Chronic Kidney Disease (Chronic Renal Failure)
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Chronic Kidney Disease – CKD (previously – chronic renal failure) involves a long-standing and often deteriorating reduction in renal function. It is irreversible and generally appears over a period of years. Initially, CKD begins as only biochemical abnormalities, but eventually it will result in clinical symptoms. When it does so, it is often referred to as uraemia.
Once reaching a stage where death is imminent without renal replacement therapy, it is referred to as ESRF – end-stage renal failure.
The definition and diagnosis of CKD is based on the presence of protein in the urine (albuminuria) and / or a reduced estimated glomerular filtration rate of <60ml/minute for a period of at least 3 months.
Detecting kidney disease can be difficult. Almost cases will be asymptomatic, and symptoms will only develop once 90% of kidney function has been lost. Most patients only become symptomatic once they reach CKD stage 5. Therefore, screening plays an important role in detecting CKD in earlier stages.
In most cases, nothing can be done reverse the damage that has already occurred.  Exceptions involve cases of urinary tract obstruction, Goodpasture’s syndrome, and cases where narrowing of the renal arteries can be corrected.
However, there is good evidence that early treatment can reduce the rate of disease progression and prevent the complications of end stage CKD. The earlier the intervention, the greater the impact of treatment. The goal is to prevent the need for dialysis.
Most patients can be managed in primary care, and will never develop significant disease. Those with an eGFR <30 (CKD stage 4 and 5) are considered to have more serious disease and should be referred to a renal specialist.
Early detection of CKD allows for lifestyle modifications, and the initiation of an ACE-inhibitor or angiotensin receptor blocker (ARB) , which reduces the risk of progression, and reduces the risk of associated cardiovascular complications by up to 50%.


  • Strongly correlated with other chronic diseases – such as diabetes and cardiovascular disease
  • Stage 3 to 5 CKD has a prevalence of about 8%
    • 10% in women
    • 6% in men
  • Chronic kidney disease is of particular importance in terms of cost to the NHS; about 630 patients per 1 million are kept alive by renal replacement therapy, and the incidence of new patients having such treatment is about 110 per 1 million.
  • In the USA, incidence is about 3 times higher than in the UK; over half of CKD patients in the US are diabetics
  • There is a much higher incidence of ESRF in black populations than in white populations.  In this ethnic group CKD tends to be caused by hypertensive nephropathy.
  • CKD due to atherosclerotic vascular disease in the renal artery is more common in elderly patients than in young patients.
  • There is wide geographic variation in the incidence of conditions that cause CKD.
    • Malaria is the main cause of CKD throughout Africa.
    • Schistosomiasis – this is a parasitic disease caused by several species of fluke. The disease is most commonly found in parts of the Far East, Middle East and Africa where the water supply contains numerous freshwater snails carrying the parasite. After penetrating the skin, snail larvae affected by the parasite move into systemic circulation and then into portal circulation, maturing in the liver. Moving into veins surrounding the bladder, they then lay eggs which cross the urethral or bladder wall causing long-standing urinary obstruction which results in CKD.
  • The incidence of diabetes, and thus diabetic nephropathy tends to be higher in Asian populations than in white populations.

Risk factors

  • Cardiovascular disease
  • Diabetes
  • Smoking
    • Between 40% and 105% increased risk depending on pack years
  • Hypertension
  • Acute Kidney Injury (AKI)
  • Obesity
    • Risk is doubled
    • Central obesity is a greater predictor compared to total weight
  • Chronic use of NSAIDs


As there are numerous causes of CKD, only the most common ones are listed below.
Proportion accounting for all cases of ESRF
Congenital / inherited

e.g. polycystic kidney disease, Alport’s syndrome, medullary cystic disease, tuberose sclerosis

Polycystic kidney disease, Alport’s syndrome, medullary cystic disease, tuberose sclerosis
Renal artery stenosis
The wide variation here could be due to racial difference or diagnostic differences – we do not know!
Accelerated hypertension
Glomerular diseases
e.g. IgA nephropathy, Wegerner’s granulomatosis, amyloidosis, diabetic glomerulosclerosis, thrombotic thrombocytopaenic purpura, sickle cell disease
IgA nephropathy, Wegener’s granulomatosis, amyloidosis, diabetic glomerulosclerosis, thrombotic thrombocytopenic purpura, sickle cell disease
Interstitial diseases

e.g. reflux neuropathy, TB, schistosomiasis, multiple myeloma

Reflux nephropathy, tuberculosis, schistosomiasis, multiple myeloma, renal papillary sclerosis, Chinese herb nephropathy
Systemic inflammatory disease
e.g. SLE, vasculitis
SLE, vasculitis
Diabetes mellitus
There are significant racial and regional differences in numbers diagnosed with DM who go on to develop ESRF.
Other / Unknown
A very careful history needs to be collected, paying close attention to…
  • The duration of symptoms
  • Drug history – including NSAIDs, anti-inflammatories and other medication use; don’t forget to  take into account the use of herbal remedies
  • Family history of renal disease
  • Diabetes
  • Known hypertension
  • Previous occasions on which a kidney function test has been taken, e.g. for medical insurance, new job or new patient check, etc.
CKD can be caused by any pathology that destroys the normal structure and function of the kidney.
One of the most useful signs is bilaterally small kidneys on USS.

Signs and symptoms

The early stages of CKD are often completely asymptomatic.
Urea and creatinine levels are usually measured, and there is a rough correlation between these levels and the severity of disease.
Many of the symptoms of CKD are due to high urea levels.
Symptoms become apparent when serum urea concentration reaches 40 mmol/L, and this is only seen in severe CKD. However, many patients experience symptoms at lower concentrations than this.  Symptoms may include:
  • Hypertension
  • Malaise
  • Loss of appetite
  • Insomnia
  • Nocturia and polyuria due to inability to concentrate urine
  • Itching (due to high levels of urea)
  • Nausea, vomiting and diarrhoea
  • Parasthesia due to polyneuropathy
  • Restless leg syndrome
  • Bone pain due to metabolic bone disease
  • Peripheral and pulmonary oedema due to salt retention
  • Symptoms of anaemia
  • Amenorrhoea
  • Erectile dysfunction
  • Bruising
  • Shortness of breath
  • Haematuria

Signs can include:

In more advanced uraemia, i.e. 50-60 mmol/L , the aforementioned symptoms tend to be more severe, and there may be others, including CNS symptoms:
  • Mental slowing, clouding of consciousness, seizures
  • Myoclonic twitching – myoclonus is where a particular group of muscles will twitch involuntarily, e.g. hiccups are a kind of myoclonic jerk affecting the diaphragm; in severe disease, it is generally one of the last signs to show after other symptoms are already present.
Eventually there may also be oliguria, which tends to only occur in AKI and in the very late stages of CKD.
Urine output is NOT a good guide for renal function.  A low GFR can still result in a very high urine output due to failure of reabsorptive mechanisms.
  • Although urea on its own is not a particularly toxic substance, the overall effect of all the metabolites of protein metabolism is what accounts for the problematic nature of living with CKD. This is confirmed by the fact that restricting dietary protein can reduce the symptom severity.


There are generally very few signs of uraemia.  There may or may not be apparent:
  • Short stature – due to chronic renal failure in childhood
  • Pallor – i.e. pale colour due to anaemia
  • Increased photosensitive pigmentation – which may make the patient appear misleadingly healthy
  • Brown discolouration of the nails
  • Scratch marks – the patient may feel itchy due to the high levels of urea in the body
  • Signs of fluid overload – peripheral oedema, pulmonary oedema (crackles at the lung bases on auscultation)
  • Pericardial friction rub
  • Glove and stocking sensory loss – rare
The kidneys themselves are generally not palpable unless they are enlarged from polycystic disease, obstruction or tumour.
Consider rectal and vaginal examination if indicated – this may disclose the underlying cause of the disease, for example, urinary tract obstruction.
There may also be signs of other underlying conditions, such as retinopathy in diabetes, evidence of peripheral vascular disease, evidence of spina bifida, and other causes of neurogenic bladder.


A diagnosis of CKD can be made with either of:

  • eGFR <60 on two occasions at least 2 weeks apart
    • Make sure to repeat within 1 week to rule out AKI, and then usually repeated at 2-3 months after this to confirm CKD
  • Albuminuria (ACR >30 [UK] or 2.5 for men and 3.5 for women [AUS]) on two occasions within 3 months (first void urine specimens)

CKD itself is not a primary diagnosis – further attempts should be made to identify the underlying cause (see Investigations below).


It is important to consider at risk populations for renal disease. The RACGP “Red Book” [AUS] recommends:

  • Blood pressure
  • U+Es – for creatinine (and eGFR)
    • If eGFR <60 mL/min – repeat within 7 days
  • Urine for albuminuria
    • If positive – arrange two further samples over 2 months

On the following at risk patients every two years:

  • Obese (BMI >30)
  • Smoker
  • Known cardiovascular disease
  • Aboriginal or Torres Straight Islander peoples aged >30
    • These patents are 4-5x more likely to have CKD
  • History of acute kidney injury
  • Family history of CKD
  • Known renal tract disease – e.g. stones, prostatic hypertrophy
  • Multi-system disease known to affect kidneys – e.g. SLE
  • Haematuria
  • Malignancy
  • Aged >60

And annually to all patients with:

  • Hypertension
  • Diabetes


In addition to blood pressure, U+Es and urine ACR, many further investigations may be performed to identify the underlying cause.

The following is a list of tests that may be considered to look for an underling cause of CKD.


  • FBC
  • ESR – if this is raised it suggests myeloma or vasculitis
  • U+E – raised urea and raised creatinine
    • Urea in particular is a poor marker of CKD. Levels vary according to hydration and diet
    • Creatinine levels can remain normal up to the point of loss of 50% of renal function
  • eGFR – is usually calculated by most laboratories based on age, urea and creatinine
  • Glucose – check for diabetes
  • Sodium – often low
  • Potassium – may be raised – and if it is raised – is often a sign of severe disease and requires urgent management
    • Hyperkalaemia in the main indication for dialysis
    • Urea and creatinine are only secondary considerations, and patients are not routinely dialysed without abnormalities of potassium
  • Calcium – can be low, normal or high!
  • Increased phosphate
  • Raised parathyroid
  • Albumin – often low – due to loss via the kidney
  • Serology
    • Consider hepatitis B and C as well as HIV serology
    • Consider antibody screen


  • Haematuria – can differentiate glomerulonephritis from chronic renal failure; also rules out other conditions.
    • Patients with haematuria should have urine MC+S performed, to rule out UTI
    • If no UTI, but persistent haematuria and NO evidence of renal failure, then refer to urology for investigation for cause of haematuria (e.g. RCC or TCC)
  • Proteinuria – if this is heavy it is strongly suggestive of glomerular disease.
  • Glycosuria – this is common even with normal blood glucose in CKD.
  • Casts – suggestive of renal disease; highly suggestive of glomerulonephritis.
  • White cells – suggestive of infection / nephritis
  • Red cells – can come from anywhere along the urinary tract, so their presence is not particularly useful in diagnosing CKD.
  • 24-hour creatinine clearance – useful in determining the level of renal failure. Urine ACR is the recommended investigation (as opposed to “protein” which is less sensitive)
    • Single urine sample for ACR is preferred (first void of the day) for convenience and compliance, and can be used to estimate the 24-hour value
    • The degree of proteinuria strongly correlates to the level of kidney disease
    • Reference ranges:
      • Normal – 30 mg albumin / 1g creatinine
      • Microalbuminaemia – 30 – 300mg albumin / 1g creatinine
      • Macroalbuminaemia – >300 mg albumin / 1g creatinine
    • Confirms the diagnosis of CKD (Even if eGFR is normal) with 2 positive samples within 3 months
  • Urinary electrolytes – an unhelpful investigation.
  • Urine osmolality – this is low in cases of high fluid intake, but it is also low when fluid intake is inadequate in renal disease; demonstrates that the kidney is unable to concentrate urine.


  • ECG – to look for signs of underlying cardiac dysfunction – e.g. left ventricular hypertrophy
  • Renal USS
    • Kidney often large in early stage of CKD and become small as disease progresses
    • Often multiple cysts are visible
    • May spot signs of renal tract disease (e.g. hydroneophrosis)
    • Indications
      • Have accelerated progression of disease
      • eGFR <30
      • Persistent haematuria
      • Any symptoms of urinary tract obstruction
      • Strong FHx of polycystic kidney disease
    • In Australia, recommended to perform USS on all CKD patients once diagnosis is confirmed
  • Renal nucleotide scan
    • Can assess the presence of renal artery stenosis
  • CT
    • May spot renal cysts and masses – but these are better visualised with USS
    • The best investigation for suspected renal tract pathology
  • MRI
    • May be rarely used if CT is contraindicated – e.g. if allergic to IV contrast

Tests that should always be performed upon diagnosis of CKD:

  • Renal tract USS
  • Urine ACR
  • Fasting lips and glucose
  • Urine microscopy for dysmorphic red cells, red cell casts or crystals


The GFR is the glomerular filtration rate. The estimated GFR (eGFR) is calculated using the patients creatinine level, age, sex and a formula. There are several formulas which are used, the most common being the CKD-EPI equation.

The eGFR strongly correlates with the level of kidney disease, however, up to 50% of renal functions an be lost before creatinine begins to rise.

Other factors that can affect the eGFR include:

  • Consumption of a meal containing meat within the 4 hours before U+Es was taken
  • Extremes of body size
  • Patient is on a high protein diet (or taking protein supplement)
  • High muscle mass
  • Severe lives disease
  • Drugs – particularly fenofibrate and trimethoprim
  • Pregnancy
  • Patient is on dialysis

eGFR and drugs

Some drug doses should be altered in patents with a low eGFR. Common examples include metformin and other diabetes drugs.

Drugs than are known to affect renal function include:

  • NSAIDs
    • Especially when in combination with an ACE-inhibitors (or ARB) and a thiazide diuretic – the triple whammy – is known to precipitate AKI, especially if combined with dehydration / volume depletion
  • Lithium
  • Radiographic contrast agents
  • Aminoglycosides
  • Gadolinium

Albuminuria and ACR

Protein in the urines a key marker of kidney damage. Most of the protein found in urine is albumin. A “first void” specimen should be take – i.e. the first part of the urine stream. Repeat tests (typically 3 within 3 months) are required to confirm the presence of albuminuria. A patient is said to have albuminuria if 2 out of 3 tests are positive. CKD is present if the albuminuria persists for 3 months.

  • Elevated ACR is a more sensitive sign than low eGFR
  • 8% of adults will have an abnormal urine ACR, whilst 4% will have an low eGFR

Dipstick testing is not recommended for diagnosis as it is not accurate enough.

Several other non-CKD factors can cause albuminuria:

  • UTI
  • High dietary protein intake
  • Heart failure
  • Acute febrile illness
  • Heavy exercise within the last 24 hours
  • Menstruation
  • Genital infection
  • Drugs – especially NSAIDs

Differentiating AKI and CKD

The following factors can help differentiate between chronic and acute renal failure (more properly – AKI – acute kidney injury), but remember they are not always present!
Acute renal failure (ARF)
Chronic renal failure (CKD)
Normal sized kidneys
Small kidneys, increased echogenicity
No anaemia
Anaemia, i.e. normochromic, normocytic – check Hb
No diabetes
Low BP
Raised BP
Rapid change in urea/creatinine
Gradual onset of symptoms
Oliguria normally present
Oliguria only present in later stages; polyuria and nocturia often present in less advanced disease
Not often CNS symptoms
CNS symptoms in later disease
Symptoms a bit like “shock”
Symptoms more like serious extensive disease
Renal ultrasound is the most useful investigation to differentiate between AKI and CKD. AKI will frequently be normal, whilst CKD is associated with the following ultrasound findings:
  • Small kidneys (often secondary to chronic glomerulonephritis)
  • Cysts

Acute-on-chronic kidney disease is also a common presentation and can be especially difficult to assess the extent of acute and chronic injury.

Disease Staging

There are 5 stages of CKD. Symptoms only usually occur once stage 4 is reached.
GFR (ml/min/1.73cm2)
Some sort of kidney damage present which has been detected by urine test (albuminuria) or imaging studies.  GFR is normal or high
Investigate more thoroughly – check for proteinuria and haematuria.
Kidney damage with slightly low GFR
Renoprotection control blood pressure and modify diet, i.e. low protein.
Moderate reduction in GFR. Sometimes divided into:
  • 3a – eGFR 45-59
  • 3b – eGFR 30-44
Severely low GFR
Prepare for renal replacement therapy if appropriate. Many medications require a reduced dosage with an eGFR <30
Kidney failure
<15 or dialysis

The suffix (p) is used to denote co-existing proteinuria

Progression of CKD

CKD progression can be monitored by examining creatinine levels.  Normal creatinine is 70-150 μmol/L. Once levels exceed 300 μmol/L there is usually trouble!  Beyond this stage, creatinine levels tend to rise exponentially; thus, by plotting  1/creatinine vs time, a straight, declining line graph will result, parallel to a straight, declining line graph of GFR.  The rate of decline varies between individuals, but will be fairly constant for one particular individual.  This graph can be used to predict when dialysis will be needed.


Quick overview

Review annually – check weight, eGFR and urine ACR. Bloods for lipids and T2DM (usually an HbA1c).

  • Control hypertension
  • Smoking cessation
  • Aim for healthy BMI (18.5 – 24.9)
  • Avoid nephrotoxic medications
  • Lifestyle factors
    • Exercise
    • Diet
    • Alcohol
  • If eGFR 30-60 with albuminuria, or 30-45 without albuminuria (moderate disease)
    • All of above
    • Review every 3-6 months
    • Check calcium, phosphate and parathyroid hormone
  • If eGFR <30
    • All of above
    • Review every 1-3 months
    • Monitor for oedema
    • Refer to renal physician
    • Discuss advanced care plan, dialysis and renal transplant

The details

  • Explain to patients what a CKD is and reassure that the vast majority of patients will not require dialysis
  • Most important factors in management are to:
    • Control hypertension
    • Control diabetes
    • Prevent and treat urinary tract obstruction
  • Avoid NSAIDs
  • Provide influenza and pneumococcal vaccinations
  • Advise about the link between CKD and cardiovascular disease
  • Repeat urea and creatinine within 5 days of initially abnormal results to ensure there is no rapid progression
    • Repeat again at 90 days to confirm diagnosis of CKD
  • Assess urine ACR annually
  • Urea and electrolytes annually. More regularly in more severe or rapidly advancing disease
  • The three mainstays of preventative health are discussed in further detail below and include:
    • Management of blood pressure
    • Prevention of cardiovascular disease
    • Lifestyle factors
  • Consider giving patients an information factsheet, e.g. Australia or UK

Lifestyle factors

  • Important to monitor for weight loss and undernutrition
  • Weight and perform BMI annually. Undernutrition defined as:
    • Actual body weight is 85% of ideal body weight
    • BMI <20 kg/m2
    • 5% weight loss in 3 months or 10% in 6 months (if not due to oedema)
  • Consider supplementation if undernutrition present
    • If weight loss continues, the NG feeding or PEG feeding may be indicated
  • Consider protein supplementation
    • In later stages of CKD albumin is lost in the urine in large amounts and can result in weight loss
    • 0.75g/Kg of ideal body weight daily for CKD 4-5
    • 1.2g/Kg ideal body weight if on dialysis
  • Supplement vitamin D
  • Advise regular moderate exercise
    • 30 minutes daily of moderate intensity exercise (equivalent to a brisk walk) on at least 5 days per week
    • This should include 2 days (60 minutes per week) of strengthening activities
    • Consider referral to an exercise physiologist for a personalised plan – especially if severe co-morbidities
    • A gradual increase in physical activity from a sedentary lifestyle is safe and beneficial for the vast majority of patients
  • Advise mediterranean style diet
    • A varied diet that should be rich in vegetables, nuts, fruits, wholegrain, cereals, lean meat, poultry, fish, eggs, beans, legumes and low-fat dairy products
    • Limit salt intake to <6 per day
    • Limit added sugars
    • Limit saturated and trans fats
  • Alcohol – advise within safe drinking limits, total cessation probably better

Prevention of cardiovascular disease

  • Statins
    • Should be offered as primary and secondary prevention for all patients with CKD
    • If eGFR <30 – consult with renal specialist regarding the dose
  • B12 and Folate supplementation
    • Consider in all patients
    • Check serum folate and B12 in all stage 4 and 5 CKD patients every 6 months, and every 3 months if patient is on dialysis
  • Aspirin
    • Recommended for secondary prevention only
  • Oral anticoagulatns
    • When indicated (e.g. in non-valvular AF), rivaroxaban is generally preferred to warfarin in CKD. Discuss with renal specialist if eGFR <30

Manage blood pressure

  • Aim for <130/80 mmHg
  • ACE inhibitors are first line
    • Always check U+Es before starting – particularly potassium
    • Repeat 2 weeks after starting medication, and 2 weeks after any dose changes
    • Contra-indicated if potassium is >6 mmol/L (stop treatment immediately)
    • Do not start treatment if potassium is >5 mmol/L
  • For dialysis patients
    • Low salt diet (<5g/day)
    • Hypertension usually managed by ultrafiltration

Indications for referral for specialist care

  • eGFR <30
  • Albumin creatinine ration (ACR) >70mg/mmol, OR
    • ACR >30 mg/mmol WITH haematuria
  • Accelerated progression of diseaseDefined as:
    • Decrease of eGFR 25% or more + change in category of disease within less than 12 months, OR
    • Decrease in eGFR of >15 within less than 12 months
  • Hypertension that is not controlled with at least 4 anti-hypertensive medications
  • Known or suspected genetic cause of CKD
  • Renal artery stenosis (proven or suspected)
  • Renal outflow obstruction – refer to urology rather than renal team

Mineral and Bone disorders

  • Disorders of the parathyroid axis (parathyroid hormone, calcium, phosphate and vitamin D) can occur in CKD
    • Typically there is secondary hyperparathyroidism – where PTH is chronically increased – usually in response to high phosphate – which is not properly excreted by the diseased kidney. This rise in PTH causes changes in calcium metabolism
    • CKD is the main cause of parathyroidism
    • Supplementation with vitamin D is frequently required in severe CKD
    • The disruption in this axis, and the subsequent mobilisation of calcium from bone predisposes CKD patients to osteoporosis. Offer treatment for this where appropriate
  • Is it not routinely recommended to check levels of PTH, calcium or phosphate unless eGFR <30
    • In patients with eGFR <30, then check PTH, calcium and phosphate at regular intervals – the exact interval will depend on the extent of the abnormality of these levels
    • If abnormalities are present – treat with vitamin D first (cholecalciferol). If this is unsuccessful use a vitamin D analogue (e.g. calcitrol) instead
  • In haemodialysis patients – be wary to always check the “adjusted” calcium – and keep in the range of 2.2 – 2.5 mmmol/L – be wary of hypercalcaemia
  • Hyperphosphateaemia is also common in CKD
    • Occurs due to decreased filtering of phosphate by the kidneys
    • This causes increases in PTH – causing secondary hyperparathyroidism
    • Secondary hyperparathyroidism causes increased mortality and morbidity, and increased risk of fractures
    • Consider a referral to a dietician to come up with a personalised diet plan which is low in phosphate
    • If protein supplements are required, use ones that are low in phosphate
    • If phosphate still remains high – treat with a phosphate binder –e.g. calcium acetate. This is frequently not tolerated by patients, calcium carbonate is a suitable alternative
      • If hypercalcaemia develops (usually only in CKD stages 4 and 5) then use a non calcium based binder
      • Take phosphate binders with food

Renal replacement Therapy

There are several treatment methods that fall under the category of renal replacement therapyThis includes:

  • Peritoneal dialysis – can be performed either in a hospital environment, or at home, after patient training
  • Haemodialysis
  • Renal transplant

When to start dialysis is a contentious issue. A rough guide would be:

  • eGFR <10 ml/minute, OR
  • eGFR <15 ml/minute in patient with diabetes

There is no evidence that early dialysis improves outcomes. However, late dialysis often results in marked malnutrition (perhaps due to protein loss).

Refer patients to a renal specialist when eGFR <30 ml/minute to consider their options

Dialysis is also frequently used in AKI. In this circumstance, the on of the main indications is the potassium level (usually >6.5mmol/L for AKI, but 7.0 mmol/L in CKD). In AKI, other considerations include:

  • Sodium >155 mmol/L or <120 mmol/L
  • Severe acidosis (pH <7.0) – not responsive to bicarbonate
  • Severe renal failure – e.g. creatinine >500, urea >30 mmol/L
  • Drug toxicity with drugs than can be dialysed


  • Anaemia
  • Left ventricular hypertrophy
  • Impaired cognitive functioning
  • Coagulopathy
  • Hypertension, leading to:
    • Cardiovascular disease
    • Heart failure
  • Calcium phosphate loading can cause
    • Cardiovascular disease
    • Soft tissue calcification
  • Bone changes secondary to hyperparathyroidism
    • Bone pain
    • Fractures
  • Uraemic encephelopathy
  • Fluid overload
    • Pulmonary oedema
    • Worsens hypertension
  • Malnutrition and weight loss
  • Low protein
  • Glucose intolerance

CKD and T2DM

  • Those with both CKD and T2DM are more than twice as likely to have hypoglycaemic episodes
  • The lower the eGFR the more likely the patient is to have hypoglycaemia
  • Many medications used in the treatment of diabetes require dose reductions or cannot be used in patients with low eGFR – e.g.:
    • Metformin should be reduced when eGFR 30-60 and is contraindicated when eGFR <30
    • SGLT2 inhibitors require dose reduction
    • DPP-4 inhibitors – sitagliptin requires dose reduction, linagliptin does not
    • Sulphonylureas require dose adjustment when eGFR <30
    • GLP1 receptor antagonists – e.g. injectable agents Byetta and Trulicity – contraindicated when eGFR <30
    • Insulin does not require specific dose adjustment but be aware of the increased risks of hypoglycaemia

CKD and Hypertension

  • Maintain BP <130/80 for all patients
  • Lower BP may have improved outcomes – especially for those at high risk of cardiovascular disease
  • ACE-inhibitors and ARB are first line
    • ACE-inhibitor (or ARB) + calcium channel blocker is likely the most effective combination are reducing cardiovascular disease risk
    • ACE-inhibitors cause a reduction in glomerular blood-flow, and there may be a decline in eGFR when ACE-inhibitors are started. If this is <25% reduction, no further action is required. If it is >25% cease the medication and refer to a renal physician
    • Avoid thiazide diuretics if eGFR <45
    • Beta-blockers can also be considered
  • Be wary of the risk of hyperkalaemia – especially if diuretics are used in combination with an ACE
    • Cease ACE, ARB and spironolactone in patients with a K+ >6

CKD and medications

  • Many drugs require reduced doses once eGFR <60, and some are contraindicated, especially once eGFR <30


Preventing AKI is an important part of the management of CKD. In particular, avoiding medications that are known to precipitate AKI or worsen renal function is very important during an acute illness or acute episode of dehydration. Medications that should be a voided can be remembered with the SAD-MANS mnemonic:

  • S – Sulphonylurea
  • A – Ace-inhibiotrs
  • D – Diuretics
  • M – Metformin
  • A – ARBs
  • N – NSAIDs
  • S – SGLT2 inhibitors

Managing fluid and electrolytes

  • Patients with CKD typically produce normal amounts of urine until the very end stages. Fluid restriction is only required in end stage disease. In fluid restriction, recommended intake is:
    • Urine output PLUS 500mls
  • Avoid binge drinking
  • Be vigilant to replace losses through sweat – e.g. hot weather
  • Dietary restriction of sodium and potassium is sensible but best achieved with good dietary advice (involve dietician)
  • Loop diuretics can be helpful to improve sodium balance and hypertension
  • Hyperkalaemia
    • If >7 mmol/L – requires dialysis
    • If <7 mmol/L, try to treat the cause. Often dietary; too much:
      • Fruit
      • Chocolate
      • Coffee
    • Also consider GI bleed and ACE inhibitors as causes
  • Acidosis
    • This is a common complication in end stage disease and is due to bicarbonate loss
    • Consider oral bicarbonate supplementation
    • It can exacerbate hyperkalaemia, calcium loss from bone, and inhibits protein synthesis – aggravating low protein levels
  • Neurological side effects
    • Thought to be a consequence of build of of some toxins
    • Symptoms often alleviated by dialysis
    • Symptoms include:
      • Restless leg syndrome
      • Peripheral neuropathy
      • Sleep disorders
      • Cognitive impairment


  • Most patients do not progress to end stage disease
  • However, even moderate disease is associated with an increased falls risk, increase fracture risk, increased risk of AKI and increased mortality


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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