the direction of GFR change predicted by estimating equations was discordant with the true direction of GFR change in 28 to 40 percent of patients (depending upon the equation used). This may reflect changes in GFR in both the treated kidney and reversal of compensatory hypertrophy in the contralateral kidney [14]. It may also be related to exaggerated variability of the serum creatinine caused by changes in extracellular fluid volume or systemic blood pressure superimposed upon partial vascular occlusion.

DIAGNOSIS — In patients with clinical manifestations of ischemic nephropathy (see 'Clinical manifestations' above), a presumptive diagnosis of ischemic nephropathy can be made if there is radiologic documentation of significant stenosis (usually more than 70 percent luminal occlusion) of both renal arteries or of one renal artery to a solitary functioning kidney. Indications and options for radiographic imaging of renal artery stenosis and the interpretation of these tests are presented elsewhere. In general, these imaging tests to diagnose renal artery stenosis are warranted if a corrective procedure would be performed should significant renovascular lesions be identified and should the kidneys appear to be salvageable. (See "Establishing the diagnosis of renovascular hypertension".)

As a practical matter, there are two diagnostic elements to consider in patients who could have ischemic nephropathy; these diagnostic elements can impact treatment decisions:

Is the vascular occlusive disease posing critical hemodynamic limitation to kidney function? In general, luminal occlusion of at least 60 to 75 percent is required to limit blood flow and reduce perfusion pressure [38,39]. This degree of stenosis is usually associated with a measurable translesional pressure gradient of 10 to 15 mmHg [40,41]. Doppler ultrasound criteria conventionally require peak systolic velocities above 180 to 200 cm/sec to identify more than 60 percent luminal occlusion that is verified by pressure gradients [40]. Identifiable levels of cortical hypoxia (measured by blood oxygen level dependent magnetic resonance [BOLD-MR]) are usually associated with translesional velocities above 385 cm/sec [11] or reduction of single kidney glomerular filtration rate (GFR) in the range of 20 to 25 mL/min [12].

Is the condition of the kidneys such that restoring renal blood flow is likely to benefit function? The condition of the kidneys can be assessed by considering the renal resistive index, the six-month trajectory of kidney function, and the size of the kidneys, or by performing a kidney biopsy (which is not usually done). None of these factors predict the outcome of revascularization with certainty. Improved and validated methods to evaluate the salvageability of kidney function in this disorder are sorely needed. Some that have been proposed are as follows:

Renal resistive index – Some studies indicate that elevated resistive indices in segmental vessels (above 0.80) measured by duplex ultrasound denote poor prognosis for kidney function recovery [42] while a low resistive index is a favorable sign [43].

Trajectory of kidney function – The most consistent predictor of good recovery of kidney function after revascularization has been a recent deterioration of kidney function (ie, in the prior six to twelve months) [44].

Kidney size – Very small kidneys (less than 7 cm in longest diameter) are usually considered unlikely to recover after revascularization [45].

Kidney biopsy – Previous studies suggest that biopsy demonstrating preexisting atheroembolic changes and interstitial fibrosis indicate a limited potential for recovery [46]. Biopsies are not usually performed.

Comparison of kidney morphology with kidney function – Some investigators recommend assessing morphologic parameters, such as renal parenchymal volume and cortical thickness with MRI, and comparing these parameters with kidney function measured by radionuclide scanning [47,48]. In a stenotic kidney, apparently normal morphology combined with reduced function may indicate a "hibernating kidney" that could be salvaged with revascularization. In some cases, parenchymal viability is likely maintained by collateral vessels insufficient to support glomerular filtration [49].

A definitive diagnosis is not usually made before revascularization. In practice, confirmation of the diagnosis is based upon stabilization or improvement of the GFR after successful revascularization.

While endovascular or surgical revascularization can restore vessel patency and improve blood flow, these procedures are potentially hazardous, particularly within the severely diseased aorta. Potential complications of revascularization include atheroembolic kidney disease and contrast nephropathy. In addition, as noted above, restoring blood flow alone may not reverse the kidney disease. Hence, the clinical decision to pursue extensive diagnostic studies and renal artery intervention should weigh renal salvageability against comorbid diseases and risk.

DIFFERENTIAL DIAGNOSIS — Patients at risk for bilateral renal artery stenosis are also at risk for other disorders that can present with similar clinical findings but cannot be corrected by surgery or angioplasty; these include hypertensive nephrosclerosis and atheroembolic kidney disease.

Hypertensive nephrosclerosis has a similar clinical presentation to chronic ischemic kidney disease: hypertension, slowly progressive CKD, an unremarkable urine sediment, and possible evidence of atherosclerotic vascular disease. It is only the presence of the clinical clues described above that suggests the presence of renovascular disease. (See "Clinical features, diagnosis, and treatment of hypertensive nephrosclerosis".)

Atheroembolic kidney disease can be precipitated by aortic manipulation or can occur spontaneously. It can generally be distinguished from bilateral renal artery stenosis or nephrosclerosis by an abrupt decline in kidney function, evidence of extrarenal emboli (manifested by digital gangrene, livedo reticularis, or abdominal pain), and the transient presence of hypocomplementemia, eosinophilia, and/or eosinophiluria. Arteriography is contraindicated in this setting since there is a high risk of inducing further embolization. (See "Clinical presentation, evaluation, and treatment of renal atheroemboli" and "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

TREATMENT — Once a presumptive diagnosis of ischemic nephropathy is made, the management issues are as follows:

All patients should receive medical therapy to control their hypertension in addition to routine CKD care and surveillance. Since these individuals have atherosclerotic cardiovascular disease, they should also be aggressively treated for secondary prevention of cardiovascular morbidity with aspirin, statins, cessation of smoking, and, in patients with diabetes, glycemic control. (See "Overview of the management of chronic kidney disease in adults" and "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)

In addition to medical therapy and risk factor reduction, some but not all patients should undergo revascularization, depending upon the hemodynamic severity and likely recoverability of kidney function, as discussed above (usually achieved with percutaneous transluminal renal angioplasty plus a stent or, in selected patients, with surgery). This issue and the corresponding treatment recommendations are discussed elsewhere in detail. (See "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney", section on 'Treatment'.)

Results from studies of selected patients with ischemic nephropathy subjected to revascularization suggest that 25 to 30 percent will recover kidney function to a meaningful degree, sometimes avoiding progression to end-stage kidney disease (ESKD) and/or the need for kidney replacement therapy. Approximately 50 percent will have little immediate change in kidney function but will "stabilize," whereas approximately 20 percent will have a progressive deterioration of kidney function, sometimes related to the procedure [2]. Prospective trials such as CORAL reported fewer complications in experienced centers (2 to 5 percent) than previously reported (9 percent) [8]. (See "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney", section on 'Treatment'.)

SUMMARY AND RECOMMENDATIONS

Many but not all patients with atherosclerotic renal artery stenosis have chronic kidney disease (CKD) that is primarily due to a reduction in blood flow induced by the stenosis. In general, clinically apparent or progressive CKD (marked by an increase in the serum creatinine) occurs when the stenosis threatens the entire kidney mass. Hence, patients with CKD resulting from atherosclerotic renal artery stenosis usually have high-grade stenosis of both renal arteries or stenosis to a solitary functioning kidney. However, renal artery stenosis may be an "incidental" finding in patients who have CKD that is caused by a separate disorder (eg, diabetic nephropathy). It can be difficult to distinguish between patients whose disease is induced by renal artery stenosis and those who have an alternative cause of CKD. (See 'Introduction' above.)

CKD that results from atherosclerotic renal artery stenosis is frequently called ischemic nephropathy. Broadly speaking, "ischemic nephropathy" can refer to a reduction in glomerular filtration rate (GFR) produced by any cause of diminished renal blood flow. However, the term ischemic nephropathy is most commonly applied in patients who have CKD due to partial or complete obstruction of one or more extrarenal arteries, usually in patients with atherosclerotic disease. (See 'Definition and terminology' above.)

Despite a moderate reduction in renal perfusion pressure (up to 40 percent) and in renal blood flow (mean 30 percent), glomerular filtration is reduced but tissue oxygenation within the kidney cortex and medulla can adapt without the development of severe hypoxia. However, more advanced vascular occlusion, corresponding to a 70 to 80 percent narrowing of the renal artery, leads to demonstrable cortical hypoxia. In animal studies, this tissue hypoxia produces rarefaction of microvessels, as well as activation of inflammatory and oxidative pathways that lead to interstitial fibrosis. Although vascular occlusion can initiate these processes, long-standing parenchymal injury characterized by inflammation and fibrosis eventually becomes an irreversible process. (See 'Pathogenesis' above.)

Patients with ischemic nephropathy typically present as follows (see 'Clinical manifestations' above):

A persistent and progressive reduction in GFR (ie, CKD).

Lack of evidence supporting an alternative cause of kidney disease, such as an abnormal urinalysis, proteinuria, a paraprotein, or use of a nephrotoxic drug.

Findings that suggest the presence of renovascular disease (table 1), for example: severe hypertension that may be treatment resistant, an acute rise in serum creatinine following the administration of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), significant variability of serum creatinine concentration that may be due to changes in volume status, recurrent episodes of flash pulmonary edema and/or refractory heart failure, and deterioration of kidney function after placement of an endovascular aortic stent graft.

In addition, risk factors for atherosclerotic disease are often present, such as hyperlipidemia, cigarette smoking, and age greater than 50 years. Patients with ischemic nephropathy frequently have coronary artery disease or peripheral arterial disease in other vascular beds.

In patients with clinical manifestations of ischemic nephropathy, a presumptive diagnosis of ischemic nephropathy can be made if there is radiologic documentation of significant stenosis of both renal arteries or of one renal artery to a solitary functioning kidney. As a practical matter, there are two diagnostic elements to consider in patients who could have ischemic nephropathy; these diagnostic elements can impact treatment decisions (see 'Diagnosis' above):

Is the vascular occlusive disease posing critical hemodynamic limitation to kidney function? In general, luminal occlusion of at least 60 to 75 percent is required to limit blood flow and reduce perfusion pressure. This degree of stenosis is usually associated with a measurable translesional pressure gradient of 10 to 15 mmHg. Doppler ultrasound criteria conventionally require peak systolic velocities above 180 to 200 cm/sec to identify more than 60 percent luminal occlusion that is verified by pressure gradients.

Is the condition of the kidneys such that restoring renal blood flow is likely to benefit function? The condition of the kidneys can be assessed by considering the renal resistive index, the six-month trajectory of kidney function, and the size of the kidneys, or by performing a kidney biopsy (which is not usually done). None of these factors predict the outcome of revascularization with certainty.

A definitive diagnosis is not usually made. In practice, confirmation of the diagnosis is based upon stabilization or improvement of the GFR after successful revascularization. (See 'Diagnosis' above.)

Patients at risk for bilateral renal artery stenosis are also at risk for other disorders that can present with similar clinical findings but cannot be corrected by surgery or angioplasty, including hypertensive nephrosclerosis and atheroembolic kidney disease. (See 'Differential diagnosis' above.)

Once a presumptive diagnosis of ischemic nephropathy is made, patients should receive medical therapy to control their hypertension in addition to routine CKD care and surveillance. Since these individuals have atherosclerotic cardiovascular disease, they should also be aggressively treated for secondary prevention of cardiovascular morbidity with aspirin, statins, cessation of smoking, and, in patients with diabetes, glycemic control. In addition to medical therapy and risk factor reduction, some but not all patients should undergo revascularization (usually achieved with percutaneous transluminal renal angioplasty plus a stent or, in selected patients, with surgery). This issue and the corresponding treatment recommendations are discussed elsewhere in detail. (See 'Treatment' above and "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney", section on 'Treatment'.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Lionel U Mailloux, MD, FACP, who contributed to an earlier version of this topic review.

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Topic 3841 Version 20.0

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