aki

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ACUTE KIDNEY INJURY(AKI)

Abdirahman NourMMED

Internal Medicine

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Acute kidney injury (AKI)Definition

sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products

a designation for a heterogeneous group of conditions sharing common diagnostic features (increased (BUN) concentration (SCr))

often associated with a reduction in urine volume

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Acute kidney injury (AKI)

Absolute increase in the serum creatinine concentration of ≥0.3 mg/dL (26.4 micromol/L) from baseline

≥50% increase in the serum creatinine concentration

oliguria ≤0.5 mL/kg per hour for more than six hours

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Etiology and pathophysiology

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Azotemia /uremia

Definitions Asymptomatic increase in serum urea

and Cr Usually caused by inability of the kidney

to excrete urea, Cr and other nitrogen-containing compounds in the blood

Uremia: azotemia associated with symptoms of kidney failure (e.g. anorexia, nausea, itch, confusion)

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AKI: EpidemiologyAKI Complicates 5–7% of acute care hospital

admissions. Up to 30% of admissions to ICU.

Major medical complication in the developing world, particularly in the setting of diarrheal illnesses, infectious diseases

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AKI in the developing world

Etiologies for AKI are region specific such as

Envenomations from snakes, spiders, and bees;

Infectious causes such as malaria

Crush injuries and resultant rhabdomyolysis from earthquakes.

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Prerenal AKI It is the designation for a rise in SCr or

BUN concentration due to

Inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration.

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Prerenal AKI Volume depletion: poor po intake, vomiting,

diarrhea, diuretics, third-spacing Hypotension: sepsis, drugs, bleeding, maybe

liver disease? Decreased cardiac output: CHF, acute MI Poor arterial perfusion: renal artery stenosis,

embolism, thrombosis

Often multifactorial, with meds exacerbating

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Prerenal AKI

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Prerenal AKI

Prerenal azotemia involves no parenchymal damage to the kidney

is rapidly reversible once intraglomerular hemodynamics are restored

Prerenal azotemia may coexist with other forms of intrinsic AKI.

Prolonged periods of prerenal azotemia may lead to ischemic injury, often termed acute tubular necrosis, or ATN

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Compensatory renal physiologic changes

Mediators of this response includeangiotensin II, norepinephrine, and

vasopressin (ADH) Glomerular filtration can be maintained

despite reduced renal blood flow by angiotensin II–mediated renal efferent vasoconstriction, which maintains glomerular capillary hydrostatic pressure closer to normal

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Myogenic reflex within the afferent arteriole leads to dilation in the setting of low perfusion.

Intrarenal biosynthesis of vasodilator prostaglandins

(prostacyclin, prostaglandin E), nitric oxide (NO) also increase in response to low renal perfusion pressure.

tubuloglomerular feedback elicit dilation of the juxtaposed afferent arteriole

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Counterregulatory mechanisms to maintain GFR in the face of systemic hypotension have limits

Renal autoregulation usually fails once the systolic blood pressure falls below 80 mmHg

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Risk factors for prerenal azotemai HTN Atherosclerosis Age Renovascular diseases Drugs (NSAIDs,) ACE inhibitors/ARBs

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Intrinsic AKI

The most common causes are Sepsis Ischemia Nephrotoxins, both endogenous and exogenous Conceptualize others anatomically according to

the major site of renal Parenchymal damage Glomeruli, Tubulointerstitium, Vessels

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Intrinsic AKI

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SEPSIS-ASSOCIATED AKI complicates more than 50% of cases of

severe sepsis, and greatly increases the risk of death.

Sepsis is also a very important cause of AKI in the developing world.

most cases of severe AKI typically occur in the setting of hemodynamic collapse

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SEPSIS-ASSOCIATED AKI The hemodynamic effects of sepsis: Vasodilatation (cytokines/induced NO)The operative mechanisms may be o excessive efferent arteriole vasodilation o renal vasoconstrictiono endothelial damage( microvascular

thrombosis activation of reactive oxygen species, and leukocyte adhesion and migration)

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ISCHEMIA-ASSOCIATED AKI

kidneys receive 20% of the cardiac output and account for 10% of resting oxygen consumption,

despite constituting only 0.5% of the human body mass

kidneys are also the site of one of the most hypoxic regions in the body, the renal medulla

leukocyte-endothelial interactions in the small vessels

lead to inflammation and reduced local blood flow tothe metabolically very active S3 segment of the

proximalTubule.

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ISCHEMIA-ASSOCIATED AKI Prerenal azotemia and ischemia-

associated AKI represent a continuum of the

manifestations of renalHypoperfusion. Persistent preglomerular

vasoconstriction may be a common underlying cause of the reduction in GFR seen in AKI

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ISCHEMIA-ASSOCIATED AKI implicated factors for vasoconstriction

include activation of tubuloglomerular feedback

Increased basal vascular tone reactivity to vasoconstrictive agents Decreased vasodilator responsiveness

Other factors backleak of filtrate across ischemic andtubular epithelium and mechanical obstruction of

tubules from necrotic debris

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NEPHROTOXIN-ASSOCIATED AKI All structures of the kidney are

vulnerable to toxicinjury, including the tubules, interstitium,

vasculature,and collecting system Risk factors for nephrotoxicity include

older age Chronic kidney disease (CKD) prerenal azotemia Hypoalbuminemia

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NEPHROTOXIN-ASSOCIATED AKINephrotoxins Contrast agents Antibiotics Chemotherapeutic agents Endogenous substances (myoglobin, hemoglobin, uric acid, and

myeloma light chains)

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Drugs that contribute to acute kidney injury

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POSTRENAL ACUTE KIDNEY INJURY

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POSTRENAL ACUTE KIDNEY INJURY

The pathophysiology of postrenal AKI involves hemodynamic alterations triggered by an abrupt increase in intratubular pressures

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Initial diagnostic work-up

The distinction between AKI and chronic kidney disease is important for proper diagnosis and treatment.

Easy if recent baseline SCr concentration is availableclues suggestive of CKD radiologic studies (e.g., small, shrunken kidneys with cortical thinning

on renal ultrasound)Labs normocytic anemia secondary hyperparathyroidism with

hyperphosphatemia and hypocalcemi

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No set of tests, however, can rule out AKI superimposed on CKD since AKI is a frequent complication in patients with CKD

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Physical exam Blood pressure JVP Orthostatics Palpation of bladder for distention Exam for pulmonary and/or peripheral

edema Signs of uremia (N/V, fatigue, mental status

changes, asterixis, pericardial rub)

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History and Physical Examination

Careful history taking, and physical examination often narrow the differential diagnosis for the cause of AKI” think of prerenal in the following

Vomiting, diarrhea, glycosuria causing polyuria, and

Medications including diuretics, NSAIDs, ACE inhibitors, and ARBs

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PRE RENAL urinalysis is unremarkable

no proteinno bloodno abnormal castsno cellsspecific gravity is high

urine [Na] < 10 mEq/lkidney is normal…perfusion is not

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RENAL nephrotic range proteinuria, hematuria, RBC/WBC

casts..glomerulonephritis

low grade proteinuria, pyuria (eosinophiluria), WBC casts..

AIN

low grade proteinuria, hematuria, hemegranular and epithelial cell casts..

ATNif urine is bland, it is very unlikely that there is intrinsic renal damage

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POST RENAL urinalysis also unremarkable

physical exam: distended bladder

diagnosis usually made from imaging

ultrasound hydronephrosisdiuresis after foley insertion

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REDUCED GFR

normal normalabnormal*

PRE RENAL POST RENALRENAL

urinalysis

stones tumorsprostate

drugs

cardiacdehydratedvascularHTN

diabetesGN

ultrasoundrenal scan

serology+/- biopsy**clinical Dx

* proteinuria, hematuria, RBC casts** depends on GFR and urinalysis

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A good approach Make sure the patient is not dry or

hypotensive try giving some fluid

Put in a foley catheter … especially if male

Stop toxic drugs // adjust doses of drugs diclofenac, ibuprofen, indomethacin, gentamicin, (vancomycin)

Treat the underlying problem

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Approach to AKI

Investigations blood: CBC, electrolytes, Cr, urea (think

prerenal if increase in urea is relatively greater than increase in Cr), Ca2+ , PO·

urine volume, C&S, R&M: sediment, casts, crystals

urinary indices Foley catheterization (rule out bladder outlet

obstruction) fluid challenge (i.e. fluid bolus to rule out

most pre-renal causes)

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Approach to AKIImaging abdo U/S (assess kidney size,

hydronephrosis, post-renal obstruction)

indications for renal biopsy diagnosis is not certain prerenal azotemia or ATN is unlikely oliguria persists >4 wks

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MANAGEMENT

Disease Specific Therapies if pre-renal improve perfusion

if post renal relieve the obstruction

if renal treat the underlying GN or AIN and support the ATN

usually, prompt attention will quickly resolve renal dysfunction

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MANAGEMENTNon-Specific (Supportive) Therapies

drug management

fluid balance

electrolyte homeostasis

acid base balance

management of uremia

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FLUID BALANCE most patients with AKI lose ability to regulate volume

status

unable to dilute or concentrate urine excrete fixed amount of urine daily excrete fixed amount of sodium daily

must regulate intake or overload will occur

pulmonary edema

similarly, if pt gets dehydrated after GFR starts to improve, kidney function may not recover

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ELECTROLYTES problems can occur with:

potassium sodium calcium phosphorus magnesium

major clinical problem is hyperkalemia

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Complications Uremia Hypervolemia/ hypovolemia Hyponatremia Hyperkalemia Acidosis Hyperphosphatemia/hypocalcemia Bleeding Infectiosn/cardiac complications

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OUTCOME AND PROGNOSIS

AKI high morbidity and mortality in patients with

sustained AKI and multi-organ failure is associated with a significantly increased

risk of in-hospital and long-term mortality longer length of stay increased costs Prerenal azotemia, with the exception of the

cardiorenal and hepatorenal syndromes, and postrenal azotemia carry a better prognosis than most cases of intrinsic AKI

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THANKS

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