Chapter 125 - Renovascular disease introduction Flashcards
Rate of atherosclerotic renal artery stenosis in elderly
7%
Etiology of renal artery stenosis
1) atherosclerosis
2) FMD
3) dissection
4) aneurysm
5) trauma
6) arteritis
7) developmental abnormalities
Primary importance of renal vascular disease
1) hypertension
2) loss of renal function
Discovery of Renin
19th century
Tigerstedt, Bergman isolated from rabbit kidney
Goldblatt 1930 landmark experiment
HTN from RAS can be reversed by removing ipsilateral kidney
Leadbetter 1938 on renal artery stenosis
normalized BP after removing ectopic kidney in child with severe HTN
Freeman 1954 on renal artery stenosis
Successful renal artery reconstruction in someone with bilateral ostial stenosis
HTN normalized
Ischemic nephropathy definition
Renal insufficiency from RAS or occlusion
Wake Forest study on RAS reconstruction mortality
30 day mortality 4.6%
7% in ones with ischemic nephropathy
NIS data on renal bypass mortality
10%
Improvements in BP following renal bypass
85% improved
15% no better or worse
Post-op marker for improved dialysis free survival
eGFR stability or improvement
RCT on renal artery stenting
1) ASTRAL
2) CORAL
Characteristic of atherosclerotic RVD
1) most severe at renal ostia
2) contiguous with sheet of aortic plaque
Characteristic of FMD PVD
1) main artery and branches away from ostia
2) web-like stenosis (string of beads)
3) in children it’s mostly intimal fibroplasia subtype (no string of beads)
Pathophysiology of renovascular HTN
1) flow limiting RAS –> pressure drop
2) juxtaglomerular cells release renin
3) Angiotensinogen converted to angiotensin I
4) angiotensin I converted to Angiotensin II by ACE in pulmonary circulation
5) Ang II = peripheral vasoconstruction and blood volume expansion
Effects of angiotensin II
1) activates vasoconstriction and mitogenic response
2) forms reactive oxygen species that inactivate NO
cross talk with GF to amplify smooth muscle cell vasoconstrictor and proliferative signaling pathways
3) Upregulate NE and endothelin 1
4) renal tubules for Na and H2O reabsorption
5) adrenal release of aldosterone –> Na reabsorption
6) vasopressin release of pituitary
Non-RAAS mediated renovascular HTN
Chronic structural changes with hypertrophic remodelling
Goldblatt volume-dependent renovascular HTN
Patients with bilateral RAS or RAS in solitary kidney that cannot compensate to volume expansion
Risk factors for ischemic nephropathy
1) HTN
2) diabetes
3) atherosclerosis
4) dyslipidemia
5) smoking
Prevalence of RAS in at risk individual
7%
1/8 has bilateral disease
6% < 55 years old
40% > 75 years old
Association with RVD in presence of other stenotic arterial beds
CAD - 22%
Carotid - 27%
PAD - 40%
Anatomic progression of RAS in 3 years
43% progression, 7% occlude
How much renal function loss before creatinine rise
50%
Other measures of renal function
kidney length
Rate of progression to dialysis in RAS in 3-4 years
7-12%
Differential diagnosis in patients with renovascular HTN
1) essential HTN
2) glomerulonephritis
3) nephrotic syndrome
4) primary aldosteronism
5) cushing
6) pheochromocytoma
7) carcinoid
8) hyperthyroidism
9) coarctation of the aorta
10) sleep apnea
11) increased intracranial pressure
12) volume overload
Spontaneous hypokalemia or severe hypokalemia after diuretics suggests this disease
Conn syndrome
hyperaldosteronism
Diseases that may be associated with pheochromocytoma
1) MEN2
2) neurofibromatosis type 1
3) von Hippel-Lindau
Accuracy of US to detect RAS
> 90%
Critical stenosis of RAS defined as
PSV > 200 cm/s in main renal artery
equals > 60% stenosis
RAR = renal artery PSV / aortic PSV
significant if > 3.5
Blunted waveform with delayed systolic upstroke in RAS US
> 100 ms suggest RAS
PPV 97%; low sensitivity
Resistive index in RAS US
normal < 0.7
>0.8 critical RAS
How much more radiation does a CTA do compared to CXR
87-260 times more
How much contrast used in CTA of renal
120-140 ml
FDA black box warning on gadolinium
Not use in eGFR < 30 unless absolutely necessary
Access site bleeding for DSA for renal artery based on CORAL study
13%
Radionuclide renography key points
1) quantify uptake and excretion of radiolabeled molecules (Tc 99m-mercaptoacetyltriglycine)
2) ACEi renography (captopril renography) to unmask intrinsic renal compensation to RAS
3) diseased kidney will show decline in excretion of radiolabel; normal kidney will show increase GFR and more excertion
4) less accurate in patients with azotemia or small kidneys
Renal vein renin assay key points
1) start with low-sodium diet and stop antiHTN meds except diuretic and CCB 5 days before
2) furosemid given evening prior 40 mg
3) bedrest 4 hours prior to study
4) sample from renal veins and IVC as control
1.5 times higher renin considered positive
Medical management of RAS
1) statins
2) improve cardiovascular risks
3) ACEi and ARBs
4) diuretics
5) CCB
6) beta blockers
Patency of open repair in RAS
better than endo
> 90%
Restenosis of RAS after stenting
> 10%
Factors to lower threshold for RAS revascularization
1) children with severe RVD
2) FMD complicated by HTN
3) failure of conservative mgnt with ongoing eGFR reduction and HTN problem
4) hypertensive crisis
