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ACUTE RENAL FAILURE
Dr. Salman Ahmad Ansari(MBBS)
Kanachur Institute of Medical Sciences
ARF
● Definition
● Causes
● Pathogenesis
● Morphology
● Stages
● Clinical features
● Diagnosis, treatment
Anatomy
● Unit of kidney - nephron
● Nephron consists of glomerulus, tubule and collecting system
● Glomerulus is the filtering unit
Acute Renal Failure(ARF) or Acute Kidney Injury(AKI)
● Definition: rapid reduction of renal function,
with severe oliguria
● Usually reversible
● Now known as AKI(acute kidney injury)
● Acute Tubular Injury(ATI) is the most common
cause of acute kidney injury(acute renal failure)
● ATI →AKI/ARF
● Commonly seen in hospital setting
● Very common in ICU patients
KDIGO criteria
According to KDIGO(Kidney Disease: Improving Global
Outcomes), AKI is the presence of any of the following:
1. Increase in serum creatinine by 0.3 mg/dL or more
within 48 hours
2. Increase in serum creatinine to 1.5 times or more
baseline within the prior seven days
3. Urine volume less than 0.5 mL/kg/h for at least 6
hours
Causes of AKI
Divided into 3 categories
Pre-renal
(60%)
Intra-renal
(35%)
Post-renal
(5%)
1. Pre-renal
Any cause that reduces blood flow to kidney
● Fluid loss: due to blood loss, burns, diarrhoea,
vomiting
● Hypotension: shock, pulmonary embolism
● Medications which cause renal vasoconstriction:
diuretics, ACEI, ARBs, metformin, NSAIDs, iodinated
contrast
2. Intra-renal
Any condition which affects the tubules or glomeruli of
kidney
● Acute tubular necrosis(ATN)
● Acute glomerulonephritis(AGN)
● Medications which cause acute interstitial
nephritis(AIN):
clavulanic acid, penicillins, NSAIDs
3. Post-renal
Any obstruction to urine flow
● Renal stones
● Blocked catheter
● tumours
● BPH(benign prostatic
hyperplasia) in older men
Pre-renal Renal Post-renal
Fluid loss: bleeding,
burns diarrhoea,
vomiting
Acute tubular
necrosis(ATN)
Renal calculi
Hypotension: shock Acute
glomerulonephritis(A
GN)
Blocked catheter
Drugs:
● Diuretics
● ACEI/ARB
● Metformin
● NSAIDs
● Contrast dye
Acute interstitial
nephritis(AIN) due to
drugs like:
● NSAIDs
● Penicillins
● Clavulanic acid
BPH
Tumours
Injury to tubular epithelial cells, due to ischemia/toxins
↓
Leads to back-leakage of fluid from lumen into interstitium
↓
Damaged tubular epithelial cells detach and form casts, which blocks the lumen
↓
Block of lumen leads to: (1)increased tubular pressure, (2) decreased GFR and
(3) decreased urine flow
↓
Ischemia also causes vasoconstriction which reduces GFR and oxygen supply
to tubules
↓
Acute tubular injury
Pathogenesis of AKI
→ Acute kidney injury
Clinical course
3 stages:
1. Initiation phase
2. Maintenance phase
3. Recovery phase
Clinical course
3 stages:
1. Initiation phase
2. Maintenance phase
3. Recovery phase
● Mild ↓urine output, ↑ in BUN
● Lasts for 10-14 days
Clinical course
3 stages:
1. Initiation phase
2. Maintenance phase
3. Recovery phase
● ↓↓ in urine output(oliguria),
salt and water overload, rising
BUN, hyperkalemia, metabolic
acidosis and other features of
uremia
● Lasts for days to weeks
Clinical course
3 stages:
1. Initiation phase
2. Maintenance phase
3. Recovery phase ● Steady ↑ in urine volume
● Loss of large amounts of
water(up to 3 litres/day), Na and
K in urine(leads of hypokalemia)
Clinical features
● Decreased or no urine output
● Edema
● Nausea, vomiting
● Weight gain
● Shortness of breath(dyspnea)
● Hypertension
● Confusion
Signs:
● Edema
● Elevated JVP
● crepitations
Diagnosis
● ↓ urine volume
● Renal function tests(RFT): S. urea, S.creat ↑
● hyperkalemia
● eGFR: 🙅 not useful in AKI 🙅
Complications of AKI
● Hyperkalemia
● Metabolic acidosis
● Cardiac arrhythmias
● Seizure
● Anemia
Complications of AKI
Treatment of AKI
● AKI is often reversible
● Treatment depends upon the cause(pre/renal/post)
● Stop any nephrotoxic drugs (Mnemonic:“stop the
DAMN” drugs)
● Input/Output monitoring
● Maintain BP and urine output
● Restrict fluid intake - up to 400 ml/day
D - Diuretics
A - ACEI/ARB
M - Metformin
N - NSAIDs
● Sodium balance: sodium restriction
● Potassium balance: correction of hyperkalemia by
dietary restriction or medication(using calcium chloride
or dextrose/insulin)
● Acid-base balance: i.v sodium bicarbonate
● Phosphorous balance: controlled with aluminium
hydroxide
● Diet:
- Restrict dietary protein to 40 g/day
- Restrict salt intake
- Vitamin supplements
● If no improvement, dialysis and hemofiltration
References:
● Archith Boloor, Ramadas Nayak - Medicine Prep
Manual for Undergraduates
● StatPearls - Acute kidney injury
Questions:
salman.s.ansari92@gmail.com
For notes, click here
or scan:
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Acute Renal Failure - Medicine - RDT

  • 1. ACUTE RENAL FAILURE Dr. Salman Ahmad Ansari(MBBS) Kanachur Institute of Medical Sciences
  • 2. ARF ● Definition ● Causes ● Pathogenesis ● Morphology ● Stages ● Clinical features ● Diagnosis, treatment
  • 3. Anatomy ● Unit of kidney - nephron ● Nephron consists of glomerulus, tubule and collecting system ● Glomerulus is the filtering unit
  • 4.
  • 5.
  • 6.
  • 7. Acute Renal Failure(ARF) or Acute Kidney Injury(AKI) ● Definition: rapid reduction of renal function, with severe oliguria ● Usually reversible ● Now known as AKI(acute kidney injury) ● Acute Tubular Injury(ATI) is the most common cause of acute kidney injury(acute renal failure) ● ATI →AKI/ARF
  • 8. ● Commonly seen in hospital setting ● Very common in ICU patients
  • 9. KDIGO criteria According to KDIGO(Kidney Disease: Improving Global Outcomes), AKI is the presence of any of the following: 1. Increase in serum creatinine by 0.3 mg/dL or more within 48 hours 2. Increase in serum creatinine to 1.5 times or more baseline within the prior seven days 3. Urine volume less than 0.5 mL/kg/h for at least 6 hours
  • 10. Causes of AKI Divided into 3 categories Pre-renal (60%) Intra-renal (35%) Post-renal (5%)
  • 11. 1. Pre-renal Any cause that reduces blood flow to kidney ● Fluid loss: due to blood loss, burns, diarrhoea, vomiting ● Hypotension: shock, pulmonary embolism ● Medications which cause renal vasoconstriction: diuretics, ACEI, ARBs, metformin, NSAIDs, iodinated contrast
  • 12. 2. Intra-renal Any condition which affects the tubules or glomeruli of kidney ● Acute tubular necrosis(ATN) ● Acute glomerulonephritis(AGN) ● Medications which cause acute interstitial nephritis(AIN): clavulanic acid, penicillins, NSAIDs
  • 13. 3. Post-renal Any obstruction to urine flow ● Renal stones ● Blocked catheter ● tumours ● BPH(benign prostatic hyperplasia) in older men
  • 14. Pre-renal Renal Post-renal Fluid loss: bleeding, burns diarrhoea, vomiting Acute tubular necrosis(ATN) Renal calculi Hypotension: shock Acute glomerulonephritis(A GN) Blocked catheter Drugs: ● Diuretics ● ACEI/ARB ● Metformin ● NSAIDs ● Contrast dye Acute interstitial nephritis(AIN) due to drugs like: ● NSAIDs ● Penicillins ● Clavulanic acid BPH Tumours
  • 15. Injury to tubular epithelial cells, due to ischemia/toxins ↓ Leads to back-leakage of fluid from lumen into interstitium ↓ Damaged tubular epithelial cells detach and form casts, which blocks the lumen ↓ Block of lumen leads to: (1)increased tubular pressure, (2) decreased GFR and (3) decreased urine flow ↓ Ischemia also causes vasoconstriction which reduces GFR and oxygen supply to tubules ↓ Acute tubular injury Pathogenesis of AKI → Acute kidney injury
  • 16. Clinical course 3 stages: 1. Initiation phase 2. Maintenance phase 3. Recovery phase
  • 17. Clinical course 3 stages: 1. Initiation phase 2. Maintenance phase 3. Recovery phase ● Mild ↓urine output, ↑ in BUN ● Lasts for 10-14 days
  • 18. Clinical course 3 stages: 1. Initiation phase 2. Maintenance phase 3. Recovery phase ● ↓↓ in urine output(oliguria), salt and water overload, rising BUN, hyperkalemia, metabolic acidosis and other features of uremia ● Lasts for days to weeks
  • 19. Clinical course 3 stages: 1. Initiation phase 2. Maintenance phase 3. Recovery phase ● Steady ↑ in urine volume ● Loss of large amounts of water(up to 3 litres/day), Na and K in urine(leads of hypokalemia)
  • 20. Clinical features ● Decreased or no urine output ● Edema ● Nausea, vomiting ● Weight gain ● Shortness of breath(dyspnea) ● Hypertension ● Confusion
  • 21. Signs: ● Edema ● Elevated JVP ● crepitations
  • 22. Diagnosis ● ↓ urine volume ● Renal function tests(RFT): S. urea, S.creat ↑ ● hyperkalemia ● eGFR: 🙅 not useful in AKI 🙅
  • 23. Complications of AKI ● Hyperkalemia ● Metabolic acidosis ● Cardiac arrhythmias ● Seizure ● Anemia
  • 25. Treatment of AKI ● AKI is often reversible ● Treatment depends upon the cause(pre/renal/post) ● Stop any nephrotoxic drugs (Mnemonic:“stop the DAMN” drugs) ● Input/Output monitoring ● Maintain BP and urine output ● Restrict fluid intake - up to 400 ml/day D - Diuretics A - ACEI/ARB M - Metformin N - NSAIDs
  • 26. ● Sodium balance: sodium restriction ● Potassium balance: correction of hyperkalemia by dietary restriction or medication(using calcium chloride or dextrose/insulin) ● Acid-base balance: i.v sodium bicarbonate ● Phosphorous balance: controlled with aluminium hydroxide ● Diet: - Restrict dietary protein to 40 g/day - Restrict salt intake - Vitamin supplements ● If no improvement, dialysis and hemofiltration
  • 27. References: ● Archith Boloor, Ramadas Nayak - Medicine Prep Manual for Undergraduates ● StatPearls - Acute kidney injury Questions: salman.s.ansari92@gmail.com For notes, click here or scan: For PPT, scan: