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Histopath Tutorial 2:
Renal Pathology
Christiane Riedinger 6/3/14
Today’s Contents
●
●
●

●

●

organising renal pathology
major symptoms of renal pathology
kidney failure (acute kidney INJURY, chronic renal DISEASE)
○ acute vs. chronic
○ causes, clinical phases
sites of renal pathology
○ glomeruli
○ tubules
○ interstitium
○ collecting system
biochemical abnormalities
Today’s Contents
●
●
●

●

●

organising renal pathology
major symptoms of renal pathology
kidney failure
○ acute vs. chronic
○ causes, clinical phases
sites of renal pathology
○ glomeruli
○ tubules
○ interstitium
○ collecting system
biochemical abnormalities
Overview of Renal Pathology
●

many different ways of organising this topic

●

mnemonic

●

hereditary vs. acquired

●

structure/anatomy

●

outcome: acute vs. chronic
Overview of Renal Pathology ctnd.
●

mnemonic - surgical sieve: (e.g. A vitamin CDE)
● Acquired: Diabetic kidney disease
● Vascular: Particularly susceptible, renal artery stenosis, arterionephrosclerosis,
hypertension
● Infectious: nephritis (glomeruli vs. tubules, potentially post-infectious), TB,
abscesses
● Trauma: shock
● Autoimmune: Particularly susceptible, SLE, vasculitides, amyloidosis
● Malignant: benign tumours, tubular or transitional cell carcinoma, nephroblastoma
● Idiopathic: many glomerulonephritides, e.g. minimal change
● Neoplastic: renal carcinoma, Wilm’s tumour, multiple myeloma
● Congenital: PKD, Alport’s, Fabry’s, von Hippel-Lindau
● Drugs: toxicity
Overview of Renal Pathology ctnd.
●

structure/anatomy

tubule
glomerulus

macroscopic

systemic

collecting
system

vessels
http://www.sclerodermasociety.co.
uk/Theheartandscleroderma1.php

tubulointerstitial

http://www.baileybio.
com/plogger/?
level=picture&id=1486
Overview of Renal Pathology ctnd.
●

outcome:

acute
vs.
chronic
kidney failure
Today’s Contents
●
●
●

●

●

organising renal pathology
major symptoms of renal pathology
kidney failure
○ acute vs. chronic
○ causes, clinical phases
sites of renal pathology
○ glomeruli
○ tubules
○ interstitium
○ collecting system
biochemical abnormalities
1* Symptoms of Renal Pathology
●

●

●
●
●
●

haematuria
○ with or without symptoms
○ microscopic or macroscopic
proteinuria
○ via leakage - glomerular damage
○ defective reabsorption in tubules
■ heavy metal damage
■ Fanconi syndrome
■ Hartnup disease AA absorption disease
○ overflow
■ haemolysis
■ intravascular haemolysis
NEPHRITIC (both) vs NEPHROTIC syndrome (prOtein Only)
oligo/anuria
renal pain
endocrine changes
1* Symptoms of Renal Pathology ctnd.
●
●

●

always also think about what is happening in the blood, not just the urine!
nephritic syndrome
○ haematuria
○ proteinuria
○ in blood: azotemia
○ oedema, hypertension
nephrotic syndrome
○ proteinuria
○ lipiduria
○ in blood: hypoalbuminuria, hyperlipidaemia
○ oedema
○ increased clotting
○ risk of infection
Today’s Contents
●
●
●

●

●

organising renal pathology
major symptoms of renal pathology
kidney failure
○ acute vs. chronic
○ causes, clinical phases
sites of renal pathology
○ glomeruli
○ tubules
○ interstitium
○ collecting system
biochemical abnormalities
Kidney Failure: Definitions
Acute deterioration in kidney function (over <48h) with
increase in creatinine (>0.3mg/dL) and decrease in
urine output (<0.5mL/kg/h).
Long-term degeneration of kidney function defined by
persistently low or decreasing GFR or abnormal
structural or functional findings.
Kidney Failure: Causes (acute)
●

●

pre-renal
○ all vascular + contents of vessels
○ low blood volume
○ low BP
○ CHF
○ renal artery stenosis
○ ischaemia
○ renal vein thrombosis
renal
○ glomerulonephritis (deposition, vasculitis)
○ acute tubular necrosis (toxins, antibiotics, contrast)
○ acute interstitial nephritis (distal obstruction)
Kidney Failure: Causes (acute) ctnd.
●

post-renal:
○
○

○

○

○

○

think OBSTRUCTION!

again many ways to organise e.g. extrinsic vs intrinsic, here: structural
parenchyma
■ clot
■ mass
■ papillary necrosis
ureters
■ kidney stones
■ AAA
■ retroperitoneal fibrosis
bladder
■ bladder stone, tumour, clot
■ neurogenic bladder
prostate
■ BPH
■ prostate carcinoma
urethra
■ stone
■ stricture
Kidney Failure: Causes (acute) ctnd.
●

summary:

80% pre-renal and tubular necrosis
(other statistics: 85% ATN, 10% interstitial nephritis, 5% GN)
Kidney Failure: Causes (chronic)
●
●
●

diabetes mellitus 30%
hypertension 15%
glomerulonephritis 25%

●
●
●
●
●
●
●

together 75%!!!!!
vascular: renal artery stenosis, vasculitis, HUS
infectious: HIV nephropathy, parasites
toxins
congenital: Alport’s syndrome, Fabry’s disease, Polycyst. kidney d. (5%)
systemic (see earlier slide)
post-renal obstruction (see earlier slide)
Kidney Failure: Causes (chronic) ctnd.
●

summary:

75% diabetes, hypertension, GN
Kidney Failure: Acute v. chronic
summary
Today’s Contents
●
●
●

●

●

organising renal pathology
major symptoms of renal pathology
kidney failure
○ acute vs. chronic
○ causes, clinical phases
sites of renal pathology
○ glomeruli
○ tubules
○ interstitium
○ collecting system
biochemical abnormalities
Sites of Renal Pathology

The Glomeruli:
Glomerulonephritis
Glomerular Pathogenesis

Think DEPOSITION and VASCULAR!
Glomerular Pathogenesis: DEPOSITION
● immune complexes
● glycoprotein deposition, glycation
● amyloid deposition
● paraprotein deposition (MM)
Glomerular Pathogenesis: IMMUNE COMPLEXES
●

whole immune complexes get trapped
○ 3 locations:
■ mesangium
■ between endothelium and GBM
■ between GBM and podocytes
○ (GRANULAR PATTERN)

●

in situ reaction
○ ABs attack “planted’ non-glomerular antigens
■ SLE nucleosomal complexes, bact. products, protein
aggregates
○ ABs attack glomerular AGs (LINEAR PATTERN)
■ anti-GBM, anti-podocyte
Glomerular Pathogenesis: IMMUNE COMPLEXES
Glomerulonephritis: DISTINGUISH
●

global vs. segmental

(entire glomerulus or part)

●

diffuse vs. focal

(all glomeruli or patches)

●

proliferative vs. non-proliferative

(proliferation of endothelial and/or

mesangial cells, often a result of inflammation, but does not have to be. I
don’t think BM thickening counts as proliferative)
●

nephrotic, nephritic syndrome or both? (how big are the holes?)

●

pathological entity vs. clinical syndrome!
Glomerulonephritis
The following slide is the way I have organised GNs to
memorise them more easily - it may not be the best/most
correct way as different books group them differently.
For resources used see my Histopath notes.
Renal Pathology Tutorial
(post-)
infectious
GN
global, diffuse!
global, diffuse!
global, diffuse!
global, diffuse!
Histology of Glomerulonephritis
●

note: For an excellent overview, also see Wheater’s Basic Pathology Chapter 15 page 180ff

post-infectious GN

membranous GN

membranoprolif. GN

crescenteric GN
note: GN can cause ischaemia
which then causes tubular injury!
Sites of Renal Pathology
The Tubules:
(Acute) Tubular Necrosis
Pathogenesis of Tubular Necrosis

f
Sites of Renal Pathology
The Interstitium
Tubulointerstitial Pathology
Sites of Renal Pathology
The Collecting System:
Kidney Stones
Path. of the Collecting System: STONES!
●
●
●
●
●
●

80% Calcium oxalate
- absorptive hypercalcinuria
10% Magnesium/Ammonium phosphate - alkaline urine from UTIs
<10% uric acid or cystine
- urate from gout
- cystine from defect in transport
all stones contain 2.5% mucoprotein
stone formation around nidus, e.g. bacterial debris or desquamated
epithelium
blockage of urine flow => hydronephrosis:
compression => tubules affected => can’t concentrate urine => even more urine!!

Therefore polyuria if partial obstruction
Anuria if complete and bilateral (80% of stones unilateral)
Today’s Contents
●
●
●

●

●

organising renal pathology
major symptoms of renal pathology
kidney failure
○ acute vs. chronic
○ causes, clinical phases
sites of renal pathology
○ glomeruli
○ tubules
○ interstitium
○ collecting system
biochemical abnormalities
Biochemistry of Renal Disease
●
●

think about what kidney does and then derive it!
In general potential abnormalities in the following tests

○

blood
■ FBC
■ U&E
■ BUN
■ LFTs
■
■
■

ESR/CRP
clotting screen
CK

○

urine
■ output
■ urinalysis
■ electrolytes
■ creatinine
■ osmolality
■ Bence-Jones
■ culture

○

○

○
○
○

special
■ GFR
■ tubular function
imaging
■ US, CT, MRI
■ radioisotope scan
pathology
■ biopsy
immunology
ECG!
Biochemistry of Renal Disease: prerenal
INADEQUATE PERFUSION = ACCUMULATION/RETENTION
●
●
●
●
●
●
●

urea
creatinine
H+
compounds containing N
anuria/oliguria/polyuria
changes in GFR
activation of RAAS

=> uraemia
=> acidosis
=> azothemia

=> Na+ retention

=> U&E’s
=> U&E’s+
=> U&E’s, ABG?
=> BUN, BUN/Cr
=> urine output
=> GFR
=> U&E’s, urine
blood: hi Na+,also hi K+?
urine: low Na+
Biochemistry of Renal Disease: renal
REDUCED FUNCTION => ELECTROLYTE IMBALANCE AND LEAKAGE
●

=> Hyponatraemia

(Na+ loss)
●

opposite of RAAS

hyperkalaemia

retention of H+

=> metabolic acidosis

=> ABG

=> hyperphosphataemia

=> U&E’s

=> hypermagnesaemia

=> U&E’s
=> urinalysis
=> urinalysis
=> urine output

retention of phosphate
●
●
●
●

retention of Mg2+
proteinuria
haematuria
anuria/oliguria/polyuria

=> U&E’s
Biochemical abnormalities: chronic kidney d.
●
●

●
●
●

initially compensated
one nephron hypothesis of Bricker 1960:
○ as nr of nephrons decrease, remaining nephrons must perform greater
fraction of total renal excretion
disturbances we mentioned in previous slides
starts with polyuria
endocrine effects
○ hyperphosphataemia/hypocalcaemia => renal osteodystrophy
○ decreased calcitriol cynthesis
○ decreased T, Oe
○ thyroid abnormalities
○ disorders of glu metabolism
○ anaemia
○ dyslipidaemia
The end.

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Renal Pathology Tutorial

  • 1. Histopath Tutorial 2: Renal Pathology Christiane Riedinger 6/3/14
  • 2. Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure (acute kidney INJURY, chronic renal DISEASE) ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities
  • 3. Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities
  • 4. Overview of Renal Pathology ● many different ways of organising this topic ● mnemonic ● hereditary vs. acquired ● structure/anatomy ● outcome: acute vs. chronic
  • 5. Overview of Renal Pathology ctnd. ● mnemonic - surgical sieve: (e.g. A vitamin CDE) ● Acquired: Diabetic kidney disease ● Vascular: Particularly susceptible, renal artery stenosis, arterionephrosclerosis, hypertension ● Infectious: nephritis (glomeruli vs. tubules, potentially post-infectious), TB, abscesses ● Trauma: shock ● Autoimmune: Particularly susceptible, SLE, vasculitides, amyloidosis ● Malignant: benign tumours, tubular or transitional cell carcinoma, nephroblastoma ● Idiopathic: many glomerulonephritides, e.g. minimal change ● Neoplastic: renal carcinoma, Wilm’s tumour, multiple myeloma ● Congenital: PKD, Alport’s, Fabry’s, von Hippel-Lindau ● Drugs: toxicity
  • 6. Overview of Renal Pathology ctnd. ● structure/anatomy tubule glomerulus macroscopic systemic collecting system vessels http://www.sclerodermasociety.co. uk/Theheartandscleroderma1.php tubulointerstitial http://www.baileybio. com/plogger/? level=picture&id=1486
  • 7. Overview of Renal Pathology ctnd. ● outcome: acute vs. chronic kidney failure
  • 8. Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities
  • 9. 1* Symptoms of Renal Pathology ● ● ● ● ● ● haematuria ○ with or without symptoms ○ microscopic or macroscopic proteinuria ○ via leakage - glomerular damage ○ defective reabsorption in tubules ■ heavy metal damage ■ Fanconi syndrome ■ Hartnup disease AA absorption disease ○ overflow ■ haemolysis ■ intravascular haemolysis NEPHRITIC (both) vs NEPHROTIC syndrome (prOtein Only) oligo/anuria renal pain endocrine changes
  • 10. 1* Symptoms of Renal Pathology ctnd. ● ● ● always also think about what is happening in the blood, not just the urine! nephritic syndrome ○ haematuria ○ proteinuria ○ in blood: azotemia ○ oedema, hypertension nephrotic syndrome ○ proteinuria ○ lipiduria ○ in blood: hypoalbuminuria, hyperlipidaemia ○ oedema ○ increased clotting ○ risk of infection
  • 11. Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities
  • 12. Kidney Failure: Definitions Acute deterioration in kidney function (over <48h) with increase in creatinine (>0.3mg/dL) and decrease in urine output (<0.5mL/kg/h). Long-term degeneration of kidney function defined by persistently low or decreasing GFR or abnormal structural or functional findings.
  • 13. Kidney Failure: Causes (acute) ● ● pre-renal ○ all vascular + contents of vessels ○ low blood volume ○ low BP ○ CHF ○ renal artery stenosis ○ ischaemia ○ renal vein thrombosis renal ○ glomerulonephritis (deposition, vasculitis) ○ acute tubular necrosis (toxins, antibiotics, contrast) ○ acute interstitial nephritis (distal obstruction)
  • 14. Kidney Failure: Causes (acute) ctnd. ● post-renal: ○ ○ ○ ○ ○ ○ think OBSTRUCTION! again many ways to organise e.g. extrinsic vs intrinsic, here: structural parenchyma ■ clot ■ mass ■ papillary necrosis ureters ■ kidney stones ■ AAA ■ retroperitoneal fibrosis bladder ■ bladder stone, tumour, clot ■ neurogenic bladder prostate ■ BPH ■ prostate carcinoma urethra ■ stone ■ stricture
  • 15. Kidney Failure: Causes (acute) ctnd. ● summary: 80% pre-renal and tubular necrosis (other statistics: 85% ATN, 10% interstitial nephritis, 5% GN)
  • 16. Kidney Failure: Causes (chronic) ● ● ● diabetes mellitus 30% hypertension 15% glomerulonephritis 25% ● ● ● ● ● ● ● together 75%!!!!! vascular: renal artery stenosis, vasculitis, HUS infectious: HIV nephropathy, parasites toxins congenital: Alport’s syndrome, Fabry’s disease, Polycyst. kidney d. (5%) systemic (see earlier slide) post-renal obstruction (see earlier slide)
  • 17. Kidney Failure: Causes (chronic) ctnd. ● summary: 75% diabetes, hypertension, GN
  • 18. Kidney Failure: Acute v. chronic summary
  • 19. Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities
  • 20. Sites of Renal Pathology The Glomeruli: Glomerulonephritis
  • 22. Glomerular Pathogenesis: DEPOSITION ● immune complexes ● glycoprotein deposition, glycation ● amyloid deposition ● paraprotein deposition (MM)
  • 23. Glomerular Pathogenesis: IMMUNE COMPLEXES ● whole immune complexes get trapped ○ 3 locations: ■ mesangium ■ between endothelium and GBM ■ between GBM and podocytes ○ (GRANULAR PATTERN) ● in situ reaction ○ ABs attack “planted’ non-glomerular antigens ■ SLE nucleosomal complexes, bact. products, protein aggregates ○ ABs attack glomerular AGs (LINEAR PATTERN) ■ anti-GBM, anti-podocyte
  • 25. Glomerulonephritis: DISTINGUISH ● global vs. segmental (entire glomerulus or part) ● diffuse vs. focal (all glomeruli or patches) ● proliferative vs. non-proliferative (proliferation of endothelial and/or mesangial cells, often a result of inflammation, but does not have to be. I don’t think BM thickening counts as proliferative) ● nephrotic, nephritic syndrome or both? (how big are the holes?) ● pathological entity vs. clinical syndrome!
  • 26. Glomerulonephritis The following slide is the way I have organised GNs to memorise them more easily - it may not be the best/most correct way as different books group them differently. For resources used see my Histopath notes.
  • 33. Histology of Glomerulonephritis ● note: For an excellent overview, also see Wheater’s Basic Pathology Chapter 15 page 180ff post-infectious GN membranous GN membranoprolif. GN crescenteric GN
  • 34. note: GN can cause ischaemia which then causes tubular injury!
  • 35. Sites of Renal Pathology The Tubules: (Acute) Tubular Necrosis
  • 37. Sites of Renal Pathology The Interstitium
  • 39. Sites of Renal Pathology The Collecting System: Kidney Stones
  • 40. Path. of the Collecting System: STONES! ● ● ● ● ● ● 80% Calcium oxalate - absorptive hypercalcinuria 10% Magnesium/Ammonium phosphate - alkaline urine from UTIs <10% uric acid or cystine - urate from gout - cystine from defect in transport all stones contain 2.5% mucoprotein stone formation around nidus, e.g. bacterial debris or desquamated epithelium blockage of urine flow => hydronephrosis: compression => tubules affected => can’t concentrate urine => even more urine!! Therefore polyuria if partial obstruction Anuria if complete and bilateral (80% of stones unilateral)
  • 41. Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities
  • 42. Biochemistry of Renal Disease ● ● think about what kidney does and then derive it! In general potential abnormalities in the following tests ○ blood ■ FBC ■ U&E ■ BUN ■ LFTs ■ ■ ■ ESR/CRP clotting screen CK ○ urine ■ output ■ urinalysis ■ electrolytes ■ creatinine ■ osmolality ■ Bence-Jones ■ culture ○ ○ ○ ○ ○ special ■ GFR ■ tubular function imaging ■ US, CT, MRI ■ radioisotope scan pathology ■ biopsy immunology ECG!
  • 43. Biochemistry of Renal Disease: prerenal INADEQUATE PERFUSION = ACCUMULATION/RETENTION ● ● ● ● ● ● ● urea creatinine H+ compounds containing N anuria/oliguria/polyuria changes in GFR activation of RAAS => uraemia => acidosis => azothemia => Na+ retention => U&E’s => U&E’s+ => U&E’s, ABG? => BUN, BUN/Cr => urine output => GFR => U&E’s, urine blood: hi Na+,also hi K+? urine: low Na+
  • 44. Biochemistry of Renal Disease: renal REDUCED FUNCTION => ELECTROLYTE IMBALANCE AND LEAKAGE ● => Hyponatraemia (Na+ loss) ● opposite of RAAS hyperkalaemia retention of H+ => metabolic acidosis => ABG => hyperphosphataemia => U&E’s => hypermagnesaemia => U&E’s => urinalysis => urinalysis => urine output retention of phosphate ● ● ● ● retention of Mg2+ proteinuria haematuria anuria/oliguria/polyuria => U&E’s
  • 45. Biochemical abnormalities: chronic kidney d. ● ● ● ● ● initially compensated one nephron hypothesis of Bricker 1960: ○ as nr of nephrons decrease, remaining nephrons must perform greater fraction of total renal excretion disturbances we mentioned in previous slides starts with polyuria endocrine effects ○ hyperphosphataemia/hypocalcaemia => renal osteodystrophy ○ decreased calcitriol cynthesis ○ decreased T, Oe ○ thyroid abnormalities ○ disorders of glu metabolism ○ anaemia ○ dyslipidaemia