renal

• fluid loss

  GI losses: diarrhoea, vomiting

  Bleeding: trauma, surgical, haemorrhage, burns

  Diuresis: medication, diabetes

  Sepsis: fever, hypotension

  Hyperventilation

  increased drain output: biliary drain, pancreatic drain, ileostomy
• Reduced fluid intake

  Nil by mouth, e.g post-stroke

  fluid supplementation error
• Fluid overload

  Heart failure, Liver cirrhosis and failure, nephrotic syndrome, renal failure, excess fluid administration
• Thirst, dizziness

  Tachycardia

  Low BP, postural drop

  HR>90 bpm

  Hypo-perfusion: Hypotension systolic <100 mmHg, Prolonged CRT

  Dry: Reduced skin turgor , Dry mucous membranes

  JVP not visible

  Oliguria, decreased urine output <30ml/h

  Weight loss

  Elevated urea and creatinine

  Decreased GCS

  negative fluid balance on chart

  Other sources of fluid loss (e.g. rectal bleeding, diarrhoea, vomiting)

  Hypovolaemic
• Ankle swelling, abnormal swelling

  Breathlessness RR>20, decreased SpO2

  Hypertension

  Raised JVP

  Inspiratory crepitations, bilateral crackles

  Pleural effusion

  Ascites, peripheral oedema

  Weight gain

  Increased urine output

  positive fluid balance on fluid chart


  Hypervolaemia
• Resuscitation fluids


  0.9% sodium chloride, plasmalyte
• maintenance fluids


  0.18% sodium chloride+ 4% glucose, 5% glucose. 0.9% sodium chloride with added potassium
• Hypovolaemic no cardiogenic shock


  500ml plasmalyte or 0.9% sodium chloride over 15 min
• Hypovolaemic, no cardiogenic shock, still hypovol after 15 min 500ml

  check response for perfusion, BP, pulse fall, CRT shorten, Urine output and give max 2000ml IV
• Hypovolaemic, given 15 min 500ml plasmolyte and BP rises, pulse falls etc.

  What next?

  Continue maintenance fluids plus ongoing losses, manage underlying problem
• hypovolaemic patient still hypo after max 2000ml IV fluids

  what to do next?

  Senior input
• Maintenance fluids

  daily requirements are:

  • 30 ml/kg/day of water,
  • 1 mmol/kg/day of sodium and potassium
  • 50–100g/day of glucose to limit starvation ketosis
• Maintenance fluid regime


  • e.g: 1000ml 0.18% NaCL/4% glucose with 40mmol/L K+
  • 1000ml 0.18% NaCL/4% glucose with 20mmol/L K+
  • Run at 1.25 mL/kg/hour
  • no more than 100 mL/hour (risk hyponatraemia)
  • Check U&Es and creatinine daily if IV fluids
• danger of 0.18% sodium chloride/4% glucose maintenance


  • hypotonic once glucose used up, risk hyponatraemia and cell bursting,
  • if sodium <132 mmol/L (use 0.9%sodium chloride instead)
• Potassium >5.0 mmol/L but needs maintenance fluids


  do not add potassium, recheck the potassium
• increased creatinine>25 in 48h or 50% in 7 days, or urine output < 0.5ml/kg/h over 6h


  renal injury
• pre-renal AKI

  impaired perfusion, hypotension:

  • cardiac failure/ reduced cardiac output
  • Shock: sepsis, blood loss
  • dehydration
  • vascular occlusion
  • meds
  • oedematous states: liver disease, heart failure, nephrotic syndrome
  • selective renal ischaemia
• renal AKI

  • Intrarenal vascular injury: Systemic vasculitis, Accelerated (malignant hypertension), Emboli
  • Glomerulonephritis
  • Tubular injury: Acute tubular necrosis, Rhabdomyolysis (massive muscle necrosis), Interstitial nephritis especially drugs, Drug induced tubular injury, Myeloma (tumour of plasma cells)
  • Haemolytic uraemic syndrome
• post-renalAKI

  • Obstruction of flow
  • kidney stones, urinary calculi (bilateral)
  • retroperitoneal fibrosis
  • benign prostatic hypertrophy
  • bladder, prostate, cervical cancer
  • urethral stricture/ valves
  • meatal stenosis/ phimosis
  • neurogenic bladder
• prolonged hypoperfusion can cause?

  acute tubular injury

  acute tubular necrosis
• nephrotoxins

  gentamicin, radiocontrast agents, cisplatin
• proteinuria (>=3.5g/day), hypoalbuminuria (serum<=30g/L)

  nephrotic syndrome
• haematuria, proteinuria (<3.5g/L/day), hypertension, oliguria, red cell casts

  nephritic syndrome
• nephrotic syndrome, > child than adult, no visible abnormalities on microscope,

  • Electron microscopy: loss of visceral epithelial cells’ foot processes, vacuolation, and growth of microvilli on the visceral epithelial cells

  minimal change glomerulonephritis
• management for minimal change glomerulonephritis?

  • Supportive care: nutritional support, salt and fluid restriction
  • Corticosteroids
  • immunosuppressants (e.g. calcineurin inhibitor, mycophenolate mofetil, rituximab)
• • nephrotic syndrome, adults, genetic or HIV/lupus/reflux nephropathy
  • renal biopsy are segmental scarring of some glomeruli

  Focal segmental glomerulosclerosis (FSGS) (primary genetic) (secondary disease)
• management of FSGS

  • Supportive care: salt restriction and fluid management
  • High-dose prednisolone
  • Cyclophosphamide or ciclosporin is used in some cases to reduce proteinuria
• nephrotic syndrome, slowly progressing, 30-50, idiopathic, hep B, malaria, SLE

  thickened glom basement membrane

  IgG uptake diffuse

  Membranous glomerulonephritis
• Membranous glomerulonephritis management

  • Supportive care: salt restriction and fluid management
  • Corticosteroids
  • prognosis, 1/3 chronic, remission, end-stage
• nephritic syndrome (macroscopic) 24-48h after URTI, IgA deposition

  IgA nephropathy
• IgA nephropathy management?

  • High-dose prednisolone
  • immunosuppressants
• 2 weeks post-infection (streptococcal ) nephritic syndrome

  renal biopsy: Diffuse proliferative and exudative, D3 staining

  Post-infectious glomerulonephritis
• Post-infectious glomerulonephritis management?

  supportive, monitor fluid balance
• hep C, SLE,

  renal biopsy:

  • Thickened basement membrane
  • Thickened mesangium
  • “Tram tracking” appearance

  IgG subendothelial deposition

  Membranoproliferative glomerulonephritis
• Membranoproliferative glomerulonephritis management?

  • Children (with nephrotic-range proteinuria): corticosteroids
  • Adults: dipyridamole and aspirin
  • Kidney transplantation for patients with end-stage renal disease
• acute nephritic syndrome, 20-50 yo, microscopic glomerular crescent formation with progression to renal failure within weeks to months

  Rapidly progressive glomerulonephritis
• antibody attack against lung and kidney, rapid progression to renal failure, sudden nephritic syndrome,

  IgG deposits along basement membrane of glomerulus

  Anti-glomerular basement membrane antibody disease (Anti-GBM) (Goodpasture's syndrome)
• Anti-GBM management?

  high dose immunosuppression: IV prednisolone, cyclophosphamide and plasmapheresis.
• rapidly progressive glomerulonephritis, acute nephritic syndrome 2 types?

  Vasculitic disorders, Anti-GBM
• formation of granulomas and vasculitis (small and medium vessels: URT, lungs, kidneys), c-ANCA,

  biopsy: leukocytoclastic vasculitis with necrotic changes and granulomatous inflammation 

  Granulomatosis with polyangiitis (GPA)