Chronic Kidney Disease Pathway Document Description Presented ...

Chronic Kidney Disease Pathway
Document Description
Document Type
Service Application
Version 2.0
Ratification date October 2009
Review date October 2011
Clinical Pathway
Clinicians Included in the Management of Renal
Disease
Lead Author(s)
Name
Position within the Organisation
CVD/Renal Disease Lead nurse
Pharmaceutical Advisor
Presented for discussion, approval and ratification to
Core Policies and Procedures Group
Change History
Version Date Comments
1.0 Dec. 2007 Chronic Kidney Disease Register Validation Toolkit
1.1 July 2009 Draft of CKD pathway circulated for consultation
1.2 Sept 2009 Amendments agreed following consultation process
2.0 Oct. 2009 Chronic Kidney Disease Pathway ratified
Link with Standards for
Better Health Domains
Link with Trust Purpose
and Values statements
C6:Clinical and Cost Effectiveness
We will work to continuously improve services
We will support and empower people to
contribute to improving their health and that of
their community
1

Summary Sheet
This pathway is intended to provide information on the management of people
with Chronic Kidney Disease (CKD) to reduce their risks and to identify, prevent
or delay the progression of associated co-morbid vascular and metabolic
conditions. It is also intended to identify people who are deemed to be at high risk
of developing CKD, to promote active screening of these people and to reduce or
eliminate individual risk factors to reduce their overall level of risk.
This policy applies directly to all staff members employed by NHS Dudley and
Dudley Community Services who are involved in the management of people with
CKD and is recommended as good practice guidance for each of the
independent contractor professions. National and local guidance, policies, reports
and/or papers which this particular document should be read in conjunction with:
Local Guidance:
• Best practice Guidelines for Lifestyle Assessment
• Cardiovascular Risk pathway
• Hyperlipidaemia Guidelines
• Dudley Guidelines for the Pharmacological Management of Hypertension
National Guidance: NICE Guidelines for:
• Management of Chronic Kidney Disease
• Secondary Prevention of Myocardial Infarction
• Management of Patients with Heart Failure
• Management of Hypertension
• Lipid Modification
• Management of Obesity
National Service Frameworks for:
• Coronary Heart Disease
• Renal Services Part II
• Diabetes
This document will be subject to formal review in October 2011 led by the
Vascular Programmes Local Implementation Team.
2

Pathway for the Identification and Management of
Chronic Kidney
Disease
In the Primary Care Setting
Implementation date: October 2009
Review date: October 2011
Pathway overview
3

This CKD pathway has been produced by the CKD pathway group, a sub-group
of the Dudley Renal LIT. It is intended to be used by practice and community
teams, GPs, practice nurses, HCAs and administrative/I.T staff to:
• Build and validate accurate CKD registers in line with the Quality and
Outcomes Framework of the GMS contract and nationally expected
prevalence rates.
• Promote an awareness of CKD and the need for reduction of risk, early
identification and diagnosis.
• Inform the management of people with CKD in line with best practice as
demonstrated in local and national guidelines
• Support the appropriate referral to acute services and/or promotion of
joint working with acute and community services to provide optimum
outcomes in terms of management and patient choice.
Consultation has included:
• Renal LIT
• Diabetes DIP
• Vascular LIT
• Nephrologists at DGoH
• Diabetologists at DGoH
• Consultant Chemical Pathologist
• Dudley Clinical Commissioning Forum (DCF)
• Dudley Clinical Executive Team
• Community Diabetes Team
• Renal Dieticians
• Dudley Kidney Patients’ Association
This pathway may be used wholly electronically by downloading onto the practice
system, or in paper form. Practices may wish to use the pathway in either way, or
may wish to download certain sections only.
For further information on the development of the CKD pathway please contact:
Cardiovascular and Renal Disease Lead Nurse Tel. 01384 366880
Falcon House Fax. 01384 366460
The Minories Mob. 07786 338072
Dudley
DY2 8PG Courier 114
4

Contents
Introduction ……………………………………………………………………….7
Renal Pathway Overview ……………….……………………………………. ..9
High Risk Groups ……………………………………………………………….10
Read Codes ……………………………………………………………………..12
Identification of CKD in patients not in a High Risk Group …………………14
Acute Renal Failure …………………………………………………………….15
Contact Details ……………………………………………….. ………………. 17
Diagnosis of CKD ……………………………………………………………... 18
CKD Stages ……………………………………………………………………. 19
Prevalence of CKD ……………………………………………………………. 20
Practice Action Plan Template ………………………………………………. .21
Stages 1 and 2 …………………………………………………………………. 30
Patient information ……………………………………………… 30
Cardiovascular risk ……………………………………………… 31
Hypertension …………………………………………………….. 33
Initiating ACE Inhibitor …………………………………………… 36
Salt intake ………………………………………………………… 36
Nephrotoxic drugs ……………………………………………….. 36
Renal Artery Stenosis …………………………………………… 37
Urinalysis …………………………………………………………. 40
Diet ………………………………………………………………... 44
Diabetic Control …………………………………………………. .45
Hepatitis B ……………………………………………………… 48
5

Influenza/Pneumococcal Vaccination ……………………….. 49
Follow-up ……………………………………………………….. 50
Stage 3 …………………………………………………………………………… 51
Anaemia ……………………………………………………….. 51
Stage 4 …………………………………………………………………………… 54
One-Stop Renal Clinic ………………………………………. 54
Bone Metabolism …………………………………………….. 56
Annual Review ……………………………………………….. 57
Stage 5 ………………………………………………………………………….. 59
Referral ……………………………………………………….. 60
Renal Ultrasound ……………………………………………. 61
Abbreviations …………………………………………………………………… 62
Appendix 1:
Calcium and Phosphate Balance pathway …………………………………. 63
6

Introduction
Chronic kidney disease (CKD) describes abnormal kidney function and/or
structure. It is common, frequently unrecognised and often exists together with
other conditions (for example, cardiovascular disease and diabetes). When
advanced, it also carries a higher risk of mortality. The risk of developing CKD
increases with increasing age, and some conditions that coexist with CKD
become more severe as kidney dysfunction advances. CKD can progress to
established renal failure in a small but significant percentage of people.
CKD is usually asymptomatic, but it is detectable, and tests for detecting CKD
are both simple and freely available. There is evidence that treatment can
prevent or delay the progression of CKD, reduce or prevent the development of
complications and reduce the risk of cardiovascular disease. However, because
of a lack of specific symptoms, people with CKD are often not diagnosed, or
diagnosed late when CKD is at an advanced stage.
http://www.nice.org.uk/nicemedia/pdf/CG073NICEGuideline.pdf
Normal Kidney Ageing
A normal estimated glomerular filtration rate (eGFR) is about 100 ml/min in young
adults. However, this may be somewhat lower, some young adults with normal
kidneys may have an eGFR as low as 75 ml/min. Normal kidney function
deteriorates with age and falls by about 1 ml/min per year. Therefore as people
get older, many healthy people aged 75+ may have an eGFR of < 60 ml/min.
Recent research suggests that 1 in 10 of the population may have chronic kidney
disease (CKD), but it is less common in young adults, being present in 1 in 50
people. In those aged over 75 years, CKD is present in 1 out of 2 people.
However, many elderly people with an eGFR < 60 mls/min may not have
‘diseased’ kidneys, but have normal ageing of their kidneys. Although severe
kidney failure will not occur with normal ageing of the kidneys, there is an
increased chance of high blood pressure and heart disease or stroke.
It is recommended that all patients with CKD stage 1 – 5, including elderly
patients are added to the CKD register for the GMS Contract Quality and
Outcomes Framework and undergo annual screening to monitor the rate of
progression, blood pressure, proteinuria and development of associated
cardiovascular risk factors.
http://www.kidney.org.uk/Medical-Info/ckd-info/index.html
Late referral of patients with CKD requiring renal replacement therapy (RRT) to
specialist renal services is associated with significant cost and poor clinical
outcomes. On average 30% of people with advanced kidney disease are
referred late to nephrology services from both primary and secondary care,
causing increased mortality and morbidity.
http://www.nice.org.uk/nicemedia/pdf/CG073NICEGuideline.pdf
7

The great majority of patients starting RRT have progressed from earlier stages
and most could therefore have been identified, managed and referred more
appropriately at an earlier stage from primary care. Early CKD is common
however and referral of all patients with early CKD would completely overwhelm
existing specialist services. The great majority of patients with early CKD do not
progress to end-stage renal disease (ESRD), but do have a substantially
increased risk of cardiovascular morbidity and mortality. Optimal management of
the risk factors for cardiovascular disease, such as hypertension and proteinuria
will reduce the risk of progression from early CKD to ESRD and can be managed
effectively in primary care.
CKD Stages According to Established Estimated Glomerular Filtration Rate
(eGFR)
CKD Stage
Description
1 Normal eGFR > 90 mL/min/1.73m 2
*With other evidence of chronic kidney damage present
2 Mild Impairment - 60-89 mL/min/1.73m 2
*With other evidence of chronic kidney damage present
3 Moderate Impairment - 30-59 mL/min/1.73m 2
3A 45 - 59
3B 44 - 30
4 Severe Impairment – 15-29 mL/min/1.73m 2
5 Established Renal Failure (ERF)
< 15 mL/min/1.73m 2 or on dialysis
*Other Evidence of Chronic Kidney Damage
• Persistent microalbuninuria, proteinuria or haematuria (after exclusion of
other causes)
• Structural abnormalities seen on X-ray (e.g. polycystic kidney disease)
• Biopsy proven chronic glomerulonephritis
8

CKD Pathway
D
I
A
G
N
O
S
I
S
Ensure annual assessment
of people in high risk groups
Introduction
1. Confirm diagnosis
2. Identify CKD stage 1 - 5
3. Enter onto practice system with appropriate
read code compatible with GMS contract to form
register.
4. Check register prevalence
5. Consider use of practice action plan template
Suspicion of Chronic Kidney Disease
(CKD) following investigation for other
unrelated condition
Is it Acute Renal
Failure
Urgent
Admission
M
A
N
A
G
E
M
E
N
T
CKD stage 1 and 2.
Patient information and
education
Address progressing factors:-
CV risk
Hypertension
lifestyle
Initiation of ACE/ARB
Drugs with high salt content
Nephrotoxic/renally excreted
drugs, inc. OTC medication
Renal Artery Stenosis
Urinalysis
Diet in CKD
Glycaemic control
Flu/pneumo vac
Hepatitis B immunisation
Follow-up
Stage 3 (3A 3B)
As stage 1 and 2
plus:
Management of
anaemia
ESA pathway
CKD stage 4
As I, 2 and 3 plus shared
care plan initiation. Refer to
"One-Stop" Renal clinic
Bone metabolism
Pathway for the
Management of Calcium
and Phosphate Balance
CKD stage 5
Urgent referral
if clinically
appropriate
exceptions
Annual
review in
primary
care
R
E
F
E
R
R
A
L
Criteria for referral to
Specialist Nephrology
services
Renal Ultrasound
Information to include
with referral
Palliative care trust protocol
Prescribing /symptom control in advanced
renal disease
Seeking Advice from
Nephrologist / Renal
Dept. DGOH
Contact information
Frequently asked
questions
9

High Risk Groups
Renal function should be measured and recorded annually for all patients who
fall into a high risk group. This is measured by Estimated Glomerular Filtration
Rate (eGFR). Measurement of eGFR is available from the pathology department
at Dudley Group of Hospitals. It accompanies the report following any request for
Urea and Electrolytes (U+E), being calculated from the serum creatinine assay.
Patients in the high risk groups are considered to be at a higher than normal risk
of developing renal impairment due to co-morbities and/or medical history.
Ethnicity also increases risk with black and minority ethnic (BME) groups in the
U.K having up to 4 times greater risk of developing CKD.
http://www.britishrenal.org/conferences/brs2007/posters/CKD%20General-48.doc
The high risk groups fall into 3 main categories, morbidity, drug related and
urinary.
Morbidity:
• Patients with Vascular disease
o Coronary Heart disease
o Stroke
o Peripheral Vascular disease
• Heart Failure
• Hypertension
• Diabetes
• Multi-system diseases which involve the kidney, e.g. systemic lupus
erythematosus, rheumatoid arthritis.
• A first-degree relative with CKD stage 5.
Drug related:
• Patients on ACE inhibitors or angiotensin receptor blockers (ARBs)
• Patients on NSAIDs, including COX II
• Patients on diuretics
• Patients on lithium carbonate
• Mesalazine and other 5-aminosalicylic drugs
• Calcineurin inhibitors (cyclosporin, tacrolimus)
Urinary:
• Recurrent Urinary Tract Infections
• Bladder outflow obstruction
• Recurrent kidney stones (>1/year) or predisposing condition, e.g. primary
hyperoxaluria
• Neurogenic bladder
• Past surgical urinary diversion
• Polycystic kidney disease
• Reflux nephropathy
• Biopsy proven chronic glomerulonephritis
• Persistent proteinuria
• Urologically unexplained persistent haematuria
10

Kidney function deteriorates naturally with age. However the conditions above
may cause the kidneys to deteriorate more rapidly. Careful management of
progressing factors (see pathway) could ensure a normal or close to
normal/expected pattern of deterioration.
Kidney function by eGFR measurement should be monitored annually in the high
risk groups identified above.
Frequency of monitoring of Kidney function in CKD is indicated by the table
below.
Frequency of Monitoring of Kidney Function in Established CKD
K/DOQI eGFR
Frequency
Stage mls/min
1 > 90 Annually
2 60 - 89 Annually
3 30 - 59 Annually
(6 monthly if newly diagnosed or progressive**)
4 15 - 29 6 monthly
(3 monthly if newly diagnosed or progressive**)
5 < 15 3 monthly
Stable kidney function is defined as a change of < 2mls/min in 6 months
** Progressive kidney function is defined as a change of > 2mls/min in 6 months
Any patient assessed with a progressive condition should receive assessment of
progressing factors and discussion/referral to nephrology services.
Stage 3 Classification
The UK Consensus Conference on early CKD has recommended that the Kidney
Disease Outcomes Quality Initiative (KDOQI) classification should be modified by
dividing CKD stage 3 into CKD 3A and 3B and that a suffix “p” should be used for
all stages to denote patients with urine protein to creatinine ratio >100mg/mmol,
who are at increased risk for progression and/or the development of
cardiovascular disease e.g. CKD stages 2p, 3Bp.
CKD stage 3 is sub-classified into 2 groups, 3A and 3B.
Stage eGFR Progression to ESRD
3A 45 - 59 Lower risk
3B 44 - 30 Higher risk
11

Using the existing classification at least 4% of the adult population have stage 3
CKD, many of whom are elderly. They are at increased risk of cardiovascular
disease but most will not progress to end stage kidney disease. The priority
should therefore be to identify those at risk of kidney disease progression.
Persistent proteinuria (protein:creatinine ratio (PCR) > 100 mg/mmol) is the
best indicator of risk of progression to ESRD.
In diabetic patients urinary albumin /microalbumin estimations should be used.
It is recommend that all patients with suspected early CKD should have a urine
dipstick for proteinuria and, if positive, quantification of the PCR. This is included
in the Quality and Outcomes Framework. Urine albumin:creatinine ratio (ACR)
should be used in line with national guidelines in people with diabetes.
(Patients undergoing dialysis have the suffix D added to their CKD stage, e.g.
5D. Those who have had a transplant should be classified according to eGFR but
have the suffix T added, e.g. 3T)
Read Codes
1Z15. CKD stage 3A
1Z16. CKD stage 3B
1Z17. CKD stage 1 with proteinuria / 1P
1Z18. CKD stage 1 without proteinuria
1Z19. CKD stage 2 with proteinuria / 2P
1Z1A. CKD stage 2 without proteinuria
1Z1B.
1Z1C.
1Z1D.
1Z1E.
1Z1F.
1Z1G.
1Z1H.
1Z1J.
1Z1K.
1Z1L.
CKD stage 3 with proteinuria / 3P
CKD stage 3 without proteinuria
CKD stage 3A with proteinuria / 3AP
CKD stage 3A without proteinuria
CKD stage 3B with proteinuria / 3BP
CKD stage 3B without proteinuria
CKD stage 4 with proteinuria / 4P
CKD stage 4 without proteinuria
CKD stage 5 with proteinuria / 5P
CKD stage 5 without proteinuria
http://www.renal.org/CKDguide/consensus.html
References
12

Joint Speciality Committee - Royal College of Physicians, The Renal Association
(2006) Chronic Kidney Disease in Adults, UK Guidelines for Identification,
Management and Referral.
http://www.renal.org/CKDguide/full/CKDprintedfullguide.pdf
University Hospital – Leicester (2005) Renal Guidelines Adults with Chronic
Kidney Disease http://www.britishrenal.org/Other/RenalGuideline.pdf
Department of Health (2005) The National Service Framework for Renal
Services: Part Two: Chronic Kidney Disease, Acute Renal Failure and End of Life
Care.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicy
AndGuidance/DH_4101902
Return to overview
13

Identification of CKD in Patients who are not in a High Risk Group
There are few specific signs or symptoms which would alert suspicion to the
possibility of CKD in groups who are not routinely tested due to the presence of
morbidities which would put them at high risk. As a result these patients often
present at a late stage. Another reason for this would be the lack of
understanding of clinical staff on the significance of kidney function testing when
relying only on measurements of serum creatinine concentration. It is therefore
recommended that eGFR be requested as this gives a more accurate picture of
decline in kidney function than rising serum creatinine alone. Currently at Dudley
Group of Hospitals any request for urea and electrolytes (U+E) will automatically
have eGFR calculated and will accompany the results.
Any patient with an eGFR of < 60 mls/min should be investigated following
the renal pathway.
An eGFR of > 60 without other evidence of renal disease should not be
considered significant and these patients should not be subject to further
investigation. However, a diagnosis of Acute Renal Failure should be considered.
In many cases the possibility of renal impairment only comes to light when a
patient receives routine monitoring at a well person clinic, insurance medicals or
during routine investigations for acute illness or any assessment which involves
the monitoring of serum creatinine and/or U+E and/or urinalysis. It is worth
remembering that the majority of these patients will feel well and therefore the
diagnosis of renal impairment will be unexpected, especially if it comes to light as
part of a routine assessment.
Joint Speciality Committee - Royal College of Physicians, The Renal Association
(2006) Chronic Kidney Disease in Adults, UK Guidelines for Identification,
Management and Referral.
http://www.renal.org/CKDguide/full/CKDprintedfullguide.pdf
Return to overview
14

Acute Renal Failure
Acute Renal Failure (ARF) is a medical emergency as deterioration can be rapid
and fatal in many cases. Prognosis for recovery of kidney function is dependent
on the time delay between presentation and diagnosis. It is therefore extremely
important that people with suspected ARF are identified and investigated
promptly to ensure best possible outcomes. These patients should receive
prompt admission to acute nephrology services/emergency department.
ARF is characterised by rapid deterioration in renal function over a period of
hours or days. It should be suspected in the presence of an acute illness with
the following signs/symptoms:
• A 50% rise in serum creatinine concentration
• A 25% fall in eGFR (if baseline unknown, assume 75mls/min)
N.B. eGFR should be interpreted with caution as it should be calculated in
stable creatinine concentrations
• Oliguria (urinary output

Management of a Previously Undiagnosed Patient with eGFR <
60mls/min
Is the YES patient acutely unwell
NO
YES
Manage illness as appropriate.
Repeat eGFR within 1-5 days
(Go to *)
Symptoms of outflow
obstruction**
YES
Palpate for bladder
Urgent renal ultrasound
(Renal ultrasound scan if history
suggestive of urological disease)
NO
* Has a reduced eGFR (< 60mls/min) or
raised creatinine been measured
previously
NO
Repeat eGFR within 5 days
Suspect ARF in the presence of
any of the following:
eGFR < 30 ml/min
eGFR fall of 25%
Creatinine rise of 50%
Blood and Protein in urine
YES
Check previous eGFR results.
Calculate eGFR using the 4-
variable MDRD formula from
previous creatinine results.
Compare results and track rate of
progression chronologically.
Suspect ARF if there is:
• A fall in eGFR of 25%
• A rise in Creatinine of 50%
• eGFR < 30 ml/min
• Blood and Protein in urine
URGENT
ADMISSION
Refer to/
Discuss with
nephrologist.
Contact details
**People with CKD and renal outflow obstruction should normally be referred to urological
services, unless urgent medical intervention is required.
16

Next Steps
Any patient suspected to have ARF should be admitted urgently to nephrology
services/emergency department with as much information as possible, including
all previous results available for:
• Creatinine
• eGFR
• Blood pressure
• Urinalysis
• HbA1C (if diabetic)
To include a list of current medication (including OTC) and any relevant medical
history.
Further information upon which to make a clinical decision should be sought
urgently by contacting the nephrology department.
Contact details:
On call renal consultant:
(Advice/Urgent admission)
01384 244432 (direct line)
(or 01384 456111 to switchboard at
RHH and ask for on-call renal
consultant)
Fax./urgent paper referral 01384 244543
Haemodialysis 01384 244384
(Nursing Station Renal Unit)
CAPD 01384 244388
(Nursing Station Renal Unit)
Return to overview
Diagnosis of CKD
17

The diagnosis of CKD is made by assessment of kidney function using estimated
Glomerular Filtration Rate (eGFR). eGFR is calculated from serum creatinine
levels, but depends on the method of creatinine assay used by each pathology
department. Therefore independent calculations of eGFR from previous
creatinine results will not give reliable results, as a correction factor needs to be
applied for the method used by Dudley group of hospitals pathology dept.
There is no need for 24-hour urine collection to measure creatinine clearance in
primary care.
The method for calculating eGFR is the 4-variable MDRD formula:
eGFR (mL/min/1.73m 2 )= 186 x [Serum Creatinine (umol/L) x 0.0113] -1.154 x
Age(years) -0.203 (x 0.742 if female) and 1.21 if African Caribbean.
An online calculator can be downloaded from:
http://www.renal.org/eGFRcalc/GFR.pl
N.B. The 4-variable MDRD formula:
• Is suitable for adults only (>17 years of age)
• Results are unreliable for eGFR > 60 mL/min/1.73m 2 .
• Results will NOT reflect true GFR if patient is receiving dialysis therapy.
• The formula has not been validated for Asian people.
• Results may deviate from true GFR values with extremes of body
composition, dietary intake or severe liver disease.
• The formula has NOT been validated for drug dosing. Use the Cockcroft
and Gault formula
Diagnosis of CKD should be made during a period of wellness by
measurement of eGFR.
Advise the person not to eat meat for at least 12 hours before the eGFR blood
test.
If the eGFR is < 60 mls/min then the guidance in this pathway should be followed
to exclude acute renal failure.
A diagnosis of renal impairment should not be made on the basis of
one result; at least 2 results should be considered which should be at
least 3 months apart.
If both of the results are< 60 mls/min then the patient should be considered to
have CKD and be added to the practice register. The patient should then be
managed following the guidance in this pathway.
18

Return to overview
CKD Stages
CKD Stage
Description
1 Normal eGFR > 90 mL/min/1.73m 2
With other evidence of chronic kidney damage
2 Mild Impairment - 60-89 mL/min/1.73m 2
With other evidence of chronic kidney damage
3 Moderate Impairment - 30-59 mL/min/1.73m 2
3A 45 - 59
3B 44 - 30
4 Severe Impairment – 15-29 mL/min/1.73m 2
5 Established Renal Failure (ERF)
< 15 mL/min/1.73m 2 or on dialysis
*Other Evidence of Chronic Kidney Damage
• Persistent microalbuminuria
• Persistent proteinuria
• Persistent haematuria (after exclusion of other causes)
• Structural abnormalities seen on X-ray (e.g. polycystic kidney disease)
• Biopsy proven chronic glomerulonephritis
Patients found to have an eGFR of 60-89 mls/min without one of the markers
above should not be considered to have CKD as these levels are considered
normal and therefore should not be subject to further investigation unless there
are additional reasons to do so, e.g. belonging to a high risk group.
Prevalence of CKD
The prevalence of CKD in at stage 3-5 in the UK based on neoErica data is
4.9% 1
19

(Where stage 4 = 0.7%, and stage 5 = 0.2%)
Screening of patients with hypertension, diabetes and > 55 would yield approx.
93% of the CKD register, with this approach being the most effective strategy to
detect patients with CKD 2 .
Based on an expected prevalence of 4.9%:
• For a practice population of 2000:
The approx. number of patients with CKD = 94
(4 pts. at stage 4 and 4 pts. at stage 5)
• For a practice population of 5000
The approx. number of patients with CKD = 245
(10 pts. at stage 4 and 10 pts. at stage 5
• For a practice population of 10 000
The approx. number of patients with CKD = 490
(20 pts. at stage 4 and 20 pts. at stage 5)
For guidance on building and validating a practice CKD register see practice
action plan - compiling a chronic kidney disease register.
References
1. de Lusignan S, Chan T, Stevens P, O'Donoghue D, Hague N, Dzregah B,
Van Vlymen J, Walker M and Hilton S. Identifying patients with chronic
kidney disease from general practice computer records. Family Practice
2005; 22: 234–241
http://fampra.oxfordjournals.org/cgi/content/full/22/3/234
2. Hallan S et al. Screening strategies for chronic kidney disease in the
general population: follow-up of cross sectional health survey BMJ
2006;333(7577):1047. http://www.bmj.com/cgi/con
Return to overview
20

Practice Action Plan
Compiling a Chronic Kidney Disease Register
Name of Practice …………………………………………………………………………………………………………………………
Aim: To build a register of patients with Chronic Kidney Disease to meet the requirements of the Quality and
Outcomes Framework of the GMS contract: CKD1
This action plan sets out the method and rationale behind each action in a step wise approach, assigning responsibility to
each part of the task. Practice expected prevalence should be calculated, allowing for assessment of the completeness of
the final register.
Support for completing these actions is available from the Cardiovascular and Renal Disease Lead Nurse, (address
below)
Shelagh.cleary@dudley.nhs.uk Tel. 01384 362754
Please sign below and send a copy of this front sheet to:
Cardiovascular and Renal Disease Lead Nurse
Service Development Dept. 5 th Floor, Falcon House, The Minories, Dudley. DY2 8PG. Courier no. 114, Fax 01384 366460
Signed ………………………………………………. Position ………………………………………...
Print …………………………………………………. Date ……………………………………………
21

Practice Demographics
Population size ……………………………….
Estimated CKD prevalence at stage 3-5 = 4.9%
Stage 4 = 0.7%, and stage 5 = 0.2%
(Based on UK figures from NeoErica 1 )
Estimated practice prevalence of CKD stage 3-5 = ……………………. patients
(Stage 4 = ………. patients
Stage 5 = ……….. patients)
Number on practice system with read coded CKD diagnosis ……………………………….
(Read codes compatible with QoF)
This information can be found from population manager or clinical audit facility on the practice system. Or a practice query
can be run as outlined on p.4
22

Action Rationale Responsible
Run a search on the practice system to identify
all patients with an eGFR

one

eGFR

3.1.07 eGFR = 35
26.1.07 eGFR = 41
3.3.07 eGFR = 38
4741 30.6.06 eGFR = 50
10.10.06 eGFR = 56
22.5.07 eGFR = 46
Last BP 139/71
On ACE
Achieving all 4 clinical indicators.
Diagnosis confirmed CKD 3. Added to register.
Last BP 144/70
Not on ACE
Achieving CKD 1,2 and 3
26

CKD Stages
CKD Stage Description Read Code
1 Normal GFR > 90 mL/min/1.73m 2
*With other evidence of chronic kidney damage
2 Mild Impairment - 60-89 mL/min/1.73m 2
*With other evidence of chronic kidney damage
3 Moderate Impairment - 30-59 mL/min/1.73m 2 1Z12
4 Severe Impairment – 15-29 mL/min/1.73m 2 1Z13
5 Established Renal Failure (ERF)
< 15 mL/min/1.73m 2 or on dialysis
eGFR
(estimated glomerular filtration rate)
1Z14
451E
*Other Evidence of Chronic Kidney Damage
• Persistent microalbuminuria
• Persistent proteinuria
27

• Persistent haematuria (after exclusion of other causes)
• Structural abnormalities seen on X-ray (e.g. polycystic kidney disease)
• Biopsy proven chronic glomerulonephritis
Patients found to have an eGFR of 60-89 mls/min without one of the markers above should not be considered to have
CKD and should not be subject to further investigation unless there are additional reasons to do so, e.g. belonging to a
high risk group.
References
de Lusignan S, Chan T, Stevens P, O'Donoghue D, Hague N, Dzregah B, Van Vlymen J, Walker M and Hilton S.
Identifying patients with chronic kidney disease from general practice computer records. Family Practice 2005; 22: 234–
241 http://fampra.oxfordjournals.org/cgi/content/full/22/3/234
Return to overview
28

References
Joint Speciality Committee - Royal College of Physicians, The Renal Association
(2006) Chronic Kidney Disease in Adults, UK guidelines for Identification,
Management and Referral.
http://www.renal.org/CKDguide/full/CKDprintedfullguide.pdf
Department of Health (2005) The National Service Framework for Renal
Services: Part Two: Chronic Kidney Disease, Acute Renal Failure and End of Life
Care.
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicy
AndGuidance/DH_4101902
University Hospital Leicester (2005) Renal Guidelines – Adults with Chronic
Kidney Disease http://www.britishrenal.org/Other/RenalGuideline.pdf
British Medical Association (2007) Chronic Kidney Disease Frequently Asked
Questions. NHS Employers
http://www.primarycarecontracting.nhs.uk/uploads/QOF/june_07/qof__faq_in_chr
onic_kidney_disease.pdf
Return to overview
29

Stages 1 and 2
Patient Information and Education
The following websites are useful for downloading information and materials for
patients and for use in clinics.
It is worth noting however, that a diagnosis at stage 3/4 CKD may have been
made on blood test results alone. The patient will most likely have not had any
symptoms and therefore will not be expecting the diagnosis.
Kidney Patient Guide
Web: www.kidneypatientguide.org.uk
The Kidney Patient Guide provides web-based patient information for renal
patients, their families, health professionals and others interested in kidney
disease. The site is described as follows: "It includes information not only on
physical aspects of kidney failure - how the kidneys function, what happens when
they don't, and the treatments available - but also on wider issues such as
emotional, social and financial implications.
The site is designed primarily with a UK focus but will be of value to anyone who
is affected by the condition." Information is included on the following topics.
• What patients say.
• The physical aspects of kidney failure.
• The treatment of kidney failure.
• Emotional effects.
• Diet.
• Financial implications.
• Holidays.
• Carers, partners, family & friends.
• Support groups.
Kidney Health Information
http://www.kidneyresearchuk.org/index.phpoption=com_content&task=view&id=
15&Itemid=32
Kidney Health Information is a service for kidney patients, their families and
carers, as well as medical professionals and researchers. The service is provided
by Kidney Research UK and the information is available to everyone at no
charge. It has a downloadable factfile section.
Return to overview
30

Cardiovascular Risk
All patients with CKD have a greatly increased risk of developing heart disease
and other diseases of blood vessels, including strokes. For many, this is more
important than the danger of progressing to end-stage renal disease due to the
10 fold increase in cardiovascular events and mortality at CKD stage 3.
Furthermore, when events occur, mortality is higher for people with CKD and
they have less favourable outcomes from intervention such as angioplasty. This
increased risk begins at the very earliest stages, for example when there is
microalbuminuria without a reduced eGFR. The prevalence of CKD at stage 3-5
in the population is currently approximately 4.9%. However the prevalence of
CKD at stages 4-5 is approximately 0.9%. The chief reason for the reduction of
the numbers of people going on to stage 4 or 5 is due in the most part to their
cardiovascular mortality at an earlier stage. For this reason reducing
cardiovascular risk is of crucial importance to impact on mortality and as a
progressing factor for further renal deterioration.
For this reason, CVD risk calculators, including JBS2, are not recommended for
use in calculating risk in patients with CKD. CKD at stage 3-5 is in itself a marker
for CVD, therefore no calculation is needed and these patients should be
considered high risk.
Dyslipidaemia
Patients with established macrovascular disease should receive treatment for
hyperlipidaemia according to the current PCT Hyperlipidaemia Guidelines. Treat
with simvastatin 40mg, aim for cholesterol of < 4mmol/l.
Patients with diabetes and CKD but no established macrovascular disease
should be offered lipid-lowering drug treatment according to the current PCT
Hyperlipidaemia Guidelines.
Patients with CKD who do not have diabetes and who do not have established
macrovascular disease should be offered the options of lipid-lowering treatment
according to the current PCT Hyperlipidaemia Guidelines if estimated 10-year
risk of cardiovascular disease is ≥20%.
Health Economy Formulary Drug of Choice - simvastatin 40mg.
For further information see Dudley Guidelines for the Drug Treatment of
Hyperlipidaemia. http://joint.dudley.nhs.uk/cmsextra/documents/cms/222-2008-2-
22-5663216.pdf
It would follow that patients with CKD should receive lipid therapy if they are
considered to be at high risk. However, studies evidencing benefit from the use
31

of statins such as HPS and ASCOT excluded patients with CKD therefore
reliable evidence is not available. The Study of Heart and Renal Protection
(SHARP) with a cohort of over 9000 patients will hopefully provide the evidence
required. Until then, patients with CKD and no cardiovascular disease or diabetes
should be treated with a statin if their 10 year CVD risk is > 20% (Renal
Association). However, tables for calculating risk of CVD are not recommended
for use in patients with CKD, but it would follow that due to their presenting
condition, they would be considered at high risk of cardiovascular disease.
Antiplatelet therapy
Aspirin should be considered for all patients with an estimated 10 year risk of
Cardiovascular (CVD) disease of >20%, so long as blood pressure is 50
o Calculated to have a 10 year CVD risk of > 20%
Health Economy Formulary Drug of Choice - aspirin dispersible 75mg OD
See Aspirin Initiation Protocol
Also see:
Hypertension
Lifestyle
Primary Prevention of Cardiovascular Disease Protocol
Return to overview
32

Hypertension
Blood pressure should be measured by a health care professional who has
undergone training, using a machine which is regularly serviced and calibrated.
The patient should be seated comfortably and relaxed with:
• arm supported at chest level
• ensuring correct cuff size is used ie. inner bladder fits 80 – 100% of the
circumference of the upper arm.
On the first visit:
• BP should be measured in both arms and the arm with the higher
reading used. This arm can then be noted and used for each
subsequent visit.
• At least 2 readings should be taken, with an interval of at least a
minute between readings and an average of the readings recorded.
• If the BP is above treatment threshold, (either systolic, diastolic, or
both) check the BP again at the end of the consultation or after a short
interval of 5 – 10 minutes, where patient remains seated comfortably.
Target BP Range in CKD
Aim for: Systolic of

If BP is above threshold, check this reading on 2 more visits 2 – 4 weeks apart or
check home readings.
If the BP trend is found to be above the treatment threshold as stated, a decision
on initiating pharmacological management should be made. Inhibition or
blockade of the renin/angiotensin/aldosterone system with ACE inhibitors or
ARBs has been found to confer renal and cardio protection over and above the
effects of their BP lowering effect. For this reason they are recommended as first
line treatment for people with CKD.
See Initiation of ACE/ARB.
See Renal artery stenosis
For non-pharmacological management discuss lifestyle measures as detailed in
the “Best Practice Guidelines for Lifestyle Assessment” with particular attention
to salt content in the diet and also in prescribed or OTC drugs.
Note that in the checklist below for those with CKD the dietary advice differs from
that which is usually recommended:
• Fruit and vegetables are to be at a maximum of 5 portions a day due to
their potassium content
• Oily fish should be one portion only per week due to high phosphate
levels.
Lifestyle Measures Checklist
• Stop smoking
• Correct dyslipidaemia
• Screen for diabetes
• Maintain normal weight for adults (body mass index 20-25 kg/m2)
• Avoid central obesity

Further information on the pharmacological management of hypertension can be
found in the:
“Dudley Guidelines for the Pharmacological Management of Hypertension”,
http://joint.dudley.nhs.uk/cmsextra/documents/cms/222-2007-12-19-5392411.pdf
For further information on taking blood pressure measurements, guides using
electronic machines and anaeroid and mercury sphygmomanometers may be
downloaded from the british hypertension society www.bhsoc.org
For patients with T2 diabetes, please refer to NICE Guidelines, Inherited
Guideline H “Management of Type 2 Diabetes: Management of Blood Pressure
and Blood Lipids”
http://guidance.nice.org.uk/page.aspxo=38564
Return to overview
35

Initiation of ACE Inhibitor / ARB
ACE inhibitors and ARBs reduce hypertension in renal disease, but also confer
major prognostic benefits over that which can be attributed to the reduction in
blood pressure alone. For this reason they are recommended for use in CKD.
Threshold for initiation – see hypertension
Dual blockade with combinations of ACE and ARB should only be initiated under
specialist supervision.
Serum creatinine and potassium concentration should be checked
• prior to starting ACE and/or ARB
• within two weeks of initiation
• two weeks after any subsequent dose increase
• during severe intercurrent illness, particularly if there is a risk of
hypovolaemia
• annually (or more frequently if indicated, according to kidney function, see
follow-up.)
A rise of serum creatinine concentration of >20% or fall in estimated GFR of
>15% after initiation or dose increase should be followed by a further
measurement within two weeks.
If deterioration in kidney function is confirmed, before the ACE or ARB is
discontinued, a specialist opinion should be sought (not necessarily by
formal referral) on whether the drug treatment should be stopped or the
patient subjected to investigation for renal artery stenosis.
If hyperkalaemia is present (K >6.0 mmol/l)
• Stop relevant drugs, such as NSAIDs, K sparing diuretics.
• Check diet, e.g. “low-salt” salt substitute discontinue use.
If hyperkalaemia persists despite these measures, then advice should be sought
from the nephrology dept on management with the ACE/ARB. Contact details
Health Economy Formulary Drugs of Choice
Lisinopril*
Ramipril capsules
Candesartan (not specific CKD licence)
36

Irbesartan*
Valsartan
Losartan*
*Specifically licensed for patients with type 2 diabetes and
nephropathy/microalbuminuria.
ARBs should be used as a second line treatment, only in patients who do not
tolerate ACE inhibitors (usually due to development of persistent dry cough which
does not disappear within two months of starting the ACE – check no other
caveats).
N.B Heart Failure
The commonest fear for not using an ACE/ARB in patients with Heart Failure
(HF) is the potential for worsening renal function. However, although the
CONSENSUS trial demonstrated a 30% rise in Creatinine; the subsequent
follow-up showed 19% returned to baseline and the ACE was generally well
tolerated.
Drug treatment with an ACE or ARB can contribute to hyperkalaemia, which can
also be exacerbated by treatment with spironolactone (indicated in the treatment
of heart failure).Severe hypovolaemia, may complicate the treatment of heart
failure with high dose diuretics, as it may also cause hyperkalaemia in the
presence of CKD, although in the presence of volume overload, diuretic
treatment may be a logical treatment for hyperkalaemia. For these reasons,
working out the cause and appropriate treatment of hyperkalaemia can be
difficult, and a good reason for referral to / advice from a nephrologist.
NSAIDs are associated with worsened outcomes in Heart Failure because they
oppose the benefits of ACE by inhibiting the production of prostacyclin.
Spironolactone should be avoided in patients with a GFR < 30 but can be used
with caution in patients where eGFR is between 30 – 60 ml/min. It should be
withheld in patients with diarrhoea and vomiting, who have heart failure and
CKD, due to dehydration and hyperkalaemia.
Spironolactone, ACE and ARB should be reduced or stopped if the serum
potassium is greater than 6.0 mmol/l. This includes potassium sparing diuretics.
http://www.renal.org/CKDguide/ckd.html
37

K/DOQI Recommended Monitoring Intervals
Salt Intake
All patients with hypertension should be advised to reduce dietary sodium intake
to

• Diuretics
• Lithium carbonate
• Mesalazine and other 5-aminosalicylic drugs
• Calcineurin inhibitors (cyclosporin, tacrolimus)
For further information see appendix 3 of the BNF.
http://www.bnf.org/bnf/bnf/current/41003.htm
or contact the Dudley Medicines Management team:
CKD clinical services lead clair.huckerby@dudley.nhs.uk
P.A. for the team Tel. 01384 366589
Patients with CKD should be offered a 6 monthly medication review by a Practice
Based Pharmacist if on 4 or more medicines. This could be more or less frequent
depending on the needs of the individual patient.
Return to overview
Renal Artery Stenosis
Suspect Atherosclerotic Renal Artery Stenosis (ARAS) in patients whom:
• There is a rise in serum creatinine of > 20% or a fall in eGFR of > 15%
during the first 2 months after initiation of ACE or after any dose increase.
• A rise in serum creatinine of > 20% or a fall in eGFR of > 15% in a 12
month period where there is evidence or suspicion of widespread
atherosclerosis.
• Refractory hypertension – where BP remains >150/90 despite 3
antihypertensives.
• Recurrent episodes of pulmonary oedema despite normal LV function on
echocardiogram (flash pulmonary oedema)
• Unexplained hypokalaemia with hypertension.
These patients should receive referral to nephrology for further investigation and
specialist management.
Return to overview
39

Urinalysis
Protein
No diabetes
Proteinuria is a significant risk factor for progression in renal disease and for
cardiovascular morbidity and mortality. Unlike haematuria, proteinuria almost
always has a renal origin. Management should include assessment of:
• Albumin/creatinine ratio (ACR) / Protein/creatinine ratio (PCR)
• Haematuria
• Serum creatinine and eGFR
To detect and identify proteinuria, use ACR in preference, as it has greater
sensitivity than PCR for low levels of proteinuria. For quantification and
monitoring of proteinuria, PCR can be used as an alternative. ACR is the
recommended method for people with diabetes.
http://www.nice.org.uk/nicemedia/pdf/CG073QuickRefGuide.pdf
Urine should be tested for protein annually in stage 3, and 6 monthly in stages 4
and 5 if stable. If protein is detected, exclude infection (only if symptoms suggest)
and retest.
Measurements should not be made during acute illness.
Send an early morning urine specimen for microalbumin and ACR level.
Persistent proteinuria is defined as 2 or more positive tests, ACR > 30
spaced by 1-2 weeks.
A positive ACR test (>30) in the presence of hypertension indicates
initiation of an ACE inhibitor
http://www.nice.org.uk/nicemedia/pdf/CG073QuickRefGuide.pdf
However, patients with CKD have an increased risk of CVD mortality.
Consideration should be given to initiating ACE inhibitors in patients with CKD,
positive microalbumin (< 30mg/day) and increased CVD risk, due to their
cardioprotective effect.
http://www.sign.ac.uk/pdf/sign103.pdf
40

Recommendation:
Therefore consider ACE inhibitor therapy regardless of established proteinuria for
patients with CKD and:
• Hypertension
• Heart failure
• Coronary, cerebral or peripheral vascular disease
• Diabetes mellitus
• Multi-system disease including SLE, rheumatoid arthritis, vasculitis
For many in this patient group, the cardiovascular impact of their renal disease is
more significant than the risk of continuing to end stage renal failure.
http://renux.dmed.ed.ac.uk/edren/Unitbits/CKDmanagement.html
see initiation of ACE/ARB
Protein/creatinine ratio PCR
PCR is the best test to confirm clinical proteinuria at higher levels. ACR at higher
levels (> 45) may be inaccurate. If using PCR, then proteinuria is defined as
Positive results: PCR > 50
In 2 separate specimens spaced by 1-2 weeks.
http://www.nice.org.uk/nicemedia/pdf/CG073QuickRefGuide.pdf
ACR >70 (PCR 70 (PCR >100)
• Refer to nephrologist.
41

Diabetes
All people with diabetes should receive annual assessment of microalbumin and
albumin/creatinine ratio.
If raised ACR :
• ACR >2.5mg/mmol (male)
• ACR >3.5mg/mmol (female)
or
• Microalbumin level > 30 mg/day
Repeat test at next two clinic visits over 3–4 months
Microalbuminuria is confirmed if at least one out of two or more results is also
raised. http://www.nice.org.uk/nicemedia/pdf/CG66T2DQRG.pdf
Microalbuminuria with eGFR >60ml/min/1.73m 2 is stage 1 / 2 CKD.
In patients with diabetes (type 1 or type 2), microalbuminuria/proteinuria is an
indication for:
• Treatment with ACE inhibitors (or Angiotensin receptor blockers if those
are not tolerated), with titration up to maximum dose or maximum
tolerated dose irrespective of initial blood pressure
• Control of hypertension to target
• Tight glycaemic control
• Monitoring of ACR, serum creatinine and eGFR.
• Consider referral to / discussion with the diabetic team or joint
diabetic/nephrology clinic for review
• Consider referral to Nephrologist. See referral criteria
Blood
Microscopic haematuria without proteinuria, eGFR >60ml/min
• Age >50, refer to Urology
• Age 50 with negative urological investigations, treat as CKD
stage
Microscopic haematuria with proteinuria eGFR >60ml/min
• Refer nephrology
42

Lower levels of proteinuria should be monitored annually and patients managed
according to CKD stage.
Macroscopic haematuria
(Use reagent strips and not microscopy)
• Fast track Urology referral
• If deteriorating function (eGFR), urgent nephrology referral; urgent
imaging to exclude obstruction
• If GFR

Diet in CKD
Information on nutritional recommendations can be found on EdREN, the
website of the Renal Unit of the Royal Infirmary of Edinburgh.
http://renux.dmed.ed.ac.uk/EdREN/EdRenINFObits/Diet_CRF.html
Summary of Downloads
Keeping salt intake down
Cutting Down Potassium
A short leaflet about Fluid
Controlling phosphate
Increasing your calorie intake
Weight control
Renal Diets for Christmas and other holidays
Return to overview
44

Glycaemic Control
CKD and Diabetes
Diabetes mellitus is the most common cause of chronic kidney disease
worldwide (Burrows-Hudson 2005) (Levy et al 2006) and at least 20-30% of
people with diabetes will have some evidence of the disease (Audit Commission
2002). There is a variation in the incidence of diabetes among racial and ethnic
groups, with people of South Asian, African and African-Caribbean descent
having a higher than average risk of type 2 diabetes (DOH 2001). The risk of
nephropathy is related to the duration of diabetes with microalbuminuria being
the first sign, progressing to albuminuria then nephropathy. The presence of
urine albumin whether microalbuminuria or albuminuria strongly increases the
person’s cardiovascular risk (University Hospital of Leicester 2006). Thereby a
person with diabetes should not be assessed in isolation for kidney disease but
also for lipid lowering, anti-platelet therapy and hypertension in tandem. Optimal
glycaemic control should be the cornerstone of all treatment for diabetes care.
For guidance please see Dudley Diabetes Management Guidelines for Adults
2006.
Persistent hyperglycaemia results in the thickening of the basement membranes
and accumulation of proteins in the glomeruli (Levy et al 2006). Research studies
suggest that intensive glycaemic control can reduce the rate of microalbuminuria,
proteinuria and nephropathy (Gross et al 2005) and improvement in glycaemic
control may reduce the risk of patients with diabetes developing both
macrovascular and microvascular complications (DOH 2001). Studies relating to
hypertension control also suggest similar results in relation to prevention of renal
failure (DOH 2001) recommending the use of ACE inhibitors (Angiotension
Converting Enzyme Inhibitors) or ARBs (Angiotension Receptor Blockers) to
delay the onset of diabetic nephropathy in people with microalbuminuria.
45

Screening and Management for People with Diabetes
Annual urine analysis: Protein or
Albumin Creatinine Ratio + U&Es
and eGFR
Follow
urology/
nephrology
guidelines.
Does patient have
persistent haematuria
YES
NO
Does patient have proteinuria YES Present on repeat
test >2 weeks
later
NO
Does patient have eGFR

References
Audit Commission (2002) Testing Times: A Review of Diabetes Services in
England and Wales.
Burrows-Hudson (2005) Chronic Kidney Disease: an overview. American Journal
of Nursing.
DOH (2001) National Standard Framework for Diabetes: Standards. The
Stationary Office. London
Gross J.L., de Azevedo MJ, Silveiro S.P., Canani L.H., Caramori M.L.,
Zelmanovitz T. (2005) Diabetic Nephropathy: Diagnosis, Prevention, and
Treatment. Diabetes Care. 28, 1l 164-176.
Levy J., Pussey C., Singh A. (2006) Fast Fact: Renal Disorders. Health Press,
Oxford
University Hospitals of Leicester NHS Trust (2006)
Return to overview
47

Immunisation Against Hepatitis B
National Guidelines:
“Immunisation against HBV is recommended for patients on dialysis or in
transplantation programmes. Patients with chronic renal failure should be
immunised as soon as it is anticipated that they may require dialysis or
transplantation. Vaccine and, if appropriate, hepatitis B immunoglobulin should
be given to susceptible patients who have been exposed to HBV.”
Department of Health
Good Practice Guidelines for Renal Dialysis/Transplantation Units 2002
Prevention and Control of Blood-borne Virus Infection
“Patients with CKD in whom dialysis is anticipated, should be screened for
hepatitis B and C as well as HIV infection. Patients who are hepatitis B surface
antigen and hepatitis B surface antibody negative should be immunised and their
antibody levels measured post vaccination.”
UK Renal Association Clinical Practice Guidelines 4th Edition 2007
Clinical Practice Guidelines for the Care of Patients with Chronic Kidney
Disease
Immunisation Programme
• Use standard course (0, 1, 6 months) and titre level taken 6 weeks after
last dose
• Recommended dose 40mcg
• Intramuscularly in the upper arm
Return to overview
48

Influenza and Pneumococcal Vaccine
All patients with CKD should be advised to have an influenza vaccine by the
practice at the appropriate time each year. Efforts should be made to target the
patients who appear on the CKD register.
Pnuemococcal vaccine should also be offered to patients who remain
unimmunised. This may be given at the same time as the influenza vaccine, but
patients who have not received pneumococcal vaccine may be immunised at any
time during the year.
Contraindications, criteria and schedule for the flu and pneumococcal vaccine
and can be found in product literature and in the British National Formulary
• Influenza - http://www.bnf.org/bnf/bnf/current/6509.htm
• Pneumococcal - http://www.bnf.org/bnf/bnf/current/6490.htm
Guidelines for administration of the flu vaccine can be found in the “green book”,
“Immunisation Against Infectious Diseases”.
Return to overview
49

Follow-up
Suggested follow-up plan
Stage Description Frequency
3 eGFR 30 – 59 mls/min 6 monthly
(12 monthly if
stable*)
4 eGFR 15 – 29 mls/min 3 monthly
(6 monthly if
stable*)
5 eGFR < 15 mls/min 6 weekly
*Stability = < 5mls/min fall in eGFR over 12 months
Take the following steps to identify progressive CKD:
• Obtain a minimum of three eGFR estimations over a period of not less
than 90 days.
• Define progression as a decline in eGFR of > 5 ml/min/1.73 m 2 within
1 year, or > 10 ml/min/1.73 m 2 within 5 years.
• Focus particularly on those in whom a decline of eGFR continuing at the
observed rate would lead to the need for renal replacement therapy within
their lifetime (eGFR

Stage 3
Management at stage 3 should include all of the interventions as
detailed for stages 1 and 2 plus the following section/s for stage 3.
Management of Anaemia
Lower levels of kidney function have been proven to be associated with lower
haemoglobin levels and a higher prevalence and severity of anaemia.This is
especially true in patients with diabetes and CKD. Anaemia can occur early in
the course of diabetic kidney disease and is associated with inappropriately low
erythropoietin concentrations 1 .
In patients with chronic renal disease, normochromic normocytic anaemia may
develop from decreased renal synthesis of erythropoietin. The anaemia becomes
more severe as the GFR decreases 2 . No reticulocyte response occurs, red blood
cell survival is decreased, and there is an associated increased bleeding
tendency due to uraemia-induced platelet dysfunction.
An eGFR of less than 60 ml/min (stage 3 onwards) should trigger investigation
into whether anaemia is due to CKD. When the eGFR is greater than or equal to
60 ml/min (stage 1 and 2) anaemia is more likely to be related to other causes 3 .
All patients at stage 3 CKD should have an annual measurement of
haemoglobin (Hb)
If the Hb is < 11 g/dl
Not all anaemia in patients with CKD will be ‘renal anaemia’ and causes of
anaemia other than CKD should be actively excluded before a diagnosis of
anaemia associated with CKD can be made 3 .
Other causes:
• Chronic blood loss
• Iron deficiency
• Vitamin B 12 or folate deficiency
• Hypothyroidism
• Chronic infection or inflammation
• Hyperparathyroidism (consider referral for assessment)
• Aluminum toxicity
51

• Malignancy
• Haemolysis
• Bone marrow infiltration
• Pure red cell aplasia
(Iron deficiency anaemia is the most common cause of anaemia either due to
negative iron balance through blood loss (most commonly gastrointestinal or
menstrual), inadequate nutritional intake, or related to poor gastrointestinal
absorption).
Check:
• full blood count (if not already done)
• serum ferritin
• total iron binding capacity
• B 12 and folate
• Other investigations will be determined by the likely alternative diagnoses
and cardiovascular effects of anaemia, e.g. thyroid function test,
echocardiography, cause of GI bleeding
Serum ferritin
Serum ferritin levels may be used to assess iron deficiency in people with CKD.
Because serum ferritin is an acute-phase reactant and frequently raised in CKD,
the diagnostic cut-off value should be interpreted differently to non-CKD
patients 4 .
Iron-deficiency anaemia should be:
• diagnosed in people with stage 5 CKD with a ferritin level of less
than 100 micrograms/l
• considered in people with stage 3 and 4 CKD if the ferritin level is
less than 100 micrograms/l.
In people with CKD who have serum ferritin levels greater than100 micrograms/l,
functional iron deficiency, (and therefore those patients who are most likely to
benefit from intravenous iron therapy) should be defined by:
• percentage of hypochromic red cells greater than 6%, where the
test is available, or
• transferrin saturation less than 20%, when the measurement of the
percentage of hypochromic red cells is unavailable.
Supplements of vitamin C, folic acid or carnitine should not be prescribed
specifically for the treatment of anaemia of CKD.
52

If all other causes for the anaemia have been excluded, (or where diagnosis
is unclear) then referral may be indicated for assessment and possible
initiation of Erythropoietin Stimulating Agent (ESA).
References
1. El Achkar et al. Higher prevalence of anemia with diabetes mellitus in
moderate kidney insufficiency: The Kidney Early Evaluation Program
(KEEP). Kidney International 2005; 67: 1483-8.
2. National Health and Nutritional Examination Survey III (NHANES III) data
cited in Royal College of Physicians. Anaemia Management in CKD:
National Clinical Guideline for Management in Adults and Children.
http://www.nice.org.uk/nicemedia/pdf/Anaemia_Management_full_guideline.pdf
3. NICE clinical guideline 39: Anaemia Management in People with CKD
http://www.nice.org.uk/nicemedia/pdf/AMCKD_NICE_guideline_v8.1.pdf
4. Royal College of Physicians. Anaemia Management in CKD: National
Clinical Guideline for Management in Adults and Children.
http://www.nice.org.uk/nicemedia/pdf/Anaemia_Management_full_guideline.pdf
Return to overview
53

Stage 4
Management at stage 4 should include all of the interventions as
detailed for stages 1, 2 and 3 plus the following section/s for stage 4.
Patients at CKD stage 4 should be referred for specialist nephrology opinion. For
most patients management at this stage can be achieved by a shared care
programme between the nephrology dept. and primary care, with the provision of
a detailed shared care management plan from the nephrology team.
Referral for patients at this stage with no other referral indication should be to the
"One-Stop" renal clinic.
“One-Stop” Renal Clinic
Introduction:
The “one-stop” renal clinic is an innovative and modern concept delivering health
services designed around patients' needs and lifestyles. The clinics are an
integral part of the drive towards building a patient-centred NHS, providing care,
which minimises waits and delays, and removes unnecessary hospital visits.
The service is committed to raising individual and community health status and
awareness through high quality, evidence based screening, advisory, therapeutic
and support services.
A patient referred to a “one-stop” clinic will typically receive a specialist
consultation, undergo diagnostic testing e.g. renal ultrasound, doppler,
blood tests, basic echocardiography etc., receive their results in the clinic
and have treatment initiated where appropriate.
Clinic aims:
• To provide seamless care and patient flows from primary to secondary care
and vice versa.
• Quicker, more convenient and timely diagnosis and investigation. Faster and
better care, same day diagnostic tests etc.
• Reduction in the number of hospital visits.
• Reduction in patient anxiety levels associated with disease.
• Smoother and quicker access to other specialties and health care
professionals (eg. renal specialist dietician) if required.
54

Clinic inclusion criteria:
Patients can be referred directly by the GPs (Choose and book or paper
referrals). Patients waiting for conventional appointment may be transferred to
the “one-stop” clinic by the GP or Consultant if appropriate.
The clinic is suitable for:
• Elderly patients
• Those with borderline eGFR where diagnosis may be unclear
• Patients with borderline referral criteria
• A specialist second opinion requested by the GP
• A specific question requested rather than a formal referral
Exclusion criteria
The clinic is not suitable for established and/or advanced renal disease,
which requires many diagnostic tests and long-term follow up.
All patients who attend the “one-stop” clinic are sent a leaflet with their
appointment letter explaining the range of tests they may have, how long the
tests will take and when they can expect results. They are informed that they are
very welcome to bring someone with them. The leaflet also contains contact
numbers for the clinic coordinator should patients wish to access any further
information or alter their appointment time.
Patients benefit by completing their outpatient appointment with a timely and
clear understanding of their diagnosis and management plan rather than
experiencing weeks of uncertainty and apprehension whilst waiting for individual
tests and results. Where immediate treatment is not feasible, the patient will be
given a date for a further appointment before they leave and the referring primary
care clinician informed.
The clinic is currently held at Russells Hall hospital twice monthly with future
plans for further expansion.
For housebound patients this service can be requested as a domiciliary visit from
the Community CKD Team, as an outreach service from Dudley Group of
Hospitals. Portable scanning equipment is available for use by the team. It is
recommended that patients are supported by a member of the primary care
team, usually district nursing services, who meet the CKD team in the patient’s
home. An individual shared care management plan is developed by the CKD
team for use by primary care. Referral is by referral letter to Nephrology Services
at Dudley Group of Hospitals.
55

Contact details:
Clinic co-ordinator
Lead Clinician
Renal Administrative Secretary
Tel. 01384 244432, Fax. 01384 244543
Claire.miles@dgoh.nhs
Senior Consultant Renal Physician
Tel. 01384 244432, Fax. 01384 244543
Claire.miles@dgoh.nhs
Consultants Tel. 01384 244432, Fax. 01384 244543
Claire.miles@dgoh.nhs
Renal Dieticians Tel. 01384 244017, Fax. 01384 244017
Christine.morgan@dgoh.nhs
Radiology Support Tel. 01384 456111 ext. 2541
Peter.oliver@dgoh.nhs
Out-Patient Manager Tel. 01384 456111 ext. 2406
Rose.tonty@dgoh.nhs
Return to overview
Bone Metabolism
Patients at stage 4 and 5 should have regular calcium, phosphate and
parathyroid hormone (PTH) concentrations measured. Specimens need to be in
path lab within 1 hour. Therefore it would be recommended that the specimens
are taken at the phlebotomy clinic at Russells Hall Hospital. Blood requests
should include:
• Calcium phosphate
• PTH
• Bicarbonate (in selected patients)
• Serum calcium and phosphate plus alkaline phosphatase (in selected
patients)
• 1,25 dihydroxycholecalciferol (in selected patients)
It is recommended that the management of bone metabolism is carried out by
specialist nephrologist, unless practices are confident to do so under advice from
the nephrology dept. Investigations into bone metabolism are included in the
one-stop clinic assessment and in the shared management plan with primary
care.
56

Where vitamin D supplementation is indicated:
Stage 1 – 3A
Initiate alfacalcidol 0.25mcg alternate days and titrate according to PTH and
serum calcium and phosphate. Consider adcal / calcichew D3 1 twice daily in
patients at risk of osteoporosis.
Stage 3B - 5
Initiate alfacalcidol, dose titrated according to PTH, serum calcium and
phosphate and continue to monitor calcium and phosphate levels
See Appendix 1 - Pathway for the Management of Calcium and Phosphate
Balance in Chronic Kidney Disease
Osteoporosis – initiate biphosphonates in stages 1 – 3B
Dudley PCT formulary drug of choice - Alendronate 70mg weekly
N.B. Avoid if eGFR

At CKD stage 4 and 5:
• Measurement of serum calcium, phosphate and PTH levels
Return to overview
58

Stage 5
Patients identified at CKD stage 5 should be referred urgently for
specialist management unless they are already known to the nephrology
dept. Shared management plans should be agreed between primary and
secondary care, especially for patients who chose to be treated
conservatively and for those who are being worked up for renal
replacement therapy.
Exceptions to Referral
• Patients with deteriorating kidney function as a consequence of another
terminal illness
• Patients for whom further investigation and management is clearly
inappropriate
• Patients with stable function with all appropriate investigations and
interventions completed who have agreed and understood their individual
care pathway.
Shared care management should include:
• 3 monthly follow-up where serum creatinine, eGFR, Hb, calcium, phosphate,
PTH are monitored and acted upon including correction of acidosis.
• Dietary assessment and advice/referral
• Hepatitis B immunisation
• Information and support for patient and family in treatment options
• Timely provision of renal replacement therapy depending on patient choice
Return to overview
59

Referral
Criteria for Referral to Specialist Nephrology Services According to eGFR
eGFR mls.min
Indication
< 15
Stage 5
15 – 29
Stage 4
Urgent referral (exceptions)
Referral to “one stop” clinic for assessment, investigations and
shared management plan
30 – 59
Stage 3
Routine referral/advice indications:
• Where condition is not shown to be stable ie. progressive
deterioration in kidney function
• Microscopic haematuria
• PCR >45 mg/mmol (ACR > 70mg/mmol)
• Unexplained anaemia (Hb < 11)
• Continuing abnormal potassium, calcium or phosphate levels
despite advice in this pathway
• Suspected systemic illness, e.g. SLE
• Uncontrolled hypertension (>150/90 on 3 agents)
> 60
Stage 1 and 2
Indications
irrespective of
eGFR
Referral not required unless other problems present (see below)
Immediate referral:
• Accelerated hypertension
• Hyperkalaemia (K > 7.0 mmol/l)
Urgent referral
• Nephrotic syndrome (proteinuria, oedema and low serum
albumin)
Routine referral
• Dipstick proteinuria present and PCR >100 mg/mmol
• Dipstick proteinuria and microscopic haematuria present
• Macroscopic haematuria with negative urological testing
• People with, or suspected of having, rare or genetic causes
of CKD
• Suspected renal artery stenosis.
60

Information to include with referral
• General medical history and details of co-morbidities
• Urinary symptoms
• Medication
• Current blood pressure reading and all blood pressure readings over the
last 2-3 years or back to normal levels, in date order, in graph form if
available. If incomplete, send as much information as available
• Current eGFR and serum creatinine levels and all levels over the last 2-3
years or back to normal levels, in date order, or graph if available. If
incomplete, send as much information as available.
• Examination findings, e.g. oedema, palpable bladder
• Urine dipstick results for blood and protein
• PCR if proteinuria present. If no proteinuria present, microalbumin for all
patients, plus ACR for diabetic patients.
• U and E, FBC, albumin, calcium, phosphate, cholesterol. HbA1c if
diabetic.
• Results of any renal ultrasound scan if available.
Once a referral has been made and a plan jointly agreed, consider routine
follow-up in primary care rather than in the specialist clinic.
Specify criteria for future referral / re-referral and when to seek advice.
Renal Ultrasound
Renal ultrasound is indicated in:
• progressive CKD
• visible or persistent invisible haematuria
• symptoms of urinary tract obstruction
• family history of polycystic kidney disease and are aged over 20
• stage 4 or 5 CKD
• nephrologist recommendation for renal biopsy.
Advise people with a family history of inherited kidney disease about the
implications of an abnormal result before arranging the scan.
Return to overview
61

Abbreviations
ACE
ARB
ARF
BP
CAPD
CKD
DGoH
DIP
eGFR
ERF
ESA
FBC
GI
GMS
Hb
KDOQI
LIT
MDRD
NSAID
OTC
QMAS
QOF
RHH
U+E
UTI
Angiotensin Converting Enzyme
Angiotensin Receptor Blocker
Acute Renal Failure
Blood Pressure
Continuous Ambulatory Peritoneal Dialysis
Chronic Kidney Disease
Dudley Group of Hospitals
Diabetes Improvement Partnership
estimated Glomerular Filtration Rate
Established Renal Failure
Erythropoietin Stimulating Agent
Full Blood Count
Gastrointestinal
General Medical Services
Haemoglobin
Kidney Disease Outcomes Quality Initiative
Local Implementation Team
Modified Diet in Renal Disease
Non- Steroidal Anti-Inflammatory Drug
Over The Counter
Quality Management and Analysis System
Quality and Outcomes Framework
Russell’s Hall Hospital
Urea and Electrolytes
Urinary Tract Infection
Return to overview
62

Appendix 1
The Dudley Group of Hospitals
NHS Trust
Pathway for the Management of Calcium and Phosphate balance in
Chronic Kidney Disease within Dudley Health Economy
Rationale: Hyperphosphataemia (elevated serum phosphate) is recognised as an important risk factor for many adverse outcomes in dialysis
patients, including vascular calcification, calciphylaxis, secondary hyperparathyroidism and mortality. Retention of phosphate occurs much earlier in
the course of CKD. Serum phosphate concentration increases when eGFR falls below 30 mls/minute (CKD 4).
Aim: To maintain phosphate levels between 0.9-1.5 mmol/L (1) and between 1.1 and 1.8 mmol/L in dialysis patients.
Dietary Modification: Patients with CKD may need to follow a reduced phosphate diet. Phosphate rich foods include chocolate, nuts, dairy, eggs,
meat and fish. This needs to be balanced carefully and so referral to a specialist dietitian is essential.
If phosphate or intact PTH levels cannot be controlled within target range despite dietary phosphate restriction then prescribe a phosphate binder.
Calcium containing phosphate binders
1 st Line Choice:
Calcium Carbonate (Calcichew®) 1.25g
(Contains 500mg elemental calcium per tablet)
Dose: To be titrated starting at 1 bd up to 2 tds
with meals
S/E: diarrhoea, hypercalcaemia
Alternatives: Adcal ® 1.5g
(Contains 600mg elemental calcium per tablet)
or add D3 in those at risk of Osteoporosis with
CKD stages 1-3
2 nd Line Choice:
Calcium Acetate (Phosex®) 1000mg
Indication – hyperphosphataemia and
intolerance to calcium carbonate or contraindicated.
NB - contains less elemental calcium
compared to calcium carbonate for the same
phosphate binding capacity; this is also
affected less by gastric pH.
Dose: 1g tds with meals titrated according to
serum phosphate levels, max 12 daily.
S/E: nausea and vomiting, constipation.
NB - Prescribing should be in line with an
effective shared care agreement (ESCA)
Calcium Acetate.doc
* MONITORING
Parameter
Serum
Phosphorous
concentration
Serum
calcium
concentration
Frequency
of
Monitoring
Every 2-4
weeks until
stable levels
are reached
and then 1-3
months as
directed by
the clinician
Target (KDOQI,
Renal Association,
recommendations
for stages of CKD)
CKD Stage 3/4 0.9 –
1.5 mmol/l
Dialysis 1.1 – 1.8
mmol/l
1-2 monthly CKD Stage 3/4 2.1 -
2.6 mmol/l
Dialysis 2.2 – 2.5
mmol/l
Ca x P CKD Stage 3/4 2.6 mmols/l
SEVELAMER (RENAGEL®) 800mg
Indication: hyperphosphataemia as monotherapy
or in combination with calcium containing
phosphate binder. May also decrease total and
LDL cholesterol.
Dose: 1 tds with meals, titrate dose according to
calcium and phosphate balance, max 5 per
meal.
SE’s/CI: CI in hypersensitivity,
hypophosphataemia, bowel obstruction, young
children, gastroparesis, swallowing disorders.
NB – Prescribing should be in line with an ESCA
Sevelamer.doc
OR
LANTHANUM (FOSRENOL®)
Indication: hyperphosphataemia
NB – May be beneficial in those who are
intolerant to sevelamer or where it is desirable to
reduce the pill burden.
Dose: 500mg, 750mg or 1000mg with meals
titrated to 1500mg or 3000mg daily.
S/E’s: Abdominal pain, constipation, diarrhoea,
nausea and vomiting.
NB – Prescribing should be in line with an ESCA
Lanthanum.doc
PRESCRIBING COSTS:- / DRUG
INFORMATION
Phosphate binders
Calcichew 2tds £15.67
Phosex 2tds £18.47
Sevelamer 3tds £171.86
Lanthanum 1tds 750mg £142.03
Cost of 28 days
treatment (BNF 56)
63

SUPPORTING INFORMATION:
Introduction:
Phosphate retention occurs in chronic kidney disease due to the reduction in the glomerular filtration rate. Hyperphosphataemia leads to a series of changes
resulting in secondary hyperparathyroidism. This is a major concern because the high parathyroid hormone (PTH) levels play an important role in the
development of renal osteodystrophy and considered as a “uraemic toxin” as well.
From the viewpoint of calcium and phosphate balance, initially the hypersecretion of PTH may be appropriate. This would increase the calcium and phosphate
release from bone and enhances urinary phosphate excretion as well. It can thus correct the hypocalcaemia and to some extent hyperphosphataemia. However,
when the glomerular filtration rate (GFR) falls below 30 mls/min, this physiological change is no more maintained. At this stage, dietary phosphate restriction
may still reduce the plasma phosphate and PTH levels to an extent but may not normalise the values. As a result, oral phosphate binders are more often
required. This problem gets worse once the renal failure is advanced, especially in dialysis patients. In end stage renal disease (CHD 5), there is essentially no
phosphate excretion by the kidneys and oral phosphate binders are a must to limit the dietary phosphate absorption.
The combination of hyperphosphataemia and calcium product (determined by multiplying plasma, calcium and phosphate in mmol/L) when in excess of 4.4,
there is a tendency for calcium to precipitate in soft tissues such as arteries, joints and viscera. This phenomena can lead to various vascular complications
including coronary artery disease and peripheral vascular disease. Thus both morbidity and mortality rate increases with these advanced complications.
Phosphate restriction: Restricting phosphate intake can be attempted with about 800 to 1000mgs per day (1)which some patients find acceptable. However,
care must be exercised as limiting phosphate intake significantly can reduce protein intake resulting in malnutrition which can also increase the morbidity and
mortality. A Specialist Renal Dietitian’s advice will be very useful in balancing such a diet. Most often in dialysis patients, we encourage them to avoid
unnecessary dietary phosphate products such as colas, certain vegetables and excessive dairy products. At the same time, high biological value protein
sources must also be increased to avoid malnutrition. Lengthening the dialysis or using larger and high efficiency dialysers may influence very marginally the
phosphate removal. Many patients with chronic Kidney disease and all dialysis patients require the administration of oral phosphate binders to limit the
absorption of dietary phosphate. Agents used to regulate phosphate balance include calcium salts and more recently Sevelamer and Lanthanum carbonate.
Magnesium and Aluminium containing binders are now avoided because of safety concerns.
Phosphate binders – bind phosphate in the gut and prevent its absorption. They must be taken with phosphate containing foods to be effective, they should
not be taken at the same time as iron preparations and some antibiotics because together they form insoluble compounds in the gut – which reduces the
efficacy of both drugs.
There is some evidence that calcium containing phosphate binders are related to arterial/vascular calcification when compared to non-calcium containing
binders. Hypocalcaemia can also cause soft tissue calcification.
Produced by:
Jane Elvidge, Senior Renal Pharmacist, RHH
Clair Huckerby, Pharmaceutical Adviser, Dudley PCT
Dr K A Shiva Kumar, Consultant Renal Physician, RHH
Christine Morgan, Senior Specialist Renal Dietitian, RHH
Alison Whitlock, Clinical Pharmacist
Lucy White, Administration, Public Health Dept. Dudley PCT
In consultation with:
AMMC
Renal LIT
References:
1. Renal Association Guidelines for the treatment of adult patients with renal failure; 4th Edition.
2. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. AM J Kidney Dis 2003;
42(Suppl 3): S1-S202.
3. Summary of product characteristics for Sevelamer (Renagel).
4. Block GA, Hulbert-Shearon TE, Levin NW, Port FK. Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic
haemodialysis patients: a national study. AM J Kidney Dis 1998; 31: 607-617.
5. Goodman WG, Goldin J, Kuizon BD et al. Coronary-artery calcification in young adults with end stage renal disease who are undergoing dialysis. N
Engl J Med 2000; 342: 1478-1483.
6. Guerin AP, London GM, Marchais SJ, Metivier F. Arterial stiffening and vascular calcifications in end stage renal disease. Nephrol Dial Transplant
2000; 15: 1014-1021.
7. Hutchison A, Webster I. Lanthanum carbonate, a novel, non-aluminium, non-calcium phosphate binder, is effective and well tolerated in
hyperphosphataemia. Poster presented at the 9 th Asian Pacific Congress of Nephrology, 16-20 February 2003, Pattaya, Thailand.
8. Wilson J. ARIF request on the risk of cardiovascular problems in patients using calcium versus metal- free (non- calcium) phosphate binders to treat
hyperphosphataemia. ARIF. University of Birmingham.
64