News Release

Chronic kidney disease -- most with condition in rich countries more likely to die of cardiovascular causes, not kidney failure, while those in poorer settings will probably die from kidney failure

Peer-Reviewed Publication

The Lancet_DELETED

Because availability of renal replacement therapies (dialysis or transplant) is limited in countries of low and middle income, most patients around the world with chronic kidney disease (CKD) will die from kidney failure without receiving dialysis or transplantation. In developed countries, many more people will die from cardiovascular disease rather than progress to kidney failure requiring renal replacement. But early recognition and prevention of CKD is vital in all settings, says the second paper in The Lancet Series on Renal Medicine—written by Dr Marcello Tonelli, University of Alberta, Edmonton, AB, Canada, and colleagues.

The ageing of populations along with the growing global prevalence of diabetes and other chronic non-communicable diseases has led to corresponding worldwide increases in prevalence of CKD and kidney failure. CKD is defined by a sustained reduction in glomerular filtration rate (GFR—the rate at which fluids are filtered through the kidneys) or evidence of structural or functional abnormalities of the kidneys on urinalysis, biopsy, or imaging. When defined by a GFR of 60 or less in standard GFR units (mL min–¹ 1•73 m𔃀) approximate CKD prevalence across Europe, Asia, North America and Australia is 2-11% of the population.

In developed countries, age, hypertension, diabetes, increased body-mass index, and smoking are associated consistently with CKD, as is a history of established cardiovascular disease. Poorer countries have the same causes as high-income nations but with the added burden of extra CKD cases due to bacterial and viral infections (most continents) and heavy metal poisoning (Asia, Africa, Middle East). Cardiovascular disease is the leading cause of mortality in CKD, and even mild reductions in glomerular filtration rate are associated with excess cardiovascular risk. At any given level of kidney function, raised amounts of proteinuria are associated with increased cardiovascular morbidity and mortality. In patients with cardiovascular disease, diabetes, or hypertension, presence of CKD (especially with proteinuria) is a so-called risk multiplier that identifies the subset of individuals who are most likely to have adverse outcomes.

Early identification of patients with CKD is desirable because interventions can then be implemented to reduce risk of cardiovascular events or progression to kidney failure. The high prevalence of CKD, absence of symptoms until disease is advanced, accessibility of laboratory tests for diagnosis and prognostication, and availability of treatments that prevent complications suggest that screening for CKD could be worthwhile. However, the role of population-based screening remains controversial. Screening for proteinuria is appealing because it is easy to undertake, predicts cardiovascular morbidity and mortality, and might be a better predictor of future decline in GFR than a reduction in estimated GFR.

Diagnostic testing for CKD is advocated for several groups of patients who seek medical attention for other reasons, especially those with diabetes, hypertension, cardiovascular disease, structural renal-tract disease, autoimmune diseases with potential for kidney involvement, and a family history of CKD or hereditary kidney disease.

Initial management of CKD entails identification of reversible disorders (such as urinary-tract obstruction, infection, or autoimmune disease) that could respond to specific treatment and lead to stabilisation or improvement in kidney function. Irrespective of underlying cause, typical goals of management for all patients with CKD include prevention of cardiovascular events and reduction of the rate of progression of the disorder (thereby delaying or preventing kidney failure and other complications). Reduction of high blood pressure using an angiotensin-converting-enzyme (ACE) inhibitor, is a treatment frequently given to patients with non-diabetic or diabetic CKD. Statins and aspirin could also be of benefit. But their role is less clearly defined. Stopping smoking, and sodium bicarbonate supplementation are other interventions that show benefit.

Adherence to treatment for CKD can be poor. In the UK, only a fifth of patients with diabetes and chronic kidney disease had a blood pressure of 130/80 mm Hg or less, and fewer than half were receiving an ACE inhibitor or angiotensin-receptor blocker. The authors add: "Furthermore, only 50% of those with stage 3 chronic kidney disease were prescribed an antiplatelet agent or a lipid-lowering treatment, suggesting that the management of these patients in primary-care settings could be enhanced considerably."

Depsite the availability of drugs to slow CKD progression, many patients do develop kidney failure—the authors call for more research into new drugs and treatments. They conclude: "Further research on the merits of novel methods for case-identification and care delivery in diverse settings is needed because of the high and growing global prevalence of chronic kidney disease. In view of the severely restricted availability of dialysis in countries of low and middle incomes, such research is especially urgent outside the developed world. For all health systems (irrespective of resources), multi-intervention clinics and programmes that enhance care of patients in primary practice settings are attractive alternatives to conventional models that merit further study."

###

See also World Report for details of a CKD screening programme in middle-income and low-income countries.

Dr Marcello Tonelli, University of Alberta, Edmonton, AB, Canada. T) +1 780 407 8520 E) mtonelli-admin@med.ualberta.ca

For more details of the programme in the World Report, please contact Giuseppe Remuzzi, Mario Negri Institute for Pharmacological Research, Bergamo, Italy. T) +39-035 319888 E) giuseppe.remuzzi@marionegri.it

Or alternatively William G. Couser, Head of ISN-COMGAN, T) +1-425 415 8436 E) wgc@u.washington.edu

For full Series paper 2, see: http://press.thelancet.com/renal2.pdf

For World Report, see: http://press.thelancet.com/wr1004.pdf


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.