3. Definition
• Acute kidney injury (AKI) is abrupt reduction of renal
function which happens for less than 3 months,
leading to decrease the elimination of nitrogenous
waste products and other uremic toxins resulting to
increased blood urea nitrogen and creatinine,
electrolytes and acid base disturbances, water
retention.
• It was known as renal failure
7. Pathophysiology and etiology prerenal
AKI
• Impaired renal perfusion with a resultant fall in
glomerular capillary filtration pressure is a common
cause of AKI
• A marked reduction in renal perfusion may
overwhelm autoregulation and precipitate an acute
fall in GFR
8. Pathophysiology…
• With lesser degrees of renal hypoperfusion,
glomerular filtration pressures and GFR are
maintained by afferent arteriolar vasodilation
(mediated by vasodilatory eicosanoids) and efferent
arteriolar vasoconstriction (mediated by angiotensin
II)
• AKI may be precipitated by agents that impair
afferent arteriolar dilation (nonsteroidal
antiinflammatory drugs [NSAIDs]) or efferent
vasoconstriction (angiotensin-converting enzyme
[ACE] inhibitors, angiotensin receptor blockers
[ARBs])
9. Pathophysiology…
• Prerenal AKI is often secondary to extracellular fluid
volume depletion as a result of;
– gastrointestinal losses (diarrhoea, vomiting,
prolonge NGT grainage)
– renal losses (diuretics, osmotic diuresis in
hyperglycemia),
– dermal losses (burns, extensive sweating), or
sequestration of fluid, sometimes known as third-
spacing (e.g., acute pancreatitis, muscle trauma)
10. Pathophysiology…
• Prerenal AKI can be corrected if the extrarenal
factors causing the renal hypoperfusion are rapidly
reversed
• Failure to restore renal blood flow (RBF) during the
functional prerenal stage will ultimately lead to
tubular cell injury
11. Pathophysiology and etiology of
postrenal AKI
• Obstruction must be excluded in any patient with AKI
because prompt intervention can result in
improvement or complete recovery of renal function
• Obstruction of the extrarenal collecting system at any
level (renal pelvis, ureters, bladder, or urethra) can
increase intratubular pressure, which opposes
glomerular filtration pressure and decreases GFR
12. Pathophysiology…
• All types of renal obstruction are also associated with
inflammation and fibrosis and can result in
permanent injury if the obstruction is prolonged
22. Other causes of AKI
• Artheroembolic renal deseases
• Renal artery or vein occlusion
• Glomerular diseases
• Thrombotic microangiopathy
• Acute interstitial nephritis
23. Management of AKI
History
• Detailed hx taking including symptoms, duration, risk
factors and possible causes
• Assessing daily urine volume can narrow the
differential diagnosis, dividing AKI into oliguric (<500
ml/day) and nonoliguric causes
• Underlying diseases eg. Heart failure, hypertension,
CKD, diabetes
• Family hx of renal diseases
• Medicines use and herbs
• Drugs of illicit
• Dietary etc
24. Management…
Physical examination
• General examination including weight, height and BMI
• Vital signs
• Hydration status
• Skin
• Systemic examination
• eGFR estimation is important
Cockcroft-Gault formular (140-age)xweight(kg)/(72xserum
creatinine in mg/dl)
• Ans x 0.85 if female
25. Management…
Investigations
• 3-RFT; BUN, creatinine
• 2-Electrolytes-K+,Na+
• ECG; look for hyperkalemia
• pH
• Arterial blood gases; partial pressure of carbondioxide
and oxygen, pH, bicarbonates
• 1-Urinalysis and microscopy; dipstick check for
proteinuria, hematutia, glucose, nitrates, WBCs,
26. Treatment…
Aim of treatment
• Haemodynamic stabilization and maintaining
adequate renal perfusion
• Treatment of the underlying medical condition
• Management of complications
• Avoid further kidney injury
• Renal replacement therapy (RRT) in most severe
forms
27. Treatment…
Haemodynamic stabilization
• Crystalloids; RL, NS, blood
– aim is restoration of renal blood flow and maintain
adequate perfusion
– Given if dehydration
– Diuretics are not indicated unless there is fluid
overload
– Vasoactive agents if indicated; norepinephrine
29. Treatment…
• Treatment of the underlying medical condition
eg. Sepsis, cardiac failure, malignancy,
obstructive uropathy etc.
• Avoid further kidney injury
– Avoid nephrotoxic agents eg. Aminoglycosides,
NSAIDs etc.
30. Treatment…
Management of complications
Fluid overload
• Limit fluid intake
• Iv loop diuretics as bolus or infusion
• Morphine and nitrates can be used to reduce distress
• Possitive pressure ventilation can be used
• Dialysis if refractory to medical therapy
33. Treatment…
Management of complications…
• Calcium, magnesium and phosphorus
disorders to be managed
– Avoid food high in phosphorus like dairy products,
canned food ( for hyperphosphatemia)
– Calcium containing phosphorus binders can be
used in case of hypocalaemia
34. Treatment…
Provide appropriate nutrition
• Nutritional assessment is important
• Patients have increased risk of PEM
• Patients with AKI should receive a basic intake of 0.8
to 1.0 g of protein/kg/day if not catabolic and a total
energy intake of 20 to 30 kcal/kg/day(KDIGO
guidelines)
• Enteral feeding if possible
• Parenteral feeding in case of difficult if enteral is not
possible
35. Treatment…
Renal Replacement therapy
• Aim to remove endogenous and exogenous toxins
and to maintain fluid, electrolyte and acid-base
balance until renal function return
36. Treatment…
Indications of renal replacement therapy
• Acidosis
• Uremic encephalopathy
• Intoxication with dializable chemical eg. Diethyl
glycol, lithium, barbiturates, phenytoin
• Refractory hyperkalemia
• Severe edema not responding to diuretics
• Uremic pericarditis
• Pericardial effusion
37. Modes of dialysis
• Peritoneal dialysis
• Intermittent hemodialysis
Most commonly is hemodialysis in aki and
peritoneal dialysis in CKD
38. Adverse outcomes of AKI
• Mortality; 15% to 80% in critically ill patients
for those patients developed AKI in Hospital
• Increased hospital stay
• Progression to CKD
39. References…
• Comprehensive Clinical Nephrology 6th edition
• José António Lopes and Sofia Jorge. In Depth Review; The RIFLE and AKIN
classifications for acute kidney injury: a critical and comprehensive review. Clin
Kidney J (2013) 6: 8–14
• The Kidney Disease Improving Global Outcomes (KDIGO) Working Group. KDIGO
Clinical Practice Guideline for Acute Kidney Injury. Kidney International
Supplements. 2012;2(1):1–138.
Editor's Notes
Note ckd can cause aki. So risk factors are old age,chronic diseaes like dm,ckd and HTN,chronic use of drugs like nsaids,aminogycosides,ace inhibitors,liver disease,abdominal surgery(increase intraabdominal pressure)
Infections like malaria,dengue fever.Toxins like from snakebite,arthropods,scorpions,smoking,alcohol etc.systemic disease like SLE
Amikacin,kanamycin,gentamycin,streptomycin-aminoglycosides-ear defects as most side effect
Nsaids-asprin,diclophenac,acetaminophen,ibuprofen,meloxicam
Dehydration-
These are due to high levels of urea causing uremic syndrome.There are early and late uremic markers.Early one(to be asked in hx) include 1.bilateral loin pain due to hydronephrosis,2.hiccups due to increased creatinine 3.uremic gastroparesis-nausea,vomiting and anorexia 4.uremic coagulopathy-is due to urea as toxin impares platelets aggregation hence hematemesis,blood in stool 5.uremic encephalopathy due to penetration thru bbb-loc,convulsions,coma,drowsy
Late uremic markers(observed when gfr is <50ml/min include-1.cardiac arrythmia due to hyperkalemia and uremic pericarditis 2.anemia-due to impared epo hormone production by the kidney 3.metabollic acidosis-due to failure to secrete h+ and impared excretion of ammonium.1 and 3 can lead to cardio respiratory failure
4.Renal bone disease(osteodystrophy) due to hyperphosphatemia,hypocalcemia and increased PTH levels—cunajua hyperphosphatemia is due to renal injury causing stimulation of pth hence hypocalcemia as result 5.malnutrion occurs-weight loss,anorexia,wasting
Never give fluids that contain K+ like KCl,RL may worsen hyperkalemia.So give NS is safe
Malnutrition is due to uremia causes anorexia and vomiting,reduced absorption of nutrient from edematous gut,metabollic acidosis
A-acidosis,ph<7.1 E-electrolyte mbalance-resistant hyperkalemia I-intoxification-eg lithium,alcohols O-overload of fluid,not responding to diuretics –pericardial effusion,pulmonary edema leading to pulmonary renal syndrome U-uremic syndrome esp encephalopathy and uremic pericarditis
