Acute Kidney Injury [ Acute Renal Failure]

Definition :- 

AKI Previously called Acute Renal Failure is an abrupt loss of kidney functions that develops within 7 days.

It is characterized or manifested by decrease glomerular filtration rate, level of serum creatinine and urea nitrogen rise and oligourea or anurea. 

 Etiology :-

It's cause are numerous. Generally it occurs because of damage to kidney tissue caused by decreased blood flow (ischemic kidney), low blood pressure or hypotension, exposure to substance harmful to kidney, inflammatory process or an obstruction of the urinary tract.

The causes of AKI can be categorized by into 3 major area's :-

1. Pre-Renal cause
2. Intra-Renal cause
3. Post Renal cause

     1. Pre-Renal Cause :-

• Pre-Renal causes are those that decrease effective blood flow to the kidney and cause to decrease in GFR.
• Low blood volume in the body (hypovolemia) [due to vomiting, diarrhea, hemorrhage, burns and excessive use of diuretics.]
• Hypotension
• Decreased cardiac output
• Heart failure
• Renal artery stenosis

      2. Intra-Renal / Intrinsic cause :-

Process which directly damage kidney itself :

• Glomerular Nephritis
• Tubular Necrosis
• Renal Surgery
• Injury, Trauma, Crush
• Electric Shock
• Diabetes Malitus
• Infectious Disease
• Rejection of transplant kidney
• Genetic Factors

      3. Post Renal cause :-

Caused by disease states / condition down stream of the kidney.

• Urinary tract obstruction.
• Uritral or urethral structures (stenosis)
• B.P.H.
• calculi
• cancer or tumor of bladders & uretor's
• Surgical Accidents
• Spinal cord injury leads to decrease bladder emptying of functional obstruction.

Mechanism / Pathogenesis :- 

The mechanism of AKI is not specific or not clear there are some mechanism which are :-

• Ischemic kidney
• Activation R.A.S.
• Tubular injury or infection
• Fibrosis and scare formation
• Renal Calculi
• Decreased osmotic pressure

Clinical Manifestation :-

• Headache 
• Fatigue
• Nausea , Vomiting
• Diarrhea
• Constipation 
• Loss of Apetite
• Flank pain
• Edema
• Shortness of breath
• Hematuria
• Oligurea or Anurea 
• Hypertension
• Hand tremors
• Decrease G.F.R.
• Increase Serum Keratinine
• Acidosis
• Ureanitrogen level Increase
• Fluid and Electrolyte Imbalance
• Hyperkelemia
• Hyponatriemia
• Hypocalcemia
• Hyperattrisemia

Investigation :-

• Serum Creatinine level (increases)
• Blood ureanitrogen
• Serum pottasium
• Urine analysis
• Radiological study (CT, MRI, X-ray)

Management :-

The management of AKI is divided into 4 stages or phases :-

1.  Initiating / onset phase :-  This phase covers the period from the precipitation event to the development of renal manifestation and continue until the sign and symptoms.It can last for few hours to week.
2. Oliguric phase :- The most common initiative manifestation of AKI is oligurea caused by a reduction in the G.F.R. oligurea usually occur within 24 hours. The longer oliguric phase clast the poor prognosis for recovery of complete renal function. (1 to 8 week).
3. Diuretic phase :- The diuretic of AKI begin with a gradual increase of urine output of 1 to 3 lit. per day but may reach to 3 to 5 liter per day or more although output increased in case nephrones are still  not fully functioning. At this stage the uremia may still be serve as infected by the low creatinine clearance , elevated serum creatinine, BUN level, and persistent sign and symptoms of dehydration because of large of loss of fluid and electrolyte . ( 25- 30 % of death dehydration)
4. Recovery phase :- The recovery phase begins when the GFR increases allowing the BUN and serum creatinine level decrease some individual do not recover or progress to chronic kidney failure. The older adults patient are less likely recovery to fully kidney function.The treatment of recovery phase last for some month or a year in severe cause dialysis or kidney transplantation may be prescribed.

Medical Management :-

• Avoidance of substance that are toxic to the kidneys called Nephrotoxics, it include NSAID.
• Iodinated contrast or contrast medium use in radio-graphic examination specially CT scan and MRI.
• Antibiotics 
• In lower BP :- Non epinephrine, Inotrops, steroid, Dobutamine
• In high BP :- calcium channel blocker, ACE inhibitor, Diuretics.
• In metabolic acidosis administer sodium bicarbonate 

Surgical management :-

• Nephrotomy
• Catheterization
• Dialysis
• Renal Transplantation

Nursing Management :-

• Fluid volume excess related to inability to kidney to promote or excrete urine.
• Fluid volume deficit.
• Altered  nutrition level .
• Risk for infection.
• Disturb thought process.
• Risk for impaired normal skin integrity related to edema.