michigan hypertension core curriculum - State of Michigan

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