Kidney disease 1

Question 1

How prevelant is kidney disease

Answer 1

In the UK up to 100000 deaths each year in hospital are associated with acute kidney injury with up to 30% being preventable with the right care and treatment
A 2012 paper concluded that AKI occurred in over 1 of 5 hospitalisations and was associated with more than a 4x increase likelihood of death
Also in 2012, Dr Selby etal in Derby found that approximately 65% of AKI started in the communi

Question 2

What is the think kidney campaign

Answer 2

A campaign which provides info to hcps and professionals about the warning signs and risks of kidney disease

Question 3

What is acute kidney injury (AKI)

Answer 3

AKI not Acute Renal Failure
Characterised by a sudden decline in kidney function
Can occur without symptoms and is detected by either a blood test (serum creatinine) or sudden decrease in urine output.
Many different potential causes but often secondary to other serious illness eg sepsis or hypovolaemia resulting in a (sustained) drop in blood pressure.

Question 4

Which criteria do we use to characterise AKI

Answer 4

AKI is defined when one of the following criteria is met.

Serum creatinine rises by > 26micromol/L within 48 hours Serum creatinine rises by > 1.5 fold from the reference value *which is known or presumed to have occurred within one week
Urine output is <0.5mls/kg/hour for >6 consecutive hours

The reference serum creatinine should be the lowest creatinine value recorded within 3 months of the event

Question 5

If a patient meets the criteria for an AKI what system do we use to treat them

Answer 5

The KDIGO staging system for acute kidney
It has 1 (least severe) - 3 stages depending on the severity of disease and is dependent on urine output and serum creatinine (the higher of which is used to place them into a category)

Question 6

Who is at risk of AKI

Answer 6

People at risk of AKI
Older patients
Chronic medical conditions eg Chronic kidney disease, diabetes mellitus, heart failure, cancer
Nephrotoxic medicines or medicines that could cause hypoperfusion

Question 7

What are the mechanisms behind AKI

Answer 7

Mechanisms of AKI are threefold - pre-renal, intrinsic renal and post renal.

Kidney function is dependent upon adequate blood pressure to provide renal perfusion in addition to having adequate nephrons.

Question 8

Who is most at risk for having pre-renal failure

Answer 8

It is often precipitated by a lack of blood entering the nephrons. Pre-renal failure is seen in patients with sepsis, increased fluid loss, those with a risk of dehydration and those with reduced cardiac output or heart failure

Question 9

Give some intrinsic causes of AKI

Answer 9

Prolonged pre-renal AKI (where cel damage has occured due to the decrease in blood pressure in the nephron)
Medicines that exacerbate hypovolaemia and hypotension (ace inhibitors, loop diuretics, CCBs, nitrates)
Medicines that can be harmful to the kidneys in the setting of acute illness (non-steroidals, anti-infetives (gentomycin))
Toxins - contact media (eg myoglobin released in reaction to muscle damage)
Kidney disease - glomerulonephritis, tubulointerstitial nephritis
Systemic disease processes - myeloma, vasculitis, lupus

Question 10

What factors can cause post-renal aki

Answer 10

Obstruction to urinary flow within the renal tract
Enlarged prostrate
Pelvic or abdominal masses eg bowel or ovarian cancer
Kidney stones
Congenital obstructive uropathy (in children)

Question 11

Who are the most at risk groups for developig an aki in secondary care

Answer 11

Any patient with acute illness
Sepsis
Frail/ elderly
Multiple co-morbidities (diabetes, heart or liver disease)
History of AKI
Neurological or cognitive impairment (less able to manage their own fluid intake)
Patients undergoing surgery – particularly intraperitoneal surgery (nul by mouth, prophylactic antibiotics), emergency surgery in sepsis

Question 12

What are the key facts to remember when prescribing for patients at risk of aki

Answer 12

Medicines can exacerbate an episode of AKI through direct toxicity or indirectly due to hypotension.
Risk of accumulation of parent drug or metabolites resulting in adverse effects
Avoid using the term “nephrotoxic” unless referring to direct toxicity.

Question 13

When conducting a medicines review, what must we try to do to minimise exacerbating the aki

Answer 13

Eliminate potential causative factors
Eliminate contributory factors
Avoid inappropriate combinations (using 2 diuretics)
Reduce adverse events
Ensure that doses of prescribed medication are appropriate and individualised
Start-stop – ensure that all medicines continue to be clinically appropriate

Question 14

What are the key mantras to think while conducting an mur

Answer 14

What should be stopped
What should be suspended
What must continue
What can be used with caution
Are there suitable alternatives with less risk

We must amend doses according to renal function 
If possible consider value of checking blood drug concentrations
Monitor duration (try to reduce the course if possible)

Question 15

What must be considered in the ongoing management of patients post AKI

Answer 15

Think about reintroduction of suspended or stopped medicines

Communication with patient and primary care teams

Question 16

Which patients must be reintriduced onto their usual medication asap after an aki episode

Answer 16

Patients previously stabilised on drugs for the treatment of heart failure (ace, arbs or diuretics)– these should be restarted asap and retitrated to achieve the best control of fluid balance and bp unless there is a specific contraindication.
Medicines will often be recommenced in 2ndry care (hosptial) but will require titration in the community
If patients are under the heart failure service –they should be involved in the drug titration

Question 17

What are the 3 ratios whereby patients who were previously on medicines contraindicated for aki can be restarted onto these for continued management of other conditions

Answer 17

Patients previously stable on ACEi or ARB for chronic kidney disease with albuminuria should be identified as theyre high risk ptientts

• Diabetes with albumin/ creatinine ratio >3mg/mmol
• Hypertension with albumin/creatinine ratio >30mg/mmol
• Alumin/creatinine ratio >70mg/mmolIrrespective of hypertension or cardiovascular disease

These patients should be restarted unless there is a new contraindication (eg potassium >5mmol/l)

Question 18

For patients previously stable on a single BP lowering agent, how do we bring them back into therapy for that condition

Answer 18

Patients previously stable on a single BP lowering agent – therapy should be brought into line with NICE/ BHS guidance CG127 (particlar care being taken around black/afro-carribean patients who wil be placed on a ccb even if they were previously stable on an arb)

Question 19

What is the theory behin ACEs and ARBs being beneficial in the treatment of akis

Answer 19

There is a theoretical possibility that ACE and ARB treatment might reduce the severity or duration of AKI The drugs cause efferent arteriolar vasodilation which increases blood flow to the renal tubules.
Tubular injury causes perisstent AKI and increases the risk of subsequent chronic kidney disease.

Question 20

What is sick day guidance

Answer 20

For patients who are well, there is controversy around the use of sick day rules where patients are advised to withold specific medicines if they feel they are experiencing symptoms.
The evidence that this advice reduces harm is weak
There are potential harms of patients coming off medications without medical guidance