Acute tubular necrosis = A.T.N.

Causes :
1- Prerenal factors if not corrected rapidly.
2- Toxins endogenous Hb H. An.
Myoglobin crush $
bilirub. Nephropathy
exogenous dye of I. V. P.

contrast nephropathy
Drugs aminoglycosides
Toxins of gram - ve septicemia
Path of tubular N.:

1- necrosed epith. Cells

to the lumen of tubules

epith. Cast will formed

tub. obstruction will occur
2-Glomerular microthrombi
surface area available
for filtration.
3-Peritubular leakage
leakage of the glomerular
filtrate to
gl. Filtration peritubular. Plexus

¯ urine volume
1, 2, 3,4 oliguria
4-reflex afferent arteriolar spasm.
Late, recovery relief of tub. obstr.
will occur relief of g. thrombi.
due to regeneration of tubules but kidney.
Tubules still unable to concentrate urine for a time
Ü Ischaemia diffuse affection of all kid. tub.
Ü Toxins mainly P.C.T.

N.B.v The initial insult in ATN causes disruption of the cell
Membrane ca influx disturbs mitochondrial respiration anaerobic glycolysis intra cellular acidosis also there is
¯ Na - K Atpase and there is production of O2 free radicals.
Cortical blood flow may be reduced by thromboxane vasopressin angiotensin these counter balanced by the intrarenal P.G.

C/P 3 stages

Oliguric phase:
(2-4 wks)

♦Causes: (seebefore.)

♦C/P: (do not forget manifestation of the cause).
-oligurea < 400 c.c. (minimal amount of urine can
excrete waste products) urine volume
- Anuria < 50 or < 100 c.c.
- Vomiting, nausea GIT
-Hypert. heart f. pulm. Edema.
- Hypervolaemia CVS
¯ Ca boney ache
­ ms weakness arrythmia metabolic
- Acidosis acidotic breathing errors
♦Investig.: Cr.
­- urea­ - PH¯, K­
( Ca ¯ - P­ - Hb¯) sometimes normal.
Urine Granular casts or tubular casts.
Sonar almost normal kid.
ttt:(diet - fluid - 4 H)
* Protein
¯¯ < 40 gm/ d * Acidosis Na HCO3.
* Low K diet. *
­ K glucose & insulin
* Fluid chart. * Ca supplements & Al hydroxide to
¯ P.
* Hypert ttt.
* Hr. failure ttt.

Q : indicat. of haemodialysis
bad G. condition
S.K. > 7 m Eq / L
marked acidosis (HCO3 < 15) / Nr (22-26).
volume over load ultrafiltration.

Polyuric phase : (for 3 - 4 Ds)
1- Relief of tub. obstr. & gl. Thrombi
2-Regeneration of kid. tub. but still unable to conc.urine.
3- Urea retension (osmotic diuresis)

- improvement of G. condition.
¯ Na, ¯ K due to diuresis
-urine out put 3-5 L / d

♦ttt: Fluid Na & K supplements.

Post diuretic phase:

pt clinically kid function urine output
free normal
normal volume concentrated urine

How can you differentiate prerenal, renal&post renal uraemia?
1-Bladder outflow obstruction is ruled out by insertionof a urethral catheter or flushing of an existing catheter.

2-Absence of upper tract dilatation on renal ultrasonography can rule out urinary tract obstruction in most cases.

3-if there is no diuresis after fluid intake ±frusemide or low dose dopamine , acute intrinsic renal failure is present.the following table is to defferentiate prerenal failure from failure due to intrinsic renal disease.:
-urine Na > 20 mmol/L
-urine osmolarity <500m.osmol/L
-high BUN:creatinine ratio

< 40 mmol/L
low ratio

How to differentiate Acute from chronic renal failure?
A rapid rate of change of serum urea & creatinine suggesting an acute process.
Small kidneys with increased echogenisity diagnostic of chronic process.
Evidence of renal osteodystrophy is indicative of chronic disease.
Measurment of carbamylated HB(a product of non enzymatic reaction between urea & HB) if high suggesting a chronic disease.
HB, Ca, P may suggest a chronic disease.

Source: Internal Medicine Book of Dr.Osama Mahmoud (Ain Shams University)