Transcript Document

Hypertention
Dr. Mojgan Mortazavi
Nephrologist
Isfahan university of medical sciences
Renal Parenchymal Hypertension
• Renal parenchymal diseases are the most common secondary or reversible
cause of hypertension and their incidence will continue to increase as the
population grows older and fatter
CHRONIC KIDNEY DISEASE
• Of the various discernable primary causes of ESRD among patients starting
dialysis in the United States, diabetic nephropathy is the most common,
comprising about 40%, followed by vascular diseases, including hypertensive
nephrosclerosis (20%), primary glomerular disease (18%), tubulointerstitial
diseases (7%), and cystic diseases (5%)
Practical Solutions
• First, increase the performance of spot urine testing for albuminuria and
estimated glomerular filtration rate (eGFR) from a serum creatinine (Lee et
al., 2009).
• Second, encourage primary caregivers to treat those with stage 1 or 2 disease
more intensely. There are not enough nephrologists to care even for those
with stage 3 disease, which is the level of CKD that is now the criterion for
referral to a nephrologist.
The Role of Hypertension
• Hypertension accelerates the progression of renal damage, regardless of the cause.
• In patients with CKD, ambulatory BP monitoring, which often identifies a loss of
nocturnal dipping, is better than office readings in predicting progression of renal
damage and mortality
• Outof-office BP measurements in patients with CKD are also critical to identify the
considerable proportion with white-coat hypertension, 32% in one series (Minutolo
et al., 2007a), to avoid unnecessary and potentially harmful overtreatment.
Mechanisms
TABLE 9.3 Features Associated with High Blood Pressure in Chronic Kidney Disease
Preexisting primary (essential) hypertension
Extracellular fluid volume expansion
Arterial stiffness
Renin-angiotensin-aldosterone system stimulation
Increased sympathetic activity
Endothelin
Low birth weight with reduced nephron number
Decrease in vasodilatory prostaglandins
Obesity and insulin resistance
Sleep apnea
Smoking
Mechanisms
Hyperuricemia
Erythropoietin administration
Parathyroid hormone secretion/increased intracellular calcium/hype rcalcemia
Renal vascular disease and renal arterial stenosis
Aldosterone-induced fibrosis and sodium retention
Advanced glycation end products
Chronic allograft dysfunction
Cadaver allografts, especially from a donor with a family history of hypertension
Immunosuppressive and corticosteroid therapy
Heritable factors
Proteinuria
• The degree of proteinuria serves as a strong predictor of the rate of
progression of CKD
Management
• Reduction of BP and proteinuria has been clearly shown to slow the rate of
progression of CKD
An algorithm for treating patients with CKD.
Lifestyle Changes
• All hypertensives with or without CKD, with or without diabetes, should be
intensively encouraged to change their unhealthy lifestyles and given as much
help as possible to achieve these changes.
• Cessation of smoking is paramount, since smoking is a major risk for
progression of CKD
• Sodium reduction to the range of 1 to 2 g per day
• Weight reduction: Obese hypertensive people are now likely to develop CKD
• Glycemic control: If only they could lose their excess weight, most type 2
diabetics would likely avoid their subsequent risk of CKD.
Renin-Angiotensin System (RAS) Inhibitors
• Both ACEIs and ARBs reduce proteinuria and slow the progression of CKD
equally
• The renoprotective effect has been shown in CKD caused by diabetes
nondiabetic disease and in patients with polycystic disease
• Despite their benefits, neither ACEIs nor ARBs have been found to reduce
all-cause mortality, in patients with CKD
Diuretics
• In practice, thiazides diuretics in usual doses (12.5 to 50 mg) are usually not
adequate when eGFR falls to below 50 mL per minute per 1.73 m2
• Fortunately, loop diuretics can be safely given at high enough doses to cross
the secretory barrier and exert a diuresis, even with much lower eGFR.
Aldosterone Blockers
• Aldosterone is now recognized to be an accelerator of renal damage by
stimulating inflammation and fibrosis
• When an aldosterone blocker is added to an ACEI or ARB in CKD patients,
proteinuria decreases from the level achieved by the RAS inhibitor by 15% to
54% and a significant fall in BP occurs in 40% of the patients (Bomback et
al., 2008
Calcium Channel Blockers
• In conclusion, non-DHP-CCBs may be preferable to DHP-CCBs but either
type of CCB can safely and effectively be used when added to an ACEI or
ARB in patients with CKD
β-Blockers
• β-blockers should be used only for secondary prevention of cardiac
problems, e.g., post-MI, CHF, or tachyarrhythmias.
• The α/β agents carvedilol and labetalol will cause less metabolic mischief
than a β-blocker, and carvedilol has been shown to reduce proteinuria in
CKD patients (Bakris et al., 2006).
Minoxidil
• In the past, those with refractory hypertension and CKD were successfully
treated with minoxidil (Toto et al., 1995). However, when added to a regimen
that included maximal doses of an ACEI or ARB, proteinuria increases,
despite the lower BP (Diskin et al., 2006).
Timing of Therapy
• The potential for additional adverse effects of the persistently elevated
nocturnal BP, i.e., nondipping, that is frequently present in patients with
CKD has prompted studies comparing a shift in the timing of
antihypertensive drug intake from morning to evening.
Restriction of Dietary Protein
• A protein-restricted diet has been recommended for predialysis patients
Correction of Anemia
• Anemia is a risk factor for progression of CKD and left ventricular
hypertrophy (Rossing et al., 2004). However, treatment with erythropoietin
to achieve a hemoglobin level above 12 g/L has been found to increase
serious adverse events, so the current recommendations are to maintain a
level of 11 g/L (Moist et al., 2008
Lipid-Lowering Agents
• In view of the common presence of dyslipidemia in CKD patients and the
high rate of atherosclerotic vascular disease they suffer, the use of lipidlowering agents seems appropriate.
Renovascular Hypertension
Fibromuscular Dysplasia
Aneurysm
• Aneurysms are common with medial fibroplasia. Saccular aneurysms, usually
at the bifurcation of the renal artery, may induce hypertension by various
mechanisms. They rarely rupture and need not be ablated if less than 2.0 cm
in diameter in the absence of symptoms or severe hypertension (English et
al., 2004).
Emboli
• Most commonly seen as a complication of angiography or vascular surgery,
renal cholesterol emboli can induce renal failure or RVHT (Scolari et al.,
2007). Cutaneous, ocular, and other visceral lesions are usually seen, and the
diagnosis may be documented by biopsy of skin lesions.
Renal atheroembolus
• Thin section, toluidine blue stain shows the characteristic
cholesterol clefts of an atheroembolus in the small renal artery.
Courtesy of Helmut Rennke, MD.
Blue toe syndrome
• Blue toes are a classic manifestation of peripheral embolization of atheromatous
material from proximal arterial sources (eg, aorta); the pedal pulses are often normal.
This patient, who has a 30-year history of type 1 diabetes and severe peripheral
vascular disease, presented with foot pain and discoloration. Cholesterol microemboli
from the aorta were suspected to be the cause. Reproduced with permission from
Lawrence B Stack, MD. Copyright © Lawrence B Stack, MD.
Livedo reticularis
• Patient with livedo
reticularis (manifested by a
reddish-cyanotic, reticular
pattern of the skin) which
has resulted in ulcer
formation (arrows). Courtesy
of Samuel Moschella, MD.
Hollenhorst plaque (cholesterol cyrstal,
arrow) in retinal artery
• Reproduced with permission
from: Digital Reference of
Opthalmology, Edward S.
Harkness Eye Institute,
Columbia University, NY.
Arteritis
• Progressive aortic arteritis (Takayasu arteritis or pulseless disease) is seen infrequently in
North America and Europe but is a common cause of RVHT in China, India, Japan,
Mexico, and Brazil (Weaver et al., 2004). It is seen mainly in children and young adults and is
often associated with signs of chronic inflammation (Cakar et al., 2008).
• RVHT is common in various vasculitic syndromes with renal involvement, including
Wegener granulomatosis (Woodrow et al., 1990), systemic lupus erythematosus (Ward &
Studenski, 1992), and the antiphospholipid syndrome (Riccialdelli et al., 2001). These
patients may enter into an acute, severe hypertensive phase, usually associated with markedly
elevated plasma renin levels, likely reflecting intrarenal stenosis from multiple arteriolar
lesions. The hypertension can sometimes be rather remarkably reversed by ACEI therapy
Aortic Dissection
• RVHT was found in nearly 20% of patients with aortic dissection (Rackson
et al., 1990).
CLINICAL FEATURES
History
Onset of hypertension before age 30 in women with no family history (fibromuscular dysplasia)
Abrupt onset or worsening of hypertension
Severe or resistant hypertension
Symptoms of atherosclerotic disease elsewhere
Smoker
Worsening renal function with ACE inhibition or All receptor blockade
Recurrent flash pulmonary edema
Examination
Abdominal bruits
Other bruits
Advanced hypertensive retinopathy
Laboratory
Secondary aldosteronism
Higher plasma renin
Low serum potassium
Proteinuria, usually moderate
Elevated serum creatinine
>1.5cm difference in kidney size on sonography
Cortical atrophy on CT angiography
Additional Features
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Hyperaldosteronism
Nephrotic Syndrome
Polycythemia
Dyslipidemia
Cortical Atrophy
Ischemic Nephropathy
The possibility of bilateral renovascular disease should be
considered in the following groups (Chonchol & Linas, 2006):
• Young women with severe hypertension, in whom fibroplastic disease is common.
• Older patients with extensive atherosclerotic disease who suddenly have a worsening
of renal function.
• Azotemic hypertensives who develop multiple episodes of acute pulmonary edema.
• Any hypertensive who develops rapidly progressive renal failure without evidence
of obstructive uropathy.
• Patients in whom renal function quickly deteriorates after treatment with an ACEI,
ARB, or DRI.
THERAPY
• Medical Therapy
• As these data reconfirm, careful monitoring of renal function is mandatory
in patients who are either known to have renovascular disease or who are
more likely to have renovascular, i.e., when an ACEI, an ARB, is started.
• If the serum creatinine rises beyond 30% of baseline, the reninangiotensin
inhibitor should be stopped and revascularization considered (Cohen &
Townsend, 2008).
Angioplasty
• After at least 1-year follow-up, there were no differences in BP, changes in
serum creatinine, rates of acute renal failure, or cardiovascular events
between the revascularized or the medically treated halves.
The Choice of Therapy
• Patients with fibroplastic disease do better than do those with atherosclerotic disease
when treated medically or by revascularization (Slovut & Olin, 2004). Their better
response likely reflects their younger age, less prolonged hypertension, and less
atherosclerosis in other organs. Those who do not respond well to medical therapy
should have percutaneous transluminal angioplasty (PTA), usually without a stent.
Angioplasty cures or improves 70% to 90% (Slovut & Olin, 2004).
• For atherosclerotic RVHT, medical therapy, usually with an ACEI or ARB and often
with a calcium channel blocker, may be effective over many years (Hackam et al.,
2007).
The Choice of Therapy
• Angioplasty with a stent should be performed in patients who do not tolerate or
respond to medical therapy or who have progressive renal impairment (Textor,
2008).
• Surgical revascularization is much less commonly indicated, except when angioplasty
with stenting is not feasible or is unsuccessful or when abdominal vascular surgery is
required.
• Revascularization or angioplasty may be indicated for ischemic nephropathy, more
to preserve renal function than to control hypertension (Levin et al., 2007).