Acute Renal Injury Flashcards by Chloe Mackle

What is the traditional definition of acute renal failure?

The rapid loss of glomerular filtration and tubular function over hours-days

How well did you know this?

Not at all

Perfectly

What are the features of acute renal failure according to the traditional definition?

Retention of urea/creatinine due to a failure of homeostasis
Can be oliguric or non-oliguric
Potentially recoverable

How well did you know this?

Not at all

Perfectly

What are the problems with the traditional definition of acute renal failure?

Lack of standardisation
Absolute creatinine, changes in creatinine, urine output and need for dialysis are not determined
Creatinine is an insensitive and late marker
RRT is a hard end-point but very late marker
There is a wide spectrum of renal injury

How well did you know this?

Not at all

Perfectly

What are the features of acute renal failure according to the current definition (KDIGO)?

Increase in serum creatinine by ≥ 0.3 mg/dl (25.5mol/l) within 48 hours or
Increase in serum creatinine by ≥ 1.5 times the baseline, which is known or presumed to have occurred within the prior 7 days, or
Urine volume < 0.5 ml/kg/hour for 6 hours

How well did you know this?

Not at all

Perfectly

In normal/increased risk stages of acute kidney injury outcome, what measures should be taken?

Preventative

How well did you know this?

Not at all

Perfectly

Once damage and progression occur to the kidneys, what should the treatment strategy be focussed on?

Managing the disease

How well did you know this?

Not at all

Perfectly

How many hospital admissions are complicated by acute kidney injury?

Between 1/7 and 1/5

How well did you know this?

Not at all

Perfectly

What is the mortality in hospital with dialysis-requiring AKI? In what patients is the mortality worse?

45-75%

Worse in older patients and in those with multi-organ failure

How well did you know this?

Not at all

Perfectly

What is the mortality in hospital of non-dialysis requiring AKI? (AKIN classification)

2% of people
8% with AKIN 1
25% with AKIN 2
33% with AKIN 3

How well did you know this?

Not at all

Perfectly

What is the incidence of long-term renal replacement therapy (RRT) following AKI?

Around 20% at 90 days post-discharge of those who had RRT

5/100 per year with AKI

How well did you know this?

Not at all

Perfectly

What is the incidence of long-term chronic kidney disease following AKI?

8/100 per year with AKI (both with and without dialysis)

How well did you know this?

Not at all

Perfectly

What are pre-renal causes of AKI?

Drugs

NSAIDs
ACEIs/ARBS
Beta-blockers
Diuretics
Immunosuppressants

Problems with the blood flow to the kidney

Sepsis
Hypovolaemia e.g. haemorrhage, burns
Hepatorenal syndrome
Congestive cardiac failure
Hypotension
Renal artery occlusion/vasoconstriction

How well did you know this?

Not at all

Perfectly

What are renal causes of AKI?

Damage to renal parenchyma

Acute tubular injury e.g. haemoglobinuria, rhabdomyolysis
Tubulointerstitial injury
Glomerulonephritis
Myeloma
Vasculitis

How well did you know this?

Not at all

Perfectly

What are post-renal causes of AKI?

Obstruction to urine exit

Kidney stones
Prostatic hypertrophy
Tumours
Retroperitoneal fibroids

How well did you know this?

Not at all

Perfectly

What can happen in pre-renal AKI?

There is reduced effective circulation volume due to volume depletion, hypotension, cardiac failure etc. and arterial occlusion

How well did you know this?

Not at all

Perfectly

What can happen in renal AKI?

Acute tubular necrosis
Acute interstitial nephritis
Acute glomerulonephritis
Intra-renal vascular obstruction e.g. vasculitis, thrombotic microangiopathy

How well did you know this?

Not at all

Perfectly

What can happen in post-renal AKI?

Obstruction

Intraluminal e.g. calculus, clot
Intramural e.g. malignancy, ureteric stricture
Extramural e.g. malignancy

How well did you know this?

Not at all

Perfectly

What is the most common cause of AKI?

Poor perfusion leading to established tubule damage

How well did you know this?

Not at all

Perfectly

How does damage occur in pre-renal AKI?

There is failure of the circulation to provide sufficient plasma flow to maintain blood chemistry due to volume/pressure loss, and fluid imbalance occurs

How well did you know this?

Not at all

Perfectly

What can pre-renal AKI lead to if sustained?

Intrinsic renal failure (acute tubular necrosis)

How well did you know this?

Not at all

Perfectly

What is intrinsic renal failure exacerbated by?

Toxic injury e.g. drugs

How well did you know this?

Not at all

Perfectly

What are the stages in the course of acute kidney injury?

Initiation
Maintenance
Recovery

What happens in initiation of AKI?

Exposure to toxic/ischaemic insult
Real parenchymal injury evolves
Potentially preventable

What happens in maintenance of AKI?

Established parenchymal injury
Usually maximally oliguric at this stage
Typical duration of 1-2 weeks (can be up to several months)

What happens in recovery of AKI?

Gradual increase in urine output Fall in serum creatinine If GFR recovers more quickly that tubular resorptive capacity excessive diuresis may result

What are potential sources of harm to the kidneys?

Drugs e.g. ACEI, NSAIDs Toxins e.g. drugs, radiocontrast Sepsis Myeloma

What is radiocontrast nephropathy?

AKI following administration of iodinated contrast agent

What happens in radiocontrast nephropathy?

Usually transient renal dysfunction, resolving after 72 hours May lead to permanent loss of function

What are small reductions in renal function associated with?

Significant increase in mortality

What are the risk factors for radiocontrast nephropathy?

``` Diabetes mellitus Renovascular disease Impaired renal function Paraprotein High volume of radiocontrast ```

What is myeloma?

Cancer arising from plasma cells - monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains Second most common haematological malignancy

What is the median age of diagnosis of myeloma and the median survival?

Median age of diagnosis - 68 | Median survival - 5 years

What are the clinical features of multiple myeloma?

``` Anaemia Back pain Weight loss Fractures Infections Cord compression Markedly elevated ESR Hypercalcaemia ```

How is myeloma diagnosed?

Bone marrow aspiration (> 10% clonal plasma cells) Serum paraprotein +/- immunoparesis Urinary Bence-Jones protein Skeletal survey

List the causes of AKI

``` Cardiac failure Haemorrhage Sepsis Vomiting and diarrhoea Prostate disease Tumours Stones Glomerulonephritis Vasculitis Radiocontrast Myeloma Rhabdomyolysis Drugs ```

What investigations are done for AKI?

``` U&Es Bicarbonate LFTs Bone scan FBC Clotting screen Blood gas ANCA Urine dipstick Urine PCR/ACR if indicated Renal biopsy Ultrasound X-ray ```

What are important features of the history when suspecting AKI?

``` PMH of systemic disease New rash, nose bleeds, sore eyes, joint pain Drug exposure Uraemic symptoms Timing of symptoms ```

What are some common complications of AKI?

``` Acidosis Electrolyte imbalance Intoxication Overload Uraemia complications ```

What is the management of AKI?

Remove or treat cause if possible Pre-renal - consider fluid replacement, BP support Renal - remove precipitant if possible Post-renal - consider catheterisation ``` Volume resuscitation or fluid restriction (deplete vs overload) Treat sepsis Vasopressors Stop nephrotoxic drugs e.g. NSAIDs, ahminoglycosides Dopamine Furosemide Atrial natriuretic peptide IGF 1 ```

What are the "five Rs for IV prescribing" in AKI?

``` Resuscitation Routing maintenance Replacement Redistribution Reassessment ```

What are some of the possible ECG changes in hyperkalaemia?

``` Peaked T waves Tall tented T waves Widened and flattened P wave Lengthened PR segment P waves eventually disappear Prolonged QRS interval ```

What is the treatment of hyperkalaemia?

Stabilise myocardium - calcium gluconate Shift potassium intracellularly - salbutamol, insulin-dextrose Remove - diuresis, dialysis, anion exchange resins

What indications for dialysis in AKI are particularly important?

Decreased HCO3- Increased K+ Pulmonary oedema Pericarditis

What is haemodialysis?

Solute removal by diffusion | Intermittent therapy with sessions lasting 3-5 hours

What is haemofiltration?

Solute removal by convection Larger pore size Continuous therapy

What concepts are important in dialysis?

Ultrafiltration Diffusion Osmosis

What is ultrafiltration?

Solution moves by pressure gradient, blood enters glomerulus at a high pressure

What are the advantages of haemodialysis?

Rapid solute removal Rapid volume removal Rapid correction of electrolyte disturbances Efficient treatment of hypercatabolic patients

What are the disadvantages of haemodialysis?

Haemodynamic instability Concern if dialysis is associated with hypotension - may prolong AKI fluid removal only during short treatment time

What are the advantages of continuous renal replacement therapy?

Slow volume removal associated with greater haemodynamic stability Absence of fluctuation in volume and solute control over time Greater control over volume status

What are the disadvantages of continuous renal replacement therapy?

Need for continuous anticoagulation May delay weaning/mobilisation May not have an adequate clearance in hypercatabolic patients

What are the risk events for AKI?

``` Post-surgery Volume depletion Hypovolaemia Hypotension Rhabdomyolysis Radiocontrast Sepsis Toxins ```

What are patient-related AKI risk factors?

``` Age > 75 Previous AKI Heart failure Liver disease Chronic kidney disease Vascular disease Cognitive impairment Acutely unwell e.g. MI Co-morbidities e.g. diabetes mellitus ```

How can you reduce the risk from contrast?

Saline hydration Sodium bicarbonate N-acetyle cysteine Osmolarity of radiocontrast