Page 703 - Textbook of Pathology, 6th Edition

2. ENDOCRINE HYPERTENSION. A number of hormonal 687
secretions may produce secondary hypertension. These are:
i) Adrenal gland—e.g. in primary aldosteronism, Cushing’s
syndrome, adrenal virilism and pheochromocytoma.
ii) Parathyroid gland—e.g. hypercalcaemia in hyperpara-
thyroidism.
iii) Oral contraceptives—Oestrogen component in the oral
contraceptives stimulates hepatic synthesis of renin substrate.

3. COARCTATION OF AORTA. Coarctation of the aorta
causes systolic hypertension in the upper part of the body
due to constriction itself (Chapter 15). Diastolic hypertension
results from changes in circulation.
4. NEUROGENIC. Psychogenic, polyneuritis, increased
intracranial pressure and section of spinal cord are all
uncommon causes of secondary hypertension.

EFFECTS OF HYPERTENSION

Systemic hypertension causes major effects in three main
organs—heart and its blood vessels, nervous system, and
kidneys. The renal effects in the form of benign and malignant
nephrosclerosis are discussed below, whereas hypertensive
effects on other organs are described elsewhere in the
respective chapters. An important and early clinical marker
for renal injury from hypertension and risk factor for CHAPTER 22
cardiovascular disease is macroalbuminuria (i.e. albuminuria
> 150 mg/day or random urine albumin/creatinine ratio of
>300 mg/gm creatinine), or microalbuminuria estimated by
radioimmunoassay (i.e. microalbumin 30-300 mg/day or
random urine microalbumin/creatinine ratio of
30-300 mg/gm creatinine).
Figure 22.34 The renin-angiotensin mechanism.
Benign Nephrosclerosis
i) Control of blood pressure by altering plasma concen- Benign nephrosclerosis is the term used to describe the
tration of angiotensin II and aldosterone. kidney of benign phase of hypertension. Mild benign
ii) Regulation of sodium and water content. nephrosclerosis is the most common form of renal disease in
iii) Regulation of potassium balance. persons over 60 years of age but its severity increases in the
The renin-angiotensin mechanism is summarised in presence of hypertension and diabetes mellitus. The Kidney and Lower Urinary Tract
Fig. 22.34.
b) Sodium and water retention. Blood volume and cardiac MORPHOLOGIC FEATURES. Grossly, both the kidneys
output, both of which have a bearing on blood pressure, are are affected equally and are reduced in size and weight,
regulated by blood levels of sodium which is significant for often weighing about 100 gm or less. The capsule is often
maintaining extracellular fluid volume. Blood concentration adherent to the cortical surface. The surface of the kidney
of sodium is regulated by 3 mechanisms: is finely granular and shows V-shaped areas of scarring.*
i) Release of aldosterone from activation of renin-angiotensin The cut surface shows firm kidney and narrowed cortex
system, as already explained. (Fig. 22.35).
ii) Reduction in GFR due to reduced blood flow as occurs in Microscopically, there are primarily diffuse vascular
reduced renal mass or renal artery stenosis. This results in changes which produce parenchymal changes secondarily
proximal tubular reabsorption of sodium.
iii) Release of atriopeptin hormone from atria of the heart in
response to volume expansion. These peptides cause *The various acquired causes of ‘small contracted kidney’ and their
increased GFR and inhibit sodium reabsorption. characteristic gross macroscopic appearance may be recollected here.
These are: 1. Chronic GN (granular appearance); 2. Chronic pyelonephritis
c) Release of vasodepressor material. A number of vaso- (U-shaped scars); and 3. Benign nephrosclerosis (V-shaped scars).
depressor materials and antihypertensives counterbalance Although granular, U- and V-shaped scars correspond to the respective
the vasopressor effect of angiotensin II. These substances macroscopic patterns, acronym to remember is: ‘granular’ for glomerular
scars of chronic GN; ‘U-scars’ for uneven scars of chronic pyelonephritis;
include: prostaglandins (PGE2, PGF2, PGA or medullin) and ‘V-scars’ for vascular scars of benign nephrosclerosis. Less common
released from interstitial cells of the medulla, urinary causes are: amyloidosis of the kidney, myeloma kidney and diabetic
kallikrein-kinin system and platelet-activating factor. nephropathy.