The Kidney II.pdf pathology slides part 2

Kidney part 2 pathology slide

1. The Kidney and
Lower Urinary Tract -II
DrA Rapsang

2. Glomerular diseases

3. •Glomerular diseases - diseases that primarily invol ve
the renal glomeruli.
•2 groups:
–Primary glomerulonephritis
•The glomeruli are the predominant site of involvement.
–Secondary glomerular diseases
•Systemic and hereditary diseases which secondarily
affect the glomeruli.
•Clinical manifestations
•Usually presented with
–Proteinuria
–Haematuria
–Hypertension
–Disturbed excretory function
•Diagnosis
–Renal biopsy

4. The following are six major glomerular syndromes
commonly found in different glomerular diseases
•Nephritic syndrome
•Nephroticsyndromes
•ARF
•CRF
•Asymptomatic proteinuria
•Haematuria.

5. ACUTE NEPHRITIC SYNDROME.
•Acute onset following an infective illness
•Haematuria
-generally slight
–Urine
•Smoky appearance
•Erythrocytes detectable by microscopy
•Red cell casts
•Proteinuria
-mild (less than 3 gm per 24 hrs)
•Hypertension
-generally mild.
•Oedema
-usually mild
–Results from sodium and water retention
•Oliguria
- variable and reflects the severity of glomerular
involvement.
•The underlying causes may be
–Primary glomerulonephriticdiseases
•Acute glomerulonephritis
–Systemic diseases

6. NEPHROTIC SYNDROME
•Nephroticsyndrome is a constellation of features in
different diseases having varying pathogenesis
Characterisedby
•Heavy proteinuria
(protein loss of more than 3 gm per 24
hrs)
•Hypoalbuminaemia
-due to urinary loss of albumin and
inadequate hepatic synthesis of albumin.
•Oedema
–Usually peripheral but in children facial oedemamay be more
prominent
–Due to
•Fall in colloid osmotic pressure consequent upon
hypoalbuminaemia.
•Sodium and water retention

7. •Hyperlipidaemia
•Lipiduria
-due to excessive leakiness of glomerular
filtration barrier.
•Hypercoagulability
–due to loss of anti-coagulants
In children, primary glomerulonephritis is the main
cause
In adults, systemic diseases (diabetes, amyloidosis and
SLE) are more frequent causes

9. PATHOGENESIS OF GLOMERULAR INJURY

11. PRIMARY GLOMERULONEPHRITIS

12. Acute Glomerulonephritis
•Acute GN follows acute infection and
characteristically presents as acute nephritic
syndrome.
•2 main groups:
–Acute post-streptococcal GN
–Acute non-streptococcal GN
Acute post-streptococcal gn
•Usually affects children between 2 to 14 years
•Onset of disease is sudden after 1-2 weeks of
streptococcal infection (streptococcal pharyngitis)
•Etiopathogenesis.
–Group A β-haemolyticstreptococci infection

13. Grossly •Kidneys are
symmetrically enlarged
•Petechial haemorrhages
-appearance of flea-
bitten kidney

14. M/E •Glomeruli -enlarged
and hypercellular
(inflammatory cells)
•Tubules -swelling and
hyaline droplets with
red cell casts.
•Interstitium-edema
and leucocytic
infiltration.
•Vessels –no change

15. Acute glomerulonephritis
(Electron microscopy)
•Irregular deposits
(‘humps’) on the
epithelial side of the
GBM (represent
immune complexes)

16. Clinical features.
•Usually young children presenting with acute
nephritic syndrome
•Sudden and abrupt onset following an episode of
sore throat or skin infection 1-2 weeks prior to th e
development of symptoms.
•The features include
–Microscopic or intermittent haematuria
–Red cell casts
–Mild proteinuria (less than 3 gm per 24 hrs)
–Hypertension
–Periorbital oedema
–Oliguria.

17. •In adults
–Sudden hypertension
–Edema
–Azotaemia.
•Complications
–Rapidly progressive GN
–Chronic GN
–Uraemia
–Chronic renal failure.

18. Membranous Glomerulonephritis
•Widespread thickening of the glomerular capillary
wall
•Causes
–85% -idiopathic
–15% -secondary to an underlying condition (e.g.
SLE, malignancies, infections such as chronic
hepatitis B and C, syphilis, malaria and drugs).
Grossly
•Kidneys are enlarged, pale and smooth.

19. M/E •Glomeruli –diffuse
thickening
•‘duplication’ of GBM
•No cellular proliferation
•Tubules –vacuolation
•Interstitium–fibrosis
and scanty chronic
inflammatory cells.
•Vessels -hypertensive
changes of arterioles
may occur.

20. Membranous GN
Electron microscopy
•Subepithelialdeposits
of electron-dense
material so that the
basement membrane
material protrudes
between these
deposits.

21. Clinical features.
•Insidious onset of nephroticsyndrome
•Proteinuria
•Microscopic haematuria
•Hypertension
•Progression to impaired renal function and endstage
renal disease with progressive azotaemiaoccurs in
approximately 50% cases
•Renal vein thrombosis -due to hypercoagulability.

22. IgA Nephropathy (Synonyms: Berger’s Disease, IgA
GN)
•Characterisedby aggregates of IgA, deposited
principally in the mesangium .
Etiopathogenesis.
•Idiopathic in most cases.
•Immune-mediated
•Increased mucosal secretion of IgA.
•HLA-B35 association
•Genetically-determined

23. Clinical features.
•Common in children and young adults
•Recurrent bouts of haematuria(often precipitated by
mucosal infections)
•Mild proteinuria
•Occasionally nephroticsyndrome may develop.

24. Chronic Glomerulonephritis (Synonym: End-Stage
Kidney)
•Irreversible impairment of renal function.
•Caused by different glomerular diseases which may
progress to chronic GN
–Rapidly progressive GN
–Membranous GN
–MembranoproliferativeGN
–Focal segmental glomerulosclerosis
–IgA nephropathy
–Acute post-streptococcal GN
•About 20% cases of chronic GN are idiopathic
without evidence of preceding GN of any type.

25. Grossly •Short contract kidney
•The capsule is adherent
to the cortex and has
diffusely granular
cortical surface.
Cut section
•Cortex is narrow and
atrophic
•Medulla is
unremarkable.

26. M/E •Glomerular tufts are
acellularand
completely hyalinised.
•Blood vessels in the
interstitiumare
hyalinisedand
thickened
•Interstitiumshows fine
fibrosis and a few
chronic inflammatory
cells.

27. Clinical features.
•The patients are usually adults.
•The terminal stage of chronic GN is characterisedby
–Hypertension
–Uraemia
–Progressive deterioration of renal function.
–Systemic manifestations of uraemia
•These patients eventually die if they do not receiv e a
renal transplant.

28. Diabetic Nephropathy
•Complication of diabetes mellitus.
•More frequently in type 1
•Patients present with
–Asymptomatic proteinuria
–Nephroticsyndrome
–Progressive renal failure
–Hypertension.
•Morphologic features -4 types of renal lesions
–Diabetic glomerulosclerosis
–Vascular lesions
–Diabetic pyelonephritis
–Tubular lesions (Armanni-Ebsteinlesions).

29. Diabetic glomerulosclerosis.
•Pathogenesis
–Hyperglycaemia→ glomerular hypertension → renal
hyperperfusion→ deposiEon of proteins in the
mesangium→ glomerulosclerosis→ renal failure.
•Can be
–Diffuse
–Nodular
Diffuse glomerulosclerosis.
•Involvement of all parts of glomeruli.
•There is thickening of the GBM
•Diffuse proliferation of mesangialcells.
•Capsular drop -eosinophilic hyaline thickening of t he
parietal layer of Bowman’s capsule and bulges into
the glomerular space.

30. Nodular glomerulosclerosis. •Also called as Kimmelstiel-Wilson (KW) lesions -
nodules in the glomerulus.
•Nodule
–Ovoid acellularmass
–Surrounded peripherally by glomerular capillary loops
–Contain lipid and fibrin.
•As the nodular lesions enlarge, they compress the
glomerular capillaries As a result of glomerular an d
arteriolar involvement, renal ischaemiaoccurs
leading to tubular atrophy and interstitial fibrosi s and
grossly small, contracted kidney.

31. Diabetic nephropathy
•Nodular (Kimmelstiel-
Wilson or KW) lesions.

32. Vascular lesions
•Renal ischaemia
–Atheroma of renal arteries
–Arteriolosclerosis affecting the afferent and efferent
arterioles of the glomeruli
•This results in
–Tubular atrophy
–Interstitial fibrosis

33. Diabetic pyelonephritis
•Caused by bacterial infections.
•Papillary necrosis result in acute pyelonephritis.
•Chronic pyelonephritis can also develop.
Tubular lesions (Armanni-Ebsteinlesions)
•Epithelial cells of the proximal convoluted tubules
develop extensive glycogen deposits appearing as
vacuoles (k/a Armanni-Ebsteinlesions)
•The tubules return to normal on control of
hyperglycaemicstate.

34. Assignment
•What are glomerular diseases? How many types of
glomerular diseases are there?
•Differentiating features of nephritic and nephrotic
syndrome
•Pathogenesis, pathological and clinical features of
–Acute glomerular nephritis
–Chronic glomerular nephritis
•Short notes on
–IgA nephropathy
–Diabetic nephropathy
•What are Armanni-Ebsteinlesions?