Acute kidney injury

1. Acute kidney injury
Yousaf khan
Lecturer Renal dialysis
IPMS- KMU

2. Acute kidney injury
 Acute renal failure (ARF)
 Abrupt loss of Kidney function that develops within 7
days.
 Increase in serum creatinine
 AKI may lead to a number of complications,
 metabolic acidosis
 high potassium levels
 Uremia
 changes in body fluid balance
 Effects on other organ systems
 including death
 People who have experienced AKI may have an
increased risk of chronic kidney disease in the future.

3. Diagnostic Approach
 Time of onset – prior serum creatinine
 Careful review of history and physical
exam
◦ Comorbidities
◦ Medications
◦ Current illness (vomiting, diarrhea, blood
loss, etc)
◦ BP, volume status, skin lesions,
flank/abdominal signs

4. Signs and symptoms
 Accumulation of urea and other nitrogen-
containing substances in the bloodstream
lead to
 Fatigue
 loss of appetite
 Headache
 Nausea
 Vomiting
 Marked increases in the potassium level can
lead to irregularities in the heartbeat, which
can be severe and life-threatening
 Fluid balance is frequently affected, though
blood pressure can be high, low or normal

5. Stages of acute injury

6. Consistent Risk Factors
 Age
 Hypovolemia
 Hypotension
 Sepsis
 CKD
 Hepatic dysfunction
 Cardiac dysfunction
 DM
 Exposure to nephrotoxins

7. Differential Diagnosis of AKI
 Pre-renal
 Renal
 Post-renal

8. Prerenal
 Decrease effective blood flow to the kidney
 low blood volume
 low blood pressure
 heart failure
 liver cirrhosis
 renal artery stenosis
 renal vein thrombosis
 Renal ischaemia can result in depression of GFR
 inadequate cardiac output

9. Intrinsic
 Glomerular
◦ Rapidly progressive GN, post-strep GN,
 Interstitial nephritis
◦ Infection-related, inlammation, drug-induced,
infiltrative (lymphoma, leukemia, sarcoidosis)
 Tubular Lesions
◦ Post-ishemia, nephrotoxic (drugs, contrast,
anesthetics, heavy metals), pigment
nephropathy, light chain, hypercalcemia

10. Postrenal
 Bladder flow obstruction
◦ Urethral, bladder neck (BPH), neurogenic
bladder
 Ureteral obstruction (bilateral or single
kidney)
◦ Stones, clots, tumours, papillary necrosis,
retroperitoneal fibrosis, surgical ligation

11. Urine Output and AKI
 Anuric
◦ < 100 cc / 24 hrs
 Oliguric
◦ < 300 cc / 24 hrs
 Non-olguric
◦ Normal urine output, but inadequate
clearance
◦ GFR 2 ml/min will produce ~3L of
urine/day if there is no tubular
reabsorption

12. Diagnosis
 Clinical history
 Urea and creatinine
 Urine sediment analysis
 renal ultrasound
 renal biopsy
 Indications for renal biopsy in the setting of
AKI include
 Unexplained AKI, in a patient with two non-
obstructed normal sized kidneys
 AKI in the presence of the nephritic syndrome
 Systemic disease associated with AKI
 Renal transplant dysfunction

13. Principles of AKI Management
 Identify AKI
 Avoid further nephrotoxic injury
 Optimize renal hemodynamics
 Treat complications
◦ Fluid balance, electrolytes, uremia
 Nutritional support
 Renal Support (RRT)
 Monitoring after AKI

14. Treatment
 Identification and treatment of the underlying cause.
 (1) to prevent cardiovascular collapse and death
 (2) to call for specialist advice.
 In addition to treatment of the underlying disorder,
management of AKI routinely includes the avoidance of
substances that are toxic to the kidneys, called
nephrotoxins. These include NSAIDs such as ibuprofen,
iodinated contrasts such as those used for CT scans,
many antibiotics such as gentamicin, and a range of
other substances
 Monitoring of renal function, by serial serum creatinine
measurements and monitoring of urine output, is
routinely performed. In the hospital, insertion of a
urinary catheter helps monitor urine output and relieves
possible bladder outlet obstruction, such as with an
enlarged prostate.

15. Specific therapies
 In prerenal AKI without fluid overload
 administration of intravenous fluids is typically the first step to
improve renal function.
 Volume status may be monitored with the use of a central
venous catheter to avoid over- or under-replacement of fluid.
 Should low blood pressure prove a persistent problem in the
fluid-replete patient, inotropes such as norepinephrine and
dobutamine may be given to improve cardiac output and
hence renal perfusion.

 Intrinsic AKI require specific therapies.
 If the cause is obstruction of the urinary tract, relief of the
obstruction (with a nephrostomy or urinary catheter) may be
necessary.

16. Renal replacement therapy
 Renal replacement therapy such as
with
 Hemodialysis
 Peritoneal dialysis
 CRRT

17. Thank you