Renal Disease

Document Sample

Renal Disease





Chronic Kidney Disease

GP Management



Ross Bills

Prevalence

 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

• 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

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

The Kidney Screen

 Simple screen at presentation.

 If risk factors present:

• Check BP

• Dipstick for protein

• Creatinine level for eGFR

 If eGFR > 60, normal BP, No proteinuria, low

risk. Review opportunistically.

 Caution if other evidence of renal disease -

haematuria, casts etc.

eGFR

 The new measure of renal function, using

prediction equations based on age, sex and

creatinine clearance



 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

 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

 eGFR has not been validated or shown to have acceptable

accuracy in:

• 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

 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:

• BP

• Lipids

• Diabetes

• Smoking

• Weight

• Exercise

Signs/Symptoms Stage I - II

 Bugger all

Complications Stage I - II

 Usually just hypertension if anything

Presentations 2

 Stage 3 - moderate loss kidney function



 eGFR 30-59



• Look at modifiable risk factors

• Monitor eGFR (three monthly

• Consider referral to nephrologist

Stage III Clinical Findings

 Nil or

 nocturia

 mild malaise

 anorexia

Stage III Complications

• Hypertension

• Hyperparathyroidism

• Renal Osteodystrophy

• Anaemia

• Sleep Apnoea

• Restless legs

• CVD

• Malnutrition

Management Stage III

 Diagnosis

 Cardiac and kidney risk factor

modification

 Treat complications

Modifiable Risk Factors

• Avoid nephrotoxic drugs

• Consider ACE Medication (inhibitors/blockers) -

(antiproteinuric effect)

• Address co-morbidities:

• BP

• Lipids

• Diabetes

• Smoking

• Weight

• Exercise

• Correct:

• Anaemia

• Acidosis

• Hyperparathyroidism

• Ensure appropriate drug doses for renal function

Non-modifiable Risk Factors

 Can’t change:

• Age > 50 years

• Family History of renal disease

• ATSI heritage

Presentations 3

 Stage 4 - severe decrease renal function



 eGFR 15-29



 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

Stage IV Complications

• 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

Referral to Nephrologist

 Indications for Referral to a Nephrologist

• eGFR 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 30 mins/day physical activity

• BMI 1g/day





• ACEI and/or ARB first-line

• lifestyle modification

Proteinuria

 > 50% reduction of baseline value



• ACEI and/or ARB first-line

Cholesterol

 Total Cholesterol 6.0 mml/L

• 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







 Calcitriol

 Phosphate binders (calcium carbonate,

aluminium hydroxide, magnesium

trisilicate, sevelamer)

 Cinacalcet

Malnutrition

 Albumen < 35 g/L

 Dietary advice

Sleep apnoea

 Prevent apnoeac episodes

 Manage condition:

• Weight reduction

• Avoid CNS depressants

• CPAP therapy (if obstructive pattern

Restless legs

 Correct iron deficiency

 Dopaminergic agents



 Herbal options: Crampeze,



 Exercise/stretches

Drugs to reduce or cease

• 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.


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