michigan hypertension core curriculum - State of Michigan

~70 hours) will function down to a EGFR in the mid 30’s ml/min/1.73m 2 . As with all thiazide diuretics,
dosing is once daily.
Plan: Taper off the beta blocker over the next few weeks as there is no absolute medical indication
for the use of a beta blocker. Begin lisinopril 20 mg qd (indicated because EGFR 30%) would lead us to reduce the dose of the ACE-I or, possibly, discontinue the ACE-I. In this
scenario, evaluation for bilateral renal artery stenosis, which is a contraindication to the use of ACE-I
or ARB’s, should be undertaken. Furthermore, we must keep in mind that the rise in creatinine is likely
secondary to the significant drop in her BP and/or overdiuresis (due to the diuretic). Lisinopril may
also be contributing to the rise in creatinine. In the setting of reduced nephron mass/reduced kidney
function, the local intra-renal RAS system is activated. This results in efferent > afferent glomerular
arteriolar dilation. When indicated RAS blockade is initiated, this may result in a global reduction in
GFR that is detectable with a rise in creatinine. This is partly how RAS blockers protect the kidney.
Over the long-term the creatinine may stay above baseline, return to baseline, or sometimes even
fall below baseline levels. A marked drop in BP in patients with CKD, even without the use of RAS
blockade, is commonly followed by a rise, a least transiently, in the serum creatinine level because
of impaired renal autoregulation that has become more dependent on systemic pressure levels to
maintain glomerular filtration, at least over the short-term.
Case 10
Ms. LN returns 4 weeks after addition of an ACE-I and diuretic, and is symptomatic. What may be
causing these symptoms, and how would you handle?
Ms. LN is complaining of fatigue and generalized weakness. She denies any headaches or
lightheadedness. Currently her BP is 130/78 mm Hg seated and 126/76 mm Hg standing
with a pulse rate of 64 beats/minute.
NKFM & MDCH 279