Chronic kidney disease (CKD) is defined as a persistent reduction in glomerular filtration rate (GFR) due to underlying renal disease, or haematuria, proteinuria or radiological abnormalities of the renal tract.
The incidence and prevalence of CKD is increasing, and is in part being fuelled by the increasing prevalence of diabetes and hypertension.
CKD is an independent risk factor for cardiovascular disease, which is the main cause of death for patients with CKD.
There is little reliable data on aetiology of CKD among patients in the UK. However, data from the UK Renal Registry indicate glomerulonephritis accounts for 16 per cent, pyelonephritis 13 per cent, diabetes 12 per cent, renovascular disease 9 per cent and hypertension 7 per cent of CKD.
CKD is staged according to eGFR (see box). This system gives a guide to the severity of renal disease.
The eGFR equation uses the patient’s age, gender and serum creatinine, and gives a result in ml/min/1.73m2 (average body surface area).
Evidence of chronic kidney damage includes persistent microalbuminuria, persistent proteinuria, persistent haematuria (after exclusion of other causes such as urological disease), biopsy-proven chronic glomerulonephritis and structural abnormalities of the kidney detected on imaging, such as polycystic kidney disease.
Initial investigations should aim to identify possible causes for CKD. Urine dipstick tests should be performed; if proteinuria is detected, a protein/creatinine ratio should be ordered to quantify this.
A renal ultrasound can assess bilateral renal size and symmetry, possible hydronephrosis and exclude congenital abnormalities such as polycystic kidneys.
Early recognition of CKD is important because steps can then be taken to reduce the rate of decline in eGFR.
Management should optimise the patient’s cardiovascular risk profile; control of hypertension, lipid profile and diabetes mellitus and lifestyle modification such as smoking cessation and weight loss are therefore important. Reducing cardiovascular risk is important in these patients with target BP of <130/80mmHg (or <125/75mmHg if proteinuria >1g/24hours) is present, target cholesterol <4.0mmol/l with LDL <2.0mmol/l and target HbA1c <6.5 per cent.
There is good evidence that use of ACE inhibitors or angiotensin II antagonists can slow progression of CKD.
To achieve target BP it is often necessary to use at least three different antihypertensive agents.
Attention should be given to addressing complications related to renal failure, such as anaemia and renal bone disease. It is therefore important to monitor haemoglobin, ferritin, calcium and phosphate.
The Renal Association has issued suggested guidelines for referral to secondary care for patients with CKD.
When making a referral it is useful to include serial creatinine levels, dating back to a time when levels were normal, to give an indication of rate of decline of renal function.
Detection of CKD and efforts to optimise risk factors can slow disease progression, reduce cardiovascular complications and improve prognosis for these patients.
Dr French is SHO in renal medicine and Dr Banerjee is consultant nephrologist at St George’s Hospital, London
Further information can be obtained from The Renal Association website: www.renal.org