Renal Failure        Mark HallClinical Teaching Fellow      pathways for clinical learning
Objectives• Revise renal physiology• Understand nephrotic and nephritic  syndromes• Revise the symptoms of acute kidney  i...
Renal physiology    pathways for clinical learning
medulla                    cortex                        ureterpathways for clinical learning
afferent  proximal                 arteriole   tubule                                                      distal tubule  ...
What do kidneys do?•   Excretion of uremic toxins•   Na+/H20 homeostasis•   K+ Homeostasis•   H+ Homeostasis•   Produce hu...
Glomerular Function• GFR – efficiency of the kidney in waste product  disposal• Inversely proportional to creatinine  – Cr...
pathways for clinical learning
What happens where?• Glomerulus  – Excretion  – Conservation of normal blood products  – Hormone control/BP control• Tubul...
What happens where• Tubules  – Acid Base control in distal and proximal    tubules, renal failure = retention of acids  – ...
Proteinuria• If glomerular function is disturbed• Occasionally if tubular function is disturbed                          G...
Acute Kidney Injury     pathways for clinical learning
Why do kidneys fail?• Pre-renal  – blood supply• Renal  – Glomerulonephritis  – Acute tubular necrosis  – Interstitial nep...
Acute Kidney Injury• Rapid fall in glomerular filtration rate• Leading to:  – Abrupt rise in urea and creatinine  – Fluid ...
Causes                    Pre-Renal– Usually in the critically ill patient– < 70mmHg – renal autoregulation impaired   • H...
Causes              Intrinsic RenalIntrinsic means damage to the glomerulus,  renal tubules or interstitium– Glomeruloneph...
Causes                Post Renal• Usually revealed on renal US• Ureteric obstruction  – Hydronephrosis (usually unilateral...
Symptoms•   May be none•   Frank haematuria•   Proteinuria (frothy urine)•   Oliguria/anuria•   Lower urinary tract sympto...
Uraemic syndrome•   Neuro    – Fatigue, malaise, depression, cognitive impairment    – Involuntary movements, fits, coma  ...
Signs• Likely to reflect the cause in AKI• Assess fluid balance• Look for effects of hyperkalaemia                pathways...
When to dialyse acutely• Persistent K+ > 6.0 mmol/L• Acidosis pH <7.2• Pulmonary oedema and unable to obtain  diuresis• Pe...
Glomerular Disease• Non proliferative (no increase in cells)  – Causes Nephrotic Syndrome• Proliferative (increase in cell...
Nephrotic Syndrome• Proteinuria                                                   damage occurs  – >3.5g/24 hrs           ...
Causes of nephrotic syndrome• Glomerular Disease  – Commonly glomerulonephritis    • Minimal change glomerulonephritis    ...
History Taking - Symptoms of          nephrotic syndrome•   Frothy urine•   Effects of hypoalbuminaemia•   Drugs•   Allerg...
Signs of nephrotic syndrome•   Facial swelling•   Xanthelasma•   Xanthomata•   Hypertension•   Pleural effusions•   Ascite...
Complications• Thromboembolism  – ↑ procoagulant factors  – ↓anticoagulant factors  – Abnormal platelet function  – Altere...
Complications• Susceptibility to infection  – ↓ serum IgG  – ↓ complement activity  – Immunisation to pneumococcus• Hyperl...
Investigations•   FBC, Coag screen•   U&E, LFT, bone profile, lipid profile, glucose•   CRP•   Urine    – Dipstick    – Sp...
Investigations• Microbiology  – Hep B/C/HIV  – Urine culture (and blood cultures if febrile)• Immunology  – ANA, dsDNA, C3...
Treatment• Treat the cause• Salt restricted diet (<100 mmol/day)• Fluid restriction• May need diuretics (be cautious)• ACE...
Proliferative Glumerular Disease• Acute renal illness• Haematuria and Mild Proteinuria –  insufficient to cause a decrease...
Causes• Primary post-infectious  – Bacterial     • Streptococci – group A beta-haemolytic strep     • Typhoid  – Viral    ...
Causes• Secondary  – SLE  – IgA nephropathy  – Wegener’s granulomatosis  – HSP  – Haemoltyic uraemic syndrome             ...
Treatment• Treat the cause• Treat any consequences of renal  impairment               pathways for clinical learning
pathways for clinical learning
When to dialyse acutely• Persistent K+ > 6.0 mmol/L• Acidosis pH <7.2• Pulmonary oedema and unable to obtain  diuresis• Pe...
Investigations• Urinalysis  – dipstick, microscopy (casts, crystals)• Biochemistry  – Urea, creatinine, K+,Na+,Ca++,PO4-  ...
Investigations• Haematology  – FBC, blood film  – Coagulation• Immunology  – ANA; dsDNA  – ANCA  – Complement levels  – An...
Investigations• Virology  – Hepatitis B,C & HIV• Radiology  – Renal US                 pathways for clinical learning
Treatment•   Correct pre and post renal factors•   Optimise cardiac output/renal blood flow•   Treat cause•   Review medic...
Questions? pathways for clinical learning
Summary• Revised renal physiology• Understood nephrotic and nephritic syndromes• Revised the symptoms of acute kidney inju...
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Renal failure and potassium

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An undergraduate summary of renal failure

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  • At rest the kidneys receive 20-25% of cardiac output Renal vein drains to the IVC Renal arteries branch from the aorta
  • PR3 Wegener’s; MPO microscopic polyangiitis
  • Renal failure and potassium

    1. 1. Renal Failure Mark HallClinical Teaching Fellow pathways for clinical learning
    2. 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. 3. Renal physiology pathways for clinical learning
    4. 4. medulla cortex ureterpathways for clinical learning
    5. 5. afferent proximal arteriole tubule distal tubule collectingglomerulus duct efferent arteriole thick descendingthin descending limb of the loop oflimb of the loop Henle of Henle vein pathways for clinical learning
    6. 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. 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. 8. pathways for clinical learning
    9. 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. 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. 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. 12. Acute Kidney Injury pathways for clinical learning
    13. 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. 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. 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. 16. Causes Intrinsic RenalIntrinsic 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. 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. 18. Symptoms• May be none• Frank haematuria• Proteinuria (frothy urine)• Oliguria/anuria• Lower urinary tract symptoms• Uraemic syndrome pathways for clinical learning
    19. 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. 20. Signs• Likely to reflect the cause in AKI• Assess fluid balance• Look for effects of hyperkalaemia pathways for clinical learning
    21. 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. 22. Glomerular Disease• Non proliferative (no increase in cells) – Causes Nephrotic Syndrome• Proliferative (increase in cells) – Causes Nephritic Syndrome pathways for clinical learning
    23. 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. 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. 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. 26. Signs of nephrotic syndrome• Facial swelling• Xanthelasma• Xanthomata• Hypertension• Pleural effusions• Ascites• Peripheral oedema pathways for clinical learning
    27. 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. 28. Complications• Susceptibility to infection – ↓ serum IgG – ↓ complement activity – Immunisation to pneumococcus• Hyperlipidaemia pathways for clinical learning
    29. 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. 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. 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. 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. 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. 34. Causes• Secondary – SLE – IgA nephropathy – Wegener’s granulomatosis – HSP – Haemoltyic uraemic syndrome pathways for clinical learning
    35. 35. Treatment• Treat the cause• Treat any consequences of renal impairment pathways for clinical learning
    36. 36. pathways for clinical learning
    37. 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. 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. 39. Investigations• Haematology – FBC, blood film – Coagulation• Immunology – ANA; dsDNA – ANCA – Complement levels – Anti-GBM – ASO titre pathways for clinical learning
    40. 40. Investigations• Virology – Hepatitis B,C & HIV• Radiology – Renal US pathways for clinical learning
    41. 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. 42. Questions? pathways for clinical learning
    43. 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

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