THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

Focal
Diffuse

TERMS

Global
segmental
proliferative
membrane
alterations
crescent formation

GLOMERULONEPHRITIS

only a portion of glomeruli affected

all glomeruli affected
whole glomerulus affected
only a part of the glomerulus is affected (most
focal lesions are also segmental)
^cell numbers due to hyperplasia of one or more of the
resident glomerular cells
capillary wall thickening
epithelial cell proliferation with mononuclear cell
infiltration in Bowmans space

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

1.

Common cause of ESRF in adults

2.

Inflammation of the glomeruli and nephrons which leads to;

a.

Damage to the glomerulus restricts blood flow, leading to compensatory ^BP

b. Damage to the filtration mechanism

allows protein and blood to enter urine.
c.

Loss of the usual filtration capacity leads

to acute kidney injury

3.

Looking for degree of damage and potential cause

a.

Blood: FBC, U&E, LFT, ESR, CRP;

immunoglobulins, electrophoresis,
complement (C3, C4); autoantibodies
(p555): ANA, ANCA, anti-dsDNA, antiGBM; blood culture, ASOT, HB A , antis

HCV (p406).
b. Urine: RBC casts, MC&S, Bence Jones
protein, ACR (see p286).
c.

Imaging: CXR, renal ultrasound.

d. Renal biopsy
Presentation
IgA Nephropathy

altered regulation
of IgA

Diagnosis

Treatment

Prognosis

Common cause of GN

Mesangial

Control BP

~20% -> ESRF.

in adults

proliferation,

with ACEi,

POOR

Young man (20-30 yo),

immunofluorescenc

immunosuppr

prognosis:

^IgA possibly due

Asians and Caucasians

e (IF) shows

ession may

Male, ^BP,

to infection, which

with episodic

deposits of IgA and

slow decline

proteinuria or

forms immune

macroscopic

C3

of renal

renal failure at

complexes and

haematuria, recovery is

function.

presentation.

deposits in

often rapid between

mesangial cells.
Henoch-Schonlein

attacks

Purpura (HSP)

purpuric rash on

+ IF for IgA and C3

same as IgA

~15% -> ESRF.

extensor surfaces

in skin or renal

nephropathy

If both

biopsy.

Systemic IgA

Arthralgias

nephritic and

nephropathy, causing a

Purpura

nephrotic 50%

small vessel vasculitis.

Abdominal pain, GI

-> ESRF

bleeding

Hematuria

Systemic lupus

Cough, chest pain, nasal congestion

~1/3 SLE have renal disease

erythematous (SLE)

Maculopapular rash over her chest

with vascular, glomerular and

Haematuria, proteinuria,

tubulointerstitial damage.

Pulmonary

A/b develop against

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-

AKI may occur within

IgG along GBM

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.

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

IV collagen an essential
component of the GBM

symptoms

ELISA

Malaise, fatigue,

ANCA

anorexia, weight loss,

capillary loop

arthralgias, myalgias

staining with IgG

and C3 and
extensive crescent
formation

Post-streptococcal

Occurs 1-12 wks after

Urinalysis

Complication

Strep. Ag is deposited

a sore throat or skin

Inflammation

Severe HPT,

on the glomerulus

infection

rxn affecting

renal failure,

Nephritic syndrome

mesangial and

primary

endothelial cells

disease (SLE)

causing a host rxn and

immune complex form.

IF: IgG and C3

deposits

Rapidly progressive

AKI +- systemic

^ASOT ^C3

ANCA +ve

Aggressive immunosupresion

patients

with high-dose IV steroids and

Most aggressive GN.

features (fever,

Could cause ESRF over

myalgia, weight loss,

cyclophophamide +- plasma

days.

haemoptysis)

exchange

Pulmonary

haemorrhage is the
commonest cause of
death

5 year survival 80%

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

NEPHROTIC SYNDROME
Criteria
PROTEINURIA (> 3.5 G/DAY/1.73 M2)
-

Structural damage to the glomerular

compartment is secondary to the

increase in the size and number of

accumulation of sodium in the

pores -> allow more and larger

extracellular compartment.

This is due to an imbalance between

Fixed negatively charged components

oral (or parenteral) sodium intake and

are present in the glomerular capillary

urinary sodium output, as well as

wall, which repel negatively charged

alterations of fluid transfer across

protein molecules.

capillary walls.

Reduction of this fixed charge occurs in

Elevated TNF- levels in nephrotic

glomerular disease and appears to be a

syndrome activate protein kinase C,

key factor in the genesis of heavy

which changes phosphorylation of

proteinuria.

occludin and capillary permeability

HYPOALBUMINAEMIA (< 3.5G/DL)

-

Expansion of the interstitial

basement membrane leads to an

molecules.
-

OEDEMA

Urinary protein loss of the order 3.5g

HYPERLIPIDAEMIA (C > 250 MG/DL)

Hyperlipidaemia is the consequence of

daily or more in adult required to cause

increased synthesis of lipoproteins in

hypoalbuminaemia

the liver, abnormal transport of

Increased of catabolism of reabsorbed

circulating lipid particles, and decreased

albumin in the proximal tubules though

catabolism.

actual albumin synthesis is increased.

Nephrotic syndrome is NOT a diagnosis. Therefore, the underlying cause should always be sought.

Histological patterns of NS
1.

Minimal change disease

PAEDS: common cause, MALE good prognosis. X leads to
CKD, facial oedema
ADULT: asso. With drugs (NSAIDs, lithium, antibiotics
(cephalosporins, rifampicin, ampicillin) , bisphosphate and
sulfasalazine) or paraneoplastic (Hodgkins lymphoma)
Glomeruli appear normal on light microscopy but on EM,
fusion of podocytes could be seen
Tx: high dose corticosteroid therapy with prednisolone 60
2

mg/m daily (up to a maximum of 80 mg/day) for a

2

maximum of 46 weeks followed by 40 mg/m every other

day for a further 46 weeks corrects the urinary protein
leak in more than 95% of children
Two-thirds children have relapse and further courses of corticosteroids are required.
One-third of these children regularly relapse on steroid withdrawal, so that cyclophosphamide
should be added after repeat induction with steroids. A course of cyclophosphamide 1.52.0
mg/kg daily is given for 812 weeks with concomitant prednisolone 7.515 mg/day.

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

2.

Membranous nephropathy (common cause, 20-30% in adult)

75% are primary or idiopathic form but can be associated to 2 to drugs (penicillamine, gold,
NSAIDs, probenecid, mercury, captopril), autoimmune disease (e.g. SLE, thyroiditis), infectious
disease (e.g. hepatitis B, hepatitis C, schistosomiasis, Plasmodium malariae), neoplasia (e.g.
carcinoma of lung, colon, stomach, breast and lymphoma) and other causes (e.g. sarcoidosis,
kidney transplantation, sickle cell disease)
At all stages, IF shows the presence of diffusely thickened GBM of IgG and C3
COMMON: Adults, males
Asymptomatic proteinuria or frank nephrotic syndrome.
May present with mocroscopic haematuria, hypertension and/or renal impairment
POOR PROGNOSIS: HPT and higher degree of renal impairment
40% develop CKD
GOOD PROGNOSIS-> Younger, females, and asymptomatic proteinuria of modest degree
3 stages

Early: deposits are small can be missed on LM. EM

reveals small electron-dense deposits in the subepithelial aspects of the capillary walls

Intermediate: deposits are encircled by basement

membrane => appearance of spikes of
basement membrane perpendicular to the
basement membrane on silver staining

Late: uniform thickening of the capillary

basement membrane

3.

Mesangiocapillary GN
Immune complex (IC)

Driven by circulating immune complexes, which

deposit in the kidney and activate complement via the classical pathway. An underlying cause
can be found in most cases, eg Hep C, SLE and monoclonal gammopathies.

Complement mediated

Less common and involves persistent activation of the alternative complement pathway

BIOPSY: mesangial and endocapillary proliferation, a thickened capillary basement membrane,

double contouring (tramline) of the capillary walls. IF can show Ig staining, complement
staining or light chains depending on cause. EM shows electron dense deposits.
4.

Focal segmental glomerulosclerosis

May be 1 or 2 (VUR, IgA nephropathy, Alports syndrome, vasculitis, sickle-cell disease)
Presentation: nephrotic syndrome or proteinuria. ~50% have impaired renal function.
BIOPSY: scarring of the glomeruli at certain segments (focal sclerosis). IF: IgM and C3 deposits at
affected area.
Tx: corticosteroid. Resistant: cyclosphamide or ciclosporin
Untreated most progress ESRF

Complication
A. DVT
a.

Hypercoagulable state due to urinary losses of anti-thrombin and thrombocytosis

b. Exacerbated by steroid therapy

c.

Increased synthesis of clotting factors

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

d. Increased blood viscosity from the raised haematocrit
e.
B.

This is usally arterial and may affect the brain, limbs, and splanchnic circulation.

Sepsis
a.

Serum: IgG, complement, T cell function

b. Steroid: immunosuppressant toxicity

C. Lipid abnormalities
D. Hypovalaemia
E.

Acute renal failure (rare)

Investigation
DIAGNOSTIC
1.

Proteinuria +1> on 2/3 dipstick

2.

P:C (> 200mg/mmol) (early morning)

3.

Serum lipid

4.

C3 level (sensitive n specific if other than

MCD)

5.

abundant hyaline cast

Haematuria (other thn MCD)

Na+ <10mmol/L in hypovolaemia

Glucose

10. LFTs; ASOT

11. Urine culture
12. Varicella status should be known in all

BP

children commencing steroids.

FURTHER INVESTIGATION
6.

Full blood count: HCT, WBC

7.

Renal profile: normal in MCD

13. Other investigations

other thn MCD

U+Es; Creatinine

8.

Serum albumin: <25g/L

9.

Urinalysis and quantification for urinary

protein excretion

complement levels: suggest

Antistreptolysin O titre and throat

swab

Hepatitis B antigen

14. Biopsy light microscopy/ EM/ IF

Management
Initial treatment

Predispose to venous thrombosis

This is due to loss of clotting factors in the

Na restriction and THIAZIDE diuretics

Unresponsive patients require

urine and increase in hepatic production of

FUROSEMIDE 40-120mg daily + amiloride

fibrinogen.

Normal protein intake

Sepsis

Albumin infusion
-

only produce a transient effect

Indication: diuretic-resistant, oliguria and

uraemia in the absence of severe
glomerular damage e.g. in minimal change
nephropathy.

Hypercoagulable states

Susceptibility to infection due to loss of

immunoglobulin in the urine

Lipid abnormalities
-

Increased CVS disease. Give HMG-CoA

ACEi
-

Reduce proteinuria by lowering

glomerular capillary filtration pressure

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

RECURRENT UTI

Same symptoms

Confirm antibiotic sensitivities

No fixed definition of recurrent

History of previous antibiotic use

2 infections in 6 months

Ultrasound is the most useful non-

3 infections in 12 months

After a single UTI there is a 30% risk of

invasive investigation

Treatment

recurrence with 6 months

Be aware of the risk of resistance

60% will be the same organism (E coli most

Non-antibiotic treatments

common)

Cranberry juice

After a first UTI 30-40% of patients will go onto

Increase fluid intake

have recurrent infections

Probiotics

Complicated or uncomplicated

Regular and/or post coital

Complicated: underlying anatomical or

physiological abnormality

complete voiding

Uncomplicated: normal urinary tract

Complicated UTIs are more likely to
recur but
Most recurrent infections occur in

use/diaphragm

Investigations

Long-term prophylaxis (1-2

yrs)

Low dose, at night

Single post-coital antibiotic

Confirm infection dipstick and MSU

Other conditions can mimic infection

Topical oestrogens

Antibiotics

otherwise healthy women with a

normal urinary tracts

Avoid spermicidal

dose

Self-treat

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

CHRONIC RENAL FAILURE

1.

CRF is a progressive tissue destruction with permanent loss of nephrons and renal function.
Acute Renal Failure (ARF)

Chronic Renal Failure (CRF)

Abrupt onset

Progresses over at least 3 months

Potentially reversible

Permanent- non-reversible damage to nephrons

2.

Definition
Impaired renal f(x) >3 months based on abnormal structure or function or

GFR <60mL/min/1.73m for >3 months w/ or w/o evidence of kidney damage

2

3.

ESRF: GFR <15mL/min/1.73m or need for renal replacement therapy (RRT dialysis or transplant)

4.

Progressive destruction of nephrons leads to;

Decreased glomerular filtration, tubular reabsorption & renal hormone regulation
Remaining functional nephrons compensate
Functional and structural changes occur
Inflammatory response triggered
Healthy glomeruli so overburdened they become stiff, sclerotic and functionless

5.

Factors influence eGFR; GENDER, AGE, CREATININE, ETHNIC

6.

Symptoms of severe CKD (stage 4-5)

CKD stage 4-5

7.

Later stages of uraemia (to be avoided)

Nausea

Pruritus

Anorexia

Encephalopathy

Tiredness

Asterixis / flap

Breathless

Pericarditis

Oedema/ fluid retention

Neuropathy

Unreliable eGFR reading

<18 yo
Severe malnutrition or obesity
Disease of skeletal muscle, paraplegia, or quadriplegia, amputees
Vegetarian diet

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

Acute renal failure
Prior to dosing drugs w/ significant toxicity that are excreted by the kidneys
8.

9.

Stages of CKD
Stage

GFR

Description

Treatment stage

90+

Normal kidney function but urine or other

Observation, control BP and CV risk

abnormalities point to kidney disease

factors

60-89

Mildly reduced kidney function, urine or other

Observation, control BP and CV risk

abnormalities point to kidney disease

factors

30-59

Moderately reduced kidney function

Observe, BP control, RF

15-29

Severely reduced kidney function

<15

Very severe, or endstage kidney failure

Planning for ESRF, anaemia, Ca,Pi and

PTH management
Dialysis and transplant

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

10. Causes of frequent causes of acute decline in GFR

Volume depletion
Intravenous radiographic contrast
Selected antimicrobial agents (for example, aminoglycosides and amphotericin B)
Nonsteroidal anti-inflammatory agents, including cyclo-oxygenase type 2 inhibitors
Angiotensin-converting enzyme inhibition and angiotensin-2 receptor blockers
Obstruction of the urinary tract
11. Investigation
Check previous renal function
Identify and treat underlying cause if possible - Renal biopsy
Renal imaging

May establish cause

May confirm CKD e.g. if kidneys small

May identify reversible causes e.g. RAS

Identifying complications

Blood tests

12. Treatment of advanced CKD or failed endocrine function

Clinical features
Salt and water
Hyperkalaemia
Acid-base
Hyperphosphataemia
Erythropoietin

Treatment

Oedema

Diuretics

HPT

Anti-HPT

Arrhythmias

Diet

Sudden death

Analysis

Acidaemia

Bicarbonate

Itching

Diet and binders

Anaemia

EPO and iron

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

Decreased 1,25 Vit D

Raised PTH

Vitamin D

RENAL REPLACEMENT THERAPY

1.

Aim to identify patients with progressive CKD early

2.

Timely planning for RRT

3.

Options and choices

a.

Kidney transplant

b. Dialysis
i. Peritoneal dialysis
ii. Haemodialysis
4.

Conservative care

HAEMODIALYSIS
1.

Acute indication for dialysis

A: Acidosis (metabolic acidosis)
E: Electrolyte Abnormalities (hyperkalemia)
I: Ingestants/Toxins (lithium)
O: Overload (volume overload causing respiratory distress)
U: uremia (systemic effects uremic encephalopathy, uremic pericarditis)

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)

An exchange takes about 30 minutes.

Most CAPD patients need to do between 3 and 5 exchanges a day.

Automated peritoneal dialysis (APD)

Rapid dialysate exchanges overnight (uses an automated device)

In the morning, the patient disconnects from the machine.

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

4.

Haemodialysis vs peritoneal dialysis

HD

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.

Improved patient survival (87% vs 30% 5 year survival)

2.

Correction of metabolic consequences of renal failure

3.

Improved quality of life for patient and family

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.

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

ACUTE KIDNEY INJURY

Excretion of waste products

KIDNEY

nitrogen-containing waste products e.g. urea

EPO (erythropoietin) production

stimulates red cell production

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.

It has HIGH mortality and REVERSIBILE NEED TO RECOGNISE EARLY!!

3.

Criteria

4.

Rise in creatinine > 0.3mg/dL (>26mol/L) in 48 hours

Rise in creatinine >1.5 x baseline (best figure in last 3/12)

Urine o/put <0.5mL/kg/h for >6 consecutive hours

Staging for AKI

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

5.

Consequences of sudden loss of renal function/presentation of AKI

ACCUMULATION OF

ACCUMULATION OF TOXINS

SALT & H2O

urea and other uraemic toxins

metabolic acidosis

potassium

fluid overload

nausea, vomiting, malaise

haemodynamic

muscle

(hypertension)

pericarditis, pleurisy
fitting

instability
disruption of

increased bleeding risk

cellular f(x)

weakness
cardiac
instability

increased infection risk

6.

7.

Risk factors:

Age >75

Diabetes

CKD

Drugs (esp newly started)

Cardiac failure

Sepsis

Peripheral vascular disease

Poor fluid intake/ increased losses

Chronic liver disease

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

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

8.

Investigations

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

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

10-25% of all RAS, young female (15-40 yo)

Medial diseae 90%, often involves distal RA

Atherosclerotic renovascular disease (ARVD)

Incidence increases with age

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.

Signs and symptoms

-

HPT (presents in 50%) but bear in mind, not all pts with RAS are HPT as a result.

Progressive HPT in a pt with previously stable HPT.

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

Sodium retention (ankle and pulmonary oedema)

Proteinuria (usually sub-nephrotic range)

Decreased GFR

vascular sclerosis

tubular atrophy

interstitial fibrosis with inflammatory cellular infiltrate atubular glomeruli

cholesterol emboli

secondary focal segmental glomerulosclerosis (FSGS)

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.

Predictors of Kidney salvageability

1.

Kidney size > 9 cm

2.

Resistive index < 0.80

3.

Recent increase in serum creatinine

4.

Decrease in GFR during ACE inhibition

5.

Absence of glomerular or interstitial fibrosis on kidney biopsy

Imaging
1.

MRA gold standard

2.

Radionuclide studies screening

3.

Doppler -

4.

Helical (spiral) CT scanning

Consider referral
1.

eGFR<30mL/min

2.

eGFR <60mL/min, and any of :

Progressive fall (>5mL/min in 1 year or >10mL/min in 5 years).
Microscopic haematuria.
Proteinuria (uACR >70mg/mmol, uPCR >100mg/mmol) unless known to be due to
diabetes and appropriately treated.
>15% decline in eGFR with commencement of an ACE-I or ARB (? renovascular disease).
Suspected systemic illness (e.g. SLE, myeloma).

THEMED WEEK 8: INVESTIGATION OF ABNORMAL RENAL FUNCTION

Hb <11g/dL, with no other explanation.
Abnormal calcium, phosphate, or PTH.
Refractory high BP (>150/90 despite three antihypertensive agents).
3.

eGFR >60mL/min and other evidence of renal disease/damage:

Urine Albumin-to-Creatinine Ratio (uACR) >70 or uPCR >100mg/mmol.
uACR >30 or uPCR >50mg/mmol and microscopic haematuria.
Abnormal renal imaging, e.g. renal cysts.

4.

Other indications:
Suspected acute kidney injury.

MANAGEMENT
For all stages
Non-pharmacological
1.

Exclude AKI.

2.

Explanation, education, and reassurance

regarding the causes and consequences of

Pharmacological
1.

Aspirin 75mg, according to 10-year CV risk

estimate.

2.

CKD.

Treat lipids, according to best practice

guidelines.

3.

Smoking cessation.

3.

Avoid NSAIDs and other nephrotoxic drugs.

4.

Weight reduction if obese.

4.

Limit alcohol to <3 units/day (male), 2 units/day

5.

Encourage aerobic exercise.

(female).
5.

Vaccination against influenza and

pneumococcus

PATHOPHYSIOLOGY OF CKD -> HPT

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.