ACUTE TUBULAR

NECROSIS
Mc Warsame
Amoud School Of Medicine
Dec 18, 2018
 Introduction

• Acute tubular necrosis (ATN) is the most common

cause of acute kidney injury (AKI)
• ATN is typically found in hospitalized patients due
to toxic or ischemic insult to tubular epithelium
resulting in intrinsic kidney injury.
• It is characterized by adequate renal perfusion to
maintain tubular integrity but not to sustain
glomerular filtration.
 Pathophysiology

• Ischemic or toxic injury to tubular epithelial cells leading

to intrinsic kidney injury.
• Typically severe loss of renal function with minimal
histopathologic evidence of widespread necrosis.
 • ATN is generally caused by an acute
event, either ischemic or toxic.
• Hypovolemic states: Hemorrhage,
volume depletion from
gastrointestinal (GI) or renal losses,
burn, etc

Causes • Low cardiac output states: Heart

failure and other diseases of
myocardium, valvulopathy,
arrhythmia, pericardial diseases,
tamponade
• Systemic vasodilation: Sepsis,
anaphylaxis
• Disseminated intravascular
coagulation
 • Exogenous nephrotoxins that cause
ATN
• Aminoglycoside-related toxicity occurs
in 10-30% of patients receiving
Causes of aminoglycosides, even when blood
levels are in apparently therapeutic
Nephrotoxic ranges.
• Risk factors for ATN in these patients
acute tubular include the following:
– Preexisting liver or renal
necrosis disease
– Concomitant use of other
nephrotoxins Advanced age
– Shock
– Female sex
 Cont’….
Radiographic contrast media can cause 
contrast-induced nephropathy (CIN) or radiocontrast nephropathy
(RCN);
• This commonly occurs in patients with several risk factors, such
as
• Elevated baseline serum creatinine,
• Preexisting renal insufficiency,
• Underlying diabetic nephropathy,
• Chronic heart failure [CHF], or
• High or repetitive doses of contrast media, as well as
• Volume depletion and
• Concomitant use of diuretics, ACE inhibitors, or ARBs.
Cont’…….

• Other exogenous nephrotoxins

that can cause ATN include the
following:
– Amphotericin B
– Cyclosporine and tacrolimus
– Sulfa drugs
– Acyclovir
Cont’…….

• Endogenous nephrotoxins that

cause ATN
– Myoglobinuria,
– Rhabdomyolysis
– Acute crystal-induced nephropathy
– Multiple myeloma.
 Epidemiology

• Most common cause of acute kidney injury in

hospitalized patients reported to account for;
– About 38% of all acute kidney injury cases.
– About 76% of acute kidney injury cases in intensive care
units.
 Diagnosis

• ATN is diagnosed as AKI in context of ischemic or toxic

injury to kidney generally in hospitalized patients
• Characteristic findings of ATN on laboratory tests
include
– Urine osmolality < 350-400mOsm/kg
– Urinary sediment analysis showing muddy brown casts, renal
tubular epithelial cells, granular casts.
– Fractional excretion of sodium > 2%
– Urine to plasma creatinine ration < 20
 Treatment

• Stop exposure o nephrotoxic agents if possible.

• Monitor and adjust fluid and electrolyte balance to
minimize volume depletion or overload, hyponatremia,
hyperkalemia, hyperphosphatemia and hypermagnesemia.
• Identify and treat any infectious cause
• Nutritional support
 • Diuretics not recommended
to treat AKI except in
management of volume
overload (KDIGO, Grade C).
– Furosemide in patients with
AKI does not appear to reduce
Medical mortality or improve renal
recovery but may shorten
Therapies duration of dialysis.
– High dose furosemide may
increase urine output but
does not appear to reduce
mortality or need for dialysis
in patients with AKI requiring
dialysis.
 Cont’…….

• Atrial natriuretic peptide (ANP)

– KDIGO suggests avoiding ANP to treat AKI due
to risk of hypotension outweighing limited
evidence of benefit.
– Low dose ANP might reduce need for renal
replacement therapy (RRT) in patients with AKI
• Low dose dopamine does not appear to
reduce need RRT or mortality in patients
with AKI
 Complications

• ATN reported to be the cause of AKI

– 38% of hospitalized patients with AKI
– 76% of patients in intensive care unit with AKI
• Other complications include; Hyperkalemia, volume
overload and pulmonary edema, metabolic acidosis,
anemia, CKD etc
 Prognosis

• Survival of acute tubular necrosis associated with good

prognosis for renal recovery
– 56% - 60% reported to have full recovery
– 5% - 11% of patients reported to require long-term dialysis.
• Of patients with ATN who require dialysis, reported
mortality 50% - 80%
• Prevention is strongly recommended by avoiding shock-
induced AKI, postoperative AKI, and preventing
contrast-induced AKI
END.