Chronic Kidney Disease
Definition
Chronic kidney disease (CKD) is a reduction in kidney function or structural damage (or both) present for more than 3 months, with associated health implications.
Classification
Markers of kidney damage
Raised serum creatinine
Serum estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2.
Proteinuria (a urinary albumin:creatinine ratio [ACR] of more than 3 mg/mmol).
Persistent haematuria (1+ or more of blood), after exclusion of a urinary tract infection (UTI)
Urine sediment abnormalities: red blood cells (may indicate glomerular disease); white blood cells (may indicate pyelonephritis or interstitial nephritis); or granular casts and renal tubular epithelial cells (seen in many parenchymal diseases).
eGFR (mL/min/1.73 m2)
≥90
60–89
45–59
30-44
15–29
<15
Normal
Mild reduction
Mild to moderate reduction
Moderate to severe reduction
Severe reduction
End-stage kidney failure
stage 1*
stage 2
stage 3a
stage 3b
stage 4
stage 5
* Markers of kidney damage include albuminuria (urinary ACR more than 3 mg/mmol), urine sediment abnormalities, electrolyte and other abnormalities due to tubular disorders, abnormalities detected by histology, structural abnormalities detected by imaging, or a history of kidney transplantation.
Prevalence
The age-standardized prevalence of CKD stages 3–5 was 8.5% (10.6% in women and 5.8% in men).
An exponential increase in the prevalence of CKD stages 3–5 with increasing age.
Multiple Causes
Hypertension.
Diabetes mellitus.
Glomerular disease, such as acute glomerulonephritis (typically CKD may follow on from a Streptococcal upper respiratory tract infection; may also follow hepatitis B, hepatitis C, or HIV infection).
Current or previous history of acute kidney injury (AKI). This may be triggered by severe intercurrent illness or dehydration.
Nephrotoxic drugs, such as: Aminoglycosides, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists (AIIRAs), bisphosphonates, calcineurin inhibitors (such as ciclosporin or tacrolimus), diuretics, lithium, mesalazine, and nonsteroidal anti-inflammatory drugs (NSAIDs).
Obstructive uropathy: structural renal tract disease, bladder voiding (neurogenic bladder, benign prostatic hypertrophy); urinary diversion surgery; recurrent urinary tract calculi.
Multisystem diseases with potential renal involvement, such as: Systemic lupus erythematosus (SLE) which may cause lupus nephritis; Vasculitis.
Myeloma.
A family history of CKD stage 5, or hereditary kidney disease such as autosomal dominant polycystic kidney disease, Alport's syndrome (a sex-linked recessive disease which typically causes haematuria), and familial glomerulonephritis.
Cardiovascular disease
Obesity with metabolic syndrome [Obesity alone is not a risk factor for CKD]
Complications
AKI
Hypertension
CVD
Renal anaemia
Renal mineral and bone disorder
Peripheral neuropathy and myopathy
Malignancy (risk factors may include exposure to immunosuppressive agents, and immune dysregulation caused by chronic uraemia)
End-stage renal disease (ESRD)-
People with CKD stages 4–5 may need renal replacement therapy (RRT) in the form of dialysis or kidney transplantation.
Increased all-cause mortality.
Symptoms and Signs:
Symptoms
Lethargy, itch, breathlessness, cramps (often worse at night), sleep disturbance, bone pain, or loss of appetite, vomiting, weight loss, and taste disturbance (often present with end-stage disease).
Urine output
polyuria (tubular concentrating ability is impaired)
oliguria
nocturia (due to impaired solute diuresis or oedema)
anuria (due to possible acute kidney injury [AKI]
obstructive uropathy causing urinary retention; or end-stage renal disease)
Signs
Uraemic odour (ammonia-like smell of the breath, may be present in advanced disease).
Pallor (due to renal anaemia).
Cachexia and signs of malnutrition.
Cognitive impairment (language, orientation, and attention may be particularly affected).
Dehydration or hypovolaemia (risk of AKI).
Tachypnoea (may be due to fluid overload, anaemia, or co-morbid ischaemic heart disease).
Hypertension
Palpable bilateral flank masses with possible hepatomegaly (suggests polycystic kidney disease with possible liver cysts).
Palpable distended bladder (suggests obstructive uropathy).
Peripheral oedema (may be due to renal sodium retention, hypoalbuminaemia, or co-morbid heart failure)
Peripheral neuropathy (may present with paraesthesia, sleep disturbance, and restless legs syndrome) or myopathy.
Frothy urine (may indicate proteinuria).
From history, check for predisposing factors or co-morbidities
nephrotoxic drugs, including over-the-counter or herbal medicines.
risk factors for CKD or previous history of AKI.
family history, such as autosomal dominant polycystic kidney disease.
Any associated co-morbidities or complications of CKD
Case finding: suspect CKD
Risk factors for CKD.
An incidental finding of raised serum creatinine and/or eGFR of less than 60 mL/min/1.73 m2; or markers of kidney damage (proteinuria/haematuria).
Possible clinical features of CKD (rare unless end-stage disease).
Renal investigations( + repeat within 3m)
Make a diagnosis of CKD if there is a persistent reduction in renal function (eGFR is less than 60 mL/min/1.73 m2) and/or proteinuria (urinary ACR is greater than 3 mg/mmol) lasting for at least three months.
Serum creatinine and eGFR.
Early morning urine sample to measure the ACR.
Urine dipstick test to check for haematuria.
Body mass index (BMI), blood pressure, and serum HbA1c and lipid profile to assess for cardiovascular risk factors.
A renal tract ultrasound (parenchymal renal disease, urinary tract stones or obstruction, or a family history of polycystic kidney disease).
Monitoring of CKD
Identify any underlying causes and risk factors for disease progression which will influence the frequency of monitoring.
e.g.Consider stopping any potentially nephrotoxic drugs.
Monitor renal function by checking serum creatinine and eGFR and urinary albumin:creatinine ratio (ACR)
Screen for 'accelerated progression' of CKD:
sustained decrease in eGFR of 25% or more from baseline and a change CKD category within 12 months;
or a sustained decrease in eGFR of 15 mL/min/1.73 m2 within 12 months
Full blood count to exclude renal anaemia
Serum calcium, phosphate, vitamin D, and parathyroid hormone to exclude renal metabolic and bone disorder
Referral to a nephrology specialist
Emergency admission
urinary retention; has severe hyperkalaemia (potassium greater than 6 mmol/L); severe uraemia; or signs of fluid overload or dehydration
Urology referral 2ww
Arrange an urgent 2-week wait referral if there is isolated persistent haematuria
Suspected urinary tract obstruction (for example the bladder is palpable or hydronephrosis is seen on renal tract ultrasound).
Renal physician
An eGFR of less than 30 mL/min/1.73 m2 (CKD Stage 4 or Stage 5)
Accelerated progression of CKD.
Proteinuria:
A urinary ACR ≥ 70 mg/mmol (unless known to be associated with diabetes mellitus).
A urinary ACR ≥ 30 mg/mmol with persistent haematuria, after exclusion of a urinary tract infection (UTI).Uncontrolled hypertension.
A rare or genetic cause of CKD.
Suspected renal artery stenosis.
This should be suspected if there is
a greater than 25% reduction in eGFR within 3 months of starting (or increasing the dose of) a renin-angiotensin system antagonist
refractory hypertension
pulmonary oedema
and/or a renal artery bruit.A suspected complication of CKD.
Management in primary care should include:
Providing sources of information, advice, and support.
Assessing for and managing risk factors and co-morbidities.
Advising on healthy lifestyle measures and avoiding the use of over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs).
Assessing for hypertension and CVD, and managing appropriately.
Prescribing a low-cost renin-angiotensin system antagonist lisinopril or losartan, if appropriate.
For all people with CKD, prescribe lipid-lowering therapy with a statin
Prescribe an antiplatelet drug for the secondary prevention of CVD.
Ensuring the person is offered immunizations for influenza and pneumococcal disease.