17

17 CASE 17


A 60-year-old woman being treated for hypertension returns to her physician’s office for treatment.


The patient is a smoker (45 packs/year) and social drinker and walks for exercise three times per week. She reports that her calves begin to ache 15 minutes after exercise but the pain quickly resolves when exercise stops. Past radiologic studies identified cholelithiasis, which was treated by laparoscopic surgery. Radiologic findings included an abnormal finding of an asymmetric right kidney.



PHYSICAL EXAMINATION



VS: T 37.2°C, P 70/min, R 20/min, BP 180/120 mm Hg, weight 135 lb, BMI 22

PE: Patient does not exhibit distress. She has a raspy voice due to smoking. During physical examination, the aorta is palpated superior to the navel. The patient has abnormalities of the optic fundi showing hypertensive retinopathy. She has been treated in the past for hypertension and is currently experiencing intolerance to her angiotensin I converting enzyme (ACE) inhibitor.


LABORATORY STUDIES



Abdominal ultrasound: No abdominal aortic aneurysm

Renal artery ultrasonography: Decreased size of the left kidney, increase in blood flow velocity at the left proximal renal artery, and decreased blood flow through the left renal artery

Renal arteriography: Stenosis of the left renal artery


DIAGNOSIS


Renal artery stenosis



PATHOPHYSIOLOGY OF KEY SYMPTOMS


The kidneys are a major determinant of arterial blood pressure through the regulation of body fluid volume. This regulation is evidenced by both pressure diuresis and pressure natriuresis, where a decrease in renal perfusion pressure results in the retention of both sodium and water (Fig. 17-1).


image

FIGURE 17–1 Analysis of arterial pressure regulation by equating the “renal output curve” with the “salt and water intake curve.” The equilibrium point describes the level to which the arterial pressure will be regulated.


Glomerular capillary blood pressure is determined in part by the aortic pressure and by the preglomerular vascular resistance. The preglomerular vascular resistance is predominantly at the afferent arteriole; however, a constriction in any vessel between the heart and the glomerular capillaries is also characterized as a preglomerular vascular resistance.


A stenosis in the renal artery introduces a preglomerular vascular resistance and decreases glomerular capillary pressure. The decrease in glomerular capillary pressure results in the fall in glomerular filtration rate and the shift toward retention of sodium and water. Retention of water and sodium causes an increase in systemic arterial blood pressure; and as soon as the blood pressure is sufficiently high, glomerular capillary pressure returns to normal. In this instance, sodium and water are in balance but only because the patient is hypertensive. For example, aortic stenosis above the origin of the renal arteries will result in hypertension but aortic stenosis below the origin of the renal arteries will not cause hypertension (Fig. 17-2).


image

FIGURE 17–2 Effect of placing a constricting clamp on the renal artery of one kidney after the other kidney has been removed. Note the changes in systemic arterial pressure, renal artery pressure distal to the clamp, and rate of renin secretion. The resulting hypertension is called “one-kidney” Goldblatt hypertension.

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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 17

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