Chapter 11 Diseases of Urinary System
OBSERVATIONAL METHODS OF SPECIMEN
The urinary system consists of the kidneys, the ureters, the urinary bladder and the
urethra.
Kidneys. The kidneys are a pair of bean-shaped, reddish-brown (gray-colored after
fixing) organs. The volume of normal kidney is about 11cm×6cm×3cm, weight
120g. The renal cortex is about 0.5cm in thickness, and the cut surface reveals a
clearly defined outer cortex and an inner medulla. Near the renal hilum are renal
pelvis and calyces, which are deerhorn-shaped and the mucosa is pale, smooth and
thin. The capacity of the renal pelvis is about 10 ml. When observing we should note:
①The shape, size, texture and surface color of the kidneys; ②Whether there is any
adhesion in the fibrous capsule; ③Whether the surface is smooth, or if it has any
nodes or depressions; ④whether the membrane thickened, the thickness of cortex and
whether the cortex and medulla are clearly defined; ⑤Whether there is focal
pathological change in the renal cortex and medulla, noticing the size, shape, color,
texture of the pathological change and the relationship to its surroundings; ⑥
Whether the renal pelvis is enlarged, whether there is foreign matter in the cavity of
renal pelvis, whether the mucosa is smooth (whether there is exudation) or thickened.
The glomerulus of a normal adult kidney is about 217μm in diameter, each having
48-100 nuclei (in children about 80). The afferent arteriole enters the glomerular tuft
and breaks into about 5-8 branches, which, in turn, branch into the anastomosing
capillary network of each of the eight glomerular lobules. The capillary network is
petaloid; the proximal convoluted tubule lies around the glomerulus and is lined by
single taper epithelial cells which are vague in border and cytoplasm acidophilic
(distal convoluted tubule weaker than it); the Bowman’s capsule is lined by capsular
squamous epithelial cells, and inner visceral epithelial cells which cover the external
surface of each glomerular capillary (that is podocyte); the renal interstitium consists
of connective tissue, capillary and vein. Note: ①Whether the capsule undergo
proliferation of connective tissue; ②The plentiful condition of glomerular capillary;
Whether the endothelium and the mesangial cells is swelling or proliferative, whether
inflammative cells infiltrating, basement membrane thickening, fibrous tissue
proliferating, adhesion between walls of Bowman’s capsule and renal glomerulus,
diffusive or segmental pathology; ③ Whether there is renal tubule epithelium’
degeneration, necrosis and unusual matter deposition in cavity of tubule; ④
Inflammative cells infiltrating and connective tissue proliferating; ⑤Tumor and other
changes.
Ureters. The ureters are about 20-30cm in length; 0.5-1.0cm in diameter. The wall
is thin. Note: ①Whether the cavity becomes enlarged or narrow, and whether there is
foreign matter; ② Whether mucosa is smooth (whether there is exudation); ③
Whether the wall becomes thin or thick; ④Whether there is focal pathological
change in the wall.
Urinary bladder. The urinary bladder is a hollow organ. There are many different
folds on the mucosa of its internal surface, but on the fundus of bladder there is a
smooth triangular area called the trigon of bladder. Note: ① Whether the mucosa is
smooth (whether hyperemia, hemorrhage, ulcer, neoplasm, exudation can be
observed); ②Whether the wall becomes thin or thick.
AIMS
1. To grasp the features of pathological changes and their relationship with clinical
manifestations of acute diffuse proliferative glomerulonephritis, crescentic
glomerulonephritis and chronic sclerosing glomerulonephritis.
2. To grasp the features of pathological changes, development and their relationship
with clinical manifestations of acute and chronic pyelonephritis.
3. To
understand
the
features
of
pathological
changes
of
membranous
glomerulonephritis and membranoproliferative glomerulone phritis.
4. To understand the knowledge about tumor of the kidney and the urinary bladder.
CONTENTS
Glomerulonephritis
Gross specimen
Tissue section
Acute diffuse proliferative GN
Acute diffuse proliferative GN
Crescentic GN
Crescentic GN
Chronic sclerosing GN
Chronic sclerosing GN
Membranous GN
Membranous GN
Membranoproliferative GN
Pyelonephritis
Tumor of kidney
Carcinoma of bladder
Acute pyelonephritis
Acute pyelonephritis
Chronic pyelonephritis
Chronic pyelonephritis
Renal cell carcinoma
Renal cell carcinoma
Nephroblastoma
Nephroblastoma
Carcinoma of bladder
Transitional cell carcinoma
KEY POINTS OF SPECIMEN OBSERVATION
1. Glomerulonephritis
(ⅰ) Acute diffuse proliferative glomerulonephritis
Basic pathologic changes
(1) Gross morphology
◆The
kidneys are swollen, with the fibrous capsule tense and smooth, which may
be congested, so that it is called big-red kidney; In some cases, there are many
scattered punctate hemorrhage on the surface, so that it is called louse-bitten
kidney;
◆The
cut surface reveals the thickened cortex and a clear border of cortex and a
medulla.
(2) Histopathology
◆Almost
◆The
all of the glomeruli are involved;
glomeruli are distended. Number of cell increases, which is due to the
proliferation and swelling of mesangial, endothelial and epithelial cells together
with a variable infiltration of neutrophils and monocytes. Some glomeruli may
show proliferation of cells lining Bowman’s capsule;
◆The
epithelial cells of the proximal convoluted tubule may show degenerative
changes and the tubules contain casts (such as hyaline ones, cellular ones and
granular ones);
◆
Interstitial hyperemia and edema with a variable infiltration of inflammatory
cells.
Specimen observation
Case abstract: A 8-year-old boy has suffered edema of eyelid and oliguria for 3
days.15 days ago, he suffered infection of the upper respiratory tract and had ache of
throat. Physical examination: blood pressure is17.3/12kPa; there are edema of eyelid,
hyperemia of throat and edema of both legs. Laboratory examination: urine: red blood
cell
(++),protein(+),red
blood
cell
cast
0-2/HP,uric
volume
450ml/24h,BUN21.2mmol/L(3.56-14.28mmol/L), creatinine 182µmol/L(44-132 μ
mol/L). B-ultrasonic examination: the kidneys are symmetrically swollen.
Gross specimen: (Fig. 11-01) Note:
1) Changes of the kidney volume;
2) Changes of color of the surface and cut surface;
3) Whether the cortex is thickened;
4) Whether there is a clear border between the cortex and medulla.
Tissue section: (Fig. 11-02a,b) Note:
1) Changes of the glomerular volume; whether there is increase in the number of
cells and which types they belong to;
2) Changes of tubular epithelial cells and what the tubule contains;
3) Changes of interstitium;
4) Which changes belong to alteration, exudation or proliferation?
Questions: What are the basic pathological changes of acute diffuse proliferative
glomerulonephritis? How to explain the acute glomerulonephritis syndrome in clinic
manifestation?
(ⅱ) Crescentic glomerulonephritis
Basic pathologic changes
(1) Gross morphology
◆
The kidneys are characteristically enlarged and pale;
◆
There are some petechiae in the cut surface of the cortex.
(2) Histopathology
Almost all of the glomeruli reveal formation of crescentic or annular body in
◆
the Bowman’s space;
Capsular epithelial proliferation admixed with monocytes results in the
◆
formation of capsular crescent. Some are cellular, some are cellular-fibrillar and
some are fibrillar;
◆Adhesions
of glomerular tufts to the capsule and obliteration of Bowman’s
space are common. Scaring of the glomerular tufts is striking, with few patent
capillaries remaining. Sometimes fibrosis and hyaline of some glomeruli are
seen;
◆The
tubular epithelial cells may show degenerative change and the tubules
contain cast. Some tubules show atrophy;
◆
Inflammation of lymphocyte and fibrosis proliferation can be seen in stroma.
Specimen observation
Case abstract: A 25-year-old woman has suffered edema, hematuria, oliguria for 15
days, nausea, and vomit for 3 days. Physical examination: blood pressure is
21.9/13.3kPa; he is pale complexion, and there are edema of face and both legs.
Laboratory examination: uric volume 150ml/24h, turbid, rusty, reddish brown urine,
uric protein (+++), red blood cell (+++), red blood cell cast 1-3/HP, creatinine
520µmol/L.B-ultrasonic examination: both kidneys are swollen.
Gross morphology: (Fig. 11-03) Note:
1) Changes of the kidney volume and color;
2) Changes of cortex thickness and color.
Tissue section: (Fig. 11-04a,b) Note:
1) Changes of the glomerulus, and which is the basic change;
2) Changes of the tubule and which cast is in the cavity;
3) Changes of interstitium;
4) Which changes belong to alteration, exudation or proliferation?
Questions: What is the pathological change of crescentic glomerulonephritis? Why
do these changes happen? What clinic features can be seen?
(ⅲ)Chronic sclerosing glomerulonephritis
Basic pathologic changes
(1)Gross morphology
◆The
kidneys are contracted symmetrically with a granular and pebbly surface,
lightweight and stiff texture, which is called secondary particulate contracted
kidney;
◆
The renal capsule is adherent to the surface of kidney; the border between cortex
and medulla is not clear;
◆
Adipose tissue increases near the renal pelvis.
(2)Histopathology
◆
Most of the glomeroli are fibrosis with hyalinization and renal tubules are
atrophy, fibrosis or disappear
◆
Some remaining nephrons enlarged compensatively, relevant tubules dilated and
all kinds of casts can be seen in the tubular cavity;
◆
The renal capsule is thickened; There is interstitial inflammation of connective
tissue, accompanying lymphocyte and plasma cells proliferation;
◆
Because of the interstitial fibrosis and atrophy, the involved glomeruli draw
closed and centralize, so it is called glomerular-massed phenomenon.
Specimen observation
Case abstract. A 45 year-old man has suffered edema repeatedly, proteinuria for 10
years, nausea, and vomit for 6 months, whose uric volume of nighttime are much
more than that of daytime. Physical examination: blood pressure is 21.8/12.6kPa;he is
pale complexion, and there are edema of face and both legs; the sphere of the heart is
enlarged
down
towards
left.
Laboratory
examination:
hemoglobin
60g/L
(120-160g/L),urine: granular cast 1-2/HP,protein (+),white blood cell 0-1/HP,uric
volume 2500ml/24h,SG 0.010,blood creatinine 650µmol/L.B-ultrasonic examination;
both kidneys are contracted symmetrically.
Gross specimen: (Fig. 11-05) Note:
1) Changes of uric volume and surface of kidneys;
2) The cut surface: thickness of renal cortices, whether the border between
cortex and medulla is clear and changes around renal pelvis.
Tissue section: (Fig. 11-06a,b) Note:
1) Pathological changes of nephron;
2) Changes of undamaged nephron;
3) Changes of interstitium and blood vessels.
Questions: What are the pathological changes of chronic sclerosing GN? Why does
the patient show chronic glomerulonephritis syndrome in clinic?
(ⅳ) Membranous glomerulonephritis
Basic pathologic changes
(1)Gross morphology
◆
The kidneys are slightly swollen, pale-colored, hence the use of the term
“large-white kidney”.
(2) Histopathology
◆
The basic change appears to be diffuse thickening of the GBM, forming the
spike-like projections (silver methenamine stain). Gradually the basement
membrane appears to be “worm-eaten”. Later in the disease, the narrowed
capillary cavity can be seen.
Specimen observation
Case abstract. A 46-year-old woman has suffered edema on face and both legs
accompanying with lumbago for 5 years. Laboratory examination: urine: protein
(+++), red blood cell 0-2/HP, protein cast 1-2/HP. Albumin 15g/L (36-50g/L), TC
350mg/dL (110-230mg/dL), B-ultrasonic examination: There is no obvious abnormity
in both kidney.
Gross specimen: (Fig. 11-07) Note the size and color of the kidney.
Tissue section: (Fig. 11-08) Note:
1) Changes of GBM and capillary;
2) Changes of tubules and interstitium.
Left: histological staining by sliver methenamine reveals minute “spikes” of
basement membrane. Right: PAS stain shows the pattern of “worm-eaten” of the
glomerualr basement membranes.
Questions: How do the pathological changes progress and what is the prognosis?
(ⅴ) Membranoproliferative glomerulonephritis
Basic pathologic changes
(1)Gross morphology
◆The
kidneys are swollen, pale-colored.
(2) Histopathology
◆
The glomeruli are distended, with the increase of cell.
◆There
is diffuse proliferation of mesangial cells and an increase in mesangial
matrix, causing the thickening of mesangium, exaggerating the lobular
architecture of the glomerulus.
◆
The basement membrane appears to be “double contours”(with silver
methenamine stain and PAS stain). Narrowed capillary cavity can be seen.
Specimen observation
Tissue section: (Fig. 11-09a, b) Note:
1) Changes of the glomerular volume, number of cells and capillary loops;
2) Changes of basement membrane and capillary cavity;
3) Changes of tubules and interstitium.
(a) The lobular architecture of the glomerulus is exaggerated. The mesangial
proliferate and the basement membrane reduplicate. The basement membrane appears
to be “double contours” (PAS stain). (b) Histological staining by sliver methenamine
reveals “double contours” of the glomerular basement membrane.
Questions: What is the clinical manifestation and prognosis of the disease?
2. Pyelonephritis
(ⅰ)Acute pyelonephritis
Basic pathologic changes
(1)Gross morphology
◆Pathological
◆The
changes may involve unilateral or bilateral kidneys;
affected kidney is enlarged and congested, with scattered raised,
yellowish-white abscesses on the renal surface surrounded by purplish-red
congestion zone;
◆Yellow
stripes can be seen in the medulla on the cut surface, which extending
to the cortex, and coalescing into abscesses;
◆There
are congestion and edema in the mucosa of renal pelvis, with scattered
punctate hemorrhage and purulent exudation.
(2) Histopathology
◆Renal
interstitial purulent inflammation or abscess formation, renal tubule
necrosis or degradation can be seen;
◆Ascending
infection firstly reaches the renal pelvis, characterized by
congestion and edema of the mucosa, with densely infiltration of neutrophils,
and then extends to renal tubule and the surrounding tissue, forming
abscesses;
◆The
minute abscesses are randomly distributed when the infection is
blood-borne.
Specimen observation
Case abstract: A 35-year-old woman has suffered chill, fever with urinary frequency,
urinary urgency and urodynia for 3 days. Physical examination: body temperature is
39℃, she has clear percussive pain in both kidney zones and tenderness in bladder
zone. Urine examination: white blood cell (+++), pus cell (++), protein (++), white
blood cell casts 0-3/HP, urinary culture: Bacillus coli growth.
Gross specimen: (Fig. 11-10a,b) Note:
1) Changes of volume and surface of kidney;
2) Changes of renal parenchyma on cut surface;
3) Changes of renal pelvis and calices mucosa;
Questions: Which type of infection does the specimen belong to?
Tissue section: (Fig. 11-11) Note:
1) Whether there is abscess in the renal parenchyma and the number of it;
2) Changes of the tissue surrounding the abscess;
3) Whether there is any exudation on the mucosa of renal pelvis and calices,
and which kind; changes of the mucous membrane;
4) Changes of renal interstitium;
5) Changes of renal tubules and glomeruli.
Questions: What clinical symptoms does the patient have?
(ⅱ) Chronic pyelonephritis
Basic pathologic changes
(1)Gross morphology
◆Pathological
◆Deep
changes may involve unilateral or bilateral kidneys;
irregular scars are observed, and the pathological changes are
asymmetrical if bilateral kidneys are involved;
◆The
border of cortex and medulla is not clearly defined on the cut surface,
accompanied by the contraction of renal papillae, deformation of calices and
renal pelvis, which makes the renal pelvis mucosa thickening and coarse.
(2) Histopathology
◆There
is uneven interstitial fibrosis and an inflammatory infiltration of
lymphocytes, plasma cells in the kidney parenchyma;
◆Contraction
or dilatation of tubules, with many of the dilated ones containing
eosinophilic casts known as “colloid casts”, because of the resemblance to
thyroid follicle;
◆In
the early stages, there is fibrosis around the parietal layer of Bowman’s
capsule, termed periglomerular fibrosis; eventually the glomeruli undergo
fibrosis
and
hyalinization,
and
the
remaining
nephrons
change
compensatively;
◆Large
masses of neutrophils infiltrate when acute recurrence occurs, with the
forming of minute abscess.
Specimen observation
Case abstract: A 56-year-old woman has suffered urinary frequency, urgency and
pain in urination for 15 years, nighttime uric volume increasing for 8 years, occasional
lumbago with intermittent eyelid edema for 3 years, relapsed and aggravated for 5
days. Physical examination: blood pressure is 21.9/13.8kPa, pain of both kidney zones.
Laboratory examination: urine: white blood cell (+++), SG 1.012,protein (++),
creatinine 510µmol/L, urine culture: Bacillus coli growing. B-ultrasonic examination:
both kidneys contracted asymmetrically.
Gross specimen: (Fig. 11-12)
To observe the kidney for the changes of size, shape, cortex, medulla, renal
pelvis and calices, and make diagnosis.
Tissue section: (Fig. 11-13a,b)
To observe the changes of renal glomerulus, renal tubule, renal interstitium and
the mucosa of renal pelvis, and make sure which pathological change has the
diagnostic significance.
Question: What are the main differences of pathologic changes between
pyelonephritis and glomerulonephritis?
3. Tumor of kidney
(ⅰ)Renal cell carcinoma
Basic pathologic changes
(1)Gross morphology
◆The
kidney is distorted by the tumor which most often occurs in the upper
pole, and appears as spherical masses 3 to 15cm in diameter;
◆The
cut surface reveals a solid yellowish-grey tumor with areas of
haemorrhage, necrosis, softening or calcification;
◆The
margins of tumor are well defined by pseudocapsule, and small satellite
nodules are found in the surrounding area;
(2)Histopathology
◆The
neoplastic cells are round or multilateral, whose cytoplasm are clear or
pink-granulated, with small dark stained nuclei lying in the center;
◆The
neoplastic cells arrange in disorganized masses, cords or tubules;
◆The
stroma is scanty but highly vascularized, usually accompanied by
hemorrhage, necrosis and calcification.
Specimen observation
Case abstract: A 65-year-old male smoker has suffered fever, fatigue, and weight loss
for 6 months, and lumbago in the right, hematuria for 5 days. Physical examination:
body temperature is 36.5℃; A solid immobile mass of tumor can be touched in the
kidney zone. B-ultrasonic examination: the tumor lies in the upper pole of the right
kidney, 6cm×5cm×5cm.
Gross specimen: (Fig. 11-14)
Observe the dimension, shape and color of the tumor, the secondary pathological
change and the border between the tumor and the tissue around?
Tissue section: (Fig. 11-15a,b)
To make diagnosis according to the shape and arrangement of the tumor cells,
and find out the histogenetic evidence, and make differences among renal cell
carcinoma, squamous carcinoma and adenocarcinoma.
(ⅱ) Nephroblastoma
Basic pathologic changes
(1)Gross morphology
◆Most
tumors are huge masses, with clearly defined boundary and soft
texture;
◆The
cut surface is grey or grey-red with focal hemorrhage, cystic
degeneration or necrosis, sometimes with a small quantity of bone or
cartilage.
(2) Histopathology
◆The
◆The
characteristic features are primitive or abortive glomeruli and tubules;
tumor is composed of mesenchymal tissues (fibrous tissue, mucus,
cartilage), epithelial cells (glomerular or tubular structure), and mesonephric
mesoderm cells (diffused small spindle-shaped cells).
Specimen observation
Case abstract: A 3-year-old girl has suffered an abdominal mass for 3 months,
abdominal pain and hematuria for 2 days. Physical examination: body temperature is
38℃,abdomen expands apparently, especially on the right side, and a solid immobile
glomerate mass can be touched. B-ultrasonic examination: the tumor is connected
with the right kidney, 10cm×9cm×9cm.
Gross specimen: (Fig. 11-16)
The kidney is pressed and destroyed by the huge tumor, which grows
aggressively, with hemorrhage, necrosis and the grey cut surface. Consider the
difference from renal carcinoma and give the reason.
Tissue section: (Fig. 11-17)
Observe the variety of tumor components, morphological features and their
arrangement.
4. Carcinoma of bladder
Basic pathologic changes
(1)Gross morphology
◆The
tumor can be single or multiple, different in size from millimeters to
centimeters in diameter;
◆The
tumors are papillary, ployp-like or sessile flat arising from the urothelium;
◆Tumors
may occur anywhere in the bladder, most commonly on the lateral
walls, with the trigone next in frequency;
(2) Histopathology
◆Transitional
◆Transitional
cell carcinoma has a significant proportion;
cell carcinoma are graded Ⅰ-Ⅲ according to the degree of
cytological differentiation;
① Grade Ⅰ: Tumor cells have typical papillary structure and a little atypia,
resemble the normal transitional cells. The most noticeable difference is the
increase in the number of layers of cells, over 5-7 layers, with polarity
remaining.
② Grade Ⅱ: Tumor cells have papillary structure, with more than 10
disordered layers and great loss of polarity, though still recognizable of the
transitional origin. The tumor cells have some atypia, more mitoses and form
tumor giant cells. The cells can invade into the muscle of the bladder.
③ Grade Ⅲ: The tumor cells form irregular cancer nests, and the papillary
structure scanty. The tumor cells have obvious atypia because of the loosened
arrangement and loss of polarity, which are different in size and have more
tumor giant cells as well as pathologic mitoses. The deep tissue of the bladder
can be invaded.
Specimen observation
Case abstract: A 55-year-old male dye worker has suffered painless hematuria with
urinary frequency, urgency and pain in urination for 10 days. Physical examination:
body temperature is 38.5℃,no percussive pain in the kidney area. B-ultrasonic
examination: a neoplasm in the atrium of the bladder.
Gross specimen: (Fig. 11-18)
A papillary mass protrudes from the mucosa of the bladder. Observe the
dimension, shape, color, location and invasion of the tumor. Consider the clinical
symptoms of the patient.
Tissue section: (Fig. 11-19a, b, c)
To observe the cell shape and tissue structure, and tell the grade and the
difference between transitional cell carcinoma and squamous cell carcinoma.
CASE DISCUSSION
Case abstract. A 51-year-old male, has suffered weakness, fatigue for more than 3
years, and drowsiness with nausea, emesis and anorexia for 1 month. Three years ago,
she always felt tired with low fever (body temperature 38℃ or so) and urinary
frequency. Two months ago, he felt itching of skin and 1 month ago she was drowsy
with nausea and occasional emesis. One week ago, he breath hard, and the air she
expired smelled like ammonia.
Past medical history. No special indication.
Physical examination. Chronic sickness complexion, drowsiness, pale, with body
temperature 38.5℃,pulse 106/min,breath 23/min and blood pressure 18/10kPa. Many
scratch marks for pruritus are in the skin and the superficial lymph nodes are normal.
Diffused moist rales can be heard in her two lungs, and pericardial rub at the two sides
of the manubrium of sternum. There are no abnormalities in the abdomen. No
pathological reflection of the nervous system is detected.
Laboratory examination. hemoglobin 45g/L(120-160g/L), white blood cell 9.5×
109/L, neutrophilic granulocyte 0.65, lymphocyte 0.34, eosinophilic granulocyte 0.01.
BUN 67.1mmol/L(3.56-14.28mmol/L), UA 0.5mmol/L(150-416 μ mol/L), Cr
265µmol/L(44-132 μ mol/L),CO2CP 10mmol/L(23-31mmol/L). Blood culture: no
bacteria growing. Urine: protein (+), SG 1.008, white blood cell, red blood cell and
casts can be seen; urinary culture: Bacillus growing. X-ray examination of the
breast: irregular incomplete cloudy shade can be seen in the two lungs, especially in
the lower part, and the margin of the heart doesn’t enlarge. The shadow of kidneys
contract slightly.
Although accepted supporting treatments and therapy to her symptoms, her body
temperature remained high. A week later, her temperature increased gradually. Though
the patient had blood transfusion for several times, she showed no signs of getting
better. On the10th day after hospitalization, she lost consciousness, with BUN
214mmol/L, and died on the 12th day.
Autopsy abstract
The lungs: weigh 1650g, and the cut surface of which have focal consolidated, with a
little fluid outflowed when pressed. Microscopically, there are congestion and edema
in the lungs, and a large amount of fibrin and a little monocyte can be seen in the
alveolar cavity, and no pathogen can be found by specific staining.
The heart: weigh 315g, with fibrin attaches to the pericardium. There are no
deformity and vegetation on the cardiac valves. Tissue section examination:
endocardium has no abnormality; myocardium becomes fibroid; a great amount of
fibrin attaches to the epicardium, within which a small quantity of lymphcyte
infiltration.
The kidneys: the left kidney weighs 61g, the right 72g; uneven-sized granular
changes and some irregular-distributed notched scar can be seen on the surface of
both kidneys; the cortex and medulla are not clearly defined and the mucosa of renal
pelvis is coarse. In the tissue section, most of the glomeruli are fibrosis and hyalinosis
with corresponding renal tubule loss, replaced by a large quantity of fibrous tissue,
with lymphocyte and neutrophils infiltration. Some renal glomeruli are compensatory
hypertrophy with highly dilation of the renal tubule, with the colloid casts in the
cavity.
The brain: weigh 1460g, with the shallow sulcuses, the wide gyri and the hernia of
cerebellum tonsil. Parts of the nerve cells have degenerated and the encephaledema
can be seen in the tissue section.
Discussion
1. Make the pathological diagnosis, and analyze the occurrence and
development of the disease;
2. Explain the clinical symptoms according to the pathologic changes.
3. Analyze the fatal cause of the patient.
PRACTICE REPORT
1. Illustrate the histological changes of crescentic glomerulonephritis
2. Describe the gross specimen of ①chronic sclerosing glomerulonephritis; ②
chronic pyelonephritis;
3. Write speech outline for case discussion.
QUESTIONS FOR REVIEW
1. Which diseases can cause granular atrophy of the kidney? What are the similarities
and differences in their features?
2. How does renal abscess occur? What are the deference between renal abscess and
renal tuberculosis?
3 Which diseases can lead to renal failure? What are the mechanisms?
(Hebei Medical University Liu Shuxia,
Qi Fengying)