Download Renal revision quiz - Ipswich-Year2-Med-PBL-Gp-2

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Endothelium  negatively charged endothelial
cells
Basement membrane  type IV collagen,
laminin, fibronectin, negatively charged
proteoglycans
Podocyte/pedicels  negatively charged
Estimated GFR (mL/min) =
(140-age) * weight (kg)
180 * plasma [creatinine]
Multiple this by 0.85 for women
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1.
2.
3.
4.
Dilates the afferent arteriole, leading to
decreased GFR
Constricts the afferent arteriole, leading to
increased GFR
Constricts the efferent arteriole, leading to
increased GFR
Constricts the afferent arteriole leading to
decreased GFR
1.
2.
3.
4.
Dilates the afferent arteriole, leading to
decreased GFR
Constricts the afferent arteriole, leading to
increased GFR
Constricts the efferent arteriole, leading to
increased GFR
Constricts the afferent arteriole leading to
decreased GFR
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H+ secretion  upregulated by aldosterone;
occurs in intercalated cells
HCO3- reabsorption  mostly in proximal
tubules; also thick ascending LoH and early
distal tubules
Buffers  phosphate buffer system and
ammonia buffer system
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>50% decrease in GFR in hours/days
Can also have increased BUN
Can also have decreased urine output
1.
2.
3.
4.
Hypokalaemia
Oedema
Hypertension
Anaemia
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GFR < 60mL/min/1.73m2 for > 3 months with
or without evidence of kidney damage
OR
Evidence of kidney damage with or without
decreased GFR for > 3 months
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Cardiovascular risk reduction  lifestyle, BP,
lipid-lowering, diabetic control
Monitor eGFR every 3 months
Avoid nephrotoxic drugs
Prescribe ACEI
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Retinopathy
Nephropathy
Neuropathy
MI
Stroke
Gangrene
infection
 Metabolic defect; insulin deficiency  hyperglycaemia
biochemical alterations in GBM (increased collagen type IV
and fibronectin, decreased proteoglycan) and increased ROS
( damage)
 Nonenzymatic glycosylation  inflammatory cytokines and
GF released from macrophages, ROs generation in endothelial
cells, increased procoagulant activity in endothelial cells and
macrophages, ECM synthesis and SM prolif.
 Haemodynamic changes  increased GFR, glomerular
capillary pressure, glomerular filtration area, and glomerular
hypertrophy.
 Afferent arteriole is damaged  bigger afferent than efferent 
increased GFR and pressure, causing further damage and
increased shearing forces  mesangial cell hypertrophy and
excretion of ECM products  glomerular sclerosis
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Peritoneal dialysis
Hemodialysis
Peritoneal
dialysis uses an
osmotic gradient
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Urinalysis: haematuria
Blood: electrolytes, creatinine, BUN
Paraneoplastic syndromes: FBC, ESR, LFTs, serum
calcium
LDH (prognosis)
Renal U/S or abdominal CT  cystic Vs solid
CXR  lung metastases
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One of
Incurable/irreversible terminal illness, expected to die
within a year
 Persistent vegetative state
 Permenantly unconscious
 No reasonable prospect of recovery without lifesustaining measures
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Commencing/continuing artificial
nutrition/hydration is inconsistent with good
medical practice
No reasonable prospect of regaining capacity
1.
2.
3.
4.
5.
Nephritic syndrome
Rapidly progressive
glomerulonephritis
Nephrotic syndrome
Chronic renal failure
Isolated urinary
abnormalities
a)
b)
c)
d)
e)
Acute nephritis, proteinuria, ARF
Azotaemia progressing over
months/years
Haematuria, azotemia,
proteinuria, oliguria, oedema,
hypertension
Glomerular haematuria or
subnephrotic proteinuria
>3.5g/day proteinuria,
haematuria, hypoalbuminaemia,
hyperlipidaemia, lipiduria
1.
2.
3.
4.
Postinfectious
glomerulonephritis
Crescenteric
glomerulonephritis
type I
Crescenteric
glomerulonephritis
type II
Crescenteric
glomerulonephritis
type III
a)
b)
c)
d)
Anti-GBM antibodies
Antineutrophil
cytoplasmic antibodies
Immune complexes
and
circulating/planted
antigen from bacterial
infection
Immune complexes as
a complication of other
nephropathies
1.
2.
3.
4.
Membranous
nephropathy
Minimal-change disease
Focal segmental
glomerulosclerosis
Membranoproliferative
glomerulonephritis
a)
b)
c)
d)
Effacement of podocyte
foot processes
Thickened GBM +
hypercellularity +
leukocyte infilitration
Focal and segmental
sclerosis and hyalinosos
Thickened glomerular
capillary wall
a)
b)
c)
d)
Focal segmental glomerulosclerosis
Minimal change nephropathy
Acute post-infectious glomerulonephritis
Crescenteric glomerulonephritis
1.
2.
3.
4.
Plasmaphoresis
Corticosteroids
Cyclophosphamide
Erythromycin
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Glomerular haematuria: contains bizarrelyshaped cells (each cell is different)
Non-glomerular haematuria: rbcs are smooth
disks (all the same)
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Acute tubular necrosis
1.
2.
3.
Oliguric phase (tubular obstruction)
Diuretic phase (tubules not functioning
properly)
Improving function
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Ischaemic:
Focal tubular epithelial necrosis
Multiple spots along the nephron
Toxic:
Acute necrosis
Mostly in the PCT
Both:
Occlusion of lumen (eosinophilic hyaline casts)
Detachment from BM
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Papillary necrosis
Pyonephrosis
Perinephric abscess
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Being female (more likely to get UTI ) or
elderly males (BPH)
Vesicoureteral reflux
Intrarenal reflux
Catheters
Urinary tract obstruction
Pregnancy
DM
Pre-existing renal lesions (scarring, obstruction)
Immunosuppression/immunodeficiency
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Reflux nephropathy:
Due to superimposition of urinary infection
(childhood) on congenital vesicoureteral reflux
and intrarenal reflux
Chronic obstructive pyelonephritis:
Recurrent infections superimposed on
diffuse/localised obstructive lesions 
recurrent renal inflamamtion/scarring 
chronic pyelonephritis  parenchymal atrophy
1.
2.
3.
4.
5.
Agenesis of the
kidneys
Dual induction
Hypoplasia
Horseshoe kidney
Congenital
hydronephrosis
a)
b)
c)
d)
e)
Distension and dilation of
pelvis/calyces usually due
to outflow obstruction
Either two ureteric buds or
the division of a single
ureteric bud
Failure of one/both kidneys
to develop
Reduced number of
nephrons
Fusion of kidneys during
ascent
1.
2.
3.
4.
5.
6.
7.
Adult polycystic
kidney disease
Childhood polycystic
kidney disease
Medullary sponge
kidney
Familial juvenile
nephronophthisis
Adult-onset medullary
cystic disease
Simple cysts
Acquired renal cystic
disease
a)
b)
c)
d)
e)
f)
g)
Medullary cysts on excretory
radiography
Enlarged, cystic kidneys at
birth
Corticomedullary cysts,
shrunken kidneys
Large multicystic kidneys,
liver cysts, berry aneurysms
Cystic degeneration in ESKD
Single/multiple cysts in
normal-sized kidneys
Corticomedullary cysts,
shrunken kidneys
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Dec nephron number at birth (? Low birth
weight)
Subsequent insults: nephritis, obesity, early
onset DMII
Socioeconomic and environmental
determinants
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Important health problem for individual/ community
Accepted treatment/intervention
Natural history of the disease should be understood
Latent or early symptomatic stage
Screening test or examination
Facilities for diagnosis and treatment
Policy on whom to treat as patients
Early tx should be more beneficial than late tx
Economically balanced cost
Continued case finding