Acute Kidney Injury

ACUTE KIDNEY
INJURY
SR.NIDHI JAMES
INTRODUCTION
• AKI is defined as acute retention of nitrogenous wastes such as blood
urea, uric acid, and creatinine.
• It affects 15% of hospitalized patients and can lead to morbidity and
mortality.
• Recent literature gives strong evidence that AKI is independently
associated with higher risk of cardiovascular events after hospital
discharge.
• Also associated with higher 60-day mortality in patients with septic shock.
EPIDEMIOLOGY
• AKI complicates about 5-7% of hospital admissions and about 30% of
admissions in ICU.
• The incidence of AKI has been grown four fold from1988,higher than the
incidence of stroke.
• AKI increases or worsens the development of chronic kidney disease.
• The patients who survive and require dialysis are at increased risk of later
development of dialysis requiring end-stage renal disease.
INTRODUCTION
DEFINITION
• AKI is defined as any of the following (KDIGO 2012):

Increase in S.Cr by >0.3 mg/dl (>26.5 mmol/l) within 48 hours; or
Increase in S.Cr to > 1.5 times baseline, which is known or
presumed to have occurred within the prior 7 days; or
Urine volume <0.5 ml/kg/h for 6 hours.
CRITERIAS USED FOR AKI
• RIFLE - Risk, Injury, Failure, loss of kidney function, end stage renal
disease.
• AKIN - Acute Kidney Injury Network
• KDIGO - Kidney Disease Improving Global Outcome

TYPES OF AKI
• PRE-RENAL
• RENAL
• POST RENAL
PRE RENAL
• Decreased renal perfusion accounts for 40-80% of acute kidney injury
• Etiologies:
 any cause of decreased circulating volume-GI hemorrhage, burns, diarrhea, diuretics
 volume sequestration-pancreatitis, peritonitis, rhabdomyolysis
 decreased effective arterial volume-cardiogenic shock, sepsis
 medications that interfere with renal autoregulatory responses such as NSAID, Angiotensin
blockers.
• Prompt correction of volume depletion can restore kidney function to normal, because no structural
damage to kidney has occurred.
PRE RENAL -EVALUATION
• CONTEXT-
heart failure, hepatic failure, burns, shock, post-op,dehydration,renovascular
disease,vascular drugs
• URINE OUTPUT- Oliguria(<500ml/day)
• HISTORY - trauma,shock,hypotension,burns,GI loss,sweat or renal losses
• URINANALYSIS – concentrated acid urine,hyaline casts,crystalluria
• URINE CHEMISTRY – low FENa <1%,U/P Cr>40,UNa<10,U/P osm >1
• LAB INVESTIGATIONS-High BUN/Cr ratio, usually hypercatabolic with increased
uric acid:may have hypo/hypernatremia
RENAL CAUSES
• Intrinsic renal disease can arise from processes involving large renal
vessels,intra renal microvasculature and glomeruli or tubule interstitium.
• In many cases,pre-renal azotemia advances to tubular injury if the
underlying condition is not promptly corrected.
• Antibiotics like vancomycin,Aminoglycosides,and Amphotericin B causes
tubular necrosis.
• Glomerulonephritis can lead to AKI by compromising the filtration barrier
and blood flow within the circulation.
RENAL EVALUATION
• CONTEXT - ATN,bilateral cortical necrosis,AIN,crush injuries,myoglobulinuria,hemoglobinuria,ischemia,sepsis,recent contrast drugs
• URINE OUTPUT-oliguria/normal/polyuria
• HISTORY – rhabdomyolysis,hemolysis,thrombotic microangiopathy,AIN,atheroemboli
• URINALYSIS – muddy brown granular cast,hematurai,dysmorphic RBCs,RBC cast in GN,WBC cast in AIN
• URINE CHEMISTRY – FENa 1-3%,U/P Cr <40,Uosm-isomotic
• LAB INVESTIGATIONS – high phosphate,low calcium,high PTH,metabolic acidosis

POST RENAL
• It occurs when the normal unidirectional flow of urine is acutely blocked
either partially or totally, leading to increased retrograde hydrostatic pressure
and interference with glomerular filtration.
• For AKI to occur in healthy individuals, obstruction must affect both kidneys.
• Bladder neck obstruction is the most common cause for post renal AKI which
impacts both kidneys.
• Post renal AKI accounts for <10% of AKI and rapid resolution without
structural damage can restore kidney function.
EVALAUTION
• CONTEXT-
bladder outlet obstruction,obstruction of solitary kidney,abdominal mass,b/l stones,drugs.
• URINE OUTPUT- Anuria, polyuria, both
• HISTORY - extrinsic ureteral obstruction, retroperitoneal disease, bladder outlet or urethral
obstruction by prostate or cervical cancer
• URINANALYSIS – intrarenal obstruction by uric acid or calcium phosphate in tumor lysis
syndrome, blood clots in lower urinary tract bleeding.
• URINE CHEMISTRY – Early looks like prerenal, late looks like renal.
• LAB INVESTIGATIONS- Hydronephrosis on ultrasound, extrinsic or intrinsic disease on CT scan,
tumors on MRI.
MANAGEMENT OF AKI
• Clinical assessment
 History and physical examination regarding cause of AKI,to
differentiate pre renal,intrinsic and post renal AKI.
 Drug history which causes renal injury to be obtained.
 Assessment of duration of the illness to differentiate acute from
chronic renal failure.
Investigations
• Elevated S.Creatinine
• Elevated BUN concentration
• Decreased creatinine clearecence
• BUN:Creatinine ratio - greater than 20:1 in pre-renal AKI and
less than 20:1 in intrinsic and post renal AKI
• Hyperkalemia
• Metabolic acidosis
• Estimation of urine output – oliguria/anuria
• Oliguria – Urine output <500ml/24 hour
• Anuria - Urine output <100ml/24hr

Prevention of AKI
• Hydration to prevent nephrotoxicity
• KDIGO guideline recommend using Normal saline or Sodium bicarbonate
infusion to prevent contrast induced kidney injury.
• Normal saline regimen: 1 ml/kg/hour for 12hrs before and after the
procedure.
• Sodium Bicarbonate regimen: 3ml/kg/hr for one hour before procedure
and 1ml/kg/hr for 6 hours post contrast.
• In the absence of hemorrhagic shock use isotonic crystalloids as initial
management for expansion of intravascular volume.
• Current KDIGO guidelines suggest moderate control of blood glucose
level of 110-149 mg/dl with insulin to prevent ICU induced Kidney injury.
• Use of oral NAC together with isotonic crystalloids, in patients with
increased risk of AKI before contrast.
TREATMENT
• GOAL of treatment
• minimize the degree of kidney insult
• reduce extra renal complication
• restoration of renal function to pre-AKI
Supportive care
• Adequate nutrition
• Correction of electrolyte and acid-base abnormality
• Fluid management
• Medical management of infections, cardiovascular and GI conditions and
respiratory failure.
• All drugs to be reviewed and dose adjustments to be made based on
creatinine clearance.
• Maintain adequate cardiac output and blood pressure for adequate tissue perfusion.
• Discontinue medications which causes diminished blood flow.
• Initiate appropriate fluid and electrolyte according to deficiency.
• Renal Replacement Therapy in severe AKI

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ACUTE KIDNEY

• AKI is defined as any of the following (KDIGO 2012):

• KDIGO - Kidney Disease Improving Global Outcome

• HISTORY – rhabdomyolysis,hemolysis,thrombotic microangiopathy,AIN,atheroemboli

• URINE CHEMISTRY – FENa 1-3%,U/P Cr <40,Uosm-isomotic

• LAB INVESTIGATIONS – high phosphate,low calcium,high PTH,metabolic acidosis

• Anuria - Urine output <100ml/24hr

• Discontinue medications which causes diminished blood flow.

• Initiate appropriate fluid and electrolyte according to deficiency.

• Renal Replacement Therapy in severe AKI

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