This PPT contains only a brief summery about ATN. for more information about the topic please refer to the book and site found the ppt, or you can get In touch with me .

1. BY JOSEPH NDANJI MULEBA

2. Definition
 This is a disorder characterized by destruction of
tubular epithelial cells resulting in renal function
loss….
NOTE: ATF is the most common and most important
cause of ARF characterized by sudden cessation of
renal outflow or 24hrs urine <400ml

3. Types of ATN
 Based on etiology and morphology, they are two
types of Acute Tubular Necrosis (ATN)….
1. Ischemic ATN
2. Toxic ATN

5. ISCHEMIC ATN
 Its also known as ANOXIC NECROSIS or SHOCK
KIDNEY.
 It occurs due to hypo perfusion of the kidney resulting in
focal damage to the distal part of the convoluted tubules..
 ETIOLOGY
1. SHOCK(post-traumatic, surgical, burns, dehydration
2. CRUSH INJURIES
3. Non-traumatic rhabdomyolysis induced by alcohol,
coma, muscle diseases etc
4. Mismatched blood transfusion, black-water fever
(haemoglobinuric nephrosis)

6. TOXIC ATN
 Its also known as NEPHRONTOXIC ATN or TOXIC
NEPHROSIS
 It occurs as a results of direct damage to tubular, more
marked in PCT of nephrons, its caused by ingestion,
injection or inhalation of number of toxic agents
 ETIOLOGY
1. General poison e.g. mercuric, chloride, mushroom
poisoning, insecticides etc
2. Heavy metals (mercury, lead, arsenic, gold etc )
3. Drugs e.g. anesthetic agents, certain antibiotics
4. Radiographic contrast material

7. Pathogenesis of ATN
I. Tubular damage in ischemic or toxic ATN
II. Debris of the desquamated epithelium due to necrosis cause
tubular obstruction and may block the urinary outflow and
drop in GFR & produce casts in urine.
III. This events cause increases in intratubular pressure resulting
to damage to tubular basement membrane
IV. Further increase in the pressure result to rupture of the tubular
and haematuria is seen
V. With the rupture of the tubular there is linkage of fluid into the
interstitium causing interstitial oedema.
VI. leakage of tubular fluid in interstitium ( oedema) increases the
interstitial pressure and may incites host inflammatory
response
VII. The Increased interstitial pressure causes compression of
tubules and blood vessels and setting up a cycle of accentuated
ischemia and necrosis
VIII. Ultimately, leads to reduced GFR and Oliguria

10. Difference
Feature Ischemic ATN Toxic ANT
Synonym
Frequency More common ( about
80% of cases)
Less common
Etiology Shock
Crush injury
Mismatch blood
transfusion
Poison
Heavy metal
Certain drugs
Grossly Kidney enlarged
Swollen
Cortex pale and dark
medulla
Same
Prognosis Becomes worse in most
cases
Becomes better in most
cases

11. Clinical features of ATN
 INITIATION PHASE: lasts for about 36hrs and is
characterized by decreased in urine out put and
increase in BUN.
 MAINTENCE PHASE: characterized by uriguria,
salt &water overload, hyperkalemia and increase in
BUN
 RECOVERY PHASE: Steady increase in urine
volume (up to 3l/d), hypokalemia and increase
vulnerability to infections

12. Acute Renal Failure due to ATN
(ischemic)

13. Complications of ATN
 Electrolyte abnormalities
 Intravascular volume overload
 Hypertension
 Uremic syndromes
 Anemia
 Infections

14. Diagnosis of ATN
 URINALYSIS
to look for abnormal cells, color and signs of
infection.
 BUN &CREATININE URINE TEST
both increases in kidney failure
 BIOPY
to examine the kidney tissues
 BLOOD SODIUM & CREATINE MEASURE
 CT Scans

15. Reference :
 HARSH MOHAN text book of pathology 8th edition
 www.pathology.jcu.edu.au