Transcript Renal Disease

Renal Disease
Chronic Kidney Disease
GP Management
Ross Bills
Prevalence
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1.7 million Australians with Stage three chronic
kidney disease
1 in 7 Australians has chronic kidney disease
Often asymptomatic, 80-90% of cases
unrecognised and untreated
10-20 fold increase in risk of death due to
cardiovascular events
1 nephrologist per 95,000 adult Australians
Diagnostic criteria
Chronic kidney disease (CKD) is defined as:
• A glomerular filtration rate (GFR) less than 60
mL/min/1.73m2 that is present for 3 or more months, with
or without, evidence of kidney damage
OR
• Evidence of kidney damage (with or without decreased
GFR) that is present for > 3 months, as evidenced by
any of the following
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Microalbuminuria
Proteinuria
glomerular haematuria
pathologic abnormalities (e.g. abnormal renal biopsy)
anatomical abnormalities (e.g. scarring seen on
imaging or polycystic kidneys).
GP Role
early detection of CKD
 instituting therapies which will slow or
prevent progression to kidney failure
 assessing and modifying cardiovascular
risk factors
 avoiding nephrotoxic drugs
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eGFR
The MDRD (abbreviated) equation for use
with SI units is:
GFR = 186 x {[SCr (umol/L)/88.4]-1.154} x
(age)-0.203 x (0.742 if female)
Pathologies
• Easiest to think of
– Pre-renal
• Hypertension
• Renal artery stenosis
• Phaeochromocytoma
• Multiple organ failure/shock
– Renal
• Glomerulopathies: acute and chronic, infective,
autoimmune, protein deposition (amyloidosis), chemical
(lead), drug related
• Diabetes nephropathy
• Mass - tumour (adenocarcinoma commonest adults,
nephroblastoma children), polycystic disease
– Post-renal
• Calculi and other obstructive (analgesic nephropathy)
• Strictures ureter intrinsic and extrinsic
Risk Factors
Smoking
 Diabetes
 Hypertension
 Age > 50 years
 Family History of Kidney Disease
 ATSI Patients
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The Kidney Screen
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Simple screen at presentation.
If risk factors present:
• Check BP
• Dipstick for protein
• Creatinine level for eGFR
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If eGFR > 60, normal BP, No proteinuria, low
risk. Review opportunistically.
Caution if other evidence of renal disease haematuria, casts etc.
eGFR
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The new measure of renal function, using
prediction equations based on age, sex and
creatinine clearance
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Abbreviated MDRD Formula
• GFR = 186 × (SCR + 88.4)-1.154 × AGE-0.203
• Female: multiply result by 0.742)
• When used in Afro-Americans the result should be multiplied
by 1.21
eGFR 2
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Clinical situations where eGFR results may be unreliable
and/or misleading:
• Acute changes in kidney function (eg. acute kidney failure)
• Dialysis-dependent patients
• Exceptional dietary intake (eg. vegetarian diet, high protein diet,
creatine supplements)
• Extremes of body size
• Diseases of skeletal muscle, paraplegia, those with high muscle mass
and amputees
• Children under the age of 18 years
• Severe liver disease present
• eGFR values above 60 mL/min/1.73m2
eGFR 3
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eGFR has not been validated or shown to have acceptable
accuracy in:
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Aboriginal and Torres Strait Islander peoples
Asian populations (including Japanese, Chinese and Vietnamese)
Maori and Pacific Islander peoples
Calculations for drug dosing
In these clinical situations listed, an alternative method of
estimating kidney function should be performed.
Presentations
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Stage 1 - Kidney damage, no loss of function
Stage 2 - Kidney damage with mild loss of
function
• There may be no clinical diagnostic features other than mild
impairment of Creatinine Clearance/eGFR (eGFR >60)
• Address co-morbidity:
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BP
Lipids
Diabetes
Smoking
Weight
Exercise
Signs/Symptoms Stage I - II
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Bugger all
Complications Stage I - II
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Usually just hypertension if anything
Presentations 2
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Stage 3 - moderate loss kidney function
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eGFR 30-59
• Look at modifiable risk factors
• Monitor eGFR (three monthly
• Consider referral to nephrologist
Stage III Clinical Findings
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Nil or
nocturia
mild malaise
anorexia
Stage III Complications
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Hypertension
Hyperparathyroidism
Renal Osteodystrophy
Anaemia
Sleep Apnoea
Restless legs
CVD
Malnutrition
Management Stage III
Diagnosis
 Cardiac and kidney risk factor
modification
 Treat complications
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Modifiable Risk Factors
• Avoid nephrotoxic drugs
• Consider ACE Medication (inhibitors/blockers) (antiproteinuric effect)
• Address co-morbidities:
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BP
Lipids
Diabetes
Smoking
Weight
Exercise
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Anaemia
Acidosis
Hyperparathyroidism
• Ensure appropriate drug doses for renal function
Non-modifiable Risk Factors
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Can’t change:
• Age > 50 years
• Family History of renal disease
• ATSI heritage
Presentations 3
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Stage 4 - severe decrease renal function
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eGFR 15-29
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Needs referral to nephrologist. Considering
dialysis, shunt for access, education and
transplantation
Stage IV Clinical Findings
Nil or nocturia,
 malaise
 anorexia
 nausea
 pruritis
 restless legs
 dyspnoea
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Stage IV Complications
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Hypertension
Hyperparathyroidism
Renal Osteodystrophy
Anaemia
Sleep Apnoea
CVD
Malnutrition
Hyperphosphataemia
Acidosis
Hyperkalaemia
Management Stage IV
Diagnosis
 Cardiac and kidney risk factor
modification
 Treat complications
 Dialysis education
 Dialysis access surgery
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Referral to Nephrologist
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Indications for Referral to a Nephrologist
• eGFR <30 mL/min/1.73 m2
• Rapidly declining kidney function (>15% in eGFR over 3 months
irrespective of baseline level)
• Proteinuria >1g/24 hrs
• Glomerular haematuria
• Kidney disease and hypertension that proves difficult to control
• Diabetes and eGFR <60 mL/min/1.73 m2
Presentation 4
Stage V
 End stage kidney failure
 eGFR < 15
 Referral/dialysis or transplantation
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Stage V Clinical Findings
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nocturia
mild malaise
anorexia
nausea
vomiting
pruritis
restless legs
dyspnoea
Management Stage V
Dialysis or transplantation (or
conservative medical management)
 Cardiac and kidney risk factor
modification
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Stage V Complications
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Hypertension
Hyperparathyroidism
Renal Osteodystrophy
Anaemia
Sleep Apnoea
CVD
Malnutrition
Hyperphosphataemia
Acidosis
Hyperkalaemia
Pericarditis
GIT bleeding
Encephalopathy
Neuropathy
General Management
Early Detection
 Appropriate referral
 Modify risk factors
 Treat associated complications
 Treat associated co-morbidities
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Investigations
• eGFR is a good start point
• Look for other co-morbidities (McGovern’s Law)
• Basics like BP, weight, cardiovascular assessment, BSL, urine
protein assessment are useful as early indicators
• Urea - imprecise, often elevated in dehydration/fasting
• 24 hour urine protein/creatinine clearance useful
• Imaging:
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Ultrasound (macroscopic imaging)
CT/MRI
IVP - with caution in patients with impaired renal function
(calculus)
Cystoscopy/Urethroscopy
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Biopsy for tissue diagnosis of pathology
McGovern’s Law
Number of conditions found at autopsy that
may account for the death of the patient
equals the age of the patient (years) divided
by 10, plus one.
 For a sixty year old, 6 + 1 = 7.
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Treating Hypertension
• Blood pressure reduction CKD can cause and
aggravate hypertension, and hypertension can contribute
to the progression of CKD.
• Reducing blood pressure to target levels is one of the
most important goals in management of CKD.
• Angiotensin converting enzyme inhibitors (ACEI) are
currently recommended as first line therapy, but
angiotensin receptor blockers (ARB) may provide similar
kidney protection.
• Hypertension may be difficult to control and multiple (i.e.
3 - 4) medications are frequently required.
Antiproteinuric Agents
• Antiproteinuric agents ACEI and ARB are more
effective than other anti-hypertensive agents in reducing
protein excretion and in slowing kidney function decline.
• However, these medications can cause an increase in
serum creatinine when treatment is initiated.
• If the increase in creatinine is less than 30% and
stabilises within two months of starting therapy,
medication should be continued.
• If the rise in creatinine level exceeds 30% above the
baseline value, medication should be ceased and
consideration be given to investigating the possibility of
bilateral renal artery stenosis.
Lipids
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Lipid-lowering treatments The use of
statins in people with CKD, who have
hypercholesterolaemia, slows kidney
failure progression.
Blood Glucose Levels
Glycaemic control Intensive blood
sugar control significantly reduces the
risk of developing CKD in the early
stages.
 However, the benefits in established
CKD are not known.
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Anaemia
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Correction of anaemia There is some
evidence that correction of anaemia may slow
progression of CKD. Although this has not
been proven, people certainly feel better.
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Hb < 110 g/dL
Correct iron deficiency/diet
Erythropoietin?
GIT loss?
Lifestyle
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Smoking
Nutrition
Alcohol
Physical activity
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Cease smoking
Dietary salt intake < 1 mmol/kg/day
< 2 standard glasses alcohol/day
> 30 mins/day physical activity
BMI < 25 kg/m2
WC < 102 cm (male), < 88 cm (female)
Hypertension
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Treatment goals:
• < 130/ 80 mmHg
• < 125/75 mmHg if proteinuria > 1g/day
• ACEI and/or ARB first-line
• lifestyle modification
Proteinuria
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> 50% reduction of baseline value
• ACEI and/or ARB first-line
Cholesterol
Total Cholesterol < 4.0 mmol
 LDL Cholesterol < 2.5 mmol/L
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• Dietary advice
• Statins
Blood Glucose Level
Pre-prandial BSL 4.4 - 6.7 mmol
 HbA1c < 7.0%
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• Lifestyle modification
• Oral hypoglycaemics
• Insulin
Acidosis
Acidosis
 HCO3 < 22 mmol/L
 Sodium Bicarbonate tablets
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Dietary Protein Intake
0.7 - 1.0 g/Kg body weight/day
 Dietary advice, low protein diet as indicated
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Hyperkalaemia
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K+ > 6.0 mml/L
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Dietary advice
Diuretics
Resonium???
Cease ACEI/ARB if K+ persistently > 6.0
mmol/L
Hyperparathyroidism
PO4 1.6 mmol/L
 PTH 2-5 x upper limit of normal
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Calcitriol
 Phosphate binders (calcium carbonate,
aluminium hydroxide, magnesium
trisilicate, sevelamer)
 Cinacalcet
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Malnutrition
Albumen < 35 g/L
 Dietary advice
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Sleep apnoea
Prevent apnoeac episodes
 Manage condition:
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• Weight reduction
• Avoid CNS depressants
• CPAP therapy (if obstructive pattern
Restless legs
Correct iron deficiency
 Dopaminergic agents
 Herbal options: Crampeze,
 Exercise/stretches
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Drugs to reduce or cease
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Acetazolamide
Acyclovir
Colchicine
Digoxin
Gabapentin
Lithium
metformin (significantly increased risk of lactic
acidosis when GFR < 50 mL/min/1.73m2)
• Sotalol
• sulphonylureas.
Drugs affecting renal function in
CKD
• NSAIDs and COX-2 inhibitors
• ACE inhibitors and angiotensin II receptor
antagonists
• beware, especially, the 'triple whammy' of
NSAID/COX-2 inhibitor, ACE inhibitor and
diuretic
• radiographic contrast agents
• Aminoglycosides
• lithium.
Renal osteodystrophy
• Renal osteodystrophy is multifactorial. The aetiology includes:
• Reduced production of the active form of vitamin D by the diseased
kidneys. A drop in vitamin D reduces the intestinal absorption of
calcium and causes a fall in the blood level of calcium.
• If calcium levels in the blood become too low, parathyroid hormone
(PTH) production is increased. PTH tries to keep the calcium level in
the blood normal by:
– increasing calcium resorption from bones
– increasing production of vitamin D by the kidney in an attempt to increase
calcium absorption from the intestine
– increasing resorption of calcium by the kidneys to reduce renal losses.
– Vitamin D and PTH usually work together to maintain calcium homeostasis.
However, in CKD, the kidneys have a reduced ability to produce the active
form of vitamin D and the hypocalcaemia that develops cannot be corrected.
This causes PTH levels to rise still further. Because the intestinal absorption
of calcium is impaired, the net result is resorption of calcium from the bones.