Renal and Mesenteric Flashcards
(156 cards)
Clinical Criteria for Renal Vascular Hypertension and Ischemic Nephropathy
Clinical Criteria for Renal Vascular Hypertension and Ischemic Nephropathy
Clinical Criteria for Diagnosis of Renal Vascular Hypertension
Recent onset
Resistant to drug treatment (difficult to control)
Retinopathy and end organ damage greater than for equivalent essential hypertension
Kidney dysfunction
Recurrent flash pulmonary edema
Continuous abdominal bruit
History of smoking
Other vascular disease
Clinical Criteria for Diagnosis of Ischemic Nephropathy
No intrinsic kidney disease
Recent-onset azotemia
Progressive azotemia
Hypertension
Other vascular disease
Smoking
Unequal kidney size
Anatomic Criteria for Diagnosis of Hemodynamically Significant Renal Artery Stenosis
Stenosis ≥70% diameter (∼85% cross-sectional area)
Post-stenotic dilatation
Collateral circulation
Reduced kidney size
•
Absolute length discrepancy ≥1.5 cm
•
Documented length decrease ≥1cm
Criteria for Renal Artery Intervention
Criteria for Intervention
Clinical Criteria for Ischemic Nephropathy and Renal Vascular Hypertension
Chronic progressive renal insufficiency: SCr ≥2.7 mg/dL
Drug resistance (five medications) and accelerated hypertension
Anatomic Criteria (by MRA and DSA) for Hemodynamically Significant Renal Artery Stenosis
≥80% right renal artery stenosis
≥90% left renal artery stenosis
Atrophic left kidney
Physiologic Criterion (Selective Right Renal Artery and Aortic Pressure Measurements) for Hemodynamically Significant Renal Artery Stenosis
≥25% mean arterial right renal artery pressure gradient
DSA, Digital subtraction angiography; MRA, magnetic resonance arteriography; SCr, serum creatinine.
Factor most important in predicting preservation of renal function
GFR
Those data that do show a benefit in preserving renal function also show that the groups most likely to benefit from intervention are those with stages 3A and 3B dysfunction (GFR 45-59 and 30-44). Those presenting with lower GFRs tended to progress to end-stage renal disease regardless of treatment, suggesting that the kidney is already injured beyond the point of retrieval. The degree of renal artery stenosis, patient age, preprocedural blood pressure control or number of required antihypertensive medications have not been shown to directly play a role in determining appropriate patients for intervention.
First line therapy fro treatment of renal FMD
Balloon angioplasty alone is considered to be the first line approach to renal FMD.
Indications for renal artery aneurysm intervention
- 3cm
- symptomatic
- All sizes in:
- women of child bearing age
- refractory HTN and renal artery stenosis
Diagnosis of renal vein thrombosis
CTV
Treatment of renal vein thrombosis
The treatment of renal vein thrombosis is initially anticoagulation. Unfractionated heparin followed by warfarin therapy has long been the standard. Treatment lengths vary but generally a 6-month course of anticoagulation is recommended. Thrombectomy (catheter-directed or open) or thrombolysis should be reserved for select situations, such as a threatened kidney in a young patient with acute renal failure, failure or complication of oral anticoagulation, or thrombosis of a solitary kidney with associated acute renal failure. Nephrectomy is reserved for cases of post-infarction hemorrhage. Thrombolysis typically requires both venous and arterial access. The venous access is to lyse the main renal vein and its branches, whereas the arterial catheter to drip thrombolysis agents into the renal parenchyma to clear intra-parenchymal thrombus.
Management of renal artery dissection
Spontaneous isolated renal artery dissection is rare and only represents one fourth of all renal artery dissections. There is predominance in males of 4:1. The mean age is 40 to 50 years. The presence of hypertension suggests renal ischemia and the presence of flank pain, hematuria and proteinuria suggests renal infarction. The extent of the dissection determines the optimal treatment approach. Endovascular treatment is avoided when there is branch involvement, but may be performed for focal main renal artery dissections. Renal artery bypass is utilized when there is a chance to salvage the kidney. Approaches such as in-situ repair, auto-transplantation and ex-vivo surgery may be performed for renal branch involvement. Nephrectomy is required when there is uncontrolled hypertension in the setting of irreversible renal ischemia and extensive dissection into the renal artery branches.
Narrowed Aorto-mesenteric angle is found in?
Discussion
The patient’s symptoms of painless bilious emesis after an episode of weight loss are consistent with superior mesenteric artery (SMA) syndrome. SMA syndrome tends to affect young women with a lean body type between the ages of 10 and 39 years of age. The SMA branches from the aorta at an acute angle behind the pancreas. The aorto-mesenteric space contains retroperitoneal fat, the uncinate process of the pancreas, lymphatics, third portion of duodenum and left renal vein. The adipose tissue is felt to displace the SMA anteriorly to allow for the duodenum to cross through the window without extrinsic compression. Episodes of significant weight loss are felt to reduce the adipose tissue in this space resulting in a reduction of the aorto-mesenteric angle that results in the SMA compressing on the third portion of the duodenum causing a functional obstruction. Stenosis of the SMA might result in mesenteric ischemia which is typically painful and does not improve with jejunal feeding. The celiac artery with the configuration of the J-hook is consistent with celiac artery compression; however, the hallmark of the median arcuate ligament syndrome, the clinical syndrome associated with celiac artery compression is post-prandial abdominal pain. The patient in question has painless emesis. The replaced right hepatic artery is merely an anatomic variant of the mesenteric anatomy that is important to know, but does not typically result in symptoms. Left renal vein stenosis can occur in this setting, however, patients tend to present with flank pain and hematuria.
Treatment of mesenteric vasospasm?
Vasospasm in the distribution of the SMA is the cause of nonocclusive mesenteric ischemia (NOMI). The excessive sympathetic activity that occurs during cardiogenic shock or hypovolemia, helps to maintain cardiac and cerebral perfusion at the expense of mesenteric blood flow. The treatment of NOMI is supportive therapies aimed at improving volume status and cardiac output. In some cases, intra-arterial infusion of vasodilators, especially the phosphodiesterase inhibitor papaverine at a dose of 30 to 60 mg/h, into the SMA may be employed. Operative exploration may be required if peritonitis ensues, as this may indicate presence of gangrenous bowel requiring resection.
Duplex criteria for mesenteric artery stenosis
The criteria of a PSV of greater than 200 cm/sec in the celiac artery and greater than 275 cm/sec in the superior mesenteric artery are the most accurate criteria to indicate a stenosis of 70% or greater, with a 92% sensitivity and 96% specificity as well a positive predictive value of 80% and a negative predictive value of 99%. The Bowersox criteria uses an EDV of 45cm/sec or greater to identify a stenosis in the superior mesenteric artery of more than 50%. This has a 91% specificity and 90% positive predictive value. For the celiac artery, reversed flow in the branched arteries is diagnostic of occlusion In combination with an elevated PSV in the superior mesenteric artery in a patient with abdominal pain, the diagnosis of chronic mesenteric ischemia should be considered.
How many patients have bilateral RAS? Have complete occlusion?
12%
12%
What is the natural hx of RAS?
3 years
about 8% of normal and 40% subcritical blockage progress to >60% stenosis
7% of >60% progressed to occluded
>60% will have decline in renal function, decrease renal size
10% progress to dialysis in 4 years
What factors are associated with progression?
age, high SBP, smoking, female, poorly controlled HTN
What is the pathogenesis of RAS?
athero 80%
FMD 15%
dissection 1%
How dose RAS cause HTN?
renal blood flow reduced, juxtaglomerular cells convert prorenin into renin and secrete into circulation.
renin converts angiotensinogen to angiotensin I then to angiotensis II by ACE.
AII causes blood vessel constriction and HTN. also secretes aldosterone which causes renal tubules to reabsorb NA and water into the blood (volume expansion).
What are the clinical presentations of RAS?
50% have no symptoms
ARF when starting ACEi if bilat RAS
HTN crisis
flash pulmonary edema
What blood work can support RAS?
urea and cr may be elevated
strain pattern on EKG
LVH
elevated plasmin renin
What findings on duplex can support RAS?
critical stenosis = peak systolic velocity in main RA >1.8-2.9 m/sec with post stenotic turbulence >60%
ratio renal artery to aortic peak systolic >3.5 =60%
blunted waveforms with delayed systolic upstroke are indicative of a proximal stenosis
acceleration time >100msec indicates critical stenosis within prox renal artery
resistive index
peak sys gel-end diastolic velocity/peak sys vel
>0.8 may be critical RAS
what is medical management in RAS?
ACEi-first line/ARB
then CCB/BB
statin (decrease risk of progression)
RF modification
What are indications for revascularization if RAS asymptomatic? (AHA)
IIb percutaneous
if bilat or solitary kidney and hemo signify RAS
What are indications for revasc in HTN? (AHA)
IIa
perc
hemo signif RAS, accelerated HTN, resistant HTN, malignant HTN, unexplained unilateral kidney and HTN with med intolerance
What are indications for revasc in renal dysfunction? (AHA)
IIa
progressive kidney disease and bilat or solitary kidney
IIB
chronic renal insuff and unilat RAS
