Page 704 - Textbook of Pathology, 6th Edition

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Figure 22.35 Small, contracted kidney in chronic hypertension
(benign nephrosclerosis). The kidney is small and contracted. The capsule
is adherent to the cortex and has granular depressed scars on the surface.

as a result of ischaemia. The histologic changes are, thus, and have finely granular surface. However, the kidneys
described as vascular and parenchymal (Fig. 22.36,A): of a patient who develops malignant hypertension in pure
i) Vascular changes: Changes in blood vessels involve form are enlarged, oedematous and have petechial
arterioles and arteries up to the size of arcuate arteries. haemorrhages on the surface producing so called ‘flea-
There are 2 types of changes in these blood vessels: bitten kidney’.* Cut surface shows red and yellow mottled
a) Hyaline arteriolosclerosis that results in homogeneous appearance (Fig. 22.37).
and eosinophilic thickening of the wall of small blood Microscopically, most commonly the changes are
vessels. superimposed on benign nephrosclerosis. These changes
b) lntimal thickening due to proliferation of smooth muscle are as under (Fig. 22.36,B):
SECTION III
cells in the intima. i) Vascular changes: These are more severe and involve
ii) Parenchymal changes: As a consequence of ischaemia, the arterioles. The two characteristic vascular changes seen
there is variable degree of atrophy of parenchyma. This are as under:
includes: glomerular shrinkage, deposition of collagen in a) Necrotising arteriolitis develops on hyaline arterio-
Bowman’s space, periglomerular fibrosis, tubular atrophy losclerosis. The vessel wall shows fibrinoid necrosis, a few
and fine interstitial fibrosis. acute inflammatory cells and small haemorrhages.
b) Hyperplastic intimal sclerosis or onionskin proliferation is
CLINICAL FEATURES. There is variable elevation of the characterised by concentric laminae of proliferated smooth
blood pressure with headache, dizziness, palpitation and muscle cells, collagen and basement membranes.
nervousness. Eye ground changes may be found but ii) Ischaemic changes: The effects of vascular narrowing
papilloedema is absent. Renal function tests and urine on the parenchyma include tubular loss, fine interstitial
Systemic Pathology
examination are normal in early stage. In long-standing cases, fibrosis and foci of infarction necrosis.
there may be mild proteinuria with some hyaline or granular
casts. Rarely, renal failure and uraemia may occur. CLINICAL FEATURES. The patients of malignant
nephrosclerosis have malignant or accelerated hypertension
Malignant Nephrosclerosis with blood pressure of 200/140 mmHg or higher. Headache,
dizziness and impaired vision are commonly found. The
Malignant nephrosclerosis is the form of renal disease that presence of papilloedema distinguishes malignant from
occurs in malignant or accelerated hypertension. Malignant benign phase of hypertension. The urine frequently shows
nephrosclerosis is uncommon and usually occurs as a haematuria and proteinuria. Renal function tests show
superimposed complication in 5% cases of pre-existing deterioration during the course of the illness. Azotaemia
benign essential hypertension or in those having secondary (high BUN and serum creatinine) and uraemia develop soon
hypertension with identifiable cause such as in chronic renal if malignant hypertension is not treated aggressively.
diseases. However, the pure form of disease also occurs, Approximately 90% of patients die within one year from
particularly at younger age with preponderance in males. causes such as uraemia, congestive heart failure and
cerebrovascular accidents.
MORPHOLOGIC FEATURES. Grossly, the appearance
of the kidney varies. In a case of malignant hypertension
superimposed on pre-existing benign nephrosclerosis, the *Recall the other causes of flea-bitten kidney: acute post-streptococcal GN,
kidneys are small in size, shrunken and reduced in weight rapidly progressive GN, haemolytic-uraemic syndrome, thrombotic
thrombocytopenic purpura and Henoch-Schonlein purpura.