Xn are cholesterol-filled, soft, yellowish plaques that often seen on the medial aspect of the eyelid that mostly observed in middle-aged & elderly.
Xanthelasma (Xn)
Xn are cholesterol-filled, soft, yellowish
plaques that often seen on the medial aspect of the eyelid
that mostly observed in middle-aged & elderly.
Xn are
usual associates with hypercholesterolemia
(Hc), so we should obtain a lipid profile if
ptn has not already received. Dyslipidemia can be observed in almost 50 % of adults with
Xn.
Xn are
a classic feature of primary biliary cholangitis,
a condition that usually associated with severe Hc.
Xn are
common in ptns with primary aberrations
of low-density lipoprotein (LDL) cholesterol metabolism
(e.g., familial Hc, hyperapobetalipoproteinemia). The
observation of Xn
in young subjects, particularly children,
should alert the physician the presence of an underlying inherited dyslipidemia. Ptns with a normal lipid profile, an associated Xn & atherosclerosis (AT) cannot be explained. Some reports have
found lipoprotein abnormalities other
than Hc that may augment the risk of CAD (coronary
heart disease) (e.g., low HDL (high-density
lipoprotein cholesterol) in ptns with Xn. Xn plaques often do not need ttt. Lipid-lowering agents
may induce regression of Xn in some ptns, but the effect is not
consistent. Surgical removal,
CO2 laser
therapy, or topical
trichloroacetic acid (TCA) can be applied for cosmetic appearance, but recurrent Xn is
commonly observed.
Atherosclerotic
Renal Artery Stenosis (RAS).
Frequent but not all ptns with atherosclerotic RAS
show CKD that’s primarily due
to reduced renal blood flow (RBF) induced by the stenosis. Generally, clinical progression of CKD (increasing SCr)
observed if the stenosis affects the whole renal
mass. So, ptns with CKD due
to AT-RAS
usually exhibit bilateral high-grade
stenosis of renal arteries or stenosed vessels of a single functioning
kidney. However, RAS may be an "incidental"
finding in CKD ptn induced separately
(e.g., by diabetic nephropathy). It is difficult to DD between disease induced
by RAS and
those related to other causes of CKD.
CKD caused
by atherosclerotic RAS is commonly called ischemic
nephropathy (IN). Generally, “IN
" may refer to a reduced GFR owing
to any cause inducing reduction in RBF.
However, this term is mostly applied to ptns having CKD
related to partial/complete obstruction of one or more extra-renal arteries, often with AT disease. Despite a moderate reduction in
renal perfusion pressure (up to 40 %) and in RBF (mean
30 %), GFR is reduced but tissue
oxygenation within renal cortex &
medulla can adapt with no development
of severe hypoxia. However, more intense
vascular occlusion, up to 70-80 % occlusion
of renal artery, will lead to evident cortical hypoxia. In animal reports, tissue
hypoxia may induce rarefaction of microvessels
with activation of inflammatory & oxidative
pathways that ultimately lead to interstitial fibrosis.
Long-lasting lesions , however, with inflammation & fibrosis became irreversible.
Ptns with ischemic nephropathy typically present as follows:
1) Persistent
& progressive reduced GFR (i.e., CKD).
2) Absence
of any evidence related to an alternative etiology of renal disease, e.g., abnormal
urinalysis, proteinuria, paraprotein, or nephrotoxic agent.
3) Findings
in favor of reno-vascular disease:
1. Severe
refractory HT,
2. Sudden
rise in SCr after ACEi/ARBs,
3. significantly
variable SCr
due to volume status alterations,
4. Episodic
flash pulmonary edema and/or
refractory HF &
5. Deteriorated
renal function after placing endovascular aortic
stent graft.
4) Risk factors for AT usually present, e.g., hyperlipidemia, smoking
& age > 50. Ptns with IN frequently have CAD or PVD.
Ptns with clinical suspicious of IN, a presumptive Dgx can be made if via radiologic document
of significantly stenosed both renal arteries and one of them to a single functioning
kidney. There’re 2 diagnostic criteria
to that can impact ttt decisions:
·
Presence of critical hemodynamic limitation to renal function?
Generally, luminal occlusion = 60-75 % is needed to impede blood flow & limit perfusion power. Degree of stenosis is
seen with a trans-lesional pressure gradient of 10-15 mmHg. Doppler US criteria needs
peak systolic velocity > 180-200 cm/sec to identify > 60 % luminal occlusion detected
by pressure gradient.
·
Current renal function such that
restored RBF
is likely to improve function? Condition of the kidneys can be evaluated
by recognizing:
1) Renal resistive index,
2) 6-mo serial renal function,
3) Size
of the kidneys, or by
4) Perform
kidney biopsy
(not common).
- None
of these parameters may predict the precise outcome of revascularization.
Final Dgx is not usually
established. Confirmed Dgx is relied primarily upon stabilized/improved GFR
after successful revascularization. Ptns
with risk of bilateral RAS are also at risk for many disorders with similar clinical findings but cannot be managed
by surgery/angioplasty,
e.g., HT nephrosclerosis & atheroembolic
renal disease. Once a presumptive Dgx of IN
is established, ptns should commence medical ttt to manage HT & the routine CKD care.
Since these ptns have AT CVS disease,
they should be aggressively ttt for secondary prevention of CVS with aspirin, statin, smoking cessation, and, in diabetics, glycemic control. Adding to medical therapy &
risk factor control, some but not all ptns
should proceed to revascularization (via percutaneous transluminal renal angioplasty + stenting or, in selected ptns, via surgical interference).
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