Hypertention

Dr. Mojgan Mortazavi

NephrologistIsfahan 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

HyperuricemiaErythropoietin administrationParathyroid hormone secretion/increased intracellular calcium/hype rcalcemiaRenal vascular disease and renal arterial stenosisAldosterone-induced fibrosis and sodium retention

Advanced glycation end productsChronic allograft dysfunctionCadaver allografts, especially from a donor with a family history of hypertensionImmunosuppressive and corticosteroid therapyHeritable 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 lipid-lowering 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.

• Thin section, toluidine blue stain shows the characteristic cholesterol clefts of an atheroembolus in the small renal artery. Courtesy of Helmut Rennke, MD.

Renal atheroembolus

                                            

• 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.

Blue toe syndrome

                                                                

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

HistoryOnset of hypertension before age 30 in women with no family history (fibromuscular dysplasia)Abrupt onset or worsening of hypertensionSevere or resistant hypertensionSymptoms of atherosclerotic disease elsewhereSmokerWorsening renal function with ACE inhibition or All receptor blockadeRecurrent flash pulmonary edema

ExaminationAbdominal bruitsOther bruitsAdvanced hypertensive retinopathy

LaboratorySecondary aldosteronism

Higher plasma reninLow serum potassium

Proteinuria, usually moderateElevated serum creatinine>1.5cm difference in kidney size on sonographyCortical atrophy on CT angiography

Additional Features

• 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).