Acute k idney in jury (AKI)

De f in i t ion

A rapid deterioration of parenchymal renal functions sufficiently severe to result in uremia. ◦ Usually but not invariably reversible. ◦ Oliguria is usually, but not invariably a feature.

Recently the term AKI has replaced the term ARF . De f in i t ion o f AK I based on “Acute k idney in jury network”

S tage Increase in serum creat in ine Ur ine output

1 1.5-2 times baseline OR 0.3 mg/dl increase from baseline <0.5 ml/kg/h for >6 h 2 2-3 times baseline <0.5 ml/kg/h for >12 h

3 o 3 times baseline OR o 0.5 mg/dl increase if baseline>4mg/dl OR o Any RRT given

o <0.3 ml/kg/h for >24 h OR o Anuria for >12 h

R IFLE cr i ter ia

o The RIFLE criteria consists of 3 graded levels of injury (Risky, Injury, Failure)

o Based upon either the magnitude of elevation in serum creatinine or urine output

o Two outcome measures à loss and ESRD   o The RIFLE strata are as follows

KDIGO (2012)

AKI is de f ined as any o f the fo l low ing : � Increase in SCr by X0.3 mg/dl within 48 hours; or � Increase in SCr to X1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or � Urine volume <0.5 ml/kg/h for 6 hours.  

Causes o f AK I

 

C lass i f i ca t ion o f AK I

In pre-rena l

1. Renal tissue is intact 2. Kidney biopsy shows normal renal histology. 3. Oliguria and high serum creatinine are due to functional impairment.

• Since there is no structural renal damage, early diagnosis and correction of renal hypoperfusion results in immediate diuresis and rapid drop in serum creatinine and blood urea levels.

• If hypoperfusion is severe or neglected, renal compensatory mechanisms will fail and acute tubular necrosis occurs

In post- rena l

◦ The obstruction of the urinary tract results in increasing the pressure above the level of the obstruction. ◦ When this back pressure exceeds that of the filtration pressure in the renal glomeruli, the process of urine formation will stop with progressive

accumulation of wastes and increase of serum creatinine and blood urea.

In t r ins ic Rena l

This includes: 1 . Acute tubu lar necros is (ATN) 85%

a . Tox ic b . I schaemic c . Combined

2 . Acute in ters t i t ia l nephr i t i s 10% 3. Acute g lomeru lonephr i t i s 5%

Acute tubu lar necros is (ATN)

Genera l l y

ATN can be induced by: a . Rena l hypoper fus ion ( ischemia) b . Exposure to nephrotox ins (exogenous or endogenous tox ins) c. A combinat ion o f both

Causes o f ischemic

ATN

1. Blood Loss a. Haemorrhage (post partum, surgical or GIT) b. Major trauma

2. F lu id Loss a. Gastrointestinal (vomiting or diarrhoea) b. Renal (aggressive diuresis or polyuria)

3. Th i rd Space

a. Haematoma b. Illius c. Peritonitis

4. Severe vasod i la ta t ion as in septicemia, rapid edema

formation, liver cell failure.

5. Renovascu lar d isease a. Renal artery occlusion by stenosis, embolism or

compression. b. Renal vein thrombosis or compression.

Causes o f tox ic ATN

Exogenous nephrotoxins include Endogenous nephrotoxins include 1 . Ant ib io t ics

a. Aminoglycosides , Amphotericin, Acyclovir b. Bacitracin c. Cephalosporin d. Tetracyclin e. Sulfonamide

2. Anaesthetic agents à methoxy fluorine 3. Contrast media

4. Analgesics à Phenacetin

5. Metals à mercury, lead, arsenic, bismuth, cadmium, antimony

6. Organic solvents à glycols

7. Poisons à snake bite, stings, bacterial toxins

P igments Crys ta ls • Myoglobin • Hemoglobin • Methemoglobin

• Uric acid • Calcium • Oxalate

Acute cor t ica l

necros is

� Is a subset of ATN in which there is a massive necrosis of the tubules and glomeruli of the renal cortex. � The condition may be focal or diffuse with irreversible damage of the kidneys. � It is suspected when ATN fails to recover after 4-6 weeks. � Acute cortical necrosis usually occurs with complicated pregnancy as postpartum hemorrhage and abruptio placenta

     

C l in ica l fea tures o f AK I

H is tory

Usua l ly , the pat ient g ives h is tory o f the e t io log ic cause such as :

Ø Trauma Ø Shock Ø Hemolysis Ø Drug intake Ø Infection Ø Stone disease Ø Procedure requiring contrast media Ø ICU admission

Careful history is essential • Exposure to nephrotoxin and drugs • Anuria may indicate post renal causes • Skin rashes may indicate allergic nephritis

• Evidence of volume depletion à diarrhea, bleeding

• Pelvic and per rectal examination à look for evidence of abortion • Ischemia or trauma to the legs or arms may indicate rhabdomyolysis • A history of prostatic disease, nephrolithiasis • Recent surgcial or radiologic procedures • Past and present use of medications • Family history of renal disease

CP

Changes

Pat ient may not ice a change in 1. Urine volume and character 2. Oliguria is common, but in 10-50% of cases urine volume will be normal or even higher (Non-oliguric). 3. Absolute anuria is highly suggestive of obstructive AKI (post-renal) or very severe form of ATN (cortical necrosis).

CP sa l t and

water re tent ion 1. Edema 2. Puffiness

3. Hypertension 4. Heart failure

CP o f uremia

By time, man i fes ta t ions o f uremia appear as 1 . ac idot ic breath ing , 2 . dyspnea, 3 . nausea, vomi t ing , 4 . headache, 5 . musc le tw i tches 6 . f rank encepha lopathy and coma.

Patient may present as well with complications

Compl ica t ions o f AK I

CVS • Pulmonary edema • Hypertension • Myocardial infarction

• Arrhythmias • Pericardial effusion • Pulmonary embolism

Metabo l ic

• Hyponatremia • Acidosis • Hyperphosphatemia

• Hyperkalemia • Hypocalcemia

Neuro log ic Coma , seizures G IT Gastritis, gastroduodenal ulcers

Hemato log ic Anemia, hemorrhagic diasthesis In fec t ions Pneumonia, UTI, septicemia

Invest igat ions o f AK I A- Ur inary

ind ices • May be helpful in the differentiation between pre-rena l fa i lu re and acute tubu lar necros is . • Diuretics should not be given during the preceding 48 hours for these parameters to be valid.

B- Ur inary sed iment

• Centrifugation of fresh urine sample and examination of the urinary sediment may be helpful in diagnosing different causes of AKI. • In pre-rena l fa i lu re and in ischaemic ATN ur inary sed iment is usua l ly f ree . • Ur ine sed iment in Acute Nephrot ic Syndrome and in RPGN is character is t i c .

C - Rena l Imag ing

P la in f i lm o f the abdomen This will show kidney parity, size, shape, calcification and stones.

Rena l U l t rasonography & Echo-Dopp ler o f rena l

vesse ls

◦ US safely assesses kidney size, shape and echogenicity. ◦ Cortical thinning or oedema can sometimes be seen clearly. ◦ Also, it can exc lude obstruc t ive uropathy (back pressure changes). ◦ Echo-Doppler of renal vessels can exclude occlusion of the renal arteries and veins.

Retrograde & antegrade pye lography

Provide the most reliable in format ion on the patency o f the ureter

Ang iography

Is useful mainly when an acute reversible renovascular event is suspected such as embolization, thrombosis or involvement in a dissecting aortic aneurysm. It carries the risk of exposure to contrast media which could be nephrotoxic.

C .T . s tud ies Provide reliable information on k idney par i ty , s ize , shape and presence o f hydronephros is .

Magnet ic Resonance urography

• Recently MRI urography (MRU) without use of contrast media can provide films similar to IVP. • *It is thus of great value to exc lude U .T . obstruc t ion without the risk of contrast media nephropathy. • *I t is impor tant to know that Gado l in ium an MRI contrast is nephrotox ic ,

D-Rena l b iopsy

Ind ica t ions 1. Urine: RC cast, WC cast, Proteinuria 2. Unexplained 3. Systemic disease 4. Prolonged course (more than 3 weeks).

 

 Treatment o f AK I

A- Treatment o f the cause

e.g. any condition causing renal hypoperfusion, exposure to toxic drug or chemical or systemic disease.

B- Conservat ive

measures

F lu id ba lance

• Careful monitoring of intake/output and body weight is very important to avoid overload and hypovolemia. The 1st may lead to pulmonary edema while the 2nd may aggravate renal ischemia.

• Pat ient shou ld rece ive f lu ids = da i ly ur ine output + other sens ib le losses e .g . vomi tus or d iar rhea + amount equa ls the insens ib le loss wh ich is around 600 c .c . for 60kg body we ight pat ient .

• Fluids could be given orally or (if not possible), it could be given intravenously.

E lec t ro ly tes and ac id-

base ba lance

1. Prevent and treat hyperkalemia. 2. Avoid hyponatremia. 3. Keep serum bicarbonate above 16 mmol/L. 4. Minimize hyperphosphatemia by giving phosphate binders (e.g. Ca Co3 & AL hydroxide) with meals. 5. Treat hypocalcaemia.

Treatment o f hyperka lemia

• Calcium gluconate I.V. • Glucose 50% + Insulin • Na Hco3 I.V.

• K-exchange resins (e.g. resonium) • Avoid diets and drugs causing hyperkalaemia • Dialysis

Nutr i t iona l support

� With rare exceptions, Na & K restriction is appropriate. � The place of dietary ptn restriction is controversial:

◦ Hope to avoid dialysis → 40gm/day ◦ Pt treated with HD → 70gm/day ◦ Hypercatabolic pt will need ↑ nitrogen intake

Drugs • Review all medications. • Stop magnesium-containing medications. • Adjust dosage for renal failure.

C -D ia lys is

The indications of dialysis in AKI are Based on C l in ica l observat ion Based on chemica l lab resu l ts

• Poor clinical state, nausea, confusion. • Fluid overload, pulmonary oedema. • Preoperatively

• Plasma K+ > 7 mmol/L. • Plasma bicarbonate < 12 mmol/L • Arterial pH < 7.15.

Prevent ion o f AK I

• The timing of intervention to prevent ATN is important. Protective agents must be administered at the time of, or immediately following potential renal insult. This intervention may prevent or at least blunt the severity of ATN.

• The intervention could be through the following approaches. In different combinations according to the clinical situation:

• Volume expansion by isotonic saline loading. • Diuretic as furosemide (to change ATN to polyuric-easy manageable

type) • Non dihydropyridine Calcium channel blockers as Verapamil . • Vasodilating agents as dopamine in renal dose 1-2 ug/kg/min. (are

not effective)

In case of contrast media, the following additional points should be adopted, these are

1. Avoid unnecessary contrast procedures. 2. Avoid multiple contrast exposure within a few days. 3. Avoid contrast exposure in high risk patient. 4. Use the smallest dose possible. 5. Use non-ionic , low viscosity contrast (good evidence). 6. Hydration by isotonic saline in a dose of 3ml/kg/h. for 12h

before and after contrast exposure (has the best evidence). 7. Acetyl cysteine sachets 600mg/kg tds , 2days before and

after exposure (good evidence). 8. Washing the contrast out immediately after the technique (e.g.

coronary angiography) by hemodialysis, is of no value.

Prognos is

• The mortality of AKI remains high, ranging between 50-80% in surgical and post-traumatic cases. • It is generally lower in AKI due to drugs and toxins. • About 75% of deaths occur in the first week of AKI, and 25-50% of these deaths are due to the underlying disease. • The overall prognosis is better in non-oliguric than in oliguric renal failure. • The factors influencing patient survival in AKI include the following:

o Etiology of AKI. o Severity of AKI. o Number and severity of coexisting illness. o Patient's age, Presence of complications