THE KIDNEY_4

BY DR.VENUGOPAL RAO
L.S

UROLITHIASIS
(RENAL
STONE,CALCULI)

1.

The calculi can arise at any level in the

urinary tract, frequently causing clinical
symptoms including obstruction ,
and
pain.
Theyulceration,bleeding
also predispose to renal
infection
There are 4 types of renal calculi and organic
matrix of mucoprotein.
About 70% of stones are calcium oxalate plus/
minus calcium phosphate. The calcium
containing stones are usually associated with
hypercalcaemia/hypercalciuria,hyperoxaluria
and hyperuricosuria are associated with
others.

2.About 15-20% are so called triple phosphate /

struvitestones composed of magnesium ammonium
phosphate.it is due to urea splitting bacteria that
convert urea to ammonia
3.5-10% are uric acid stones
4. 1-2% are made up of cystine.

Types of stones

1.
2.
3.

Calcium oxalate and

phosphate
Idiopathic
hypercalciuria(50%)
Hypercalciuria and
hypercalcaemia(10%)
Hyperoxaluria(5%)
Magnesium ammonium
phosphate(struvite)
Uric acid
cystine

percentage
70%

15-20%
5-10%
1-2%

pathogenesis
Increase

concentration of some
constituents, changes in urinary
PH,decreased urine volume and bacteria
all play a role in stone formation.
The loss of inhibitors of crystal
formation(eg;citrate,pyrophosphate,glycos
aminoglycans,osteopontin and an alpha
glycoprotein called nephrocalcin) may play
a pathogenic role in such cases.

nephrolithiasis

DISEASES OF RENAL BLOOD

VESSELS

1.
2.
3.
4.
5.
6.

These include
Benign nephrosclerosis
Malignant nephrosclerosis
Renal artery stenosis
Thrombotic microangiopathies
Atheroembolic renal diseases
Renal infarcts

BENIGN NEPHROSCLEROSIS;
1.

2.

3.

Benign nephrosclerosis, the term used for the

renal changes in benign hypertension, is always
associated with hyaline arteriolosclerosis.
The frequency and severity of the lesions are
increased at any age when hypertension or
diabetes mellitus are present.
It should be remembered that many renal
diseases cause hypertension, which in turn is
associated with benign nephrosclerosis.

1.

2.

3.

4.

5.

Morphology :Grossly, the kidneys are symmetrically atrophic,

each weighing 110 to 130 gm, with a surface of diffuse, fine
granularity that resembles grain leather.
MICROSCOPICALLY, the basic anatomic change is hyaline
thickening of the walls of the small arteries and arterioles, known as
hyaline arteriolosclerosis.
This appears as a homogeneous, pink hyaline thickening, at the
expense of the vessel lumina, with loss of underlying cellular detail.
The narrowing of the lumen results in markedly decreased blood
flow through the affected vessels and thus produces ischemia in the
organ served.
All structures of the kidney show ischemic atrophy. In advanced
cases of benign nephrosclerosis the glomerular tufts may become
globally sclerosed.
Diffuse tubular atrophy and interstitial fibrosis are present. Often
there is a scant interstitial lymphocytic infiltrate. The larger blood
vessels (interlobar and arcuate arteries) show reduplication of
internal elastic lamina along with fibrous thickening of the media
(fibroelastic hyperplasia) and the subintima

Clinical;This renal lesion alone rarely

causes severe damage to the kidney
except in susceptible populations, such as
African Americans, where it may lead to
uremia and death.
However, all persons with this lesion
usually show some functional impairment,
such as loss of concentrating ability or a
variably diminished GFR. A mild degree of
proteinuria is a frequent finding

Granular cortical appearance

of kidney

HYALINE
ARTERIOSCLEROSIS

MALIGNANT HYPERTENSION AND

MALIGNANT NEPHROSCLEROSIS ;
1.

2.

Malignant hypertension is far less common in the United States

than benign hypertension and occurs in only about 5% of persons
with elevated blood pressure. It may arise de novo (i.e., without
preexisting hypertension), or it may appear suddenly in a person
who had mild hypertension. In less developed countries, it occurs
more commonly.
Pathogenesis; the following sequence of events is suggested.
The initial event seems to be some form of vascular damage to the
kidneys. This most commonly results from long-standing benign
hypertension, with eventual injury to the arteriolar walls.
The result is increased permeability of the small vessels to
fibrinogen and other plasma proteins, endothelial injury, and platelet
deposition. This leads to the appearance of fibrinoid necrosis of
arterioles and small arteries and intravascular thrombosis.

Mitogenic factors from platelets (e.g., platelet-derived growth factor)

and plasma cause intimal smooth hyperplasia of vessels, resulting
in the hyperplastic arteriolosclerosis typical of malignant
hypertension
The kidneys become markedly ischemic. With severe involvement
of the renal afferent arterioles, the renin-angiotensin system
receives a powerful stimulus, and indeed persons with malignant
hypertension have markedly elevated levels of plasma renin .
This then sets up a self-perpetuating cycle in which angiotensin II
causes intrarenal vasoconstriction, and the attendant renal ischemia
perpetuates renin secretion.
Aldosterone levels are also elevated, and salt retention
undoubtedly contributes to the elevation of blood pressure.
The consequences of the markedly elevated blood pressure on the
blood vessels throughout the body are known as malignant
arteriolosclerosis, and the renal disorder is referred to as
malignant nephrosclerosis


1.
2.

3.

4.

Morphology ;
The kidney may be essentially normal in size or slightly shrunken,
depending on the duration and severity of the hypertensive disease.
Small, pinpoint petechial hemorrhages may appear on the
cortical surface from rupture of arterioles or glomerular capillaries,
giving the kidney a peculiar, flea-bitten appearance.
The microscopic changes reflect the pathogenetic events described
earlier. Damage to the small vessels is manifested as fibrinoid
necrosis of the arterioles.
The vessel walls show a homogeneous, granular eosinophilic
appearance masking underlying detail. In the interlobular arteries
and larger arterioles, proliferation of intimal cells produces an
onion-skin appearance.

4 This name is derived from the concentric

arrangement of cells whose origin is
believed to be intimal smooth muscle.
5 This lesion, called hyperplastic
arteriolosclerosis, causes marked
narrowing of arterioles and small arteries,
to the point of total obliteration.


1.

2.

3.

4.

Clinical Course:
The full-blown syndrome of malignant hypertension is characterized
by diastolic pressures greater than 120 mm Hg, papilledema,
encephalopathy, cardiovascular abnormalities, and renal
failure.
Most often, the early symptoms are related to increased
intracranial pressure and include headache, nausea, vomiting,
and visual impairment, particularly the development of
scotomas, or spots before the eyes.
At the onset of rapidly mounting blood pressure there is marked
proteinuria and microscopic, or sometimes macroscopic, hematuria
but no significant alteration in renal function. Soon, however, renal
failure makes its appearance.
The syndrome is a true medical emergency that requires prompt
and aggressive antihypertensive therapy before irreversible renal
lesions develop.

A)FIBRINOID NECROSIS
B)ONION SKIN APPEARANCE

Thank you all