Chronic Kidney Disease


Chronic kidney disease (CKD) is a common condition involving long-term damage or structural abnormality of both kidneys, resulting in reduced renal function. There are a number of possible underlying causes and it often co-exists with other chronic conditions such as cardiovascular disease and diabetes. Important issues to address in a patient with CKD are finding and treating the underlying cause, replacing functions of diseased kidneys and lifestyle modification.


CKD is usually asymptomatic and reduced renal function is most commonly an incidental finding when a urea and electrolytes blood test is done. If severe kidney damage is present, then symptoms of end stage renal failure may occur. These include:

  • Itching
  • Nausea and vomiting
  • Peripheral oedema
  • Insomnia
  • Fatigue and general malaise


As the condition is usually asymptomatic, it is less likely that a patient would seek help for CKD alone. It is more likely that a patient will present with another condition that pre-disposes to kidney disease. The most common are:

  • Diabetes mellitus
  • Hypertension
  • Cardiovascular disease - ischemic heart disease or peripheral vascular disease
  • Renal vascular disease

Less common causes include:

  • Chronic glomerulonephritis
  • Reflux nephropathy
  • Polycystic kidney disease

Patients presenting with any of these conditions should have a U+E blood test to check their renal function. Patients with diabetes should be screened annually for renal function. In patients with hypertension, cardiovascular disease, obesity or smokers, there should be awareness of the increased risk of CKD and a lower threshold to investigate.

Laboratory Investigations

CKD is defined as kidney damage which is chronic (>90 days). Kidney damage is measured by estimated glomerular filtration rate (eGFR), which is an estimate of how much blood (ml) is filtered by the glomerular apparatus of the nephron each minute. The estimate is calculated based on how much creatinine is present in the serum taken for a U+E blood test. Creatinine is a waste product of muscle breakdown which everyone produces, but muscly people produce more than small or frail people. This means that other factors are taken into account to estimate GFR. Age, gender and race are all adjusted for in the calculation (MDRD equation) but in practice it is impossible to weigh all patients and adjust for this. Therefore, eGFR is still often over-estimated for small or frail people and under-estimated for larger, muscly people.

CKD is classified based on eGFR as follows:

~CKD stage eGFR with/without other signs of kidney damage*
1 ≥90ml/min with signs of kidney damage
2 60-89ml/min with signs of kidney damage
3 30-59ml/min not required for diagnosis
4 15-29ml/min not required for diagnosis
5 <15ml/min not required for diagnosis

*Signs of kidney damage include proteinuria, hematuria (not lower tract cause such as UTI/bladder tumor) or abnormal imaging

Dipstick urinalysis can be used as an initial screening test for proteinuria or hematuria. Patients with hematuria should be investigated for UTI or urinary tract malignancy.

Urinary protein should be tested. Urinary albumin:creatinine ratio is used in diabetic patients to detect and monitor diabetic nephropathy. Urinary protein:creatinine ratio is a prognostic marker in CKD.

Radiological investigations

Patients with CKD should have a renal ultrasound to rule out any structural cause, for which management would differ


Lifestyle modification

Diet should be aimed at lowering blood pressure, achieving a healthy weight and reducing cardiovascular risk. Patients with hypertension should be advised to reduce salt intake

Patients who smoke should be advised to stop

Patients should be encouraged to lose weight and exercise regularly, and should be referred to a dietician and/or physiotherapist to help achieve this.

Blood pressure

All patients with hypertension should be treated to reduce this to under 140/90mmHg. Patients with significant hematuria (>1g/day) should have a target of 130mmHg systolic

Medical management

  • ACEi/ARB should be given to all patients regardless of BP
  • Calcium channel blockers are an alternative if intolerant of ACEi/ARB
  • Statin and low dose aspirin should be given to patients in CKD stages 1-3 with increased CV risk



The healthy kidney produces erythropoietin (EPO) which stimulates the bone marrow to produce red blood cells. In CKD this function is impaired, which can lead to anaemia.

IV iron or EPO injections can be used to treat anaemia of CKD

Bone disease

Vitamin D is hydroxylated to its active form by the kidney, another function that can be impaired in CKD. This results in reduced Calcium absorption from the GI tract, which results in secondary hyperparathyroidism when the parathyroid glands produce more PTH to counteract the low calcium levels. PTH increases osteoclast activity, meaning bone is resorbed to release calcium into the circulation. This can result in weak and painful bones and cause calcification of the arteries and heart valves.

If secondary hyperparathyroidism is present for many years, tertiary parathyroidism can develop where the parathyroid glands release PTH in an uncontrolled way not related to serum calcium. This can result in hypercalcaemia.

Bone disease can be treated with:

  • hydroxylated vit D supplement (eg alfacalcidol)
  • Gut phosphate binders (PTH also increases serum phosphate)

End stage renal disease

CKD is a progressive condition, which can be slowed or temporarily halted but not cured. Therefore, some patients will develop disease which requires renal replacement therapy (RRT) such as hemodialysis, peritoneal dialysis or kidney transplant. Usually RRT would be discussed at a eGFR of around 20ml/min and started at eGFR of under 15ml/min though this depends on each individual patient, their symptoms and their blood results (e.g. hyperkalaemia). RRT is discussed in more detail in a separate article

Key References

SIGN 103 CKD Guideline:
NICE 182 CKD Guideline:

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