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Nephrology Dialysis Transplantation 2007 22(Supplement 9):ix45-ix53; doi:10.1093/ndt/gfm449
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Speaker Abstracts

Tuesday, 6 February 2007

How common is early CKD?

 

How robust is eGFR as a measure for early CKD?

Edmund J. Lamb

Department of Clinical Biochemistry, East Kent Hospitals NHS Trust, Kent and Canterbury Hospital, Canterbury, Kent, UK, CT1 3NG

Correspondence to: Email: edmund.lamb{at}ekht.nhs.uk

Glomerular filtration rate (GFR) is accepted as the best overall measure of kidney function but measurement using reference procedures (e.g. 51Cr-EDTA) is impractical for large-scale application. Internationally there has been a recent thrust towards earlier detection of chronic kidney disease (CKD), primarily using estimated GFR (eGFR) as a tool [1]. Quality requirement one of Part 2 of the Renal NSF was aimed at prevention and early detection of CKD and to satisfy this it was recommended that clinical biochemistry laboratories report eGFR alongside all requests received for serum creatinine measurement in adults [2]. In April 2006, the Department of Health in England recommended universal eGFR reporting using the ID-MS standardized MDRD equation [3] with appropriate adjustment for assay differences and the Quality and Outcomes Framework (QOF) introduced a register of people in primary care with stages 3–5 CKD. Clinical practice guidelines to support these initiatives have been published [4].

After years of deliberation laboratory testing of kidney function seems to have taken a step forward and the age of eGFR is truly upon us. But how good is eGFR at measuring kidney function? Problems with the laboratory measurement of serum creatinine may be masked but have not disappeared following the superimposition of eGFR. Both analytical and biological variations of serum creatinine concentration contribute to imprecision of eGFR, which must be taken into account when interpreting guidelines. Is an upper reporting limit of 90 ml/min/1.73 m2 appropriate? Should the blood sample itself be obtained under fasting conditions [5]? Does eGFR using the MDRD equation predict progression of CKD? The MDRD equation was derived in a US population of middle-aged patients with CKD. A correction is applied for Black-Americans but the transferability of this to African-Caribbean (or Chinese and South Asian) populations in the UK has not been widely confirmed. Perhaps most significantly, the MDRD study did not address individuals over 75 years of age, the age group amongst which most CKD resides. This talk will review the evidence addressing some of these important issues.



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  1. National Kidney Foundation. Clinical practice guidelines for chronic kidney disease: evaluation classification and stratification. Am J Kidney Dis (2002) 39 [Suppl 1]:S1–S266.
  2. Department of Health. National Service Framework for Renal Services. In: Part Two: Chronic kidney disease, acute renal failure and end of life care. (2005) Available at: www.dh.gov.uk.
  3. Department of Health. Estimating glomerular filtration rate (eGFR): information for laboratories. Available at: www.dh.gov.uk.
  4. Joint Specialty Committee on Renal Medicine of the Royal College of Physicians and the Renal Association and the Royal College of General Practitioners. Chronic kidney disease in adults: UK guidelines for identification, management and referral. (2006) (accessed 6 December 2006). London: Royal College of Physicians. Available at: http://www.renal.org/CKDguide/full/CKDprintedfullguide.pdf.
  5. Preiss DJ, Godber IM, Lamb EJ, Dalton RN, Gunn IR. The influence of a cooked meat meal on estimated glomerular filtration rate. Ann Clin Biochem (2006) 43. in press.
 

Epidemiology of early CKD in the UK

Damian G. Fogarty1,2

1Belfast City Hospital and 2Queen's University Belfast, Northern Ireland

Chronic Kidney Disease (CKD) can manifest as either reduced kidney function or urinary abnormalities or a combination of both. Estimated glomerular filtration rate (eGFR) has emerged as the major basis for a 5-stage CKD classification [1]. Patients with an eGFR <60 ml/min/1.73 m 2 over at least 3 months are deemed as CKD stage 3, 4 or 5 and are the focus of the UK General Practice CKD quality indicators [2]. Various laboratory based surveys in the UK estimate that 3–5% of patients sampled have CKD of this degree. At present, there are no population-based studies of CKD prevalence and incidence in the UK. One study using UK General Practice data suggests ~5% may have stages 3–5 [3].

With an eGFR of 60 ml/min or greater, the diagnosis of early CKD requires the presence of other kidney damage e.g. persistent proteinuria/albuminuria, persistent microscopic haematuria or structural kidney disease. Again, few UK studies use these markers in population-based designs. In one study of middle aged London residents the prevalence of microalbuminuria varied between 2.7–7.3% depending on gender and race [4]. Given the steep decline in prevalence from stage 3 to stage 4 CKD it is clear that eGFR alone cannot best predict subsequent dialysis need. New studies are required to examine the association of classic and novel risk factors with CKD and its progression as defined by reducing GFR/increasing albuminuria. These investigations are critical for understanding the role of screening and interventions in preventing CKD progression and its associated cardiovascular disease.



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  1. Levey AS, Eckardt K-U, Tsukamoto Y, et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int (2005) 67:2089–2100.[CrossRef][ISI][Medline]
  2. Doran T, Fullwood C, Gravelle H, et al. Pay-for-performance programs in family practices in the United Kingdom. N Engl J Med (2006) 27; 355:375–384.
  3. de Lusignan S, Chan T, Stevens P, et al. Identifying patients with chronic kidney disease from general practice computer records. Fam Pract (2005) 22:234–241.[Abstract/Free Full Text]
  4. Tillin T, Forouhi N, McKeigue P, Chaturvedi N. Microalbuminuria and coronary heart disease risk in an ethnically diverse UK population: a prospective cohort study. J Am Soc Nephrol (2005) 16:3702–3710.[Abstract/Free Full Text]
 

What are the implications for the ageing population?

Peter Murchie

Department of General Practice and Primary Care, University of Aberdeen

Chronic kidney disease (CKD) is increasingly becoming an important worldwide health and social problem [1]. In the UK, CKD is under-recognized, outcomes are poor and costs high [2]. Although prevalence estimates of moderately or severely decreased kidney function in the elderly vary, rates as high as 20.6% of the over 65 population have been reported in some studies [3]. These studies also estimate that up to half of these patients will not have diabetes or hypertension [3]. Setting this in a Scottish context where 17% of the population are 65 years or older, up to 180 000 may have CKD based on current criteria [4].

For those tasked with caring for the elderly in the community this situation presents several challenges and opportunities. Increasing computerization and the development of chronic disease registers for conditions such as diabetes and hypertension will facilitate identification in the highest risk groups. Despite this, a significant proportion of elderly people with CKD, particularly those without diabetes or hypertension, will not be so readily identified. In this group several strategies are possible including opportunistic screening, screening targeted at those most likely to benefit, practice screening or population screening [5]. Research is required to ascertain the most cost-effective approach and it is likely that the new GP contract can be used to support its implementation.

In an environment of limited resources in primary care, however, the need to act must be tempered by close consideration of the costs and workload implications of whichever approach is likely to be adopted. An average general practice will have upward of 2000 elderly patients at risk of CKD [6]. The logistical issues of screening and treating such numbers are considerable.



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  1. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med (2003) 139:137–147.[Abstract/Free Full Text]
  2. Griffin SV, MacGregor MS. Facing an epidemic of chronic kidney disease. Clin Med (2005) 5:521–525.[ISI][Medline]
  3. Coresh J, Astor BC, Greene T, et al. Prevalence of chronic kidney disease and decreased kidney function in the adult US population: third national health and nutrition examination survey. Am J Kidney Dis (2003) 49:1–12.[CrossRef]
  4. Website of General Register Office for Scotland. accessed 30 November 2006. (http://www.gro-scotland.gov.uk/files/05mype-cahb-fig7.pdf).
  5. Hallan SI, Dahl K, Oien CM, et al. Screening strategies for chronic kidney disease in the general population: follow-up of cross sectional health survey. Br Med J (2006) 333:1047–1050.[Abstract/Free Full Text]
  6. Thomson R, Greenaway J, Chinn DJ, et al. The impact of implementing national hypertension guidelines on prevalence and workload in primary care: a population based survey of older people. J Hum Hypertens (2005) 19:683–689.[CrossRef][ISI][Medline]
 

What happens to patients with early CKD?

Natural history and progression of early CKD

Eberhard Ritz

Ruperto-Carola University, Heidelberg, Germany

Early Kidney disease is not the equivalent of minor renal injury and the very concept may be misleading.

The first difficulty is to recognize and quantitate early kidney disease. The is due to the fact that because of compensatory single nephron-hyperfiltration, analyses to estimate kidney function, such as eGFR and even cystatin C, underestimate the magnitude of loss nephrons/reduction in filtration capacity. In addition, histological studies showed that interstitial fibrosis (which is not necessarily reflected by either eGRF or albuminuria/proteinuria) is a more powerful predictor of progression than glomerular damage. Apart from these considerations one is confronted with the dilemma that even with standardization of chemical methods and using sophisticated equations, estimated GRF (eGFR) is too unreliable in early renal disease to base clinical decisions upon the estimate [1].

Early chronic kidney disease is clinically relevant from two perspectives: cardiovascular outcomes and progressive loss of renal function. The former are more frequent [2] and the risk starts to increase in very early stages of kidney dysfunction, as documented by prospective studies [3]. It is potentially explained by the observation that in patients with primary renal disease cardiovascular pathomechanisms (increased ADMA, insulin resistance, sympathetic overactivity, blood pressure, lipid abnormalities, etc.) are seen even before measured GFR decreases. The issue of progression of renal dysfunction is complicated by tremendous inter-individual differences documented even by very early observations [4,5], presumably to a considerable extent determined by genetic factors as illustrated by different intrafamilial courses in monogenic renal disease. A further determinant appears to be intrauterine programming. This is not to deny the importance of factors susceptible to intervention such as blood pressure [6], proteinuria [7], obesity, glycaemia, smoking as examples.

From a public health perspective the most important aspects are

  1. the factors involved in the genesis of cardiovascular events and
  2. in driving progressive loss of renal function.
A note of hope for cardiovascular intervention is the observation [8] that the cardiovascular risk factors operative in non-renal individuals have also a quantitatively similar impact in patients with early renal disease. Nevertheless, the susceptibility to intervention may be different, as illustrated by the greater response of CV-mortality to ACE-blockade in renal as compared with non-renal patients in the PEACE trial [9].

With respect to progression of renal dysfunction the factor of overriding importance is blood pressure. All intervention trials indicate that blood pressure lowering is the single-most important factor in attenuating progression.

Furthermore, there is little doubt that even in early chronic kidney disease reduction of proteinuria or albuminuria reduce the frequency of CV-events and deterioration of renal function even in the absence of overt primary kidney disease.

The issue of treatment targets has not been resolved; as to the selection of antihypertensive agents there is evidence for the efficacy of RAS blockade on albuminuria [10] and GFR loss [11] in early diabetic kidney disease, but there are few head on comparisons with alternative antihypertensive agents [12].

Factors of presumable lesser importance, but rewarding potential targets for public health intervention in early kidney disease, are smoking, obesity, high salt intake and some others whereas the previously highly rated impact of dietary protein appears to have been grossly overestimated.



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  1. Rossing. Diabetes Care (2006) 29:1024.[Abstract/Free Full Text]
  2. Keith. Arch Int Med (2004) 164:659.[Abstract/Free Full Text]
  3. Henry. Kidney Int (2002) 62:1402.[CrossRef][ISI][Medline]
  4. Mitch. Lancet (1976) ii1326.
  5. Jones. Lancet (1979) i1105.
  6. Hsu. Arch Int Med (2005) 165:923.[Abstract/Free Full Text]
  7. de Zeeuw. Kidney Int (2004) 65:2309.[CrossRef][ISI][Medline]
  8. Shlipak. JAMA (2005) 293:1737.[Abstract/Free Full Text]
  9. Salomon. Circulation (2006) 124:26.
  10. Parving. NEJM (2001) 345:870.[Abstract/Free Full Text]
  11. Barnett. NEJM (2004) 351:1952.[Abstract/Free Full Text]
  12. Ruggenenti. NEJM (2004) 351:1941.[Abstract/Free Full Text]
 

What are the implications for clinical practice?

Chris Isles

Renal Unit, Dumfries and Galloway Royal Infirmary, Dumfries, DG1 4AP

Around 10% of the adult population have early CKD as judged by the presence of microalbuminuria, proteinuria or an estimated GFR in the range 30–60 ml/min/1.73 m 2 [1]. The risks to these patients are both cardiovascular and renal with the likelihood of heart attack and stroke being much greater than that of progressive renal failure.

Cardiovascular risks have been described in detail by other speakers at this symposium. Renal risks have recently been quantified. A US population survey identified 27 998 subjects with eGFR <90 ml/min. During a five year observation period 24.3% patients with CKD3 died but only 1.3% required renal replacement therapy [2]. Similar findings have been reported by Norwegian investigators. 3069/65 604 (4.7%) subjects in a population survey had eGFR <60 ml/min. During 8 years follow-up, cardiovascular mortality was 3.5/100 person-years in subjects with eGFR 45–59 ml/min and 7.4/100 person-years with eGFR 30–44 ml/min. Corresponding incidence of ESRD was 0.04 and 0.2/100 person-years, respectively [3]. Only a minority of patients with raised creatinine in a third population survey showed progressive renal function decline during 31 months of follow up [4]. A fourth population survey has suggested that proteinuria may be more predictive of progressive renal function decline than a low GFR during 4.2 years of follow-up [5]. Both proteinuria and low GFR predicted a poor cardiovascular outcome in this study [5].

The implications for clinical practice are a huge increase in workload, not for nephrologists but for general practitioners who are being encouraged to detect, assess, manage and monitor patients with early CKD as part of their new contract. The message for GPs is that early CKD is a vascular disease. A renal opinion is only likely to be necessary if a patient has progressive renal failure and/or heavy proteinuria; a specific renal diagnosis such as polycystic kidney disease or lupus nephritis; or a specific renal complication such as anaemia or bone disease for which a nephrology referral might reasonably be expected to add value.



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  1. De Jong, et al. Nephrol Dial Transplant (2006) 21:2358–2361.[Free Full Text]
  2. Keith DS, et al. Arch Int Med (2004) 164:659–663.[Abstract/Free Full Text]
  3. Hallan, et al. Br Med J (2006) 333:1047–1050.[Abstract/Free Full Text]
  4. John, et al. Am J Kidney Dis (2004) 43:25–835.[CrossRef]
 

What are the best treatments for early CKD?

For cardiovascular prevention?

Alan Jardine

BHF Glasgow Cardiovascular Research, University of Glasgow, Glasgow G12 8TA

There are few studies on CV disease prevention in patients with early CKD. We are limited to sub-group analysis of other populations (e.g. hypertension and heart failure) that included patients with CKD (often unintentionally) and the use of data from patients with severe and end-stage CKD. Interpretation of these data is compounded by the fact that progression of CKD—per se—is associated with increased CV risk and prevention of progression will alleviate CV risk.

Sub-group analyses of studies of lipid lowering have shown that statin therapy is associated with proportional reduction in CV risk similar to that in other populations. However, in more advanced CKD the pattern of CVD outcomes changes and statin therapy reduced myocardial infarction but not CV death. Prevention of progression reduces renal failure but not CV death and there is little evidence for lifestyle modification in this population.

Overall, the evidence-base for CV risk modification is limited and further studies are required.

 

Blood pressure management in early (adult) CKD

David Goldsmith

Renal Unit, Guy's; Hospital, London SE1 9RT

Blood pressure rises with age in the UK (and other industrialized ‘wealthy’ countries) as a result of numerous environmental stimuli and adaptive responses. Elevated BP is a very important risk factor for heart disease, stroke, peripheral vascular disease and chronic kidney disease, perhaps especially so in ethnic minorities. Renovascular and renal parenchymal disease are probably the cause of around 5% of ‘hypertension’ seen in the general population. There is a relationship between mean BP and the rate of renal functional decline, and impressive evidence from trials that successful intervention to reduce BP elevation, primarily by use of drugs, can retard or arrest further renal functional decline (and of course prevent heart disease, stroke and premature death).

Intervention to alter BP as a cardiovascular and renal risk factor must take account of the patient's other risk factors and comorbidities, which should also be vigorously tackled. Advice on salt-restriction (<100 mmol Na+/day), avoiding excessive saturated fat intake, weight control, physical exercise and smoking cessation are of great importance.

In the presence of diabetes or significant proteinuria (PCR >100), (or both), elevated BP is a cardinal factor in generating progressive renal impairment. Numerous drugs, from many different ‘classes’, can reduce BP. Given the strong experimental evidence for the nephrotoxic effect of non-selective proteinuria in adults, and the strong epidemiological evidence linking micro-albuminuria, or more severe proteinuria, with adverse renal and cardiovascular outcomes, it seems sensible preferentially to use drugs which simultaneously reduce proteinuria and systemic blood pressure. These include angiotensin-converting enzyme inhibitors (ACEI), angiotensin II receptor blockers (ARBS), non-dihydropyridine calcium-channel blockers and indapamide. The most compelling evidence base, from individual trials, and from meta-analysis, is of course supportive of the use of ACEI/ARBs. Treatment should try to engineer BP values <130/80 mmHg, and even lower in the case of significant proteinuria (PCR >100). It is unlikely that one drug alone can achieve this in many (especially older) patients, so logical, easy-to-take, combinations are ideal. Reduction in proteinuria on antihypertensive therapy is a good prognostic sign for renal and cardiovascular outcomes.



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  1. http://www.bhsoc.org/pdfs/BHS_IV_Guidelines.pdf; http://www.nice.org.uk/guidance/CG34/guidance/pdf/English.
  2. Jafar TH, Stark PC, Schmid CH, et al. Progression of chronic kidney disease: the role of blood pressure control, proteinuria, and angiotensin-converting enzyme inhibition: a patient-level meta-analysis. Ann Intern Med (2003) 139:244.[Abstract/Free Full Text]
  3. Sarnak MJ, Greene T, Wang X, et al. The effect of a lower target blood pressure on the progression of kidney disease: long-term follow-up of the Modification of Diet in Renal Disease Study. Ann Intern Med (2005) 142:342.[Abstract/Free Full Text]
  4. Wright JT, Bakris G, Greene T, et al. Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK Trial. JAMA (2002) 288:2421.[Abstract/Free Full Text]
  5. Wolf G, Ritz E. Combination therapy with ACE inhibitors and angiotensin II receptor blockers to halt progression of chronic renal disease: pathophysiology and indications. Kidney Int (2005) 67:799.[CrossRef][ISI][Medline]
  6. Eriksen BO, Ingebretsen OC. The progression of chronic kidney disease: a 10-year population-based study of the effects of gender and age. Kidney Int (2006) 69:375.[CrossRef][ISI][Medline]
 

Anaemia and bone metabolism management

Mike Cassidy

Nottingham Renal & Transplant Unit, Nottingham City Hospital, Nottingham NG5 1PB

Both anaemia and perturbations in bone metabolism, due to kidney disease, can be found once glomerular filtration rate (GFR) falls to below 60 ml/min. Certain types of renal disease (e.g. chronic interstitial nephritis) and certain systemic diseases (e.g. diabetes mellitus) may be associated with more profound changes. Both complications are invariably well established once GFR falls to below 15 ml/min and by this stage add to the morbidity and mortality of kidney disease patients. It, therefore, would seem sensible to delay or prevent their onset by early treatment particularly in those patients identified as having progressive CKD.

Unfortunately though there are many good epidemiological and observational studies that clearly demonstrate the association of early CKD with anaemia and bone changes, studies to help us decide what intervention and when to institute it are lacking. Recent NICE guidance has been published providing recommendations to support clinical judgement in managing the anaemia of CKD, including early CKD. The majority of evidence for recommendations in pre-dialysis patients is class C at best. Class A evidence, however, supports the recommendation that treatment with erythropoeisis stimulating agents should be offered to people with anaemia of CKD who are likely to benefit in terms of quality of life and physical function [1]. Guidance on managing bone health in early CKD is based on even more flimsy evidence, the controlled trials that there are have been performed in relatively small numbers of patients over a short time frame [2]. Current management generally relies on class C and D evidence at best. Exciting new treatment options are becoming available, however, it will be some years before good randomized clinical trials deliver the evidence for the optimal management of this group of patients.



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  1. National Collaborating Centre for Chronic Conditions. Anaemia Management in Chronic Kidney Disease: National Clinical Guideline for Management in Adults and Children (2006) Royal College of Physicians,: London:.
  2. K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. www.kidney.org/professionals/kdoqi/guidelines_bone/index.htm.
 

Wednesday, 7 February 2007

How do we re-design the treatment?

Emerging models for care

Donal O’Donoghue

Hope Hospital, Salford M6 8HD

Caring for patients with chronic illness in an era of cost constraints and performance monitoring has led to a sharp growth in ‘disease management’ efforts by health systems. These models of care are based upon the foundation of registration, recall and review. Successful models use information systems to apply knowledge (information) in an integrated fashion and the majority have found that patient engagement is the key challenge. Education, empowerment and encouragement of self-management require clinical systems to be reconfigured specifically to address the needs and concerns of chronically ill patients. These improvements will not come easily but where disease management programmes have been established randomized trials have shown substantially better outcomes than usual care.

These models are now being adapted and applied to the management of CKD. They fall into two groups: targeting and case management and comprehensive system change. The development of pre-dialysis care for advanced CKD is an example of the former and the introduction across the UK of registers for adults with CKD provides an opportunity to develop the latter. They require a move away from an acute care culture to one where planned, regular interactions between patients and their care givers occur with a focus on function and prevention of exacerbations and complications. These interactions include systematic assessments, attention to treatment guidelines and behaviourally sophisticated support for the patient's role as self manager. These interactions should be based on clinically relevant information systems with continuing follow-up initiated by the medical practice.

Meeting the complex needs of people with Chronic Kidney Disease is a major public health challenge. The majority of individuals with CKD stages 3–5 are now being identified opportunistically by eGFR reporting. The creation of primary care-based registers as part of the Quality and Outcomes Framework can be used to facilitate a systematic approach to the implementation of the UK CKD and in due course NICE CKD guidelines. It is important that these models link with other vascular management strategies and ESRD preparation and planning.



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  1. Von Korff M, Gruman J, Schaefer J, Curry SJ, Wagner EH. Collaborative management of chronic illness. Ann Intern Med. (1997) 127:1097–1102.[Abstract/Free Full Text]
  2. Mendelssohn DC, Toffelmire EB, Levin A, et al. Attitudes of Canadian nephrologists toward multidisciplinary team-based CKD clinic care. Am J Kidney Dis (2006) 47:277–284.[CrossRef][ISI][Medline]
  3. National Kidney Foundation Kidney Early Evaluation Program. AJKD, KEEP Annual Report. Am J Kidney Dis (2005).
 

CKD and the role of the nurse

Natasha McIntyre

Nottingham University Hospital NHS Trust

It is well documented that there are still a large proportion of patients who suffer the effects of being seen too late by nephrology services, including the greater risk of mortality. With the advent of part two of the NSF for Renal Services, there is a need to improve communication and education of CKD to other clinicians outside of the renal unit. However, there are limited resources with which to do this considering patients with CKD are to be found in both primary and secondary care.

The introduction of estimated GFR and the UK guidelines for adults with CKD has been a huge organizational change for areas outside the nephrology field. To many healthcare staff it is a very new concept to have to become familiar with, in a climate where many of them, especially in primary care, have had to quickly adapt to changes in other specialist areas.

It is, therefore, important that the nurse has strategic input into planning how to implement a programme for identification, referral and management of those with CKD, to maximize use of available resources, ensuring the development of effective communication and educational processes for staff and the public.

The use of good communication and regular education can make a difference to staff outside the renal unit, looking after patients with CKD, enabling them to identify patients for referral or manage them those who do not in their own environments.

Geographical areas differ, in terms of socio-economic and healthcare requirements. It is, therefore, essential that a baseline assessment is carried out, obtaining data to identify areas that need to be targeted, but also to monitor effects of any developments introduced. This is prior to implementing new developments, ensuring that good practice is shared and equity of services not forgotten.

Nurses are in a good position to have the clinical expertise to help, influence and guide this process, and also act to bridge the gap between primary and secondary care and encourage two-way communication between the two to try to optimize the care given to our patients with CKD.

 

Can we afford it? Considerations in the cost-effectiveness of managing early CKD

Luke Vale

Health Economics Research Unit, University of Aberdeen

Using our limited health care budget one way means that we give up the opportunity to use these funds to achieve other desirable aims. This simple truth is the principle that underpins the economic notion of cost and it is intrinsically bound up with the consideration of affordability. This is because when we ask the question can we afford something we are really asking whether it is worthwhile given the other things we could do with the money. This means that we are concerned with efficiency. A judgement about whether a treatment for early chronic kidney disease is efficient for the NHS (i.e. whether its benefits are greater than its opportunity cost) requires information on the average costs and benefits of the different treatments available. So that the total cost to the NHS can be estimated, information is also required on the number of people who will be affected by chronic kidney disease and who might be eligible for the different treatments.

In this presentation, the principles of economic evaluation will be briefly outlined. This will cover what economic evaluation is and what sort of information is required to conduct an economic evaluation with special references to the prevention and treatment of early chronic kidney disease and its consequences. How this approach might be used in practice is then briefly described along with a summary and critique of the existing economic evaluations in this area. From the consideration of the existing evidence base the implication for both practice and research will be highlighted.

 

CKD around the world

John Feehally

John Walls Renal Unit, Leicester General Hospital, Leicester

The true incidence and prevalence of CKD is unknown in many parts of the world.

The number of people starting renal replacement therapy is a conventional surrogate in developed countries for the incidence of ESRD but is uninformative when renal replacement therapy is inconsistently available. Likewise, most countries lack the infrastructure or resources to undertake population-based epidemiological studies to reliably quantify early CKD. Indirect evidence suggests there are high rates of CKD due to immune-mediated glomerular disease associated with communicable disease in many parts of the developing world. It seems probable that this is now being compounded by CKD in association with the rapid emergence of non-communicable disease, particularly type 2 diabetes, which is an accelerating problem as the developing world urbanizes. Extrapolation of evidence from Europe and North America suggests that the burden of CKD in emerging countries will be disproportionate because of the increased susceptibility of their populations to CKD as a complication of diabetes. Socio-economic deprivation is also a significant risk factor for CKD.

Work in the emerging world, and among deprived indigenous populations in the developed world, suggest that low-cost screening and treatment programmes for CKD are achievable. Such programmes should be the basis of the public health strategy to combat CKD in these populations rather than unaffordable attempts to provide universal renal replacement therapy.



   References        
Top
 References
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 References   
 References    
 References    
 References    
 References    
 References    
 

  1. Modi GK, Jha V. Incidence of end-stage renal disease in India: a population-based study. Kidney Int (2006) [Epub ahead of print].
  2. Mani MK. Nephrologists sans frontiers: preventing chronic kidney disease on a shoestring. Kidney Int (2006) 70:821–823.[CrossRef][ISI][Medline]
  3. Hoy WE. Lessons in ethnonephrology. Kidney Int (2006) 70:251–257.[CrossRef][ISI][Medline]
  4. Feehally J. Ethnicity and renal disease. Kidney Int (2005) 68:414–424.[ISI][Medline]
 

Pharmacological management of CKD—a look into the future

Meguid El Nahas

Sheffield Kidney Institute, Sheffield, UK

Globally, an increased number of individuals suffer from CKD and progress to ESRD. Prevention of progression has focused so far on aggressive hypertension control and reduction of proteinuria. However, neither addresses the fundamental pathological processes involved in renal remodelling and leading to kidney fibrosis and established failure. These processes include progressive kidney cell loss, transformation into myofibroblasts, proliferation of fibroblasts and irreversible deposition of extracellular matrix (ECM). A number of interventions have addressed these steps of kidney scarring in experimental models with some promise. These include interventions aimed at the preservation of kidney cell number through the inhibition of cell death through apoptosis, the manipulation of epithelial mesenchymal transformation (EMT) of tubular cells, the reduction of fibroblast proliferation through interventions aimed at inhibiting their mediators or reducing cell responses and finally strategies to reduce ECM deposition and irreversible fibrosis. In this review, I will explore the clinical potential of some of these interventions and barriers to their clinical translation.


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