Renal failure Flashcards

1
Q

What is acute kidney injury

A

It is defined as the reversible rapid reduction of renal function (eGFR) within hours or days/weeks.

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2
Q

When does creatinine causes problems

A

when its serum levels are increased

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3
Q

Risk factors for developing AKI

A

Age >75

DIABETES
DRUGS (review newly started)
SEPSIS

Chronic kidney disease

poor fluid intake/ increase fluid loss

cardiac failure

Hx of urinary symptoms

Chronic liver disease

peripheral vascular disease

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4
Q

What are the commonest causes of AKI

A

Ischaemia to the kidneys

Sepsis

Drugs (Nephrotoxins)

above 3 are the commonest

Prostatic disease in 25% - these have very good prognosis

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5
Q

Pre-renal causes of AKI

A

these are the commonest (40-70%)

Vascular occlusion

dehydration

blood loss

sepsis

cardiac failure

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6
Q

Renal causes of AKI

A

causes 10-50% of AKI

Glomerulonephritis (commonest)

vasculitis

Acute tubular necrosis

Drugs/toxins

infection

inflammatory disease

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7
Q

Post-renal causes

A

Think from start to end

Urinary tract obstruction (Calculi)

BPH

prostatic cancer

cervical cancer

urethral stricture

meatus problems

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8
Q

AKI presentation

A

Oliguria (<500ml urine per day)

Anuria - rare and indicates obstruction

in 20% there could be normal urine output or increased (non-oliguric AKI)

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9
Q

what is uraemia

A

increased serum creatinine and urea

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10
Q

How would a patient with pre-renal AKI present

A

Hypotensive and tachycardic

with signs of hypovalaemia and postural hypotension

Confusion

can present without hypotension in patients taking NSAIDs and ACE inhibitors

Hyperkalaemia and hypocalcaemia arecommon

Dilutional hyponatraemia if patient continued to drink despite oliguria or received INAPPROPRIATE IV dextrose

signs of fluid overload –> raised JVP

peripheral oedema

CVS changes

Abdominal/flank pain

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11
Q

What is Dilutional hyponatraemia

A

Low sodium levels due to excessive fluids

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12
Q

When does metabolic acidosis develop in AKI

A

when vomiting is not controlled

or there is aspiration of gastric contents

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13
Q

What can you tell from a dipstick in AKI

A

infection +ve leukocytes and nitrates

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14
Q

What can you tell from a dipstick in AKI

A

infection +ve leukocytes and nitrates

glomerular disaese (blood+protein)

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15
Q

What investigations to carry in AKI

A

Dipstick

MC&S

U&Es for creatinine and urea

FBC

LFT

Clotting

Creatine kinase

CRP

ESR - erythrocyte sedimentation rate for inflammation

renal USS

non-contrast spiral CTKUB if obstruction suspected but not picked up by USS

CXR for pulmonary oedema

ECG in Px >40 and at risk of CVS

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16
Q

How to manage AKI

A

Establish cause and treat

If hypovalaemia is present correct with IV fluids or blood as rapidly as possible.

Stop nephrtoxic drugs

Urinary tract obstruction must be releived

correct electrolyte imbalances

nutrition - parenteral or enteral

immunosuppresion in glomereloneprhitits

renal replacement therapy (RRT) if non resolving

STOP AKI

Sepsis

Toxins - nephrtoxic drugs stop

Optimized BP

Prevent complications: hyperkalaemia, pulmonary oedaema, acidosis, pericarditis
Identify cause

17
Q

What is chronic kidney disease

A

it is the irreversible detoriartion in eGFR over years

When death is likely without RRT it is considered as end-stage renal disease (ESRD)

x4 commoner in black ethnicity because of increased risk of HTN

18
Q

CKD causes

A

Caused by any disease that causes destruction to the kidney

Diabetes 70%

HTN

atherosclerosis

renovascular disease

Interistial disaese

Glomerular disease

SLE

congenital and inherited 5%

idiopathic

19
Q

Presentation of CKD

A

patients may remain asymptomatic until eGFR <30

Pallor/ Anaemia

Uraemic

Yellow

purpura, easily bruising

excoriarations

HTN

Cardiomegaly

signs of fluid overload, rasied JVP

20
Q

What does an alkaline phosphate in LFT show

A

if increased in CKD could mean renal osteodystrophy

21
Q

Investigations in CKD

A

FBC

U&Es - reduced Ca, increased PO

LFTs

increased PTH if CKD stage 3 or more

Urine dipstick + MC&S, albumin:creatinine or protein:creatinine

USS to check kidney size –> usually smaller in CKD

Consider renal biopsy

22
Q

How to manage CKD

A

Identify causative factor

Antihypertensives therapy - target 130/80

stop nephrotoxic drugs

Reduction of proteinuria - proteinuria is worse as disease progresses. can use ACE or ARB. will cause small reduction in eGFR initially but continue unless eGFR reduction >20%.

Lipid lowering therapy - statins to control hypercholostreamia which is common with proteinuria

Dietary and lifestyle management - less protein intake. smoking cessation and exercise.

Maintain fluid and electrolyte imbalances

screen for complications - anaemia/osteodystrophy

Renal bone disease- control with VitD

ELSA BCD

Electrolyte imbalances

Life - diet exercise smoking

Stop nephrotoxins

ACE or ARB for proteinuria

BP 130/80

Complication screen

Vit D for renal bone disease

23
Q

What is the aim in managing CKD

3 Points

A

preventing further renal damage, managing and limiting metabolic and cardiovascular complications, and preparing for renal replacement therapy if required

24
Q

Stages of renal failure

A

 Stage 1 with normal or high GFR (GFR > 90 mL/min)
 Stage 2 Mild CKD (GFR = 60-89 mL/min)
 Stage 3A Moderate CKD (GFR = 45-59 mL/min)
 Stage 3B Moderate CKD (GFR = 30-44 mL/min)
 Stage 4 Severe CKD (GFR = 15-29 mL/min)
 Stage 5 End Stage CKD (GFR <15 mL/min)