michigan hypertension core curriculum - State of Michigan
michigan hypertension core curriculum - State of Michigan
michigan hypertension core curriculum - State of Michigan
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ARAS, ischemic nephropathy, and improvement in renal function after revascularization.<br />
ARAS patients with renal dysfunction may have varying degrees <strong>of</strong> nephropathy and renal ischemia.<br />
Some studies showed improvement or stabilization <strong>of</strong> Scr after stenting in 22-68 % <strong>of</strong> patients 16,63 , in<br />
contrast to a consistent deterioration after medical therapy alone. 60,63 Several studies documented<br />
improvement in Scr and in the slope <strong>of</strong> reciprocal Scr after stenting, compatible with beneficial effects<br />
<strong>of</strong> revascularization on renal function (104-106). 101-103 In a contemporary prospective study, patients<br />
with documented severe ARAS were treated with aggressive anti-hypertensive therapy and risk factor<br />
modification according to current guidelines. Renal artery stenting was recommended for increasing<br />
Scr, decline in nuclear GFR, or malignant <strong>hypertension</strong>. Despite aggressive medical therapy for 21<br />
months, there was a 7% increase in Scr, a 15% decline in GFR, and 39% <strong>of</strong> patients developed<br />
worsening stenotic-kidney GFR. In contrast, renal stenting resulted in 13-19 % improvement in total-<br />
and single-kidney GFR 36 , similar to other studies. 38,39 Nevertheless 25-30 % have deterioration in renal<br />
function despite revascularization. The key observation in prior studies <strong>of</strong> ischemic nephropathy is the<br />
crucial importance <strong>of</strong> baseline renal function 71,104-108 : Baseline Scr > 1.5 mg/dL is the single strongest<br />
predictor <strong>of</strong> late death 66 look at, and the risk <strong>of</strong> renal failure rises 3-fold for each increment <strong>of</strong> 1.0 mg/dL<br />
in baseline Scr. 88-90<br />
Failure <strong>of</strong> renal revascularization to improve renal function. The explanations for failure to improve<br />
or stabilize renal function after revascularization are multifactorial (Table 8), including revascularization<br />
<strong>of</strong> patients without renal ischemia, insensitivity <strong>of</strong> the Scr to changes in GFR when < 50 % <strong>of</strong> renal<br />
mass is revascularized (e.g. unilateral ARAS) (Figure 7), failure to identify baseline nephropathy, and<br />
procedure-induced nephropathy.<br />
The causes <strong>of</strong> procedure-induced nephropathy after revascularization include acute tubular<br />
necrosis, contrast nephropathy, and renal embolization (Table 9). Acute tubular necrosis is usually due<br />
to acute blood loss, and is characterized by progressive rise in Scr, oliguria, and increased fractional<br />
sodium excretion. Contrast nephropathy is characterized by rising Scr 2-4 days after exposure, oliguria<br />
or normal urine output, and normal urinary sodium concentration. Distal embolization may not be<br />
recognized until the Scr rises days or weeks after discharge. Urinalysis and sodium excretion may<br />
be normal, although urine eosinophils may be present. The treatment for all three conditions includes<br />
correction <strong>of</strong> underlying volume depletion and maintenance <strong>of</strong> adequate hydration.<br />
ARAS and cardiovascular outcomes. Four-year survival rates are 57% and 89% for patients with and<br />
114 Hypertension Core Curriculum