For medical students

1. ACUTE KIDNEY INJURY
CHIPATA CENTRAL HOSPITAL
PRESENTER: DR MICHAEL MUNALULA LIWELEYA
REGISTRAR, INTERNAL MEDICINE
DATE: 1ST JULY, 2022.

2. INTRODUCTION
•ACUTE KIDNEY INJURY- SUDDEN & OFTEN REEVERSIBLE REDUCTION IN KIDNEY FUNCTION,
AS MEASURED BY INCREASED CREATININE OR DECREASED URINE VOLUME (GLOMERULAR
FILTRATION RATE).
•PRESENTATION: declined in urine output, accumulation of water, electrolyte imbalances.
•Very common in hospital settings, in almost a 1/3 of ICU admissions (may be due to drugs or
contrast studies etc.).
•Carries a mortality rate of 30-50% depending on the cause.
•NO CLEAR DEFINITION OF AKI HOWEVER;
RIFLE (risk, injury, failure, loss of kidney function, & end stage kidney disease). May 2004
AKIN (Acute Kidney Injury Network). March 2007.
KDIGO (Kidney Disease: Improving Global Outcomes). 2012 & updated in 2021.

3. KDIGO
1. Increase in serum creatinine by 0.3 mg/dL or more (26.5 micromoles/L or more)
within 48 hours
2. Increase in serum creatinine to 1.5 times or more baseline within the prior seven
days
3. Urine volume less than 0.5 mL/kg/h for at least 6 hours

4. ETIOLOGY
Always Remember glomerular filtration. whatever the cause of AKI, renal blood flow
reduction is a common pathologic pathway for declining glomerular filtration rate.
•Traditionally categorized into pre-renal, renal, and post-renal.

5. PRE-RENAL
Due to any cause of reduced blood flow to the kidney. May be due to hypovolemia or
hypotension, or either by systemic hypoperfusion or selective hypoperfusion (e.g. renal
artery stenosis or aortic dissection). Tubular & glomerular function remains normal.
1. Hypovolemia: hemorrhage, severe burns, and gastrointestinal fluid losses such as
diarrhea, vomiting, high ostomy output.
2. Hypotension from the decreased cardiac output: cardiogenic shock, massive pulmonary
embolism, acute coronary syndrome
3. Hypotension from systemic vasodilation: septic shock, anaphylaxis, anesthesia
administration, hepatorenal syndrome
4. Renal vasoconstriction: NSAIDs, iodinated contrast, amphotericin B, calcineurin inhibitors,
hepatorenal syndrome
5. Glomerular efferent arteriolar vasodilation: ACE inhibitors, angiotensin receptor blockers

6. INTRINSIC RENAL
Conditions affecting the glomerulus or tubule. Pre-renal injury can convert into renal injury
when prolonged if offending factor is prolonged. This injury is associated with vasoconstrictor
release from renal afferent pathways
1. Acute tubular necrosis: ischemia from prolonged pre-renal injury, drugs such as
aminoglycosides, vancomycin, amphotericin B, pentamidine; rhabdomyolysis, intravascular
hemolysis
2. Acute interstitial nephritis: Drugs such as beta-lactam antibiotics, penicillins, NSAIDs,
proton pump inhibitors (PPIs), 5-ASA; infections, autoimmune conditions (SLE, IgG related
disease)
3. Glomerulonephritis: anti-glomerular basement membrane disease, immune complex-
mediated diseases such as SLE, post-infectious glomerulonephritis, cryoglobulinemia, IgA
nephropathy, Henoch-Schonlein purpura.
4. Intratubular obstruction: monoclonal gammopathy seen in multiple myeloma, tumor lysis
syndrome, toxins such as ethylene glycol.

7. POST-RENAL
Post renal obstruction leads to congestion of filtration system leading to a shift in
filtration driving forces
•Calculi, renal/ureteral
•Tumors
•Blood clots
•Urethral obstruction etc.

8. PATHOPHYSIOLOGY
•Pathogenesis is etiology driven. There is cellular insult due to ischemia or toxins,
which result in effacement of brush boarders and eventually cell death, thus shutting
down tubular function.
•Histopathology is used to differentiate intrinsic renal patterns from others. This is
done where renal biopsy is indicated.

9. History & Examination…
Focuses on etiology and timeline of progression.
•If hx points towards hypovolemia or hypotension then tx is guided towards volume
repletion.
•PM Hx for comorbid conditions.
•Need for thorough drug hx.
•Differentiating between AKI & CKD. The latter may present with; chronic fatigue,
anorexia, nocturia, sleep disturbances, polyuria, pruritus.
•Hx & E are extremely important as labs may not provide a cause for AKI
•A hx of urine output
•In hospital settings the most common causes of AKI are; ATN (45%), pre-renal disease
(21%), acute superimposed on CKD (13%), urinary tract obstruction (10%),
glomerulonephritis or vasculitis (4%), AIN (2%), atheroemboli (1%)

10. History & Examination…
An thorough examination is extremely important, always take orthostatic vitals.
1. Eyes & Ears- jaundice in liver disease, band keratopathy in MM, signs of DM,
atheroemboli in retinopathy, and signs of HTN. Keratitis, & uveitis in autoimmune
vasculitis. Hearing loss in Alport disease
2. CVS- BP, pulse, JVP, irregular rhythm may indicate electrolyte imbalance,
pericardial friction rub in uremic pericarditis.
3. Skin- digital ischemia, track marks in IVDA, butterfly rash, purpuras might suggest
vasculitis

11. EVALUATION
•HX & E!!!
•Lab results can be used to trace trigger for AKI in retrospect.
•Review radiologic studies that are contrast based and drugs used.
•ALL pt warrant a basic lab panel; basic metabolic panel, serum and urine electrolytes, urine
protein, urine osmolality, and urine albumin to creatinine ratios
•Those without an obvious etiology should be subjected to serum & urine protein
electrophoresis (SPEP & UPEP) to R/O monoclonal gammopathy and MM.
•Renal scan for size (normal 10-12cm), corticomedullary differentiation. Also to R/O
obstructive causes
•Urine sediment examination can reveal muddy brown casts, as seen in acute tubular necrosis
•Sterile pyuria is most sensitive for acute interstitial nephritis

12. EVALUATION
•Renal biopsy? Pros vs cons
•Although with very poor sensitivity Fractional excretion of Na⁺, and Urea & Urine
osmolality can be used to determine pre-renal from renal.
•NO SINGLE marker can be used in isolation to distinguish between pre-renal and renal
causes of AKI.
•Overall clinical picture. Assess volume status to exclude possible cardiorenal or
hepatorenal syndrome

13. TREATMENT
•FLUID CHALLENGE ANYBODY???
•The best way to determine if AKI is pre-renal or not is a fluid challenge IF THE CLINICAL
SCENARIO DOESN’T CONTRADICT IT.
•If clinical scenario doesn’t contradict all patients should receive a bolus and have a strict I/O
chart
•If renal function improves with fluids then that is the best indicator of a pre-renal AKI.
•ATN is very slow to recover, days to weeks. It may never resolve too.
•Avoid use of diuretics in anuric patients.
•Drugs need to be renally adjusted
•Diuretics can be used in volume overloaded patients. It plays NO role in converting oliguric
AKI to non-oliguric AKI.

14. TREATMENT
•Renal Replacement Therapy, dialysis (acidosis, electrolyte imbalance, intoxication, overload,
uremia)
•Vasoactive medications and colloids for treatment of hepatorenal syndrome, and cautious
diuresis in cardiorenal syndrome.
•Immunosuppressive therapy for glomerulonephritides
•Post-renal obstructions may need to be cleared.
•Peri-procedure IVF may lower risk of accelerated AKI in those with poor baseline renal
function tests.
•Hyperkalemia: Calcium Gluconate 10ml 10% over 10-15 minutes, insulin (0.1iu/kg) as bolus
with 50% dextrose (1mg/kg), beta-agonists, K⁺ binding resins and dialysis for resistant
hyperkalemia.

15. PROGNOSIS
•Old age
•Duration of illness
•Fluid balance
•Diuretic use
•Decline in urine output
•Hypotension
•Ionotropic support
•Multi organ dysfunction
•Sepsis
•Numbers of transfusions

16. END!!!!
END!!!