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Ben Savage
 Acute
◦ Causes
◦ Investigation
◦ Management
◦ Hyperkalaemia
 Chronic
◦ Cause
◦ Staging
◦ Management
 Significant reduction in renal failure in hours or days.
 Maybe no symptoms, oliguria is common
(<400ml/24hrs)
 Biochemically detected by increasing Urea &
Creatinine.
 Can occur in isolation but usually secondary to other
pathology.
 Pre Renal and acute tubular necrosis account for 80%
of acute renal failure.
 Systemic cause that reduce perfusion of the
kidney
◦ Hypovolemia
◦ Sepsis
◦ Post Surgery
◦ Shock
◦ Hepatic Failure
◦ Drugs – NSAIDs, ACEi
◦ Renal artery/vein occlusion
 Acute Tubular Necrosis
 Glomerulonephritis
 Nephrotoxic drugs
◦ NSAIDs, Gentamicin
 Rabdomyolysis
 Interstitial nephritis
 Myeloma
 Haemolytic Uremic Syndrome
 Stones
 Fibrosis
 Cancer
◦ Prostate, Cervix
◦ Bladder, Ureters
 BPH
 Urine Dip
 Bloods
 ECG
 Imaging relative to history
 Rapid diagnosis and appropriate treatment of
underlying pathology crucial.
 Crucial empirical management
◦ Oxygenation
◦ Ensure adequate circulation – fluids, blood
◦ Treatment of any hyperkalaemia
◦ Dialysis if indicated
 Indications for immediate dialysis
◦ Pulmonary oedema
◦ Potassium >6.5mM
◦ Acidosis pH<7.2
◦ Pericarditis
◦ Encephalopathy
 Normal potassium levels 3.5
and 5.0 mmol
 Treat aggressively if:
◦ Potassium >6 mmol
◦ ECG changes
 ECG changes
◦ Peaked T-waves
◦ Widened QRS
◦ Small/ absent p-waves
◦ Sine wave appearance
 Calcium Gluconate (IV)
 Insulin & Dextrose (IV)
 Calcium Resonium (PO/PR )
 Dialysis if indicated
 Causes
◦ Pre-renal
◦ Renal
◦ Post-renal
 Pre Renal and acute tubular necrosis account for 80% of
acute renal failure.
 Rapid diagnosis and treatment of underlying pathology
crucial.
 Symptomatic management and empirical treatment vital.
 Always be aware of hyperkalaemia
 Defined as kidney damage or a decreased
kidney glomerular filtration rate (GFR) of less
than 60 for 3 or more months
 ESRD aged >65, increases mortality 6x
 Usually asymptomatic in stage 1-3
 CRF alter the dose of certain drugs and
contraindicate others depending on the GFR
 Glomerular Nephritis (20%)
 Interstitial nephritis & reflux nephropathy (20%)
 Polycystic kidneys (10%)
 Diabetes Mellitus
 Renovascular disease/HTN (10%)
 Obstructive/ unknown (20%)
 Stages: -measured using GFR
1. >90 }GFR alone not sufficient for
2. 60-89 }diagnosis of stage 1&2
3. 30-59
4. 15-29
5. <15 (ESRF)
 Salt & water homeostasis
◦ Fluid overload
◦ Fluid depletion
 BP control
◦ HTN
 Removal of uraemic toxins
◦ Uraemia
 Calcium/phosphate balance
◦ Hyperphosphalipadeamia
◦ Hypocalcaemia
◦ Renal Bone disease
◦ 3ry hyperparathyroidism
 Erythropoietin production
◦ Anaemia
 Potassium Balance
◦ Hyperkalaemia
 Acid-Base balance
◦ Metabolic acidosis
 Also affect immunity – increasing infections
 Is it truly chronic?
 Treat any reversible causes or acute
exacerbations
 Treatment of consequences of chronic renal
failure
 Long term planning esp renal replacement
therapy
 Review medication during progression of
renal failure.
 Symptoms can reflect failure of any the action
of the kidneys.
 Treat any reversible causes promptly
 Plan long term therapy early
Any question

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Renal Failure

  • 2.  Acute ◦ Causes ◦ Investigation ◦ Management ◦ Hyperkalaemia  Chronic ◦ Cause ◦ Staging ◦ Management
  • 3.
  • 4.  Significant reduction in renal failure in hours or days.  Maybe no symptoms, oliguria is common (<400ml/24hrs)  Biochemically detected by increasing Urea & Creatinine.  Can occur in isolation but usually secondary to other pathology.  Pre Renal and acute tubular necrosis account for 80% of acute renal failure.
  • 5.  Systemic cause that reduce perfusion of the kidney ◦ Hypovolemia ◦ Sepsis ◦ Post Surgery ◦ Shock ◦ Hepatic Failure ◦ Drugs – NSAIDs, ACEi ◦ Renal artery/vein occlusion
  • 6.  Acute Tubular Necrosis  Glomerulonephritis  Nephrotoxic drugs ◦ NSAIDs, Gentamicin  Rabdomyolysis  Interstitial nephritis  Myeloma  Haemolytic Uremic Syndrome
  • 7.  Stones  Fibrosis  Cancer ◦ Prostate, Cervix ◦ Bladder, Ureters  BPH
  • 8.  Urine Dip  Bloods  ECG  Imaging relative to history
  • 9.  Rapid diagnosis and appropriate treatment of underlying pathology crucial.  Crucial empirical management ◦ Oxygenation ◦ Ensure adequate circulation – fluids, blood ◦ Treatment of any hyperkalaemia ◦ Dialysis if indicated
  • 10.  Indications for immediate dialysis ◦ Pulmonary oedema ◦ Potassium >6.5mM ◦ Acidosis pH<7.2 ◦ Pericarditis ◦ Encephalopathy
  • 11.  Normal potassium levels 3.5 and 5.0 mmol  Treat aggressively if: ◦ Potassium >6 mmol ◦ ECG changes  ECG changes ◦ Peaked T-waves ◦ Widened QRS ◦ Small/ absent p-waves ◦ Sine wave appearance
  • 12.  Calcium Gluconate (IV)  Insulin & Dextrose (IV)  Calcium Resonium (PO/PR )  Dialysis if indicated
  • 13.  Causes ◦ Pre-renal ◦ Renal ◦ Post-renal  Pre Renal and acute tubular necrosis account for 80% of acute renal failure.  Rapid diagnosis and treatment of underlying pathology crucial.  Symptomatic management and empirical treatment vital.  Always be aware of hyperkalaemia
  • 14.
  • 15.  Defined as kidney damage or a decreased kidney glomerular filtration rate (GFR) of less than 60 for 3 or more months  ESRD aged >65, increases mortality 6x  Usually asymptomatic in stage 1-3  CRF alter the dose of certain drugs and contraindicate others depending on the GFR
  • 16.  Glomerular Nephritis (20%)  Interstitial nephritis & reflux nephropathy (20%)  Polycystic kidneys (10%)  Diabetes Mellitus  Renovascular disease/HTN (10%)  Obstructive/ unknown (20%)
  • 17.  Stages: -measured using GFR 1. >90 }GFR alone not sufficient for 2. 60-89 }diagnosis of stage 1&2 3. 30-59 4. 15-29 5. <15 (ESRF)
  • 18.  Salt & water homeostasis ◦ Fluid overload ◦ Fluid depletion  BP control ◦ HTN  Removal of uraemic toxins ◦ Uraemia  Calcium/phosphate balance ◦ Hyperphosphalipadeamia ◦ Hypocalcaemia ◦ Renal Bone disease ◦ 3ry hyperparathyroidism
  • 19.  Erythropoietin production ◦ Anaemia  Potassium Balance ◦ Hyperkalaemia  Acid-Base balance ◦ Metabolic acidosis  Also affect immunity – increasing infections
  • 20.  Is it truly chronic?  Treat any reversible causes or acute exacerbations  Treatment of consequences of chronic renal failure  Long term planning esp renal replacement therapy
  • 21.  Review medication during progression of renal failure.  Symptoms can reflect failure of any the action of the kidneys.  Treat any reversible causes promptly  Plan long term therapy early

Editor's Notes

  1. NSAIDS constrict efferent arteriole ACEi affect afferent vessel
  2. AXR – Staghorn calcius R-side
  3. Lead my history and exam as to likely cause of renal failure ECG for hyperkalaemia
  4. http://www.pemed.com/dialysis/cobec3/cobecnt3d1.jpg
  5. 95% of the body's potassium is intracellular Aggressive Rx due to risk of arrhythmias http://upload.wikimedia.org/wikipedia/commons/4/49/ECG_in_hyperkalemia.png
  6. 1) calcium gluconate - heart membrane stabiliser, protects against arrhythmias 2) Insulin & Dextrose- Insulin moves K+ into cells thus decreasing intravasc lvls 3) Calcium resonium – Binds K+ in the gut and stops absorption
  7. Renovascular disease – NB vasculitides - wegners
  8. The deteriation in CRF is relatively predictable so long term planning can begin early to make sure that the best quality of life is maintained, esp when beginning to plan renal replacement therapy.