Renal Failure

Acute Kidney Injury (AKI)

This is a rapid deterioration in renal functioning which develops within hours.

– It is common, occurring in 50% of ICU patients – more common in men, and people with CKD.

– It is characterized by increased serum urea and creatinine combined with a low urine output.


There are many different definitions of AKI but the most widely KDIGO criteria is:

– Rise in creatinine >26uM within 48h

– Rise in creatinine >1.5 x baseline value within 1 week

– Urine output <0.5ml/kg/h for more than 6 consecutive hours



These can be divided into 3 categories: pre-renal, renal and post-renal:


i) Pre-renal:

This is due to decreased blood flow to the kidneys, decreasing renal function



– Hypovolemia (diarrhea), systemic vasodilation due to sepsis, renal artery stenosis

– Decreased blood flow decreases the GFR, causing poor excretion of urea and creatinine

– However, the kidney tubules still function and work to reabsorb sodium to preserve volume.

– They are also able to reabsorb urea and concentrate the urine

ii) Renal:

This is due to conditions giving intrinsic damage to the glomeruli, tubules or kidney interstitium.

– This gives the opposite picture where kidneys are unable to reabsorb sodium, urea and not able to concentrate the urine.


– Acute tubular necrosis

– Glomerulonephritis

– Rhabdomyolysis

iii) Post-renal:

This is due to obstructive causes which occur after the renal pelvis

– Initially the blockage increases tubule pressure which helps push the urea back into the bloodstream. Therefore, this ends up mimicking a pre-renal cause

– However, later on, the raised pressure damages the tubular cells themselves and die. This reduces their ability to reabsorb urea and sodium, mimicking a renal cause.


The etiology can be worked out by calculating the fractional excretion of sodium (FENa). This reflects the amount of sodium in the urine divided by the amount of sodium initially filtered by the kidney.

 Low FENa (<1%)

This indicates pre-renal disease –> Low excretion indicates sodium retention by the kidney

– This suggests that the body thinks the BP is too low and is trying to reabsorb sodium to increase BP and increase blood flow to the kidneys.

High FENa (>2-3%)

This indicates a renal or post-renal cause –> This suggests that the tubules are non-functional.

– This means they are unable to reabsorb sodium, and so more is lost in the urine.

Pre-Renal AKI

  Renal AKI


Fractional Excretion Na





HighPlasma Urea:Creatinine RatioNormal
<20mMUrinary Sodium>40mM


– Often can be asymptomatic

– Reduced urine output

– Pulmonary and peripheral oedema

– Arrhythmias (due to hyperkalaemia)

– Hyperuremia (pericarditis or encephalopathy)


– 1st test Urea and electrolytes

– Urinanalysis

– Imaging – Renal ultrasound in 24 hours

Grading AKI

AKI is graded on a 3-point scale depending on the serum creatinine and the urine output

Grade 1:

Creatinine = 1.5-1.9 x baseline

Urine < 0.5ml/kg/h for 6-12hours


Grade 2:

Creatinine = 2.0-2.9 x baseline                       

Urine < 0.5ml/kg/h for > 12hours


Grade 3:

Creatinine = 3 x baseline                                   

Urine < 0.3ml/kg/h for 24 hours


– For all causes, this involves diagnosis and treatment of the underlying etiology.

– Common to all causes is the need to manage fluid balance (IV + fluid chart) + acidosis + hyperkalaemia

a) Fluid balance:

– If hypovolemia –> 500mL crystalloid (0.9% saline) over 15 min, give up to 2L

– If hypervolemia –> give O2 + fluid restriction + diuretics if symptomatic

b) Acidosis:

Treatment of the underlying disorder will stop acid production

c) Hyperkalaemia:

It is necessary to treat if K+ > 6.5mM or there are ECG changes

– 10ml of 10% calcium chloride or 30ml 10% calcium gluconate –> cardioprotective

– IV insulin/dextrose infusion –> stimulates intracellular shift of K+

– Nebulized Salbutamol


Some people who have severe failure require renal replacement, commonly using hemodialysis.


One of the most important points is to stop all drugs that may exacerbate the kidney injury, or those which have increased rick of toxicity since they are renally cleared.

Safe to Continue

Worsen AKI

Toxic in AKI




Low dose aspirin




Chronic Kidney Disease (CKD)

This is used to describe a chronic decrease in renal function, primarily characterized by a low GFR.





Glomerular disease (nephrotic, nephritic syndrome).



(Can be remembered by the acronym HHONOUR)

Hypertension – Low GFR leads to excessive reabsorption of Na+ increasing ABP

Hypocalcaemia – decreased hydroxylation of Vitamin D in renal tubule cells, giving muscle cramps

Oliguria – Low urine output, leading to Hyperkalaemia with a metabolic acidosis

Normocytic/Normochromic Anemia – damage to kidney leads to decreased erythropoietin

Oedema – due to loss of protein in the urine reducing oncotic pressure

Uremia – renal failure leads to build up of urea in the blood causing nausea, anorexia, encephalopathy

Renal osteodystrophy – this is due to secondary hyperparathyroidism which also causes osteoporosis



It is graded by 3 measures (KDIGO(3)):

– GFR –> scale from G1 (>90) to G5 (<15) showing filtration rate

– Albuminuria –> scale of A1 to A3(>300) – used as a marker of kidney damage

– Underlying disease –> glomerular, vascular, cystic – indicates the type of pathology

GFR (ml/min)>9060-9045-5930-4415-29<15


This involves treating the renal disease projection as well as the complications of CKD

– Hypertension – target BP is <140/90mmHg –> use ACE-I/ARB, but monitor hyperkalemia

– Diabetes – target HbA1C of 53mM, using anti-diabetic drugs

– Anemia – treat with erythropoietin stimulating agent aiming for Hb of 100-120g/L

– Hypocalcaemia – Vitamin D supplements + Phosphate binders (Sevelamer)

– Cardiovascular disease – Statin + Antiplatelet therapy for patients at risk of atherosclerosis


If severe, treatment involves dialysis or a renal transplant. This is indicated when the risk of renal failure is 10-20% within a year.


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Image 2: 2012 International Society of Nephrology

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