medicnotes.org.uk :: Acute renal failure

Acute renal failure (ARF)

Definitions:

A potentially reversible loss of excretory renal function
Develops over hours or days

Aetiology:

Can be divided into 3 main areas:

Pre-renal
Intrinsic renal
Post-renal

Pre-renal uraemia:

Caused by impaired perfusion of the kidneys with blood
The initial physiological response to kidney hypoperfusion is Na⁺/H₂O retention:

Leads to oliguria (<0.5ml/kg/hour)

If hypoperfusion is not quickly corrected:

Acute tubular necrosis (ATN) develops

Causes of renal hypoperfusion:

Shock (MABP <80mmHg):

Hypovolaemic
Cardiogenic
Septic

Lesser degrees of hypotension + impaired renal autoregulation:

Age
Arteriosclerosis
DM
ACE inhibitors
NSAIDs

Renal vasoconstrictors:

E.g. radiocontrast agents

Measuring CVP is often invaluable in determining if the uraemia is pre-renal or not

Management of pre-renal uraemia:

If hypotension is the cause, prompt IV fluid replacement is essential
Since pre-renal and intrinsic renal uraemia can coexist and fluid challenge in the latter situation may lead to volume overload with pulmonary oedema, careful clinical monitoring is vital
BP should be checked regularly
Signs of raised JVP or of pulmonary oedema should be sought frequently

Intrinsic renal uraemia:

This is renal parenchymal disease
Is responsible for the majority of cases of CRF

The causes of intrinsic renal uraemia can be subdivided into congenital/hereditary or acquired renal diseases

Congenital/hereditary diseases:

Developmental abnormalities (hypoplasia)
Cystic diseases
Hereditary nephritis

Acquired renal diseases:

Glomerular:

Glomerulonephritis (GN)
Diabetic nephropathy

Tubulointerstitial:

Interstitial nephritis
Myeloma kidney
Nephrotoxins

Vascular:

Inflammation (vasculitis)
Occlusion (e.g. renal artery stenosis)

Post-renal uraemia:

Uraemia results from obstruction of the urinary tract at any point from the calyces to the external urethral orifice
Important to diagnose as they are readily treatable
The urinary tract is usually dilated above the level of the obstruction
Must affect both kidneys, or a single functioning kidney (or be below the level of the bladder) to cause renal failure
May cause complete anuria

Obstructions:

Are 3 types of obstructing lesion:

Intraluminal (e.g. calculi)
Intramural (e.g. stricture, tumour)
Extramural (e.g. tumour, retroperitoneal fibrosis)

Acute tubular necrosis (ATN):

Tubuloepithelial cells lose their normal morphology and may become detached from the tubular basement membrane with the formation of casts, which block the tubules
Eventually, the epithelial cells regenerate and renal function is usually restored

Urine output in ATN:

Preceding renal hypoperfusion causes physiological oliguria (which is often the first clue to the problem)
Once ATN is established, the patient often remains oliguric (but this is not invariable)
Urea and creatinine may continue to rise despite the production of urine (‘non-oliguric ARF’)
ATN has an overall mortality of ~50%

Exacerbators of ATN:

Aminoglycosides (e.g. gentamycin)
Myoglobin (from muscle breakdown, e.g. crush injury)
Paracetamol (in overdose)

Clinical features of ARF:

Uraemic symptoms:

Anorexia
Nausea
Pruritis
Lethargy

Fluid overload/volume dependent HT

Electrolyte disturbances:

Hyperkalaemia
Hyperphosphataemia

Metabolic acidosis:

Loss of acid-base balance

Raised serum urea and creatinine

Acute or chronic uraemia?

Recent record of normal renal function AFR

Normal Hb ARF > CRF

Long history of relevant symptoms CRF > ARF

Tolerating severely deranged biochemistry CRF > ARF

Low Calcium CRF > ARF

Small kidneys on US CRF > ARF

Investigations:

Urine:

Dipstick
Microscopy (RBCs, red cell casts)
Culture

Serum:

Urea
Creatinine
Calcium
Phosphate
Albumin
ALP

FBC

Blood cultures

Blood levels of nephrotoxic drugs (if appropriate)

Hyperkalaemia:

This is a life-threatening complication owing to the risk of cardiac dysrhythmias, particularly ventricular fibrillation

On the ECG:

Tall, tented, T waves
Widened QRS complexes
Loss of P waves

Management:

10mls 10% calcium gluconate IV (stabilises the myocardium)
100mls 50% dextrose IV plus 10U Actrapid IV (drives K⁺ into cells)

In many cases, hyperkalaemia will be controlled only by dialysis or haemofiltration

Pulmonary oedema:

Fluid overload causes a rise in left atrial pressure and leakage of fluid into the alveolar space

Clinical features:

Dyspnoea
Orthopnoea
Frothy sputum
Hypoxia

Management:

Sit patient up
Give high flow O₂
IV diuretics (e.g. frusemide – note higher doses needed in renal failure)
Vasodilators (e.g. IV nitrates)

If the diuretics do not induce a diuresis, dialysis or haemofiltration is necessary

Indications for haemofiltration in ARF:

Symptoms of uraemia
Complications of uraemia (e.g. pericarditis)
Severe biochemical derangement in the absence of symptoms
Hyperkalaemia not controlled by conservative measures
Pulmonary oedema not corrected by IV frusemide
Severe acidosis
For the removal of drugs causing the ARF (e.g. gentamycin)


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	Acute renal failure (ARF) Definitions: A potentially reversible loss of excretory renal function Develops over hours or days Aetiology: Can be divided into 3 main areas: Pre-renal Intrinsic renal Post-renal Pre-renal uraemia: Caused by impaired perfusion of the kidneys with blood The initial physiological response to kidney hypoperfusion is Na⁺/H₂O retention: Leads to oliguria (<0.5ml/kg/hour) If hypoperfusion is not quickly corrected: Acute tubular necrosis (ATN) develops Causes of renal hypoperfusion: Shock (MABP <80mmHg): Hypovolaemic Cardiogenic Septic Lesser degrees of hypotension + impaired renal autoregulation: Age Arteriosclerosis DM ACE inhibitors NSAIDs Renal vasoconstrictors: E.g. radiocontrast agents Measuring CVP is often invaluable in determining if the uraemia is pre-renal or not Management of pre-renal uraemia: If hypotension is the cause, prompt IV fluid replacement is essential Since pre-renal and intrinsic renal uraemia can coexist and fluid challenge in the latter situation may lead to volume overload with pulmonary oedema, careful clinical monitoring is vital BP should be checked regularly Signs of raised JVP or of pulmonary oedema should be sought frequently Intrinsic renal uraemia: This is renal parenchymal disease Is responsible for the majority of cases of CRF The causes of intrinsic renal uraemia can be subdivided into congenital/hereditary or acquired renal diseases Congenital/hereditary diseases: Developmental abnormalities (hypoplasia) Cystic diseases Hereditary nephritis Acquired renal diseases: Glomerular: Glomerulonephritis (GN) Diabetic nephropathy Tubulointerstitial: Interstitial nephritis Myeloma kidney Nephrotoxins Vascular: Inflammation (vasculitis) Occlusion (e.g. renal artery stenosis) Post-renal uraemia: Uraemia results from obstruction of the urinary tract at any point from the calyces to the external urethral orifice Important to diagnose as they are readily treatable The urinary tract is usually dilated above the level of the obstruction Must affect both kidneys, or a single functioning kidney (or be below the level of the bladder) to cause renal failure May cause complete anuria Obstructions: Are 3 types of obstructing lesion: Intraluminal (e.g. calculi) Intramural (e.g. stricture, tumour) Extramural (e.g. tumour, retroperitoneal fibrosis) Acute tubular necrosis (ATN): Tubuloepithelial cells lose their normal morphology and may become detached from the tubular basement membrane with the formation of casts, which block the tubules Eventually, the epithelial cells regenerate and renal function is usually restored Urine output in ATN: Preceding renal hypoperfusion causes physiological oliguria (which is often the first clue to the problem) Once ATN is established, the patient often remains oliguric (but this is not invariable) Urea and creatinine may continue to rise despite the production of urine (‘non-oliguric ARF’) ATN has an overall mortality of ~50% Exacerbators of ATN: Aminoglycosides (e.g. gentamycin) Myoglobin (from muscle breakdown, e.g. crush injury) Paracetamol (in overdose) Clinical features of ARF: Uraemic symptoms: Anorexia Nausea Pruritis Lethargy Fluid overload/volume dependent HT Electrolyte disturbances: Hyperkalaemia Hyperphosphataemia Metabolic acidosis: Loss of acid-base balance Raised serum urea and creatinine Acute or chronic uraemia? Recent record of normal renal function AFR Normal Hb ARF > CRF Long history of relevant symptoms CRF > ARF Tolerating severely deranged biochemistry CRF > ARF Low Calcium CRF > ARF Small kidneys on US CRF > ARF Investigations: Urine: Dipstick Microscopy (RBCs, red cell casts) Culture Serum: Urea Creatinine Calcium Phosphate Albumin ALP FBC Blood cultures Blood levels of nephrotoxic drugs (if appropriate) Hyperkalaemia: This is a life-threatening complication owing to the risk of cardiac dysrhythmias, particularly ventricular fibrillation On the ECG: Tall, tented, T waves Widened QRS complexes Loss of P waves Management: 10mls 10% calcium gluconate IV (stabilises the myocardium) 100mls 50% dextrose IV plus 10U Actrapid IV (drives K⁺ into cells) In many cases, hyperkalaemia will be controlled only by dialysis or haemofiltration Pulmonary oedema: Fluid overload causes a rise in left atrial pressure and leakage of fluid into the alveolar space Clinical features: Dyspnoea Orthopnoea Frothy sputum Hypoxia Management: Sit patient up Give high flow O₂ IV diuretics (e.g. frusemide – note higher doses needed in renal failure) Vasodilators (e.g. IV nitrates) If the diuretics do not induce a diuresis, dialysis or haemofiltration is necessary Indications for haemofiltration in ARF: Symptoms of uraemia Complications of uraemia (e.g. pericarditis) Severe biochemical derangement in the absence of symptoms Hyperkalaemia not controlled by conservative measures Pulmonary oedema not corrected by IV frusemide Severe acidosis For the removal of drugs causing the ARF (e.g. gentamycin)
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