Acute kidney failure

Presented by
19118,19119,19120
Definition
● Acute kidney injury (AKI) is defined by the impairment of kidney filtration
and excretory function over days to weeks resulting in the retention of
nitrogenous and other waste products normally cleared by the kidneys.

● AKI is not a single disease but rather a designation for a heterogeneous

group of conditions that share common diagnostic features: specifically,
an increase in serum creatinine (SCr) concentration often associated with
a reduction in urine volume.

● AKI can range in severity from asymptomatic and transient changes in

laboratory parameters of glomerular filtration rate (GFR)
 Criteria
● Abrupt decrease in renal function defined as

1. Increase in serum creatinine of greater than equal to 3mg\dl

over 48 hours or greater than equal to 50% increase from
baseline in last 7days
2. greater than 0.5ml\kg\hr reduction in urine output for greater
than 6hrs
Stages of AKI
Etiology
Pre-Renal-
● Hypovolemia
● Decreased cardiac output
● Decreased effective circulating
volume
● Congestive heart failure
● Liver failure
● Impaired renal autoregulation
● NSAIDs
● ACE-I/ARB
● Cyclosporine
Intrinsic
1-Glomerular cause
● Acute glomerular nephritis
2-Tubules and interstitium
● Ishemia
● Sepsis/ Infection
● Nephrotoxin
3- Vascular cause
● Vasculitis
● Malignant hypertension
Post-Renal
● Bladder outlet obstruction
● Bilateral pelvoureteral
● obstruction (or unilateral obstruction of a solitary
functioning kidney)
Pathophysiology
 Prerenal
• Precipitating event is renal hypoperfusion which may be due to
1. hypovolemia -hemorrhage volume depletion
2. Impaired cardiac function-congestive heart failure,acute MI
3. Systemic vasodilation-antihypertensive medications,cirrhosis
4. Increased vascular resistance-anesthesia,surgery,NSAID medications

• kidney are inadequately perfused and GFR is markedly reduced and

produce oligouria
 Renal
• it occurs due to intrinsic disease of kidney
• 1 tubuler - renal ischemia, sepsis, neprotoxic drugs
• 2 glomeruler- glomerulonephritis, wegener disease
• 3 interstitium- infection , medication- antibiotic, nsaids
• 4 vascular- vasculitis, hemolytic uremic syndrome
 postrenal
• extrarenal causes- benign prostate hypertrophy, improperly placed
catheter bladder cancer
• intrarenal causes- nephrolithiasis, blood clots,
 Investigation

• Urine findings
• Blood laboratory findings
• Renal failure indices
• Radiological evaluation
• Kidney Biopsy
• Novel Biomarkers
 Urine analysis
• Complete Anuria – (Uncommon),
may be in complete urinary tract
obstruction, renal artery occlusion,
overwhelming septic shock, vasculitis etc.

• Oliguria - more severe (worse clinical

outcomes)
• Preserved Urine output – nephrogenic DI,
tubulointerstial disease, nephrotoxicity from cisplatin or
aminoglycosides

In absence of pre-existing CKD may cause mild proteinuria

• Heavy proteinuria seen in glomerulonephritis, vasculitis
and toxins
• AKI from ATN due
to ischemic injury,
sepsis or certain
nephrotoxins have
characteristic :mu
ddy brown
granular casts and
tubular epithelial
cell casts
 Urine abnormality in ARF
Pre renal Renal Post renal

Specefi gravity >1.020 1.010 -

Urine osmolality >500 250-300 400

(mOsm\kg)
Urine\plasma >1.1 1-1.1 1-1.1
osmolality
Urinary Sodium <20 >40 <30
(mEq\L)
FENa <1% >1% Variable

Urine\Plasma >40 <20 <20

creatinine
Renal Failure Index <1 >2 >2

Urinary sediments scanty active scanty

Urinary proteins Minimal moderate to severe minimal
 Blood Laboratory findings
• Raised serum creatinine and urea levels – Consistent but not
reliable.

(as it may be influenced by age, gender, muscle mass, nutrition

status, tubular secretion
50% loss of renal function before it rises
Does not reflect true GFR)
• Other causes of raised serum creatinine
Azotemia: Prerenal, renal, post renal
large amount of consumption of meat
Hypothyroidism, acromegaly, gigantism
Rhabdomyolysis, Statins, fibrates

Anemia , thrombocytopenia, eosinophilia, schistocytes on PBS, elevated LDH and

low haptoglobin content
• Other biochemical findings are hyperkalemia, hypocalcemia,
hyperphosphatemia, and hyperuricemia
 Renal Failure indices
Etiology of acute kidney FENa(Fractional excretion BUN-to-serum creatinine
injury of sodium) ratio
Prerenal <1 % >20
Intrarenal <10-15
Tubular necrosis > or =1%
Interstitial nephritis >or=1%
Glomerulonephritis <1%
Vascular disorders <1%
Postreanal >or=1% >20
 Radiological Evaluation
• Simple bladder catheterization –to rule out urethral obstruction

• Imaging- renal ultrasound or CT scan ,to investigate obstruction and size as

Finding of obstruction –dilatation of collecting system and hydroureteronephrosis
(In CKD –kidneys smaller ,normal in AKI)
• Antegrade or retrograde pyelography

• MRI with gadolinium based contrast agents (GBCAs) : avoided (may cause
nephrogenic system fibrosis)
 Kidney biopsy
• Considered when cause not apparent on clinical context,
physical examination, laboratory studies and radiological
evaluation
• other being considered glomerulonephritis, vasculitis,
Interstitial nephritis, HUS and TTP
 Novel Biomarkers

• Neutrophil gelatinase-associated lipocalin (NGAL)

• Kidney Injury molecule -1(KIM-1)
• Interleukin-18(IL-18)
• Cystatin C
• Soluble urokinase plasminogen activator receptor (suPAR)
Complications of AKI
• Metabolic – hyperkalemia, hypocalcaemia, hyperphosphatemia,
hypermagnesemia, hyperuricemia, metabolic acidosis.
• Cardiovascular: arrhythmias, pericarditis and pericardial effusion
• Gastrointestinal : haemorrhage
• Neurological: encephalopathy, neuropathy, seizures.
• Haematological : Anaemia, platelet disfunction.
• Miscellaneous: infections
Management
• Includes assessment of fluid
• Treat underlying cause
• Electrolyte and Acid base management
• Dietary measures
• Treatment of systemic complications and screen for infections
• Withdrawal of nephrotoxic drugs.
• Dialysis
 Volume management
Optimization of systemic and renal haemodynamics through volume
resuscitation and judicious use of vasopressors.
• Assess fluid status
If hypovolemic: balanced crystalloids such as ringer’ lactate ,plasma lyte
or Hartmann’s
Once euvolaemic , match fluid intake to urine output plus an additional
500ml/day to cover insensible losses.
If fluid overload , furosemide bolus 200mg followed by intravenous drip
( 10-40mg/ h) with or without thiazides.
Specific therapy for underlying
Cause
• Intrinsic kidney disease require Immunosuppressive drugs such as
cyclophosphamide.
• Postrenal AKI : relief from obstruction
Urethral strictures -Transurethral or suprapubic bladder catheterization
Ureteric obstruction – percutaneous nephrostomy tube placement.
• Drug induced need to be withdrawn of nephrotoxic dugs.
Electrolyte and Acid- Base
Abnormalities
• Metabolic acidosis not treated unless pH<7.20 and serum
biocarbonate <15mmol/L.
• Acidosis treated by sodium bicarbonate
• Hyperphosphatemia treated by phosphate binders Like calcium
carbonate, calcium acetate , lanthanum or aluminium hydroxide.
• Hypocalcemia treated with calcium gluconate or calcium chloride.
Malnutrition management
• According to Kidney Disease Improving Global Outcomes (KDIGO)
total energy intake of 20-30kcal/day .
non- catabolic AKI without the need for dialysis; 0.8 -1.0 g/kg per day
1.0- 1.5g/kg per day in patients on dialysis and maximum to 1.7g/kg per
day
• Trace elements and vitamins supplementation.
Management of Systemic
Complications
• Infections and gastrointestinal bleeding (leading to anemia) are main
complications

• Appropiate antibiotics for infections ( urinary tract infections and

pulmonary infections.
• Proton pump inhibitors for gastrointestinal prophylaxis.
Dialysis Indications
• Fluid overload refractory to diuretics and refractory pulmonary edema.
• Severe metabolic acidosis pH < 7.1
• Complications of uremia ( pericardial effusion, encephalopathy ,
uremic bleeding).
• ESRD
• Resistant hyperkalemia.
• Tumour lysis syndrome
• Severe hyperphosphatemia > 12mg /dl
• Blood urea nitrogen more than 100mg /dl
Haemodialysis in AKI
• It can be used intermittently or continuously
• Vascular access is through the femoral , internal jugular or subclavian
vein.
• performed through a large bore , dual lumen catheter.
• Initially, 1-2 hr of dialysis prescribed.
• Later, pateints with haemodynamically stable AKI, 4-5 hr of dialysis on
alternate days or 2-3 hr per day.
• Complication- hypotension
Outcome and Prognosis
• AKI associated with a significantly increased risk of in hospital and
long term mortality ,longer length of stay.
• 50% morbidity in ICU admitted pateints.
• Increase the risk of cardiovascular diseases.
• If AKI pateints require Dialysis , increase the risk of CKD and 10%
develop End stage kidney disease.