An undergraduate summary of renal failure

1. Renal Failure
Mark Hall
Clinical Teaching Fellow
pathways for clinical learning

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
pathways for clinical learning

3. Renal physiology
pathways for clinical learning

4. medulla
cortex
ureter
pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

8. pathways for clinical learning

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
pathways for clinical learning

10. What happens where
• Tubules
– Acid Base control in distal and proximal
tubules, renal failure = retention of acids
– K+/H+ for Na+ failure = hyperkalaemia
pathways for clinical learning

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
pathways for clinical learning

12. Acute Kidney Injury
pathways for clinical learning

13. Why do kidneys fail?
• Pre-renal
– blood supply
• Renal
– Glomerulonephritis
– Acute tubular necrosis
– Interstitial nephritis
• Post-renal
– Ureteric obstruction
– Urethral obstruction
pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

17. Causes
Post Renal
• Usually revealed on renal US
• Ureteric obstruction
– Hydronephrosis (usually unilateral)
• Urethral obstruction
– Urinary retention
– Hydronephrosis (usually bilateral)
pathways for clinical learning

18. Symptoms
• May be none
• Frank haematuria
• Proteinuria (frothy urine)
• Oliguria/anuria
• Lower urinary tract symptoms
• Uraemic syndrome
pathways for clinical learning

19. Uraemic syndrome
• Neuro
– Fatigue, malaise, depression, cognitive impairment
– Involuntary movements, fits, coma
– Paraesthesia
• Cardiopulmonary
– Dyspnoea
– Kussmaul breathing
– Pleuritic chest pain
• Skin
– Pruritis
– Purpura, pallor, pigmentation
• GI
– Anorexia, nausea, vomiting
– Diarrhoea, constipation, colitis
– GI bleeding
• Haem
– Anaemia
– Bleeding pathways for clinical learning

20. Signs
• Likely to reflect the cause in AKI
• Assess fluid balance
• Look for effects of hyperkalaemia
pathways for clinical learning

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
pathways for clinical learning

22. Glomerular Disease
• Non proliferative (no increase in cells)
– Causes Nephrotic Syndrome
• Proliferative (increase in cells)
– Causes Nephritic Syndrome
pathways for clinical learning

23. Nephrotic Syndrome
• Proteinuria
damage occurs
– >3.5g/24 hrs to podocytes
• Hypoalbuminaemia
– <30 g/L
• Oedema
– Leaky capillaries
– Lose protein
• Increased cholesterol
pathways for clinical learning

24. Causes of nephrotic syndrome
• Glomerular Disease
– Commonly glomerulonephritis
• Minimal change glomerulonephritis
– No change on light microscopy, fusion of podocytes
– 1st line Steroids 2nd Line Cytotoxic
• Focal segmental glomerulosclerosis
– Sclerosis/fibrosis of glomeruli
– HIV, Heroin, Diabetes Melitus
• Membranous glomerulonephritis
– Thickened basement membrane
pathways for clinical learning

25. History Taking - Symptoms of
nephrotic syndrome
• Frothy urine
• Effects of hypoalbuminaemia
• Drugs
• Allergies
• Symptoms of vasculitis
• Symptoms of malignancy
• Chronic or recurrent infections
• Symptoms of chronic inflammation
pathways for clinical learning

26. Signs of nephrotic syndrome
• Facial swelling
• Xanthelasma
• Xanthomata
• Hypertension
• Pleural effusions
• Ascites
• Peripheral oedema
pathways for clinical learning

27. Complications
• Thromboembolism
– ↑ procoagulant factors
– ↓anticoagulant factors
– Abnormal platelet function
– Altered endothelial function
– ↓fibrinolytic activity
– Intravascular volume depletion
• Renal vein thrombosis
• DVT/PE
pathways for clinical learning

28. Complications
• Susceptibility to infection
– ↓ serum IgG
– ↓ complement activity
– Immunisation to pneumococcus
• Hyperlipidaemia
pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

33. Causes
• Primary post-infectious
– Bacterial
• Streptococci – group A beta-haemolytic strep
• Typhoid
– Viral
• CMV
• Hepatitis
• EBV
– Parasitic
• Plasmodium falciparum
pathways for clinical learning

34. Causes
• Secondary
– SLE
– IgA nephropathy
– Wegener’s granulomatosis
– HSP
– Haemoltyic uraemic syndrome
pathways for clinical learning

35. Treatment
• Treat the cause
• Treat any consequences of renal
impairment
pathways for clinical learning

36. pathways for clinical learning

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
pathways for clinical learning

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
pathways for clinical learning

39. Investigations
• Haematology
– FBC, blood film
– Coagulation
• Immunology
– ANA; dsDNA
– ANCA
– Complement levels
– Anti-GBM
– ASO titre
pathways for clinical learning

40. Investigations
• Virology
– Hepatitis B,C & HIV
• Radiology
– Renal US
pathways for clinical learning

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
pathways for clinical learning

42. Questions?
pathways for clinical learning

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
pathways for clinical learning