1. Renal Failure
Mark Hall
Clinical Teaching Fellow
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2. Objectives
• Revise renal physiology
• Understand nephrotic and nephritic
syndromes
• Revise the symptoms of acute kidney
injury
• Revise the signs of acute kidney injury
• Revise the investigation and treatment of
acute kidney injury
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4. medulla
cortex
ureter
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5. afferent
proximal arteriole
tubule
distal tubule
collecting
glomerulus duct
efferent
arteriole
thick descending
thin descending limb of the loop of
limb of the loop Henle
of Henle
vein
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6. What do kidneys do?
• Excretion of uremic toxins
• Na+/H20 homeostasis
• K+ Homeostasis
• H+ Homeostasis
• Produce humoral agents
– Erythropoietin
– Active metabolites of vitamin D
– Renin
• BP control
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7. Glomerular Function
• GFR – efficiency of the kidney in waste product
disposal
• Inversely proportional to creatinine
– Creatinine passively excreted
– From skeletal muscle bulk
• Calculated by
– (Urine creatinine x Urine flow)/Plasma creatinine
• Estimated Creatinine Clearance
– (140-age x mass)/serum creatinine
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9. What happens where?
• Glomerulus
– Excretion
– Conservation of normal blood products
– Hormone control/BP control
• Tubules
– Concentrating via osmotic gradient and
counter-current mechanism and collecting
duct via ADH
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10. What happens where
• Tubules
– Acid Base control in distal and proximal
tubules, renal failure = retention of acids
– K+/H+ for Na+ failure = hyperkalaemia
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11. Proteinuria
• If glomerular function is disturbed
• Occasionally if tubular function is disturbed
Glomerulonephritis Tubular disease
Amount of proteinuria + to ++++ + to ++
Nephrotic syndrome 0 to ++++ No
Dipstick Positive Yes No
K or lambda free chains No Yes
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14. Acute Kidney Injury
• Rapid fall in glomerular filtration rate
• Leading to:
– Abrupt rise in urea and creatinine
– Fluid volume overload
– Oligouria
– Hyperkalaemia
– Metabolic acidosis
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15. Causes
Pre-Renal
– Usually in the critically ill patient
– < 70mmHg – renal autoregulation impaired
• Hypovolaemia
– Haemorrhage, D and V
• Cardiogenic shock
• Sepsis
• Hepatorenal syndrome
– Usually causes ATN
• Recovers over 2 – 3 weeks
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16. Causes
Intrinsic Renal
Intrinsic means damage to the glomerulus,
renal tubules or interstitium
– Glomerulonephritis
– Acute Tubular Necrosis
• Toxic or Ischaemia
– Acute Interstitial Nephritis
• Infection or allergic drug reaction
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17. Causes
Post Renal
• Usually revealed on renal US
• Ureteric obstruction
– Hydronephrosis (usually unilateral)
• Urethral obstruction
– Urinary retention
– Hydronephrosis (usually bilateral)
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18. Symptoms
• May be none
• Frank haematuria
• Proteinuria (frothy urine)
• Oliguria/anuria
• Lower urinary tract symptoms
• Uraemic syndrome
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20. Signs
• Likely to reflect the cause in AKI
• Assess fluid balance
• Look for effects of hyperkalaemia
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21. When to dialyse acutely
• Persistent K+ > 6.0 mmol/L
• Acidosis pH <7.2
• Pulmonary oedema and unable to obtain
diuresis
• Pericarditis with tamponade
– Relieve tamponade first
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22. Glomerular Disease
• Non proliferative (no increase in cells)
– Causes Nephrotic Syndrome
• Proliferative (increase in cells)
– Causes Nephritic Syndrome
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28. Complications
• Susceptibility to infection
– ↓ serum IgG
– ↓ complement activity
– Immunisation to pneumococcus
• Hyperlipidaemia
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29. Investigations
• FBC, Coag screen
• U&E, LFT, bone profile, lipid profile, glucose
• CRP
• Urine
– Dipstick
– Spot urine:creatinine ratio
– 24 hour urine collection
– Bence Jones protein
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30. Investigations
• Microbiology
– Hep B/C/HIV
– Urine culture (and blood cultures if febrile)
• Immunology
– ANA, dsDNA, C3 and C4 levels, serum Igs
and electrophoresis
• Radiology
– Renal ultrasound
– CXR
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31. Treatment
• Treat the cause
• Salt restricted diet (<100 mmol/day)
• Fluid restriction
• May need diuretics (be cautious)
• ACEi/A2RB
• Consider anticoagulation when albumin
<20 g/L
• Treat persistent hyperlipidaemia
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32. Proliferative Glumerular Disease
• Acute renal illness
• Haematuria and Mild Proteinuria –
insufficient to cause a decrease in
albumin
• Inability to excrete fluids so sodium and
water retention
• Decreased GFR – uraemia
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37. When to dialyse acutely
• Persistent K+ > 6.0 mmol/L
• Acidosis pH <7.2
• Pulmonary oedema and unable to obtain
diuresis
• Pericarditis with tamponade
– Relieve tamponade first
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38. Investigations
• Urinalysis
– dipstick, microscopy (casts, crystals)
• Biochemistry
– Urea, creatinine, K+,Na+,Ca++,PO4-
– Blood gas analysis and serum bicarbonate
– CK, myoglobinuria
– CRP
– Serum immunoglobulins
– Protein electrophoresis. BJP in urine
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39. Investigations
• Haematology
– FBC, blood film
– Coagulation
• Immunology
– ANA; dsDNA
– ANCA
– Complement levels
– Anti-GBM
– ASO titre
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40. Investigations
• Virology
– Hepatitis B,C & HIV
• Radiology
– Renal US
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41. Treatment
• Correct pre and post renal factors
• Optimise cardiac output/renal blood flow
• Treat cause
• Review medications
• Optimise fluid balance; daily weight
• Identify and treat complications
• Nutritional support
• Consider dialysis
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43. Summary
• Revised renal physiology
• Understood nephrotic and nephritic syndromes
• Revised the symptoms of acute kidney injury
• Revised the signs of acute kidney injury
• Revised the investigation and treatment of
acute kidney injury
• Revised the common causes, investigation and
treatment of:
– Hypokalaemia
– Hyperkalaemia
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Notas do Editor
At rest the kidneys receive 20-25% of cardiac output Renal vein drains to the IVC Renal arteries branch from the aorta