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HYPERTENSIVE NEPHROSCLEROSIS

Systemic hypertension causes permanent damage to the kidneys in about 6% of patients with elevated blood pressure. As many as 27% of patients with end-stage kidney disease have hypertension as a primary cause. Although there is not a clear correlation between the extent or duration of hypertension and the risk of end-organ damage, hypertensive nephrosclerosis is fivefold more frequent in African Americans than whites. Risk alleles associated with APOL1, a functional gene for apolipoprotein L1 expressed in podocytes, substantially explains the increased burden of ESRD among African Americans. Associated risk factors for progression to end-stage kidney disease include increased age, male gender, race, smoking, hypercholesterolemia, duration of hypertension, low birth weight, and preexisting renal injury. Kidney biopsies in patients with hypertension, microhematuria, and moderate proteinuria demonstrate arteriolosclerosis, chronic nephrosclerosis, and interstitial fibrosis in the absence of immune deposits (see Fig. A3-21). Today, based on a careful history, physical examination, urinalysis, and some serologic testing, the diagnosis of chronic nephrosclerosis is usually inferred without a biopsy. Recent studies suggest, in the absence of diabetes, adults with hypertension and cardiovascular risk factors benefit from achieving a systolic BP <120 mmHg compared to <140 mmHg. In the presence of kidney disease, most patients begin antihypertensive therapy with two drugs, classically a thiazide diuretic and an ACE inhibitor; most will require three drugs. There is strong evidence in African Americans with hypertensive nephrosclerosis that therapy initiated with an ACE inhibitor can slow the rate of decline in renal function independent of effects on systemic blood pressure. Malignant acceleration of hypertension complicates the course of chronic nephrosclerosis, particularly in the setting of scleroderma or cocaine use (see Fig. A3-24). The hemodynamic stress of malignant hypertension leads to fibrinoid necrosis of small blood vessels, thrombotic microangiography, a nephritic urinalysis, and acute renal failure. In the setting of renal failure, chest pain, or papilledema, the condition is treated as a hypertensive emergency.

Aging patients with clinical complications from atherosclerosis sometimes shower cholesterol crystals into the circulation—either spontaneously or, more commonly, following an endovascular procedure with manipulation of the aorta—or with use of systemic anticoagulation. Spontaneous emboli may shower acutely or shower subacutely and somewhat more silently. Irregular emboli trapped in the microcirculation produce ischemic damage that induces an inflammatory reaction. Depending on the location of the atherosclerotic plaques releasing these cholesterol fragments, one may see cerebral transient ischemic attacks; livedo reticularis in the lower extremities; Hollenhorst plaques in the retina with visual field cuts; necrosis of the toes; and acute glomerular capillary injury leading to FSGS sometimes associated with hematuria, mild proteinuria, and loss of renal function, which typically progresses over a few years. Occasional patients have fever, eosinophilia, or eosinophiluria. A skin biopsy of an involved area may be diagnostic. Since tissue fixation dissolves the cholesterol, one typically sees only residual, biconvex clefts in involved vessels (see Fig. A3-22). There is no therapy to reverse embolic occlusions, and steroids do not help. Controlling blood pressure and lipids and cessation of smoking are usually recommended for prevention.

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= elevated blood pressure (>130/85).

You have different classifications:
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(elevated, stage 1, stage 2)

Different causes:
- primary/essential hypertension (85%) --> unknown cause, but risk factors (Genetic component, obesity, alcohol/sodium intake, diabetes)

- secondary hypertension (15%) --> mostly due to underlying disease (cardiovascular, cushing syndrome, diabetic nephropathy)

- White coat = when people go to the hospital and get scared, there BP increases

- Masked hypertension --> out of office constantly hypertension, but when you measure in hospital there is normal BP (snapshot)

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- formula:

Every changes in pressure can be related back to the formula. If you have more blood flow --> higher BP. If the diameter decreases --> BP increases
If the viscocity increases --> BP increases

Baroreceptors are located in the carotid and the aortic arch --> sense BP changes and send signals to the brain (neural mediation)

RAAS --> hormonal mediation
- We will now focus on the kidneys with the RAAS system
Summary: RAAS is activated when renal perfusion pressure goes down (sensed in the glomerulas; juxtaglomerular apparatus). When there is a decrease in pressure, prorenin --> renin. Renin catalyzes angiotensin 1 formation. Angiotesin 1 is converted into angiotensin 2 by ACE enzyme (in the lung capillaries). Aldosterone is then produced in the adrenal cortex. It acts on the principal cells of the distal tubule/collecting duct.  Angiotensin 2 itself causes vasoconstriction and stimulation of thirst in the hypothalamus. Aldosterone increases sodium and water reabsorption to increase BP again

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(systemic)
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Black africans have a higher risk of hypertension

Different organ systems that can be targeted by hypertension:

- Vasculature: artherosclerose (this also causes for it to sustain hypertension; loop)

- Kidney: haemoturia, proteinuria,
However, kidney can be either the effect of cause of hypertension.
Less nephrons --> less filtration --> hypertension

- Heart: thicker peripheral arteries, lower compliance, also LV hypertrophy (cardiac failure), MI, pulmonary oedema

- Brain: in the small vessels there might be an infarct (lacunae); increase risk of dementia/stroke

- Eyes: will show hypertensive retina; microdamages to the vessels in the eye.

(if you receive a kidney from someone with hypertension, you will also get hypertension)

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Changes in kidneys:
- damage to small blood vessels
- pretty common in secondary hypertension
- due to artherosclerosis/fibromuscular dysplasia (can be both result and cause)

Ofcourse, RAAS is very important in the mediation of BP in the kidney.

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-  hypertension is often asymptomatic
- risk factors (overweight, old age, male)
- symptoms: headaches, nocturnia, bleeding nose
- Cholesterol, lipidemia

Measure BP:
- patient at rest (15min sitting)
- cuff size
- arm should be supported
- 2 consistent measurements (Average)
--> ambulatory/home monitoring (can exclude white coat measurments)

Cardiac examination:
- LV hypertrophy
- sinus tachycardia
- extra aortic sounds

Measure severity:
- Level of BP
- Target organs (eyes, heart, kidneys)

Underlying causes:
- primary vs secondary
-  History (stroke, MI, etc.)

Lab tests:
- creatinine, sodium, potassium
- urine stick --> protein/blood in urine might indicate glomerular damage. (can also be kidney stone)
- White blood cell count for infections
- Creatinine also indicates GFR (elevated is bad)
- D-dimer for occlusion of renal artery

(hypertension due to decrease in renal perfusion)

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Treatment (image Marisela; stepwise plan)

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Treatment (image Marisela; stepwise plan)

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Goal is to keep BP as steady as possible to prevent target organ damage

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- assessment, risk factors, severity

-  if BP is not too high, aim to reasses per few months e.g.
-  target (130/80)

- non pharmocological treatment: lifestyle changes (diet, alcohol, activity)

Pharmacological treatment:
- ACEi and AR antagosist main treatment for young patients

- BetaBlockers main for older patients

- Diuretics: Thiazide (inhibit co-transportation of Na/CL-). Loop diuretics (not used as much). Potassium-sparing diuretics are used if hypokalemia is present (spirolactolone)

-  RAAS: ACEi, angiotensin antagonsist, ARB

- alpha adrenergic blockers (sympathetic nervous system), Betablockers (reducing cardiac output), Calcium blockers (decrease heart rate)

Prognosis:
- depends on risk factors, severity, target organ damage, age, etc.