2. Today’s Contents
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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
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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
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many different ways of organising this topic
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mnemonic
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hereditary vs. acquired
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structure/anatomy
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outcome: acute vs. chronic
7. Overview of Renal Pathology ctnd.
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outcome:
acute
vs.
chronic
kidney failure
8. Today’s Contents
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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
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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.
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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
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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.
25. Glomerulonephritis: DISTINGUISH
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global vs. segmental
(entire glomerulus or part)
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diffuse vs. focal
(all glomeruli or patches)
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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)
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nephrotic, nephritic syndrome or both? (how big are the holes?)
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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
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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
39. Sites of Renal Pathology
The Collecting System:
Kidney Stones
40. Path. of the Collecting System: STONES!
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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
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●
●
●
●
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
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think about what kidney does and then derive it!
In general potential abnormalities in the following tests
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blood
■ FBC
■ U&E
■ BUN
■ LFTs
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■
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ESR/CRP
clotting screen
CK
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urine
■ output
■ urinalysis
■ electrolytes
■ creatinine
■ osmolality
■ Bence-Jones
■ culture
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special
■ GFR
■ tubular function
imaging
■ US, CT, MRI
■ radioisotope scan
pathology
■ biopsy
immunology
ECG!
43. Biochemistry of Renal Disease: prerenal
INADEQUATE PERFUSION = ACCUMULATION/RETENTION
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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
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=> Hyponatraemia
(Na+ loss)
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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
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retention of Mg2+
proteinuria
haematuria
anuria/oliguria/polyuria
=> U&E’s
45. Biochemical abnormalities: chronic kidney d.
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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