notes-aki

1. ACUTE KIDNEY INJURY (AKI)
INTRODUCTION
Chris is a diabetic patientbut is not undergoing treatment. He doesnot buy his
maintenance medicationsbecause he believes that those could justaggravate his
condition. As monthspassed by, he began noticing changesin his urine output. He
began having decreased urine outputfor a week then was surprised to have an
outputgreater than normalin the following week. He is unusually lethargic and
has dry skin. His laboratory resultsshow an increase in creatinine and potassium.
His doctor diagnosed him with acute renalfailure secondary to diabetesmellitus.
DEFINITION
AKI is a sudden and usually reversible decreasein the glomerular filtration rate
(GFR) occurring over a period of hours to days.
(OR)
‘AKI is diagnosed by an absolute increase in SCr, at least 0.3 mg/dL (26.5 μmol/L)
within 48 hours or by a 50% increasein SCr frombaseline within 7 days, or a urine
volume of less than 0.5 mL/kg/h for at least 6 hours-KDIGO(Kidney Disease:
Improving GlobalOutcomes)
The term “Acute Kidney Injury” now replaces theterm ARF; the term Acute Renal
Failure should now be restricted to patients who have AKI and “need renal
replacement therapy”.

2. EPIDEMIOLOGY
1. Itoccurs in – 5%of all hospitalized patients and – 35% of those in intensive
care units
2. Mortality is high:
3. up to 75–90% in patients with sepsis
4. 35–45% in those without Median hospital length of stay (LOS) stratified by
single acute organ systemdysfunction (AOSD), including acuterenal failure
(ARF
CAUSES OF ACUTE KIDNEY INJURY AKI
There are numerous potential causes of AKI, mainly related to a focal mismatch
between oxygen and nutrient delivery (because of impaired microcirculation) to
the nephrons and increased energy demands (dueto cellular stress). For many
years the diagnosis and management of AKI was based on the concept of
classification to three main categories: pre-renal, intrinsic and post-renal
In Pre-renal AKI, renalhypoperfusion leads to a decreased GFR (withoutdamage
to the renal parenchyma), as an adaptive response to various extra-renal
insults. Itis known that maintaining a normalGFR is dependent on adequate renal
perfusion. The kidneys receive up to 25% of cardiac output and thus any failure of
the systematic circulating blood volumeor isolated failure of the intra-renal
circulation can have a profound impact on renal perfusion.
Prerenal Hypovolaemia Haemorrhage
Volume depletion

3. Renal fluid loss (over-diuresis)
Third space(burns,
peritonitis, muscle trauma)
Impaired cardiac
function
Congestiveheart failure
Acute myocardialinfarction
Massivepulmonary embolism
Systemic
vasodilatation
Anti-hypertensive
medications
Gramnegative bacteraemia
Cirrhosis
Anaphylaxis
Increased vascular
resistance
Anaesthesia
Surgery
Hepatorenal syndrome
NSAID medications
Drugs that causerenal
vasoconstriction (i.e.
cyclosporine)
Intrinsic renal aetiologies of AKI can be challenging to evaluate becauseof the
wide variety of injuries that can occur to the kidney. Generally, four structures of
the kidney are involved including tubules, glomeruli, the interstitium, and intra-
renal blood vessels.
Acute tubular necrosis (ATN) is the term used to designate AKI resulting from
damage to the tubules. It is the mostcommon type of intrinsic kidney injury. AKI
fromglomerular damage occurs in severe cases of acute glomerulonephritis (GN).

4. AKI fromvascular damageoccurs becauseinjury to intra-renalvessels decreases
renal perfusion and diminishes GFR and finally acute interstitial nephritis occurs
due to an allergic reaction to a variety medications or an infection
Tubular Renal ischaemia
(shock, complicationsof surgery, haemorrhage,
trauma, bacteraemia, pancreatitis, pregnancy)
Nephrotoxic drugs
(antibiotics, antineoplastic drugs, contrast
media, organic solvents, anaesthetic drugs,
heavy metals)
Endogenous toxins
(myoglobin, haemoglobin, uric acid)
Glomerular Acute post-infectious glomerulonephritis
Lupus nephritis
IgA glomerulonephritis
Infectiveendocarditis
Goodpasturesyndrome
Wegener disease
Interstitium Infections
(bacterial, viral)
Medications
(antibiotics, diuretics, NSAIDs, and many more
drugs)

5. Vascular Large vessels
(bilateralrenalartery stenosis, bilateralrenal
vein thrombosis)
Small vessels
(vasculitis, malignanthypertension,
atherosclerotic or thrombotic emboli, haemolytic
uraemic syndrome, thrombotic
thrombocytopenic purpura)
Post-renal AKI occurs after acute obstruction of the urinary flow, which increases
intra-tubular pressureand thus decreases GFR.63
In addition, acute urinary tract
obstruction can lead to impaired renal blood flow and inflammatory processes
that also contribute to diminished GFR.64
Post-renalAKI can develop if the
obstruction is located at any level within the urinary collection system(fromthe
renal tubule to urethra). In casethe obstruction is above the bladder it must
involve both kidneys (or one kidney in the case of a patient with a single
functioning kidney) to producesignificant renal failure.65
However, a patient with
pre-existing renal insufficiency may develop AKI with obstruction of only one
kidney. Urinary obstruction may present as anuria or intermittent urine flow (such
as polyuria alternating with oliguria) but may also presentas nocturia or
nonoliguric AKI. Timely reversion of pre-renal or post-renalcauses usually results
in prompt recovery of function, but late correction can lead to kidney damage
Postrenal Extrarenal
obstruction
Prostatehypertrophy
Improperly placed catheter
Bladder, prostateor cervical
cancer
Retroperitoneal fibrosis
Intrarenal Nephrolithiasis

6. obstruction Blood clots
Papillary necrosis
RISK FACTORS
Acute kidney failure almostalways occurs in connection with another medical
condition or event. Conditions that can increase the risk of acute kidney failure
include:
 Being hospitalized, especially for a serious condition that requires intensive
care
 Advanced age
 Blockages in the blood vessels in your arms or legs (peripheralartery
disease)
 Diabetes
 High blood pressure
 Heart failure
 Kidney diseases
 Liver diseases
 Certain cancers and their treatments
PATHOPHYSIOLOGY
The pathophysiology of AKI is multifactorial and complex. The most common
causeof AKI is ischaemia, which can occur for a number of reasons.
Physiologicaladaptations, in responseto the reduction in blood flow can
compensate to a certain degree, but when delivery of oxygen and metabolic
substrates becomes inadequate, the resulting cellular injury leads to organ
dysfunction. Thekidney is highly susceptible to injury related to ischaemia,
resulting in vasoconstriction, endothelialinjury, and activation inflammatory

7. processes. This susceptibility can be explained in part fromstructural
associations between renal tubules and blood vessels in the outer medulla of
the kidney, with ischaemia compromising blood flow to critical nephron
structures presenttherein. Following the reduction in effective kidney
perfusion, the epithelial cells are unable to maintain adequate intracellular ATP
for essential processes. This ATP-depletion leads to cell injury and if it is severe
enough can lead to cell death by necrosis or apoptosis. During an ischaemic
insult all segments of the nephrons can be affected but proximal tubular cells
are the mostcommonly injured. In addition, the nephron’s naturalfunction is to
filter, concentrate and reabsorb many substances fromtubular lumen, and the
concentration of these substances may reach toxic levels for the surrounding
epithelial cells
PHASES OF AKI
1. INITIATING PHASE:- Begins attime of insult until S&S seen (hours to days)
2. OLIGURICor ANURICPHASE:- Oliguria caused by GFRdecrease  Begins 1-7
days after insult depending on cause  Usually lasts usually 10-14 days (may
last up to 8 weeks)  Longer the phase, poorer prognosis of renalrecovery 
Manifestations are changes in UOP, fluid & electrolyte balances, & uremia 
 in serumlevels of urea, creatinine, uric acid, K+ & Mg
3. DIURETICPHASE: -Gradualincreaseof UOP can reach 1-2 (or more) L per
day. Nephrons are still not fully functional -Caused by osmotic diuresis and
inability of tubules to concentrate. -Recovered ability to excrete wastes, but
not concentrate. -Monitor for hypokalemia, hyponatremia & dehydration -
Hypovolemia and hypotension can occur Lasts 1-3 weeks -Acid-base,
electrolyte and wasteproductlevels begin to normalize.
4. RECOVERY PHASE:-Begins when GFR increases allowing BUN and creatinine
to reach a plateau and decreaseMay still have glycosuria and decreased
ability to concentrate urine Major improvements first1-2 weeks but may
take 12 months to stabilize.

8. CLINICAL MANIFESTATIONS
The clinical picture is often dominated by the underlying cause. The various
symptoms of acute kidney injury resultfromthe various disturbances of kidney
function that are associated with the disease.
 Decreased urine output, although occasionally urine output remains normal
 Fluid retention, causing swelling in your legs, ankles or feet
 Shortness of breath
 Confusion
 Weakness
 Chest pain or pressure
 Seizures or coma in severe cases
Accumulation of urea and other nitrogen-containing substances in the
bloodstreamlead to a number of symptoms, such as;
fatigue, loss of appetite, headache, nausea and vomiting.
Marked increases in the potassium level can lead to;
abnormal heart rhythms
DIAGNOSTIC EVALUATION
Assessmentand diagnosis of a patient with ARF include evaluation for changes in
the urine, diagnostic tests that evaluate the kidney contour, and a variety of
normal laboratory values.

9. Urine
 Volume: Usually less than 100 mL/24 hr (anuric phase) or 400 mL/24 hr
(oliguric phase), which occurs within 24–48 hr after renal insult.
Nonoliguric (morethan 400 mL/24 hr) renal failure also occurs when
renal damage is associated with nephrotoxic agents (e.g., contrastmedia
or antibiotics).
 Color: Dirty, brown sedimentindicates presence of RBCs, hemoglobin,
myoglobin, porphyrins.
 Specific gravity: Less than 1.020 reflects kidney disease,
e.g., glomerulonephritis, pyelonephritis with loss of ability to
concentrate; fixed at 1.010 reflects severerenal damage.
 pH: Greater than 7 found in urinary tract infections (UTIs), renaltubular
necrosis, and chronic renal failure (CRF).
 Osmolality: Less than 350 mOsm/kg is indicative of tubular damage, and
urine/serumratio is often 1:1.
 Creatinine (Cr) clearance: Renalfunction may be significantly decreased
before blood urea nitrogen (BUN) and serumCr show significant
elevation.
 Sodium: Usually increased if ATN is causefor ARF, more than 40 mEq/L
if kidney is not able to resorb sodium, although it may be decreased in
other causes of prerenal failure.
 Fractional sodium(FeNa):Ratio of sodiumexcreted to total sodium
filtered by the kidneys reveals inability of tubules to reabsorb sodium.
Readings of less than 1% indicate prerenalproblems, higher than 1%
reflects intrarenal disorders.
 Bicarbonate: Elevated if metabolic acidosis is present.

10.  Redblood cells (RBCs): May bepresent becauseof infection, stones,
trauma, tumor, or altered glomerular filtration (GF).
 Protein: High-gradeproteinuria (3–4+) strongly indicates glomerular
damage when RBCs and casts are also present. Low-gradeproteinuria
(1–2+) and white blood cells (WBCs) may be indicative of infection or
interstitial nephritis. In ATN, proteinuria is usually minimal.
 Casts: Usually signal renal diseaseor infection. Cellular casts with
brownish pigments and numerous renal tubular epithelial cells are
diagnostic of ATN. Red casts suggestacute glomerular nephritis.
Blood
 BUN/Cr: Elevated and usually rise in proportion with ratio of 10:1 or
higher.
 Complete blood count (CBC): Hemoglobin (Hb) decreased in presence
of anemia. RBCs often decreased because of increased
fragility/decreased survival.
 Arterial bloodgases (ABGs):Metabolic acidosis (pH less than 7.2) may
develop because of decreased renal ability to excrete hydrogen and end
products of metabolism. Bicarbonate decreased.
 Sodium: Usually increased, but may vary.
 Potassium: Elevated related to retention and cellular shifts (acidosis) or
tissuerelease (red cell hemolysis).
 Chloride, phosphorus, andmagnesium: Usually elevated.
 Calcium: Decreased.
 Serumosmolality: More than 285 mOsm/kg; often equal to urine.
 Protein: Decreased serumlevel may reflect protein loss via urine, fluid
shifts, decreased intake, or decreased synthesis becauseof lack of
essential amino acids.

11.  Radionuclide imaging: May reveal calicectasis, hydronephrosis,
narrowing, and delayed filling or emptying as a cause of ARF.
 Kidney, ureter, bladder (KUB) x-ray: Demonstrates sizeof
kidneys/ureters/bladder, presenceof cysts, tumors, ad kidney
displacement or obstruction (stones).
 Retrograde pyelogram: Outlines abnormalities of renal pelvis and
ureters.
 Renal arteriogram: Assesses renalcirculation and identifies
extravascularities, masses.
 Voiding cystoureterogram: Showsbladder size, refluxinto ureters,
retention.
 Renal ultrasound: Determines kidney size and presenceof masses, cysts,
obstruction in upper urinary tract.
 Nonnuclear computed tomography (CT) scan: Cross-sectionalview of
kidney and urinary tract detects presence/extent of disease.
 Magnetic resonanceimaging (MRI): Provides information about soft
tissuedamage.
 Excretory urography (intravenous urogramor pyelogram): Radiopaque
contrastconcentrates in urine and facilitates visualization of KUB.
 Endourology: Directvisualization may be done of urethra, bladder,
ureters, and kidney to diagnose problems, biopsy, and removesmall
lesions and/or calculi.
 Electrocardiogram (ECG): May be abnormal, reflecting electrolyte and
acid-baseimbalances.
Urine tests

12.  Urinalysis: Analysis of the urine affords enormous insightinto the
function of the kidneys.
 Twenty–four–hour urine tests: This test requires you to collect all of
your urine for 24 consecutive hours. Theurine may be analyzed for
protein and wasteproducts (urea nitrogen and creatinine). The presence
of protein in the urine indicates kidney damage. The amount of
creatinine and urea excreted in the urine can be used to calculate the
level of kidney function and the glomerular filtration rate (GFR).
 Glomerular filtrationrate (GFR): TheGFRis a standard means of
expressing overall kidney function. As kidney diseaseprogresses, GFR
falls. The normalGFR is about 100–140 mL/min in men and 85–115
mL/min in women. Itdecreases in most people with age. The GFRmay
be calculated fromthe amount of waste products in the 24–hour urine
or by using special markers administered intravenously. Patients are
divided into five stages of chronic kidney diseasebased on their GFR.
 Urine Specific Gravity: This is a measureof how concentrated a urine
sample is. A concentrated urine sample would have a specific gravity
over 1.030 or 1.040
Blood tests
 Creatinine andurea(BUN) in the blood: Blood urea nitrogen and serum
creatinine are the most commonly used blood tests to screen for, and
monitor renal disease.
o Creatinine is a breakdown productof normalmuscle
breakdown.
o Urea is the waste productof breakdown of protein.
o The level of these substances rises in the blood as kidney
function worsens.

13.  Electrolyte levels andacid–base balance: Kidney dysfunction causes
imbalances in electrolytes, especially potassium, phosphorus, and
calcium.
o High potassium(hyperkalemia) is a particular concern.
o The acid–base balance of the blood is usually disrupted as well.
 Decreasedproductionof the active formof vitaminD can cause low
levels of calcium in the blood. Inability to excrete phosphorus by failing
kidneys causes its levels in the blood to rise.
 Bloodcell counts: Because kidney disease disrupts blood cell production
and shortens the survivalof red cells, the red blood cell count and
hemoglobin may be low (anemia). Some patients may also have iron
deficiency due to blood loss in their gastrointestinalsystem. Other
nutritional deficiencies may also impair the production of red cells.
Other tests
 Ultrasound: Ultrasound is often used in the diagnosis of kidney disease.
An ultrasound is a noninvasivetype of test.
o In general, kidneys areshrunkenin size in chronic kidney
disease, although they may be normalor even large in size in
cases caused by adult polycystic kidney disease, diabetic
nephropathy, and amyloidosis.
 Biopsy: A sample of the kidney tissue (biopsy) is sometimes required in
cases in which the cause of the kidney disease is unclear. Usually, a
biopsy can be collected with local anesthesia only by introducing a
needle through the skin into the kidney.
MANAGEMENT

14. Currently, there is no definitive therapy for AKI, supportivecareis the mainstay
of management regardless of etiology.
Goal of treatment:
 Minimize the degree of kidney insult
 Reduce extrarenal complication
 Restoration of renal function to pre AKI is the ultimate goal
1. Maintain fluid and electrolyte balance:
 Fluid replacement mustbe done carefully to avoid fluid overload.
 Fluid replacement volumes are usually calculated on the basis of some
fraction of the previous day’s urineoutput plus an amount(commonly
400ml)to accountfor the usual insensiblelosses that can occur during a 24-
hr period.
 Urgent treatment of hyperkalaemia should be started if the serum
potassiumis >6.5 mmol/l, or if any ECG changes are present.
 If P waveor QRS changes are present. A bolus of 10–20 ml of 10% calcium
gluconate or chloride is given intravenously over two to five minutes.[High
serumcalcium concentrations potentiate the cardiac toxicity of digoxin—
calcium should be given as a slow infusion in hyperkalaemic patients taking
this drug (that is, 10 ml 10% calcium gluconate in 100 ml 5% dextroseover
30 minutes)]
Insulin with glucose
 Ten units of fastacting solubleinsulin should be added to 50 ml of 50%
dextrose and infused over 10–20 minutes.

15. Sodium bicarbonate
 The infusion of sodiumbicarbonate has little immediate effect on
hyperkalaemia.
Ion exchange resins
 Calcium resonium(calciumpolystyrenesulphonate) and Resonium A
(sodiumpolystyrenesulphate) are the most commonly used.
 These bind potassiumin the gastrointestinaltract, in exchange for calcium
or sodium, and result in increased potassiumexcretion in the stool.
 Given at an oral dose of 15 g up to thrice daily, together with an osmotic
laxative (for example, lactulose 10 ml) to prevent constipation. They can
also be given rectally.
The use of low dose(1–3 μg/kg/min) dopamine has been advocated to increase
renal perfusion in critically ill patients.
Atrial natriuretic peptide (ANP), an endogenous hormonesynthesized by the
cardiac atria, has been shown to improverenal function in multiple animal models
of ARF.
NUTRITIONAL THERAPY
ARF causes severenutritional imbalances (becausenausea and vomiting
contribute to inadequate dietary intake), impaired glucose useand protein
synthesis, and increased tissuecatabolism. The patient is weighed daily and can
be expected to lose 0.2 to 0.5 kg (0.5 to 1 lb) daily if the nitrogen balance is
negative (ie, the patient’s caloric intake falls below caloric requirements). If the
patient gains or does not lose weight or develops hypertension, fluid retention
should be suspected.

16.  Protein intake should be around 1.2–1.4 g/kg–20–25% of daily calories
should be provided by lipids.
 Glucoseis usually administered in a 70% solution.
 The estimated energy requirements for patients withAKI usually fall
between 30 and 40 kcal/kg normalbody weight/day.
 Water-solublevitamins should be supplemented.
RENAL REPLACEMENT THERAPY
In the absence of effective pharmacologicaltherapy, the treatment of patients
with AKI is predominantly supportive, managing haemodynamic and volume
status, correcting electrolyte and acid–base disturbances, providing adequate
nutrition and adjusting drug doses. In patients with sustained, severerenal
failure, RRT is indicated for the management of volumeoverload, hyperkalaemia,
acidosis and symptoms of uraemia while awaiting the recovery of kidney function.
Proposed Indicationsfor RRT
• Oliguria < 200ml/12 hours
• Anuria < 50 ml/12 hours
• Hyperkalaemia > 6.5 mmol/L
• Severeacidaemia pH < 7.0
• Uraemia > 30 mmol/L
• Uraemic complications (pericarditis, nausea, vomiting, poor appetite,
hemorrhage, lethargy, malaise, somnolence, stupor, coma, delirium, asterixis,
tremor, seizures)

17. • Dysnatraemias >155 or < 120 mmol/L
• Hyper/(hypo)thermia
• Drug overdosewith dialysabledrug
• Refractory hypertension
CHOICEOF RRT MODALITY
RRT can be intermittent or continuous. Continuous dialysis can be blood based or
use the peritoneal route.
Intermittent therapy is delivered as intermittent haemodialysis (IHD).
continuous renal replacement therapy (CRRT) in a number of ways, classified
according to the method of accessing the circulation and how solute removal is
achieved. Techniques based on venous access alone are mostfrequently used—
continuous venovenous haemofiltration (CVVH) and continuous venovenous
haemodiafiltration (CVVHD)—thelatter including solute removal by diffusion
(haemodialysis) in addition to fluid and solute removalby convection
(haemofiltration).

18. ADVANTAGE& DISADVANTAGEOF IRRT&CRRT
Nursing Management
The nursehas an important role in caring for the patient with ARF:
 The nursemonitors the patient’s serumelectrolyte levels and physical
indicators of these complications during all phases of the disorder.
 Parenteral fluids, all oral intake, and all medications are screened carefully
to ensure that hidden sources of potassiumare not inadvertently
administered or consumed.

19.  Intravenous solutions mustbecarefully selected according to the patient’s
fluid and electrolyte status.
 The patient’s cardiac function and musculoskeletalstatus are monitored
closely for signs of hyperkalemia.
 Assess urineoutput. Urine output varies from scanty to a normal
volume.
 Assess blood in the urine. Hematuria may be presentin patients with
ARF.
 Assess laboratory results. Laboratory results may increase, decrease, or
stabilize and these may indicate each phaseof ARF.
PREVENTION.
1. Provideadequate hydration to patients at risk for dehydration: Surgical
patients before, during, and after surgery Patients undergoing intensive
diagnostic studies requiring fluid restriction and contrastagents (eg, barium
enema, intravenous pyelograms), especially elderly patients who may not have
adequate renal reservePatients with neoplastic disorders or disorders of
metabolism (ie, gout) and thosereceiving chemotherapy
2. Prevent and treat shock promptly with blood and fluid replacement.
3. Monitor central venous and arterial pressures and hourly urineoutput of
critically ill patients to detect the onsetof renal failure as early as possible.
4. Treat hypotension promptly.
5. Continually assess renalfunction (urineoutput, laboratory values) when
appropriate.

20. 6. Take precautions to ensurethat the appropriateblood is administered to the
correctpatient in order to avoid severetransfusion reactions, which can
precipitate renal failure.
7. Prevent and treat infections promptly. Infections can produceprogressiverenal
damage.
8. Pay special attention to wounds, burns, and other precursors of sepsis.
9. Give meticulous care to patients with indwelling catheters to prevent infections
fromascending in the urinary tract. Remove catheters as soon as possible.
10. To prevent toxic drug effects, closely monitor dosage, duration of use, and
blood levels of all medications metabolized or excreted by the kidneys.
NURSING DIAGNOSES
 Excess fluid volume related to Compromised regulatory mechanism
(renal failure)as evidenced by Intakegreater than output, oliguria;
changes in urine specific gravity, Venous distension; blood pressure
(BP)/central venous pressure(CVP) changes, Generalized tissueedema,
weight gain, Changes in mental status, restlessness,Decreased
Hb/hematocrit (Hct), altered electrolytes; pulmonary congestion on x-
ray
 Risk for decreased cardiac output related to Fluid overload (kidney
dysfunction/failure, overzealous fluid replacement), Fluid shifts, fluid

21. deficit (excessivelosses), Electrolyteimbalance (potassium, calcium);
severeacidosis, Uremic effects on cardiac muscle/oxygenation
 Imbalanced nutrition; less than body requirements related to anorexia,
nausea, vomiting, dietary restrictions, and altered oral mucous
membranes.
 Activity intolerance related to fatigue, anemia, retention of waste
products, and dialysis procedure.
 Deficient knowledge regarding condition and treatment.
 Disturbed self-esteem related to dependency, role changes, changein
body image, and change in sexual function.