This lecture includes pathology of renal calculi , renal carcinoma, bladder carcinoma, bladder tumor, renal tumor etc. This lecture have been prepared in view of Nursing students according to syllabus.

1. PATHOLOGY OF
URINARY DISEASE
BY: Ms Saili Gaude
Principal
Shivam College of Nursing, Amirgadh

2. PYLONEPHRITIS
• It is inflammation of renal pelvis and kidney
• In Greek pyelum means renal pelvis and nephron is for kidney and it is is for
inflammation
• It is the inflammation of the kidney and upper urinary tract that usually
results from the bacterial infection of the bladder

5. TYPES
1) ACUTE PYELONEPHRITIS
2) CHRONIC PYELONEPHRITIS
3) XANTHOGRANULOMATOUS
PYELONEPHRITIS

7. ACUTE PYELONEPHRITIS
• A sudden development of kidney inflammation
• It is an acute suppurative inflammation

8. ETIOPATHOGENESIS
• GRAM NEGATIVE BACILLI- E. coli, Klebseilla, proteus, Enterobacter
• VIRUS- polyoma virus, adenovirus

9. Pathogen forms colonies into the urethral area
The pathogenic organism moves upward through the urinary
system
Inside the bladder the fimbria allows the bacteria to penetrate
the bladder wall
The organism replicates and forms biofilm
The ureters are infected and the bacterial toxins can alter urine
flow

10. Infection of the renal parenchyma causes inflammatory
response called pyelonephritis
Inflammatory cascade continues , tubular obstruction and
damage occur leading to interstitial edema
Interstitial nephritis occurs
Acute kidney injury

11. PREDISPOSING FACTORS
• Gender – females have a shorter vagina and are prone for infection
• Absence of antibacterial fluid like prostatic fluid
• Renal calculi
• Neurogenic bladder
• Outflow obstruction which leads to decreased flushing
• Stasis of urine
• Vesicouretral reflux

12. • In the calyces the papillae are convex and concave
• The central calyces are convex and therefore do not allow urine to go back
into the tubules, whereas the peripheral calyces are concave and hence allows
urine to enter the collecting ducts and cause pyelonephritis
• When this intra renal and vesicouretral reflux is absent then the urinary
infection is restricted to bladder (cystitis) and ureter (urethritis)

14. MORPHOLOGY
• Microscopic appearance
1) ACUTE PHASE
2) HEALING PHASE

15. 1. ACUTE PHASE
• Aggregates of neutrophilic infiltration seen in the interstitial tissue, in the
early stage.
• Later on, this reaction involves tubules and cause large areas of abscess
• Glomeruli get affected in the later stages
• In case of viral infection, tubular epithelial cells, show enlargednuclei with
intra nuclear inclusions

17. 2. HEALING PHASE
• Acute phase is followed by the healing phase of pyelonephritis
• Neutrophillic inflammatory infiltrate is replace by macrophages, plasma cells
and lymphocytes.
• The abscess areas are replaced by scars which are seen as depressed areas on
the cortical surface.

18. COMPLICATIONS OF ACUTE
PYELONEPHRITIS
• 1) Papillary necrosis
• Mainly seen in diabetes.
• Papillary necrosis involves one or more pyramids and in one or both the
kidneys.
• Microscopically – coagulative necrosis is seen.

21. • 2) Pyonephrosis :
• Caused by near complete
obstruction to urinary drainage,
therefor dilating and destroying
renal pelvis, calyces and the ureter

22. • 3)Perinephric Abscess
• Suppurative inflammation extends through the renal capsule outside into the
surrounding perinephric tissue

23. CLINICAL FEATURES
• Sudden onset fever
• Malaise
• Pain in costovertebral angle
• Dysuria
• Frequency of urination

24. LAB INVESTIGATIONS
• Urine examination
• Increased leucocytes
• Leucocyte casts that appears tubular
• Confirmed by quantitative urine culture

25. CHRONIC PYELONEPHRITIS
• Chronic inflammation of the tubulointerstitial tissue which leads to
deformity of calyces, pelvis and scarring of renal parenchyma
• Usually progresses to kidney failure

26. ETIPATHOGENESIS
• 2 reasons
• 1. Due to obstruction called as chronic obstructive pyelonephritis.
Parenchymal atrophy occurs
• 2. Vesicouretral reflux and intrarenal reflux mechanism with superadded
infections and is called Reflux Nephropathy. Common in children , leading to
scarring and atrophy of kidney

27. GROSS MORPHOLOGY
• Irregular scar either unilateral or bilateral
• Single or multiple scars usually seen in upper or lower pole of the kidney
• Cut section : scars are coarse, discrete and are seen over the calyx which
appears deformed blunt and dilated

28. MICROSCOPIC APPEARANCE
• Changes are seen in the interstitium and tubules
• Lymphocytes, mononuclear cells and neutrophils are seen
• Fibrosis in the cortico medullary region
• Tubules- hypertrophied and atrophy
• Lumen filled with eosinophilic hyaline colloid like material
• Tubular flat epithelium

29. • Glomeruli – appears normal
• Sclerotic or fibrosis maybe seen
• Blood vessels shows scarring

30. CLINICAL FEATURES
• Back pain
• Fever
• Frequent pyuria
• Bacteruria
• Polyuria and nocturia

31. XANTHOGRANULOMATOUS
PYELONEPHRITIS
• Rare form og chronic pyelonephritis
• Characteristic features are usually seen on cut section – yellowish orange
areas
• Appears as diffuse collection of foamy macrophages, intermingled with
plasma cells, lymphocytes, neutrophils and with occasional giant cell ,
forming granulomas

33. RENAL CALCULI

34. RENAL CALCULI
• Nephrolithiasis is a common clinical problem affecting men more than
women between the age of 20 to 30 years of age

35. ETIOPATHOGENESIS
• Metabolic factors
• 1) Hypercalciuria
• 2) Hyperphosphate
• 3) Oxaluria
• 4) Uric acid excess
• Dehydration
• Causing increased urinary concentration

36. • Stasis
• Obstruction to urine flow encourages salt precipitation
• Urinary pH
• Uric acid and oxalate stones from in an acidic urine while the phosphate stones
develop in an alkaline urine
• Renal disease
• Renal infection process alkaline urine
• Renal tumors produces renal stasis

37. TYPES
• 1. CALCIUM OXALATE
• 2. CALCIUM PHOSPHATE
• 3. STRUVITE
• 4. URIC ACID
• 5. CYSTINE

40. 1.CALCIUM OXALATE
• Colour- black/dark brown
• Sensitivity : Radiopaque
• Characteristics : small often possible to get trapped in ureter. More frequent
in men than in women
• Predisposing factor : idiopathic hypercalciuria, hyperoxaluria, independent of
urinary pH, family history

42. 2. CALCIUM PHOSPHATE
• Color- dirty white
• Sensitivioty : radio opaque
• Characteristics : mixed stone
• Predisposing factor: alkaline urine, primary hyperparathyroidism
• Therapeutic measures: treat underlying causes and other stones

44. 3. STRUVITE STONE
• Magnesium ammonium phosphate
• Colour : Dirty white
• Sensitivity : Radio opaque
• Characteristics: 3-4 times as common in women as men, always in association
with urinary tract infection. Large staghorn type
• Predisposing factors : Urinary tract infections

46. 4. URIC ACID
• Color : yellow / reddish brown
• Sensitivity : radiolucent
• Characteristics : Predominant in men, high incidence in jewish men
• Predisposing factors : Gout, urine acid, inherited condition

48. 5. CYSTEINE STONE
• Color : pink or yellow
• Sensitivity : radio opaque
• Characteristics: genetic autosomal recessive defect, absorption of cysteine in
GI tract and kidney, excess concentrations causing stone formation
• Predisposing Factors : acid urine

50. Pathogenesis
• Calcium and oxalate come together to make the crystal nucleus
• Supersaturation promotes their combination
• Continued deposition at the renal papillae leads to growth of kidney stone
• Kidney stones grow and collect debris
• In the case where the kidney stones block all routes to the renal papillae, this
can cause severe discomfort .
• The complete staghorn stone forms and retention occurs.

52. CLINICAL MANIFESTATION
• Sharp, severe pain of sudden onset caused by movement of calculus and consequent
irritation
• Renal colic originates deep in the lumbar region and radiates around the side and down
towards testicles in male and bladder in the female
• Ureteral colic – radiates towards the genitalia and thigh
• Severe pain
• Nausea vomiting
• Pallor
• Grunting respirations

53. • Elevated blood pressure
• Pulse
• Diaphoresis
• Anxiety

54. DIAGNOSTICS STUDIES
• A plain film of the abdomen and renal ultrasound will identify larger,
radiopaque stones.
• An IVP or retrograde pyelogram
• Ultrasonography
• CT scan
• Measurement of pH
• 24 hour urine measurement

56. RENAL FAILURE
• Renal failure is a condition in which the kidneys fail to remove metabolic end
products from the blood and regukate the fluid, electrolyte and pH balance
of the extracellular fluids
• 2 major pathologic conditions

57. ACUTE RENAL FAILURE
• It is a condition, characterized by rapid
onset of renal dysfunction that results
in nitrogenous waste accumulation in
the blood

58. CLINICAL DEFINITION
• Anuria – no urine output or less than 100 ml /24 hour
• Oliguria – less than 500 ml of urine output /24 hour
• Polyuria – more than 2.5 L /24 hour

59. ETIOPATHOGENESIS
• The causes are many and can be classified
as :
• 1) Pre- renal causes
• 2) Intra – renal causes
• 3) Post – renal causes

60. PRERENAL CAUSES
• Sudden and severe drop in blood pressure or interruption of blood flow to
the kidneys from severe injury or illness
• Any condition that significantly reduces renal perfusion pressure and causes a
decreased glomerular filtration rate may cause pre renal kidney failure

61. Problems affecting blood flow to kidneys
• 1. Dehydration: vomiting, diarrhea, water pills or blood loss
• 2. Disruption of blood flow to the kidneys
• - Major surgery with blood loss, severe injury or burns or infection in the
bloodstream
• - Blockage or narrowing of a blood vessel carrying blood to the kidneys
• - Heart failure or heart attack causing low blood flow
• - Liver Failure which affects blood flow and pressure to the kidney

62. RENAL CAUSES
• Actual damage to the nephrons and renal parenchyma characterize intrarenal failure
• Clinical conditions that result in intrarenal damage can be categorized under kidney
disease or acute tubular necrosis
• It is direct damage to the kidneys which causes renal failure
• Actual damage to the nephrons and renal parenchyma characterize intrarenal failure
• Clinical conditions that result in intrarenal damage can be categorized under kidney
disease or acute tubular necrosis
• ATN is a common type of acute renal failure in the critically ill patient

63. • The use of nephrotoxic drugs or prolonged pre renal causes may cause
ATN.
• ATN is a potentially reversible type of renal failure but it may take weeks or
months before adequate renal function returns.

64. POSTRENAL CAUSES
• Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder
tumor or injury
• Post renal failure is caused by clinical conditions that cause obstruction to urine flow
• Any problem that stops the excretion of urine may causes this type of ARF
• Common conditions associated with post renal failure are tumors, beningn prostatic
hypertrophy, kidney stones and bladder neck obstruction.
• If post renal failure is untreated it may result in actual nephron damage and
intrarenal failure.

65. STAGES OF RENAL FAILURE
1. INITIATING STAGE
2. OLIGURIC STAGE
3. DIURETIC STAGE
4. RECOVERY STAGE

66. 1. INITIATING STAGE
• This occurs when the kidneys are injured
and when diagnosis is made and treatment is
established it can last from hours to days.
• The initiation period begins with the initial
insult and ends when oliguria develops.

67. 2. OLIGURIC STAGE
• This lasts from 5 to 15 days
• The oliguria period is accompanied by a rise in the serum concentration of
substances usually excreted by the kidneys
• The minimum amount of urine needed to rid the body of metabolic waste is
400 ml.
• In this phase uremic symptoms first appear and life threatening conditions
such as hyperkalemia develops

68. • There is decrease in erythropoietin production, tubular transport , urine
formation and glomerular filtration.
• Fibrous scar tissue is formed which replaces the basement membrane and
the nephrons are clogged.
• There can be bleeding or infection during this stage.

69. 3. DIURETIC STAGE
• In the diuresis period, the third phase, the patient experiences gradually
increasing urine output, which signals that glomerular filtration has started to
recover.
• Laboratory values stop rising and eventually decrease.
• Although the volume of urinary output may reach normal or elevated levels,
renal function may still be markedly abnormal. Because uremic symptoms
may still be present.

70. 4. RECOVERY STAGE
• The recovery period signals the improvement of renal function and may take
3 to 12 months.
• Laboratory values return back to normal levels

71. CHRONIC RENAL FAILURE
• A syndrome characterised by progressive and irreversible renal function. It
occurs due to slow and prolonged destruction of renal parenchyma.

72. ETIOPATHOGENESIS
• 1. Disease causing glomerular pathology
• 2. Disease causing tubule interstitial pathology
• Though the causative disease are grouped into 2, all
parts of kidney are affected in final stage of kidney

73. 4 STAGES
1. DECREASED RENAL RESERVE
2. RENAL INSUFFICIENCY
3. RENAL FAILURE
4. END STAGE KIDNEY DISEASE

74. 1.DECREASED RENAL RESERVE
• Damage to kidney is marginal with 50 % GFR, BUN & serum creatinine are
normal and patient is asymptomatic

75. 2. RENAL INSUFFICIENCY
• About 75 % kidney function is destroyed, GFR decreases to 25 % of normal
and there is increase in BUN and serum creatinine.
• Patient presents with polyuria and nocturia.

76. 3. RENAL FAILURE
• By now renal function is destroyed by 90 % and GFR is just 10 % of
normal, causing loss of sodium and water and resulting in metabolic acidosis,
edema, and signs and symptoms of uremia.

77. 4. END STAGE KIDNEY DISEASE
• This is the end stage with GFR less than 5% of normal and picture of
uremic syndrome.

78. CLINICAL FEATURES
• Occurs as a result of metabolic acidosis.
• Kussmaul’s respiration, muscular irritability and flaccid paralysis
• Extra renal manifestation affect respiratory, cardiovascular, digestive and
skeletal system.
• Osteomalacia, osteitis fibrosa cystica, ultimately causing multiple organ
failure and later death.

79. RENAL CELL CARCINOMA
• It is the adeno carcinoma of kidney
• It arises from the tubular epithelium

80. ETIOPATHOGENESIS
• Tobacco consumption
• Obesity
• Hypertension
• Estrogen therapy
• Exposure to asbestos
• Petroleum products
• Heavy metals
• Chronic renal failfure
• Polycystic disease

81. CLASSIFICATION
• 1. Clear cell carcinoma
• 2. Papillary carcinoma
• 3. Chromophobe renal carcinoma
• 4. Collecting duct carcinoma

82. GROSS MORPHOLOGY
• Tumor may arise in any part of the kidney
• More commonly affects upper pole of
kidney
• Yellow to gray white
• Distorts the renal outline
• Large areas of hemorrhage
• Softening due to necrosis
• Multifocal or solitary

83. MICROSCOPIC MORPHOLOGY
• Cells are arranged in solid sheets to trabecular or cord like tubular pattern
• Tumor cells are mostly round to polygonal in shape with abundant clear to granular
cytoplasm.
• Nucleus show variation , bizarre nuclei and giant cells
• Cells are cuboidal or columnar with plenty of foam cells
• Cells appears to be elongated to spindle
• The cells appear clear as the lipids and glycogen present in the cells is lost during
processing.

86. TUMOR SPREAD
• Tumor may bulge into calyces and
pelvis
• Spread to the ureter
• Invade renal vein and grow as solid
cord like mass into the inferior vena
cava
• Distant metastasis occurs in lungs,
liver, adrenal and brain

87. CLINICAL FEATURES
• Pain in costovertebral region alongwith palpable mass and hematuria
• The tumor remains silent till the tumor reaches a large size of 10cm
• Fever
• Weakness
• Malaise
• Weight loss
• The tumor is associated with production of several abnormal hormone production
leading to paraneoplastic syndrome

88. CYSTITIS

89. DEFINITION
• Inflammation of the urinary bladder

90. ETIPATHOGENESIS
• Bacterial- E.coli, proteus, klebsiella and Enterobacter
• Tuberculous cystitis always occurs as a complication of renal tuberculosis
• Fungal- candida albicans, cyptococcal especially in immunocompressed
patients
• Virus, chlamydia and mycoplasma

91. PREDISPOSING FACTORS
• Bladder calculi
• Urinary obstruction
• Diabetes
• Instrumentation
• Radiation
• Urinary tract infection
• Complication of other renal disorders

92. MORPHOLOGY
• 1. Hemorrhagic cystitis : urinary bladder appears hyperemic with presence of
exudate and when there is hemorrhage it is called hemorrhagic cystitis
• 2. Suppurative cystitis: Causes of these are radiation injur, chemotherapy or
adenovirus. Large amount of suppuration is present
• 3. Ulcerative cystitis: large areas of ulceration may be seen
• 4. Chronic cystitis: inflammatory cells are lymphocytes, mononcytes, with
mucosa appearing as red, irregular, friable, granular surface with foci of
ulceration.

93. • 5. Follicular cystitis : When the lymphocytes form large aggregates with
lymphoid follicle formation which looks like a lymph node in the bladder
mucosa then it is called as follicular cystitis.
• 6. Eosinophillic cystitis : when submucosal eosinophils are present along
with fibrosis and giant cell it is called eosinophilic cystitis.

95. TRANSITIONAL CELL CARCINOMA
• Majority of urinary bladder carcinomas are transitional cell type which
constitute to 90%
• They are multicentric and are predominantly seen in the lateral and posterior
side of the bladder

96. ETIOPATHOGENESIS
• Cigarette smoking
• Industrial exposure to arylamine and
its related compound
• Long term use of analgesics
• Exposure for long duration to
cyclophosphamide.

97. GROSS MORPHOLOGY
• Flat non invasive or invasive growth
• When the tumor arises as finger like projections it is called as papillary tumor
• Papillary tumor are attached to mucosa by stalk
• Non invasive- without infiltration into the mucosa
• Invasive- infiltration of the mucosa

99. MICROSCOPICALLY
• Grade -1
• Numbers of cell layers are between 7 to 10 with definite cellular atypia and occasional
mitotic figure
• Grade 2
• The number of cell layers are more than 10 with greater degree of cellular atypia but cells
can still be recognized as urothelial type
• Grade 3
• Cellular polymorphism and hardly resembles transitional epithelium
• Large hyperchromatic nuclei are seen. Mitotic figure present. Tumor giant cells present.

100. INVASION OF TCC
• Superficial into lamina propria or deep into muscularis propria
• Invasion determines prognosis

101. SPREAD OF TCC
• Direct spread
• Lymphatic spread
• Hematogenous spread

102. CLINICAL FEATURES
• Urgency
• Frequency
• Dysuria
• Localised to bladder

103. THE END