Workup and Management of Atrophic Left Kidney
An atrophic kidney (<9 cm in length or >1.5 cm size discrepancy between kidneys) warrants immediate diagnostic evaluation for renal artery stenosis (RAS), particularly when accompanied by hypertension, as this represents a potentially reversible cause of both kidney atrophy and blood pressure elevation. 1
Initial Diagnostic Evaluation
Clinical Clues Requiring Investigation
The presence of an unexplained atrophic kidney or discrepancy in kidney size >1.5 cm is a Class I indication (Level of Evidence B) for performing diagnostic studies to identify clinically significant RAS 1. This evaluation becomes particularly urgent when accompanied by:
- Resistant hypertension (failure to achieve goal BP on 3 drugs including a diuretic) 1
- Accelerated or malignant hypertension with end-organ damage 1
- New azotemia or worsening renal function after ACE inhibitor or ARB administration 1
- Sudden unexplained pulmonary edema, especially in azotemic patients 1
Excluding Secondary Causes
Before attributing atrophy to RAS, exclude other causes through careful history 1:
- Prior pyelonephritis or reflux nephropathy - these typically have documented history
- Trauma - obtain detailed past medical history
- Congenital hypoplasia - may present with chronic symptoms 2
- Chronic obstruction - assess for ureteropelvic junction obstruction or stones 2
When such alternative explanations exist with clear documentation, additional diagnostic testing for RAS is not indicated 1.
Diagnostic Workup Strategy
Imaging Studies
Renal artery imaging is the cornerstone of evaluation for atrophic kidney with suspected RAS 1. The choice depends on institutional expertise and patient factors:
- CT angiography or MR angiography - non-invasive first-line options for anatomic assessment
- Renal duplex ultrasonography - operator-dependent but radiation-free
- Conventional angiography - gold standard when intervention is planned 1
Functional Assessment
Quantitative renal function testing is essential to determine if the atrophic kidney contributes meaningfully to overall renal function 3:
- Renal scintigraphy (MAG3 scan) - determines split renal function; kidneys contributing <10% of total function are generally considered non-salvageable 3
- Serum creatinine and eGFR - establish baseline renal function 1
- Urinalysis and urine albumin-to-creatinine ratio - assess for proteinuria and active sediment 1
Endocrine Evaluation
Selective renal vein renin sampling is critical for determining the pathophysiologic contribution of the atrophic kidney to hypertension 3, 4:
- Renal vein renin ratio >1.5 (affected/contralateral kidney) predicts favorable response to intervention 3, 4
- This test identifies patients most likely to benefit from nephrectomy when revascularization is not feasible 3, 4
- In one series, 26 of 31 patients (84%) with renin ratio >1.5 achieved normalization of BP after nephrectomy 4
Management Algorithm
Decision Framework Based on Function and Anatomy
For kidneys contributing >10% of total renal function with significant RAS (>70% stenosis):
- Endovascular revascularization is the preferred approach 3
- Expected outcomes: SBP reduction of ~26 mmHg, DBP reduction of ~14 mmHg without significant renal function deterioration 3
- This preserves nephron mass and avoids the renal function decline associated with nephrectomy 3
For kidneys contributing <10% of total renal function with renin ratio >1.5:
- Nephrectomy should be considered for refractory hypertension 3, 4
- Expected outcomes: SBP reduction of ~40 mmHg, DBP reduction of ~19 mmHg 3
- Critical caveat: Expect postoperative GFR decline of ~13 mL/min, which may exceed the predicted loss based on preoperative scintigraphy 3
- The functional threshold of 10% may be lowered to 5% in carefully selected cases to minimize postoperative renal function loss 3
For kidneys with <10% function but renin ratio <1.5:
- Medical management is preferred as nephrectomy unlikely to improve BP control 3
- Optimize antihypertensive regimen with multiple agents including diuretics 1
Special Considerations for ACE Inhibitors/ARBs
Exercise extreme caution with renin-angiotensin system blockade in patients with suspected bilateral RAS or stenosis to a solitary functioning kidney 1:
- These agents can precipitate acute renal failure by decreasing transglomerular hydrostatic pressure 1
- The mechanism involves efferent arteriolar dilation, reducing filtration fraction and shunting blood from afferent to efferent arterioles 1
- New azotemia after ACE inhibitor/ARB initiation is itself a Class I indication for RAS evaluation 1
Surgical Revascularization
When endovascular approaches fail or are not feasible, open surgical revascularization remains an option for select patients 1:
- Aortorenal bypass is most common, preferably using reversed saphenous vein 1
- Consider in younger patients or those with complex anatomy unsuitable for endovascular therapy 1
- Secondary nephrectomy is reserved for failed revascularization attempts when re-revascularization is not possible 1
Common Pitfalls to Avoid
Do not assume all small kidneys require intervention - document chronicity and exclude benign causes before pursuing invasive workup 1
Do not perform nephrectomy without renin sampling - functional assessment prevents unnecessary surgery in patients whose hypertension is unrelated to the atrophic kidney 3, 4
Do not overlook the risk of post-nephrectomy renal insufficiency - the actual GFR decline often exceeds predictions from preoperative scintigraphy 3
Do not start ACE inhibitors/ARBs empirically in patients with suspected bilateral disease or atrophic solitary kidney without first excluding hemodynamically significant RAS 1
Left-sided predominance exists - left renal atrophy is significantly more common (1.3%) than right (0.2%), possibly due to aortic pressure-induced flow disorders, left renal vein compression by splenomegaly, or anatomical factors 5