an overview of ARF&CRF

1. An Overview Of Acute &
Chronic Renal Failure
DR.TASNIM ARA JHILKY
MD Part II Phase A
Sir Salimullah Medical College
Midford Dhaka.

2. Renal Failure
•Renal failure is defined as a significant loss of
renal function in both kidneys.
•Here failure of the excretory & other functions of
kidney leading to retention of nitrogenous waste
product of metabolism & derangements of
fluid,electrolyte,acid base balance.

3. • Renal failure may occur as an acute and rapidly
progressing process or may present as a chronic
form.
• Acute renal failure has an abrupt onset and is
potentially reversible.
• Chronic failure progresses slowly over months
or years.
The major effects of renal failure all occur
because of loss of functioning nephron.

4. • Glomerular dysfunction- main function of
glomeruli is filtration.
•glomerular dysfunction leads to fall in GFR
with retention of those substances. e.g. –
glomerulonephritis.
• Tubular Dysfunction- main function of
tubules is reabsorption.
•tubular failure results in large volumes of dilute
urine (polyuria) of low specific gravity.e.g_
aminoglycoside.

5. .
•Azotemia:defined as the excess of urea,creatinine &
other nitrogenous end products of amino acid &protein
metabolism I blood that are normally excreted in
urine(biochemical changes prior to development of c/f in
CRF)
•Uremic syndrome :it is the terminal manifestation
of kidney failure .loss of excretory,metabolic,endocrine
functions of kidney ,leads to development of clinical
symptom & sign of renal failure which are reffered to as
uremia/uremic syndrome(at GFR <25% of
normal..<25ml/min with 80% nephron loss)

6. Uremic Toxin &their effects
1. Urea
2. Creatinine
3. Uric acid
4. Polyols
5. Middle
molecules(ANP,IL-
6,Cyastacin c,TNF)
6. Phenols
7. Cyanate
fatique,headache,nausea,
insulin resistance,erythrocyte
survival
Uremic pericarditis
Neuropathy
Neuropathy
Drowsiness
Drowsiness,hyperglycemia

7. Acute Renal Failure
.known as acute kidney injury.
Refers a sudden & usually reversible decline of
GFR & loss of renal function ,which develops
over a period of days or weeks & is usually
accompanied by reduction of urine volume.
 A sudden reduction of GFR expressed clinically
as elevations in blood urea and creatinine.

8. .
•Biochemically ARF is defined as having
any of followings
1. Serum creatinine>200 umol/L
2. Rise of serum creatinine by more than
50% from base line.
3. Fall of creatinine clearance by more
than 50% from base line.

9. Causes of ARF
•Pre Renal ARF
The kidney fails to receive a proper blood supply.
Hypovolemia
Hypotension
Low cardiac output
Renal artery stenosis with ACEI
Renal or Intrinsic renal disease
Intrinsic damage to the kidney tissue .this may
be due to a varity of diseases ,or the renal
damage may be consequence of prolonged pre
renal problems
Sustained pre renal causes
Glomerulonephritis

10. .
Vasculities
Acute tubular necrosis eg drug, toxin, sepsis
Nephrotoxic drugs eg NSAID
Renal artery stenosis
Interstisial nephritis
Post Renal causes
•The urinary drainage of the kidneys is
impaired beause of an obstruction ,which
produce back pressure & kidney damage
occurs.
Calculi
Tumour
Fibrosis
Prostate hypertrophy

13. .• Recovery phase
• If the pt is supported during the recovery phage tubular
cell regerate with reformation of the BM & kidney
function usually returns to normal .
• often a diuretic phage develops during recovery due to
loss of medullary hyper osmolarity.
• Medullary con. Gradient is restablished & restoration of
glomerular with tubular function .

14. .
Post Renal ARF
•Obstruction to the flow of urine leads to an
increase in the hydrostatic pressure in the
CD ,which opposes glomerular filteration.
•Obstrction is either intermittent or continuous
if untreated,
•ischemic or pressure damage to renal tissue
may cause established ARF due to ATN.

15. ATN
Develop following severe or prolonged underperfusion of
kidney & also due to ischaemia & nephrotoxic chemical.
Biochemical findings in ATN ;Like as ARF.
Plasma urea, creatinine, k+
is increased & decreased Na+
,
Ca+.
Urine volume <500 ml
Microscopically glomerular cast is present

16. Biochemical Findings in ARF
URINE PRE-RENAL RENAL POST RENAL
VOLUME <500 ml <500 ml variable
U.Sp. Gravity >1.020 ≤1.010 S
U. Osmolarity >600 LOW S
U. Na Excreation <20 mmol/L >40 mmol/L S
Fe Na% <1% >1% S
UTP normal
>1gm/d(glomerular)
<1gm/d(tubular) ±

17. ARF Cont….
SERUM PRE-RENAL RENAL POST RENAL
S. UREA ↑↑ ↑ variable
S. CREATININE ↑ ↑ “
S. URIC ACID ↑ ↑ “
BUN/S. Cr Ratio > 20 Normal “
CCR ↓ ↓ “

18. ARF Cont….
Ratio
( URINE: PLASMA)
PRE-RENAL RENAL POST RENAL
CREATININE >40 :1 <20 :1 VARIABLE
UREA >10 <10 “
OSMOLALITY >1.2 <1.2 “

19. Metabolic Consequence of ARF
Retension of nitrogenous subs./waste products
Increase s.urea& s. creatinine
Electrolytes disturbances
Hyponatremia(decreased relatively,more retention
water)
Hyperkalemia
Metabolic Acidosis
Decrease s. HCO3
Disorder of mineral metabolism
Hypocalemia(due to decrease calcitriol syn)
Hyperphasphatemia
Hypermagnesemia
Hyperuricemia
s.Uric acid increased

20. Symptoms of ARF
• Decrease urine output (70%)
• Edema, esp. lower extremity
• Mental changes
• Heart failure
• Nausea, vomiting
• Pruritus
• Anemia
• Tachypenic
• Cool, pale, moist skin

21. Acute Renal Failure Management
• Make/think about the diagnosis
• Treat life threatening conditions
• Identify the cause if possible
• Hypovolemia
• Toxic agents (drugs, myoglobin)
• Obstruction
• Treat reversible elements
• Hydrate
• Remove drug
• Relieve obstruction

23. Chronic renal failure
CRF is the progressive irreversible deteriation in
renal function which classically develops over a
period of years.
if not treated by dialysis or transplant,will result
death of the pt.
Pt with CRF may be without symptoms until the
GFR falls to very low values.
There is gradual reduction of GFR due to
progressive dystruction of renal mass.

24. CAUSES OF CRF
•DM
•Nephrotoxic Drugs
•HTN
•Glomerulonephritis
•Ch. Pyelonephritis
•Severe UTI
•PKD
•ATN( if not treated outcome is crf)
•Systemic inflammatory diease(SLE, Vasculitis)
•Amyloidosis & paraproteinaemia
•Progression for acute renal dysfunction

25. Pathogenesis of CRF
• CRF may pass through two main phases.
•An initial polyuric phase
• At first glomerular function may be adequate to maintain
plasma urea &creatinine con. within referenge range.
• Both tubular dysfunction in nephrons with functioning
glomerular and osmotic diuresis through intact nephrons
contribute to polyuria .
• Urea creatinine increase biochemically ,but other
subs.between glomerular & tubular spectrum with
metabolic acidosis usually present.

26. .
•Subsequent oliguria or anuria
• As nephron destruction continues ,the findings become
like those of pure glomerular dysfunction.
• GFR decreases significantly & urine output falls.
• Oliguria leads to steep rise in plasma urea,creatinine,
with potassium
• Metabolic acidosis becomes more severe

27. STAGE DESCRIPTION eGFR( ml/min/1.73 m² BIOCHEMICAL FEATURE
1
Normal or ↑ GFR ≥ 90 Normal
2
Early renal insufficiency 60-89 ↑plas. Urea & Cr. &
pl.TG started to ↑
3
CRF
( moderately ↓GFR)
30- 59 ↓Ca+ ,
↓LPL,Malnutrition,a
naemia
4 Severe RF
( pre end stage) 15-29 ↑TG, ↑PO4
-2
,↑K+ ,
acidosis Me.

28. Metabolic Consequence of CRF
1.Retension of nitrogenous waste products(uremic
toxin)
Urea, creatinine,uric acid phenols
2 Fluid ,Electrolytes,Acid base disturbances
Hyponatremia
Hyperkalemia
Hyperchloremia
hypermagnesemia
Hypocalcemia
Metabolic Acidosis
3 Disorder of mineral metabolism
Hyperphasphatemia
Hypocalemia
Hypermagnesemia

29. .
4.Abnormal lipid metabolism
Increased plasma triglyceride
Decreased HDL
Increased TC &LDL
5 Hyperuricemia
due to reduced urinary excretion of uric acid
6.CHO Intolarance
Insulin resistance &IGT(creatinine,cyanate)

30. .
7. Anemia
due to decreased erythropoietin synthesis
8.Altered endocrine function
2ndary hyperparathyroidism(due to dec.ca)
Osteomalacia(due to abnormal vit D meta)
Amenorrhea ,infertily( due to decreased testosterone &
increased prolactin)
9.Renal osteodystrophy

31. Laboratory finding of CRF
• S.Creatinine ………………………………high
• S.Urea ……………………………………….high
• Creatine clearance rate………………low
• U.total protein ……………………………high
•S.electrolytes
• S.potassium……………………………increased
• S.phosphate…………………………….increased
• S.sodium……………………………decreasde
• S.calcium……………………………decreased

32. Feature of metabolic acidosis
•Blood ph…………………………………low
•S.hco3-…………………………………low
•Pco2……………………………………low
•Plasma anion gap…………………high
Microscopic exam.of urine…..cells,cast
Lipid profile altered

33. Difference Between ARF & CRF
FEATURE ARF CRF
H/O onset sudden Gradual
Reversibility Reversible irreversible
Size of kidney normal Reduced
urine volume oliguria →
polyuria
polyuria oliguri→
a
Hb conc./
anaemia
normal/ absent low/ present
Change in Lipid
profile
normal ↑TG, TC, LDL,↑ ↑
HDL↓

34. FEATURE ARF CRF
Hypocalcaemia Mild Marked
Amenorrhoea,
Infertility
Absent Present
Bony Change Absent Renal
Osteodystrophy
CCR Not much low
usually <50%
↓Gradually

37. Problems Related to ESRD
• Metabolic – K/Ca
• Volume overload
• Anemia, platelet disorder, GI bleed
• HTN, pericarditis
• Peripheral neuropathy, dialysis dementia
• Abnormal immune function

38. Dialysis
• ½ of patients with CRF eventually require
dialysis
• Diffuse harmful waste out of body
• Control BP
• Keep safe level of chemicals in body
• 2 types
• Hemodialysis
• Peritoneal dialysis

39. Hemodialysis
• 3-4 times a week
• Takes 2-4 hours
• Machine filters
blood and
returns it to
body

40. Peritoneal Dialysis
• Abdominal lining filters blood
• 3 types
• Continuous ambulatory
• Continuous cyclical
• Intermittent