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Focal
Diffuse
TERMS
Global
segmental
proliferative
membrane
alterations
crescent formation
GLOMERULONEPHRITIS
2.
3.
HCV (p406).
b. Urine: RBC casts, MC&S, Bence Jones
protein, ACR (see p286).
c.
d. Renal biopsy
Presentation
IgA Nephropathy
altered regulation
of IgA
Diagnosis
Treatment
Prognosis
Common cause of GN
Mesangial
Control BP
in adults
proliferation,
with ACEi,
POOR
immunofluorescenc
immunosuppr
prognosis:
e (IF) shows
ession may
Male, ^BP,
to infection, which
with episodic
slow decline
proteinuria or
forms immune
macroscopic
C3
of renal
renal failure at
complexes and
haematuria, recovery is
function.
presentation.
deposits in
mesangial cells.
Henoch-Schonlein
attacks
Purpura (HSP)
purpuric rash on
same as IgA
extensor surfaces
in skin or renal
nephropathy
If both
biopsy.
Systemic IgA
Arthralgias
nephritic and
nephropathy, causing a
Purpura
nephrotic 50%
Abdominal pain, GI
-> ESRF
bleeding
Hematuria
Systemic lupus
erythematous (SLE)
Haematuria, proteinuria,
tubulointerstitial damage.
Pulmonary
Plasma
Relapse are
haemorrhage
3 chain type IV
exchange,
rare. Prognosis
Haematuria/nephiritc
collagen in GBM.
steroids,
is poor if
syndrome
Linear deposition of
Cyclophosph
dialysis-
amide
dependent
days of onset of
A/b detected by
Anti-glomerular
basement membrane
(GBM)
A.k.a. Goodpastures
disease caused by
auto-antibodies to type
presentation.
symptoms
ELISA
Malaise, fatigue,
ANCA
capillary loop
arthralgias, myalgias
Post-streptococcal
Urinalysis
Complication
Strep. Ag is deposited
Inflammation
Severe HPT,
on the glomerulus
infection
rxn affecting
renal failure,
Nephritic syndrome
mesangial and
primary
endothelial cells
disease (SLE)
Rapidly progressive
AKI +- systemic
^ASOT ^C3
ANCA +ve
Aggressive immunosupresion
patients
features (fever,
cyclophophamide +- plasma
days.
haemoptysis)
exchange
Pulmonary
haemorrhage is the
commonest cause of
death
NEPHROTIC SYNDROME
Criteria
PROTEINURIA (> 3.5 G/DAY/1.73 M2)
-
extracellular compartment.
protein molecules.
capillary walls.
proteinuria.
molecules.
-
OEDEMA
hypoalbuminaemia
catabolism.
Histological patterns of NS
1.
3.
Mesangiocapillary GN
Immune complex (IC)
Complement mediated
Less common and involves persistent activation of the alternative complement pathway
Complication
A. DVT
a.
This is usally arterial and may affect the brain, limbs, and splanchnic circulation.
Sepsis
a.
Investigation
DIAGNOSTIC
1.
2.
3.
Serum lipid
4.
5.
Glucose
BP
FURTHER INVESTIGATION
6.
7.
U+Es; Creatinine
8.
9.
Hepatitis B antigen
Management
Initial treatment
fibrinogen.
Sepsis
Albumin infusion
-
Hypercoagulable states
ACEi
-
RECURRENT UTI
Same symptoms
2 infections in 6 months
3 infections in 12 months
invasive investigation
Treatment
Non-antibiotic treatments
common)
Cranberry juice
Probiotics
Complicated or uncomplicated
complete voiding
use/diaphragm
Investigations
Topical oestrogens
Antibiotics
Avoid spermicidal
dose
Self-treat
CRF is a progressive tissue destruction with permanent loss of nephrons and renal function.
Acute Renal Failure (ARF)
Abrupt onset
Potentially reversible
2.
Definition
Impaired renal f(x) >3 months based on abnormal structure or function or
3.
ESRF: GFR <15mL/min/1.73m or need for renal replacement therapy (RRT dialysis or transplant)
4.
5.
6.
7.
Nausea
Pruritus
Anorexia
Encephalopathy
Tiredness
Asterixis / flap
Breathless
Pericarditis
Neuropathy
9.
Stages of CKD
Stage
GFR
Description
Treatment stage
90+
factors
60-89
factors
30-59
Observe, BP control, RF
15-29
<15
Risk factors
Worse renal function - higher serum creatinine
Proteinuria - the higher, the greater the risk of progression
Hypertension - the higher, the greater the risk
Young age - they have longer for trouble to develop
Renal biopsy shows fibrosis, or continuing inflammation
Identifying complications
Blood tests
Treatment
Oedema
Diuretics
HPT
Anti-HPT
Arrhythmias
Diet
Sudden death
Analysis
Acidaemia
Bicarbonate
Itching
Anaemia
Raised PTH
Vitamin D
2.
3.
Kidney transplant
b. Dialysis
i. Peritoneal dialysis
ii. Haemodialysis
4.
Conservative care
HAEMODIALYSIS
1.
2.
Access to circulation
Central venous dialysis catheter
Temporary
Risk of infection
Permanent
3.
Arterio-venous fistula
Arterio-venous graft
Peritoneal dialysis
Continuous Ambulatory Peritoneal Dialysis (CAPD)
4.
PD
4hrs x 3/week
Duration
Hospital or home
Venous access
Place
Complication
Infection
Continuous or at night
Home
Peritonitis
Exit site infection
KIDNEY TRANSPLANT
1.
2.
3.
4.
Cost
5.
Cold ischaemic time - the time the donor organ was kept outside the body on ice
6.
Graft prognosis
Directly related to source of donor kidney.
Recipients of cadaveric kidneys have more episodes of rejection and lower graft survival rates.
Graft survival rates for kidneys from living donor is 95% @ 1 year and 76% @ 5 years versus graft
survival from a cadaveric kidney donor is 89% @ 1 year and 61% @ 5 years.
KIDNEY
Vitamin D metabolism
healthy bones
Homeostasis
sodium and water balance
electrolyte balance; phosphate, potassium
acid-base balance
1.
Defined as rapid reduction in kidney function over hours to days. It is common especially in ageing
population and AKI prone.
2.
3.
Criteria
4.
ACCUMULATION OF TOXINS
metabolic acidosis
potassium
fluid overload
haemodynamic
muscle
(hypertension)
pericarditis, pleurisy
fitting
instability
disruption of
cellular f(x)
weakness
cardiac
instability
7.
Risk factors:
Age >75
Diabetes
CKD
Cardiac failure
Sepsis
Hx of urinary sx
Causes
Pre-renal - not enuf blood at suff. pressure to allow filtering
Impaired perfusion of the kidneys with blood, eg hypotension (hypovalaemia,
sepsis)
Due to cardiac failure, blood loss, dehydration, vascular occlusion, hypotension,
impaired cardiac pump efficiency or vascular disease limiting renal blood flow, or
combinations of these factors.
Drugs which impair renal autoregulation; ACEi and NSAIDs
Intrinsic (may require biopsy for diagnosis)
TUBULAR: ATN is the commonest cause, often a result of pre-renal damage or
nephrotoxins (aminoglycaside, radiological contrast, myoglobulinuria)
GLOMERULAR: a/immune; SLE, lymphoma, infection, 1' glomerulonephritides
INTERSTITIAL: drugs. infiltration with, eg lymphoma, infection, tumour lysis
syndrome following chemotherapy
VASCULAR: vasculitis, malignant HPT, thrombus, large vessel occlusion
Post-renal - UT obstruction
luminal: stones, clots, sloughed papillae
mural: malignancy, BPH, urethral strictures
extrinsic compression: malignancy, retroperitoneal fibrosis
8.
Investigations
CLINICAL PRESENTATION
One of many renal factors involved in the genesis of HPT is the total number of nephrons in the
kidney.
Renal artery stenosis (RAS) is an important cause of 2 HPT. 23% of malignant HPT is the result of
renovascular causes.
Aetiology of RAS
Artherosclerosis
Polyartheristis nodosa
Radiation-induced
Takayasus arteritis
Haemodynamic effects of RAS are; 1) reduction of blood
flow, 2) decreased perfusion pressure 3) activation of
pressor mechanisms.
RAS is caused by one of two pathological entities
Fibromascular disease
In most pts the atherosclerotic lesion is ostial (within 1cm of the origin of the RA) and
usually associated with SYMPTOMATIC atherosclerotic vascular disease elsewhere.
HPT (presents in 50%) but bear in mind, not all pts with RAS are HPT as a result.
Decreased GFR
vascular sclerosis
tubular atrophy
cholesterol emboli
Investigation
SCr, eGFR, U&E
Urine dipstick, uPCR or uACR
Evidence of vascular disease e.g.. ECG
difference of >1.5cm in renal length in USS kidneys
CT angiography
MRA
Formal angiography
RESULTS
Patients with abdominal audible bruits, as well as bruits over carotid arteries suggestive of generalized
arterial disease
Doppler ultrasonography showing >1.5 cm renal asymmetry,
Recurrent flash pulmonary oedema without cardiopulmonary disease
Progressive chronic renal failure in patients with evidence of generalized atherosclerosis.
2.
3.
4.
5.
Imaging
1.
2.
3.
Doppler -
4.
Consider referral
1.
eGFR<30mL/min
2.
4.
Other indications:
Suspected acute kidney injury.
MANAGEMENT
For all stages
Non-pharmacological
1.
Exclude AKI.
2.
Pharmacological
1.
2.
CKD.
3.
Smoking cessation.
3.
4.
4.
5.
(female).
5.
In renal artery stenosis, renal perfusion pressure is reduced and nephron transit time is prolonged on
the side of the stenosis; salt and water reabsorption is therefore increased.
Urine from the ischaemic kidney is more concentrated and has a lower sodium concentration than
urine from the contralateral kidney.
Creatinine clearance is decreased on the ischaemic side.