Renal calculi

1. Renal calculi
Nephrolithiasis – Stones in pelvis & calyx
Urolithiasis – Stones in ureter and bladder

2. Renal calculi
Pathogenesis:
1)Supersaturation
2)Absence of normal stone inhibitors
3)Presence of infection

3. Renal calculi
Types of stones:
1) Calcium stones (Most common) – Oxalate,
Phosphate
2) Struvite stones (Triple phosphate, Staghorn
calculi) – Mg NH3 Phosphate, proteus infection,
Alkaline pH
3) Uric acid stones – Acidic pH
4) Cystine stones - rare
All stones are Radio-opaque except “Uric acid
stones”

4. Renal Calculi
• Urinary tract calculi are usually unilateral and
about 1 to 3 mm in size. Their passage is
marked by intense abdominal or back or flank
pain. This pain can be paroxysmal, known as
renal or ureteral "colic".
• Hematuria may also be present.
• Larger stones that cannot pass may produce
hydronephrosis or hydroureter.

5. Nephrolithiasis
• Plain X-ray – Showing a
staghorn calculi
• Gross – Appearance of
triple stone resembling the
horns of an antler

6. Management of renal stones
MAJORITY : 85 to 90% of all stones can be treated by -
EXTRA - CORPOREAL SHOCK WAVE LITHOTRIPSY
(ESWL)
MINORITY : 10 to15 % SHOULD NEED MINIMALLY
INVASIVE SURGERY (PCNL / URETEROSCOPY)
(LESS THAN 1 % NEED OPEN SURGERY)

7. Congenital anomalies

8. Fetal lobulation in adult kidney
• Persistance of fetal lobulation
can be seen in routine
autopsies in certain adults
• Renal function is usually
preserved and no symptoms
occur
• At the lower right is a smooth-
surfaced, small, clear fluid-filled
simple renal cyst. Such cysts occur
either singly or scattered around the
renal parenchyma and are not
uncommon in adults.

9. Horseshoe kidney
• Its incidence is 1/500.
• Seen in Turner’s syndrome
• 90% of case there is fusion in the lower
poles
• The possible problem here is that the
ureters take an abnormal course across
the "bridge" of renal tissue and this can
lead to partial obstruction with
hydronephrosis.

10. Horseshoe kidney
• Fusion in
the lower
poles

11. Cystic renal disease

12. Multicystic Renal Dysplasia
• a sporadic disorder without familial
clustering.
• results from abnormal differentiation of the
metanephric parenchyma
• most cases - unilateral
• bilateral lesions – Potter’s Sequence, renal
failure

13. Multicystic Renal Dysplasia
• Gross -The kidney is irregular and multicystic,
the cysts are variably sized, from 1 mm to 1 cm
in size, and filled with clear fluid.
• Micro - There are few recognizable glomeruli
and tubules
• The hallmark of renal dysplasia is the presence
of "primitive ducts" lined by cuboidal to columnar
epithelium and surrounded by a collagenous
stroma. This increased stroma may contain
small islands of cartilage.

14. Multicystic Renal Dysplasia
• Gross – Multiple cyst with
distortion of the architecture
• Micro –Note cartilage & cyst
spaces

15. AD (Adult) polycystic Kidney
disease
• Incidence 1:400-1000 live births
• Presentation – Cysts not present at birth but
presents at 4th or 5th decade with Bilateral
involvement
• Genetics:
• PKD 1 gene (polycystin I)–Ch 16
• PKD 2 gene(Polycystin II) – Ch 4
• PKD 3 gene

16. ADPKD - Gross
• Kidneys are enlarged (Massive sizes) with diffuse
variably sized cysts. Cysts may contain clear fluid
or turbid

17. ADPKD
• Clinical - usually presents in 4th decade with
hypertension and hematuria-renal failure
within a decade
• Other associations :
• Berry aneurysms - may present with
subarachnoid hemorrhage
• Polycystic liver disease
• Mitral valve prolapse
• Colonic Diverticulosis

18. AR(Childhood) PKD
• Incidence – 1 in 30,000
• The kidneys are affected bilaterally
• May occur in utero, infancy & childhood
• Present with Potter’s sequence
• Genetics:
• Fibrocystin gene

19. ARPKD
• Grossly, the kidneys are markedly
enlarged
• The cysts are quite small and uniform,
perhaps 1 to 2 mm on average, arranged
at right angles to the cortex.
• Extra-renal manifestation – Congenital
hepatic fibrosis

20. recessive polycystic kidney disease
(RPKD).

21. recessive polycystic kidney disease
(RPKD).

22. Cystic diseases of Renal medulla
• Medullary sponge kidney:
• Occurs in adults
• Cysts are small representing cystic
dilatation of collecting ducts in the medulla
• Pathogenesis unknown and usually renal
function is good

23. Familial Juvenile Nephronophthisis-
Uremic Medullary Cystic Disease
• Kidneys are shrunken with cysts in the
corticomedullary junction
• Associated with cortical tubular atrophy and
interstitial fibrosis
• Renal failure, salt wasting, polyuria, tubular
acidosis, growth retardation, anemia
• Juvenile form is autosomal recessive and
presents around age 11
• Adult form is autosomal dominant and
presents around age 20
• Both together account for 10-25% of cases of
end-stage renal failure in the first 3 decades

24. Uremic Medullary Cystic
Disease
• Note cysts in the cortico-medullary areas

25. Acquired Cysts (Dialysis-
associated) Disease
• Seen in Pts with endstage renal disease
relying on dialysis
• Gross – exhibit numerous cortical and
medullary cysts 0.5 to 2 cms size often
contain calcium oxalate crystals
• Associated with renal cell carcinoma (10
yrs duration)

26. Simple cysts
• Common Post mortem finding
• Hemorrhage in the cyst occurs produce
pain
• Has to be differentiated from renal tumours
because of their massive sizes(1-5 cms) –
USG will give clue to the cystic nature with
fluid levels

27. Simple renal cyst
• Note the enormous
size of the cyst with
shiny glistening
surface

28. Tumours of kidney
Benign – Papillary adenoma
Angio-myolipoma
Oncocytoma
Malignant – Renal cell carcinoma
Transitional cell
carcinoma

29. Malignant – Renal cell carcinoma
• Also called Hypernephroma, Grawitz tumour, renal
adenocarcinoma
• Older individuals affected M:F=2-3:1
Predisposing factors: smoking, Dialysis-associated cystic
disease, tuberous sclerosis, obesity, exposure to industrial
chemicals, and autosomal dominant polycystic renal
disease
Most tumours are sporadic but some are familial
• Familial types:
• Von Hippel Lindau Syndrome – CNS tumours –
Hemangioblastoma of cerebellum + Renal carcinoma
• Hereditary clear cell ca – VHL gene mutation with renal
tumour but no CNS tumours
• Hereditary Papillary carcinoma – Mutations in MET
protooncogene

30. Gross features of RCC
• Arise in any portion – Common Upper pole
• Size -3-15 cms
• Color – solid, yellowish white
• Some are cystic with areas of necrosis
• Tumour may involve renal vein rarely
emboli to IVC and Rt heart

31. Gross - RCC
• 2 cases of renal cell ca

32. RCC
• Histological types:
• Clear cell type – VHL mutations, rounded
or polygonal cells with clear cytoplasm
• Papillary type – MET oncogene mutation,
papillary configuration lined by cuboidal
columnar cells with psammoma bodies
• Chromophobe renal ca – Cells with pale
eosinophilic cytoplasm around blood
vessels

33. RCC – Clear cell type
• Cell arranged in nest with clear cytoplasm

34. Papillary RCC
• Numerous branching papillae and small
dark structures (Psammoma bodies)

35. Chromophobe renal carcinoma
• Notice the cells showing pale eosinophilic
cytoplasm – Compare with earlier slide
with Clear cell type

36. RCC
• Clinical:
– Cost-vertebral pain, Palpable mass, Hematuria
– Occasionally fever, weakness, Weight loss
– Symptoms relating to paraneoplastic syndrome
PTH producing hypercalcemia
Erythropoietin producing polycythemia (3%)
Renin producing hypertension
Gonadotropins producing feminization or
masculinization
Cortisol producing Cushing’s syndrome

37. RCC
• Metastasis - spread to the lungs(60% have
“cannon-ball” lesions), bone, brain, liver,
and paraaortic lymph nodes
• Some cases – Involvement of the renal
vein and spermatic veins by thrombo-
embolism can cause varicocele in the
scrotum of male pts

38. Transitional Cell Carcinoma, Renal Pelvis
• This type of carcinoma constitutes 5 to
10% of all renal carcinomas.
• They are usually detected because they
produce prominent hematuria.
• They invade early through the relatively
thin wall of the pelvic mucosa.

39. TCC
 The cut surfaces of the kidney removed surgically here
demonstrate normal cortex and medulla, but the calyces show
focal papillary tumor masses of transitional cell carcinoma. Note
the multiplicity of tumors.

40. TCC
• At high power, the transitional cell carcinoma does
resemble urothelium, but the thickness is much
greater than normal and the cells show more
pleomorphism

41. Benign - Renal Papillary Adenoma
• Renal adenomas are small,usually0.5 to
1cm ,renal cortical tumors.
• They are usually papillary in histological
appearance but may be clear cell in type.
• The problem is that they are histologically
similar to renal cell carcinomas and differ
from them only in size.
• Because of increased use of imaging
studies these are now being picked up.
• The present formula is to consider tumors
from 1 to 3 cm as potentially malignant.

42. Benign - Angio-myolipoma
• Benign tumour - occurs in patients with
Tuberous Sclerosis (CNS cortical tubers
with epilepsy and MR & skin lesions) in
which cases it is often bilateral and
sometimes multifocal.
• It is made up of a mixture of fat cells,
smooth muscle and thick walled vessels.
• These often have a pleomorphic
appearance (mistaken for malignancy)

43. Angio-myolipoma
• Blood
vessels
• Smooth
muscle
• Adipose
tissue

44. Benign - Oncocytoma
• This is a benign tumor which can be
mistaken for a carcinoma.
• Gross - large Mahogany brown tumor with
a central stellate hyaline scar
• Micro – Uniform tumour cells with granular
eosinophilic cytoplasm with benign
nucleus
• With the electron microscope these cells
show markedly increased mitochondria

45. Oncocytoma
• Notice the dark
brown color and
Central scar

46. Oncocytoma
• Note the cells with uniform ,eosinophilic
granular cytoplasm and the hyaline fibrous
tissue of the central scar.

47. Oncocytoma, Electron Microscopy
• Note the markedly increased number of
mitochondria

48. • A 4 yr old child presents with painless
mass in the abdomen, hematuria and
hypertension. Diagnosis?
A)MCD
B)PSGN
C)Neuroblastoma
D)Wilms tmour
E)Renal cell carcinoma