lecture

1. KIDNEY & URETER
Dr.Bezan Baloch
Assistant Professor
SU2

2. EMBROLOGY
 ●● Kidney develops from the metanephros
 ●● Ureter sprouts from the mesonephric duct
 ●● Mesonephric duct regresses in females
 ●● Paramesonephric duct regresses in males

3. SURGICAL ANATOMY
 • Kidneys are the retroperitoneal organs, two in number on
 either side of vertebral column. Each kidney is bean or
 reniform in shape.
 Owing to the presence of liver, right kidney is 1-2 cm lower
 than the left kidney, extending from L l-L3 and the left
 kidney extends from T l2-L3
 • These relationships are very important for surgeons, as the
 structures mentioned above may get injured during
 operations on kidney (Table 39.1). Also they may get
 directly involved by renal malignancies

4. RELATION SHIP

5. DOUBLE URETER

6. DUPLEX URETERS
 Duplex ureters
 ●● Incidence 1 in 150
 ●● Unilateral more common than bilateral
 ●● More common in girls
 ●● Can be complete or incomplete
 ●● In children are associated with vesico-ureteric reflux

7.  Ureterocoele
 A ureterocoele is a cystic enlargement of the intramural ureter,
 probably due to atresia of the ureteric orifice. Ureterocoeles
 affect females more often than males (4:1)

8. URETEROCELE
 The classic sign of a ureterocoele on
excretion
 urography was of a ‘cobra head

9. ECTOPIC KIDNEY
 Ectopic kidney/crossed renal
 ectopia
 The fetal kidney arises in the pelvis and ascends to attain its
 normal position. If this process fails to any degree, the kidney
 ends up being in a lower-than-normal position. During their
 ascent, the renal pelvis also rotates from facing anteriorly to
 facing more medially. The most common anomaly is for the
 renal pelvis to face anteriorly and the more ectopic the kidney,
 the more severe is the rotational abnormality. In the majority
 of cases of renal ectopia, both kidneys are fused. In crossed
 renal ectopia both kidneys are fused and are
 on the same side – one of the ureters, therefore, crosses the
 midline to enter the bladder on the correct side of the trigone

10. PAIN
 Pain from the urinary tract
 ●● Renal pain is not synonymous with renal colic
 ●● Renal colic is a misnomer and should be referred to as
 ureteric colic
 ●● Renal pain can be distinguished from ureteric colic by careful
 history taking
 ●● Renal pain and ureteric colic may be experienced
 simultaneously
 ●● Ureteric colic may radiate to the groin/testicle/labium
 ●● Ureteric colic does not radiate to the chest or the back of the
 leg

11. HAEMATURIA
 Haematuria
 ●● Nowadays, is classified as visible haematuria (VH) or nonvisible
 haematuria (NVH)
 ●● A list of potential causes for haematuria can be rapidly
 generated by considering trauma (T), infection (I) and
 neoplasm (N) at all levels of the urinary tract from kidney to
 urethra
 ●● Haematuria is investigated with a renal USS and a flexible
 cystoscopy as a minimum

12. POL YCYSTIC KIDNEYS
(CONGENITAL CYSTIC KIDNEYS)
 • This is an autosomal dominant disease transmitted through
 chromosomes from anyone of the parents. Early onset congenital
 cystic kidneys are found to be autosomal recessive.
 • More common in women
 Types
 • ADPKD: Autosomal Dominant Polycystic Kidney Disease
 • ARPKD: Autosomal Recessive Polycystic Kidney Disease.

13. INFECTIONS
 Pyelonephritis
 ●● More common in women
 ●● Can be associated with septicaemia
 ●● Associated with pyuria
 ●● Should be treated initially with broad-spectrum antibiotics
 ●● Is potentially fatal, especially if associated with obstruction of
 the urinary tract

14. PATHOLOGY
 • During development, some of the uriniferous tubules fail
 to join with the collecting ducts. Such uriniferous tubules
 develop into cysts. The important pathological features are
 as follows:
 • Both kidneys are affected
 • They enlarge often to 3-4 times the normal size.
 • Cysts are distributed evenly throughout cortex and medulla.
 - Content of cyst varies but it is not urine.
 • The kidneys are studded with multiple large cysts
 • When the cyst ruptures into the pelvis of the kidney, it results
 in haematuria.
 • As the disease progresses, cysts progress in size which lead
 to pressure atrophy of the functional renal parenchyma
 leading to renal failure.

15. AUTOSOMAL DOMINANT POLYCYSTIC
KIDNEY DISEASE

16. HORSESHOE KIDNEY
 • During development, 2 mesonephric buds appear on the
 side of the future vertebral column and grows into
 metanephros. Mesonephric buds form ureter and
 metanephros kidneys.
 • If fusion occurs at lower pole, it results in a classical
 horseshoe kidney
 • Rarely, upper polar fusion can occur giving rise to reverse
 horseshoe kidney.
 • Inferior mesenteric artery crosses the isthmus at the level
 of L3-L4. Hence, horseshoe kidney cannot ascend. It is
 felt lower down in the abdomen.

17. ASSOCIATED ANOMALIES
• SPINA BIFIDA
• CONGENITAL HEMIVERTEBRA
• TURNER'S SYNDROME
• CLEFT LIP AND CLEFT PALATE

18. CALCULUS
 Urinary stones
 ●● The commonest urinary tract stones are calcium oxalate
 ●● Stones are best diagnosed on a non-contrast computed
 tomography kidney–ureter–bladder (KUB)
 ●● Most stones <5 mm will pass spontaneously
 ●● Medical expulsive therapy remains controversial
 ●● Indications for surgical intervention are persistent pain,
 obstruction and infection

19. RENAL STONES
 Aetiopathogenesis
 1. Infection: Organisms such as Proteus, Pseudomonas,
 Klebsiella produce recurrent UTI. These organisms produce
 urea, cause stasis of urine and precipitate stone formation.
 Nucleus of the stone may harbour these bacteriae (Fig. 3 9. 7).
 2. Hot climates cause increase in concentration of solutes,
 resulting in precipitation of calcium and formation of
 calcium oxalate stones.
 3. Dietary factors
 • Diet rich in red meat, fish, eggs can give rise to aciduria.
 • Diet rich in calcium-tomatoes, milk, spinach, rhubarb
 produce calcium oxalate stones.
 • Diet lacking in vitamin A causes desquamation of renal
 epithelium which precipitates calcium, alters it and fonns
 stones.

20. 4. Metabolic causes
• Hyperparathyroidism increases serum calcium levels
resulting in hypercalcinosis and pelvic stones.
• Gout increases uric acid levels and causes multiple uric
acid stones.
5. Immobilisation: Paraplegic patients secrete large amounts
of calcium in the urine resulting in calcium oxalate stones
(they pass skeletons in urine).
6. Decreased urinary citrate: Citric acid (300-900 mg/24
hours) keeps the urinary pH low. When citric acid levels
decrease, it promotes precipitation of urinary calcium.
Citrate excretion is under hormonal control.
7. Inadequate urinary drainage as in cases of horseshoe
kidney, unascended kidneys are more vulnerable for
development of stones due to stasis.
8. Randall's plaques: Randall has suggested that initially a
small erosion or an ulcer develops at the tip of renal papilla
on which minute concretions or minor calcium particles

21. TYPES OF RENAL STONES
 1. Calcium oxalate stone
 • Called as mulberry calculi
 • Common type of stone
 • It is irregular having sharp projections
 • Oxalate stone is bard and single
 • Produces haematuria very early, resulting in
deposition
 of blood over the stone giving a dark colour to the
stone.
 • It occurs in infected urine
 • Contains alternate layer of calcium and bacterial
 vegetation. It is visualised in plain X-ray KUB.
 2. Uric acid stone
 • Multiple, small, hexagonal, faceted, yellow coloured.
 • Contain calcium oxalate which makes them opaque.
Pure
 uric acid stones are radiolucent.
 • Occur in acidic urine
 • Common in patients who consume red meat
 • Best responsive to lithotripsy

22. TYPES
 3. Phosphate stone )
 • Smooth, round
 • Consists of triple phosphate of calcium, magnesium and
 ammonium.
 • Dirty white to yellow in colour
 • Commonly occur in renal pelvis and tend to grow in
 alkaline urine.
 • As it enlarges in the pelvis, it grows within the major
 and minor calyces and slowly fom1s staghorn calculus.
 This calculus produces recurrent urinary tract infection
 and haematuria and slowly damages the renal
 parenchyma
 4. Cystine calculus
 • Cystinuria is an inborn error of metabolism which occue
 due to decreased resorption of cystine from the rena
 tubules.
 • Occurs in young girls at puberty
 • Increased excretion of cystine in urine results in cystim
 calculus.
 • Stones are hard and radio-opaque due to sulphur

25. Clinical features
• Renal pain: Dull aching to pricking type of pain posteriorly
in the renal angle formed by the sacrospinalis and 12th rib.
Murphy's kidney punch test demonstrates tenderness at
renal angle. stones are oxalate stones. T he quantity of blood
lost is small but it is fresh blood
• Recurrent UTI: Fever with chills and rigors, burning
micturition, pyuria may occur, along with increased
frequency of micturition.
• Guarding and rigidity of the back and abdominal muscles
during severe attack of painThe same pain may some times be felt anteriorly
• Ureteric colic: When the stone is impacted in the
pelviureteric junction or anywhere in the ureter, it results
in severe colicky pain originating at the loin and radiating
to the groin, testicles, vulva and medial side of the thigh.
This may be associated with strangury. The referred pain is
due to irritation of the genitofemoral nerve.
• Haematuria is common with renal stone .

26. Complications
1. Calculous hydronephrosis occurs due to back
pressure
producing renal enlargement. Stretching of the renal
capsule
results in pain. In such cases, an associated palpable
kidney
mass suggests hydronephrosis.
2. Calculous pyonephrosis: Infected hydronephrosis
where
in the kidney is converted into a bag of pus.
3. Renal failure: Bilateral staghorn stones may not be
symptomatic until they present with uraemia and renal
failure.
4. Squamous cell carcinoma: Long-standing stones
increase
the risk of carcinoma.

27. I. Nonoperative treatment
1. Conservative: Small stones less than 5 mm in size
pass
off with intake of copious amount of fluids and at times
forced diuresis. Intravenous hydration followed by
intravenous frusemide m a y help pass the stones
spontaneously.
2. Extracorporeal shock wave lithotripsy (ESWL): After
cystoscopy, a ureteric stent (Double J stent) is placed into
the ureter on the side of a large renal stone
Shock waves are generated ( around 500-1500 shock
waves)
which blast the stone. The stones get crushed and most of
the stones will come out by the side of the stent (Key Box
. Small stones can be removed without prior crushing

28. II. Operative treatment
l . Endoscopic procedures
2. Open procedures
3. Special situations
1. Endoscopic procedures
Percutaneous nephrolithotomy (PCNL): Retrograde
pyelography (RGP) is done when the stone is located in
the pelvis of the kidney. With a small I cm incision in the
loin, the PCN needle is passed into the pelvis of the
kidney
and is confirmed by fluoroscopy. A guide wire is passed
through the needle into the pelvis of the kidney. The
needle
is withdrawn, with the guide wire left within the pelvis.
Dilators are passed over the guide wire and a working
sheath
is introduced into the pelvis. A nephroscope is passed into
the pelvis and if the stone is small, it can be taken out. If it
is big, it may have to be crushed using ultrasound probes
and the fragments are removed. Ultrasound or pneumatic
energy is used for fragmenting

29. Open surgical procedures
Depending upon the location of the stone, various types of
procedures are done. They are as follows:
A. Pyelolithotomy: When there is extrarenal pelvis.
B. Nephrolithotomy: When there is intrarenal pelvis, the
stone
has to be taken out through the kidney parenchyma.
C. Extended pyelolithotomy: By retracting the kidney
parenchyma laterally, the incision over the pelvis can be
extended over to the calyx and the stone can be extracted
from the calyx. Even a large staghom calculus can thus be
removed.
D. Pyelonephrolithotomy: Stone is extracted through an
incision in the pelvis as well as the renal parenchyma.
E. Partial nephrectomy: When the stone from a
lowermost
calyx is impacted, a lower pole neplu:ectomy can be done.
F. Nephrectomy: When the kidney is destroyed by
pyonephrosis, following obstruction by stone

30. URETERIC STONE
Stones come down from pelvis of the kidney and may get
impacted at any site of anatomical narrowing of ureter,
namely:
1. Pelviureteric junction
2. Crossing of the iliac artery
3. Crossing of the vas deferens or broad ligament.
4. Site of entry into the bladder wall
5. Ureteric orifice
This may lead to hydroureteronephrosis, renal
parenchymal
atrophy, infection and pyonephrosis

31. 1. Most of the ureteric stones pass via naturalis (urine). The
patient is asked to consume a lot of water and
antispasmodics.
2. Flushing therapy: About 2 L of IV fluid, with 20-40 mg
inj frusemide (Lasix). It can be repeated for a few days.
3. Stone in the upper ureter: ESWL is the ideal treatment.
Retrograde intrarenal surgery (RIRS) for ureteric, renal and
calyceal stones. Flexible ureteroscopy with laser fulguration
can also be done.
4. Middle ureteric stone: ESWL, ureteroscopy basketing or
open surgery (ureterolithotomy).
5. Lower ureteric stone: Ureteroscopic removal. With the
usage of ureteroscope passed through the urethra, direct
visualisation and manipulation of the stone even if it is
impacted can be done. A laser lithotripter or ultrasonic
lithotripter can be used to disintegrate the stone.
6. Vesicoureteric junction: Ureteroscopic removal or
endoscopic meatotomy of vesicoureteric junction. For a
stone impacted at ureterovesical junction, cystoscopy is
performed. Ureteric orifice is identified and a cut is given
at its mouth. Under fluoroscopic monitoring, the stone can
be manipulated and basketed out using a dormia basket or
other types of baskets available.
7. An impacted stone which is not amenable to ESWL,
fluoroscopic or ureteroscopic manipulation have to be

32. Prevention of stone disease
I. Metabolic work up of urine and blood for identifying
metabolic causes. Example: Hyperparathyroidism to be
ruled out by 24 hours urine analysis for calcium,
phosphate
and uric acid levels.
2. Fluid management: 1.5 L/day
3. Dietary adjustments: Red meat to be avoided (rich in
uric
acid).
4. Drug treatment
• Xyloric, sodium bicarbonate: Uric acid stones
Potassium citrate: Calcium stones
• Thiazides small dose: Calcium stones
• D-penicillamine: Cystine stones
• Protease inhibitors: Infection stones against E.coli
5. Ultrasound to be done once in 6 months.
HYDRONEPHROSIS

33. CAUSES OF URINARY OBSTRUCTION

34. Intrinsic causes
Intraluminal
Intratubular deposition of
crystals (uric acid, drugs)
Stones
Papillary tissue
Blood clots
Fungal ball
Reproductive system
Cervix: carcinoma
Uterus: pregnancy, tumours,
prolapse, endometriosis, pelvic
inflammatory disease
Ovary: tumour, cysts
Prostate: carcinoma
Intramural
Functional: pelviureteral or
vesicoureteral junction

35. Vascular system
Aneurysms: aorta, iliac vessels
Aberrant arteries: pelviureteral
junction
Venous: ovarian veins, retrocaval
ureter
Gastrointestinal tract
Crohn’s disease
Pancreatitis
Appendicitis
Diverticulitis
Tumours
Retroperitoneal space
Lymph nodes
Fibrosis: idiopathic, drugs,
inflammatory or lgG4-related
disease
Tumours: primary or metastatic
Haematomas
Radiation therapy
Surgical disruption or ureteral
ligation

36. RENAL TRAUMA
Ten percent of all trauma cases involve the genitourinary
tract. This is usually as a result of blunt trauma and the
injury
is usually self-limiting. Five to 10% of blunt trauma and up
to
70% of penetrating trauma are major injuries. Common
blunt
injuries result often from road traffic accidents, falls,
assaults
and sporting injuries. Common penetrating injuries are
knife
or gunshot wounds.
Major renal injury should be suspected with gross
haematuria,
shock in combination with microscopic haematuria,

37. Ureteric injury during
operation
●● Surgical trauma during pelvic
surgery is the most common
cause of ureteric trauma
●● Preoperative catheterisation
of the ureters makes them
easier
to protect
●● Injuries discovered during
surgery should be repaired
immediately

38. RENAL TUBERCULOSIS
• This is secondary to pulmonary tuberculosis/lymphatic
tuberculosis. The primary focus is often difficult to identify
- Common in males, in the 20-40 age group.
- Infection is always haematogenous. Often one may not
find any active lesion in the lung or in the lymph nodes.
- Usually unilateral.
1. Tubercles develop and coalesce over the papilla which
may
ulcerate-ulcerative form.
2. The tubercles may caseate and rupture over the renal
papilla
and communicate with the pelvis. This variety is called as
ulcerocavernous form.

39. Clinical features
1. Frequency is the earliest symptom of tuberculosis. It is due
to renal tubular inflammation and later due to tubercular
cystitis.
2. Abacterial acid pyuria: The urine is opalescent, pale or
yellow, acidic in reaction and no organisms/bacteria are
grown on repeated culture
Sterile pyuria is seen in tuberculosis, stones and in
carcinoma in situ.
3. Haematuria is not uncommon. Usually it is a small quantity
due to ulcerocavernous variety.
4. Evening rise of temperature.
5. Loss of appetite and loss of weight.
6. Evidence of pulmonary or lymph node tuberculosis (TB)
may be present.
Investigations
1. Urine for acid-fast bacilli (AFB)
• Early morning sample of urine has to be examined which
gives the highest concentration of AFB, for 3 days.
• Ziehl-Neelsen stain and Gram staining
• Lowenstein-Jensen media culture

40. Treatment
1. Conservative line of management with antituberculous
treatment is successful, provided kidneys are functioning
as in early stages.
2. Nephroureterectomy is indicated if the kidney is
nonfunctioning
3. Renal cavernotomy of Henley
• Indicated when there is stricture of calyces which results
in a hydrocalyx.
• In this operation the stricture is divided so that the
drainage becomes better.

41. RENAL NEOPLASMS
Classification
• Benign: Adenoma, cortical
adenoma, papilloma arising
from pelvis, haemangioma.
• Malignant: Nephroblastoma,
renal cell carcinoma
• Transitional cell carcinoma
(rare)
• Squamous cell carcinoma
(extremely rare

42. WILMS' TUMOUR (NEPHROBLASTOMA)
• This is a malignant tumour of the kidney occurring in
children.
• The tumour is composed of epithelial and mesothelial
elements. Thus, it may contain bone, cattilage, muscle, etc.
Hence, it is called nephroblastoma (immature embryonic
tissue).
• The tumour arises in one of the poles, distorting the
reniform
shape of the kidney. It is greyish white or pinkish white in
colour. At places, there may be areas of
haemorrhage/necrosis.
• Microscopic features include connective tissue elements
cartilage, spindle cells, smooth striated muscle cells and

43. Clinical features
• Common in female children, around 2-4 years.
- Less than I year of age carries good prognosis
- Upper limit of age is 7 years
- Rarely it may occur in adolescents
• The child is brought with abdominal distension, due to
hugely enlarged kidney which on palpation feels nodular.
• Rarely, Wilms' tumour can be bilateral
• Haematuria is a bad prognostic symptom. It is an
indication of rupture of tumour into the pelvis of kidney.
Most of such children die by 2 years of age.
• Low grade fever can occur in rapidly growing tumour due
to tumour necrosis, which releases pyrogens.

44. CT SCAN
 A 3-year-old
 male child had presented
 with left loin mass. CECT
 abdomen and pelvis was
 done which showed a
 large tumour in the left
 kidney. Left r adical
 nephrectomy was done
 and the histopathology
 was reported as Wilms'
 tumour

45. RENAL CELL CARCINOMA (RCC)
•RENAL CELL CARCINOMA
It is also called Hypernephroma or Grawitz
tumour.
• Commonly found in the age group 40-60.
• Male : female ratio 2
• Not known. Rarely familial RCC is known.
Specific
oncogenes have been identified. Smokers are
twice as often
affected than nonsmokers.
• Leather workers are more prone for RCC.
• Analgesic abusers are also more prone

46. RENAL CELL CARCINOMA:
AETIOLOGY
1. Chronic cystic disease
2. Chromosomal defect
3. Cadmium exposure
4. Cigarette smoking
5. Coffee drinking
6. Congenital disease-von
Hippel-Lindau disease
Observe6 Cs

47. PATHOLOGY
• Nearly all renal cancer in adults are adenocarcinoma
• Cell of origin: Proximal renal tubular epithelium.
• Starts in one of the poles, commonly in the upper polf
and usually ruptures outside the capsule because of which
reniform shape of kidney is maintained (Wilms' tumour
grows within the capsule. Hence, the kidney shape is los1
very early)
• On the outer surface, it is homogenous (Wilms' tumour is
pleomorphic) and yellow in colour due to position of lipids.
• A few haemorrhagic areas are common because the
tumour is very vascular
• Microscopy: Alternate clear cells and dark cells.
• Various subtypes of RCC
1. Clear cell carcinoma
• Most common type (70-80%)
• It can be familial, associated with von Rippel-Lindau
syndrome or sporadic (95%).

48. CLINICAL FEATURES
I. Triad of renal cell carcinoma
Triad is seen in only 9%, but if present, strongly indicates
metastatic disease.
1. Pain: Dragging or intermittent clot colic due to blood
clot
blocking the ureter.
2. Intermittent haematuria
3. Palpable mass: Hard, nodular, ballotable and
bimanually
palpable, loin mass moving with respiration

49. Robson's staging of renal cell carcinoma
• Stage I: Tumour limited to kidney
• Stage II: Tumour invades perinephric tissues or adrenal
gland, but does not extend beyond Gerota's fascia
Stage Ill : Tumour extends into major veins or lymph noda
involvement
• Stage IV: Tumour invades beyond Gerota's fascia or distan
metastasis.
INVESTIGATIONS
1. Urine examination is done when the patient has haematuri,
to look for malignant cells.
2. Plain X-ray KUB region: Enlarged kidney can be seen.
3. IVP: Distortion of calyces, missing of calyces or loss oJ
architectural pattern of kidney.
4. USG:
• Enlarged kidney
• Locate tumour, site and extent
• USG-guided FNAC can be done
• Can detect thrombus in inferior vena cava (IVC)

50. RENAL CELL CARCINOMA
Tx Primary tumour cannot be assessed
TO No tumour
T 1 < 7 cm, within capsule, i n greatest dimension
T2 > 7 cm, within capsule
T3a Extracapsular but within Gerota's fascia extension
T3b Into adrenal/perinephric
T3c Extension into renal vein/IVG
T4 Extension above diaphragm-direct invasion beyond
Gerota's fasica
NO No nodes
NX Cannot be assessed
N1 Single regional lymph node
N2 More than one regional lymph node
MO No metastasis
M1 Distant metastasis present

51. RCC(CT)

52. RENAL CELL CARCINOMA WITH TUMOUR
THROMBUS IN THE
RENAL VEIN, INFERIOR VENA CAVA

53. TREATMENT
1. Radical nephrectomy
• En bloc removal of entire Gerota's fascia with its
contents, i.e. kidney, proximal ureter, adrenal gland.
• Retroperitoneal lymph node dissection does not improve
the survival rate.
• Routine removal of ipsilateral adrenal gland is
uncommon. Unless tumour invovles large portion of
upper pole of kidney or there is suggestion of adrenal
gland involvement on preoperative radiologic exams.
2. Radical nephrectomy with extraction of tumour thrombus
• The tumour thrombus can extend along the renal vein
into IVC and even into the right atrium

54. PERINEPHRIC ABSCESS
It refers to the collection of pus in the perirenal area.
Causes
• Infection in a perirenal haematoma
• Pyonephrosis when it ruptures
• Tubercular perinephric abscess
• Pus from retrocaecal appendicitis can extend into loin,
perinephric area and may present as abscess.
Clinical features
• High swinging temperature
• Rigidity, tenderness, fullness in the loin
• Oedema in the loin
Investigations
• Total count: Raised above 20,000 cells/mm3
• Urine analysis: No organisms are usually foundX-ray spine: Scoliosis with concavity towards abscess
• Screening chest: Diaphragm is immobile and elevated or
the diseased side.
Treatment
• Pus is drained by an incision in the loin, breaking all tht
loculi.
• Dialysis and renal transplantation