Acute Kidney Injury &

Chronic Kidney Disease

Amir Syahmi
Derrick Ezra Ng
 AKI Definition (KDIGO)
•Increase in serum creatinine by ≥0.3mg/dl
(≥26.5umol/l) within 48 hours;
or
•Increase in serum creatinine to ≥1.5 times
baseline, which is known or presumed to have
occurred within 7 days;
or
•Urine volume < 0.5ml/kg/h for 6 hours
Classification : RIFLE and AKIN

2007
 AKI: Clinical Presentation
• Symptomatic
• Oedema
• Anuric /oliguric
• Seizure
• Hypertension
• Nausea
• Vomiting
• Ascites
• Encephalopathy
• `red urine’
• `Asymptomatic ‘
Classification AKI: Anatomical Location of Injury
 Pre-Renal Cause
● • 1. pre-renal- hypovolaemia,
● • 2. Intrinsic
● • 3. post-renal
 AKI: Intrinsic Causes
● • 1. pre-renal- hypovolaemia,
● • 2. Intrinsic
● • •3.ATN
post-renal

•AIN

•GN
 AKI- ATN
• Ischaemic
• Renal hypoperfusion (volume depletion, reduced CO)
• Nephrotoxic
– Endogenous Toxins
• Heme pigments (myoglobin, hemoglobin)
• Myeloma light chains
– Exogenous Toxins
• Antibiotics (e.g., aminoglycosides, amphotericin B)
• Radiocontrast agents
• Heavy metals (e.g., cisplatin, mercury)
• Poisons (e.g., ethylene glycol)
 AKI- AIN
• Allergic interstitial nephritis
• Drugs (penicillin, cephalosporin), NSAIDs
• Infections
• Bacterial (Legionella, Leptospirosis)
• Viral
• Sarcoidosis
 Post Renal
Causes
• 1. pre-renal- hypovolaemia,
• 2. Intrinsic
• 3. post-renal
•Anatomical – posterior
urethral valve
•Drugs – uric acid , acyclovir
 Laboratory Findings
• Rising creatinine and urea
• Rising potassium
• FBP- anaemia, MAHA
• Acidosis
• Hyperphosphatemia
• Hyponatraemia
• Hypocalcaemia
Clinical Tests
● Kidney function studies: Increased levels of blood urea nitrogen (BUN) and creatinine are the hallmarks of
renal failure; the ratio of BUN to creatinine can exceed 20:1 in conditions that favor the enhanced
reabsorption of urea, such as volume contraction (this suggests prerenal AKI)
● Complete blood count (can indicate infection; acute blood loss or chronic anemia; thrombotic
microangiopathy)
● Peripheral smear (eg, schistocytes such as hemolytic-uremic syndrome and thrombotic thrombocytopenic
purpura)
● Serologic tests: These may show evidence of conditions associated with AKI, such as in lupus nephritis,
ANCA vasculitis or anti-GBM disease or syndrome
● Complement testing: Pattern may indicate AKI related to endocarditis or various glomerulonephrities
● Fractional excretion of sodium and urea in the setting of oliguria
● Ultrasonography: Renal ultrasonography is useful for evaluating existing renal disease and obstruction of
the urinary collecting system
● Aortorenal angiography : Can be helpful in establishing the diagnosis of renal vascular diseases, such as
renal artery stenosis, renal atheroembolic disease, atherosclerosis with aortorenal occlusion, and certain
cases of necrotizing vasculitis (eg, polyarteritis nodosa)
● Renal biopsy: Can be useful in identifying intrarenal causes of AKI and directing targeted therapy
 NO The clinical evaluation of AKI includes a
AKI? Continue to monitor if high risk careful history and physical examination.

YES Drug history should include over-the-counter

formulations and herbal remedies or
recreational drugs.
History and
examinatio The social history should include exposure to
n tropical diseases (e.g., malaria), waterways or
sewage systems, and exposure to rodents
Clinical test (e.g., leptospirosis, hantavirus).
Fluid Depletion
AKI staging Physical examination should include
YES Cardiac evaluation of fluid status, signs for acute and
Insufficiency chronic heart failure, infection, and sepsis.
Reduced Renal
Perfusion? Central venous pressure are not nearly as
Renovasoconstricti
useful as dynamic variables, such as pulse-
on
pressure variation, inferior vena cava filling by
ultrasound and echocardiographic appearance
of the heart
 YES Ureteric obstruction
Ultrasound (Stone, tumor, fibrosis)
Obstruction
KUB
suspected?
Bladder neck obstruction
(BPH, Ca prostate,
neurogenic bladder, ca
bladder, stone)

Urethral obstruction
(Stricture, tumor)

Measurement of cardiac output, preload, preload responsiveness, and intra-

abdominal pressure should be considered

in the appropriate clinical context. Laboratory parameters— including SCr, blood

urea nitrogen (BUN), and electrolytes, complete blood count and differential—
should be obtained. Urine analysis and microscopic examination as well as
urinary chemistries may be helpful in determining the underlying cause of AKI.
Imaging tests, especially ultrasound, are important components of the evaluation
for patients with AKI. Finally, a number of biomarkers of functional change and
cellular damage are under evaluation for early diagnosis, risk assessment for,
and prognosis of AKI
 YES Acute Interstitial Nephritis
Specific
diagnosis
Glomerulonephritis

Thrombotic
microangiopathy

Renal Microangiopathy
Nephrotoxic drugs account for
some part of AKI in 20–30% of
patients. Often, agents like
YES antimicrobials (e.g.,
Nonspecific Ischemic
AKI aminoglycosides,
Toxic amphotericin) and
radiocontrast are used in
Infllammation (ie: Sepsis) patients that are already at
high risk for AKI (e.g., critically
ill patients with sepsis).
General management
Ultimate management of AKI
Renal replacement therapy (In case of Severe acidosis, Electrolyte imbalance,
Intoxication ,Overload, Uremia)

- Hemodialysis
- Sustained low efficiency dialysis (SLED)
- Continuous Renal Replacement Therapy (CRRT)
Discontinue RRT when it is no longer required, either because intrinsic kidney
function has recovered to the point that it is adequate to meet patient needs, or
because RRT is no longer consistent with the goals of care

In patients with AKI requiring RRT, the contact of blood with the foreign surface of
the extracorporeal circuit results in activation of both the intrinsic and the extrinsic
pathway of plasmatic coagulation and activation of platelets.

Prevention of dialyzer/hemofilter clotting often requires some form of

anticoagulation, which may represent a particular challenge in patients with AKI.
Proceed without anticoagulation if there is risk of bleeding.
Prescribe anticoagulation during RRT in AKI if a patient does not have an
increased bleeding risk or impaired coagulation and is not already receiving
systemic anticoagulation

For patients without an increased bleeding risk or impaired coagulation and not
already receiving effective systemic anticoagulation, we suggest the following:

a.For anticoagulation in intermittent RRT, we recommend using either

unfractionated or low-molecular-weight heparin, rather than other anticoagulants.

B. For anticoagulation in CRRT, we suggest using regional citrate anticoagulation

rather than heparin in patients who do not have contraindications for citrate.

C. For anticoagulation during CRRT in patients who have contraindications for

citrate, we suggest using either unfractionated or low-molecular-weight heparin,
rather than other anticoagulants.
Chronic Kidney Disease
Introduction
• Chronic kidney disease (CKD), previously termed chronic renal failure,
refers to an irreversible deterioration in renal function which usually
develops over a period of years

• Initially, it is manifest only as a biochemical abnormality but, eventually,

loss of the excretory, metabolic and endocrine functions of the kidney
leads to the clinical symptoms and signs of renal failure, collectively
referred to as uraemia
CKD is defined as:

eGFR <60 ml/min/1.73 m2 that is present >3 months with or without

evidence of kidney damage*
OR
evidence of kidney damage* that is present >3 months with or without
eGFR <60 ml/min/1.73 m2

*Markers of kidney damage are:

a. albuminuria (AER ≥30 mg/24 hours or ACR ≥3 mg/mmol)
b. urine sediment abnormalities
c. electrolyte and other abnormalities due to tubular disorders
d. abnormalities detected by histology
e. structural abnormalities detected by imaging
f. history of kidney transplantation
Spectrum of kidney injuries

AKI
CKD
Risk Factors
Clinical features
● The typical presentation is with a raised urea and creatinine found
during routine blood tests, frequently accompanied by hypertension,
proteinuria or anaemia.

● Most patients with slowly progressive disease are asymptomatic until

GFR falls below 30 mL/min/1.73 m2 (stage 4 or 5) and some can
remain asymptomatic with much lower GFR values than this.

● Early symptom is nocturia, due to the loss of concentrating ability and

increased osmotic load per nephron, but this is nonspecific.
Inx in CKD
Assessment and classification
● Renal function should be assessed using estimated glomerular filtration rate
(eGFR) based on the 2009 CKD-epidemiology (CKDEPI) creatinine equation.
● Serum creatinine should not be used alone in the assessment of renal
function.
● Kidney Disease Improving Global Outcomes (KDIGO) staging should be used
to classify chronic kidney disease.
● When GFR falls below 15–20 mL/min/1.73 m2, symptoms and signs
are common and can affect almost all body including tiredness or
breathlessness, which may, in part, be related to renal anaemia,
pruritus, anorexia, weight loss, nausea and vomiting.

● With further deterioration in renal function, patients may suffer hiccups,

experience unusually deep respiration related to metabolic acidosis
(Kussmaul’s respiration), and develop muscular twitching, fits,
drowsiness and coma.
Causes of anemia in CKD
Referral
Aims of management in CKD
● 1.to prevent or slow further renal damage.
● 2.to limit the adverse physiological effects of renal impairment on the
skeleton and on haematopoiesis.
● 3.to treat risk factors for cardiovascular disease.
● 4. to prepare for RRT.
Antihypertensive therapy
● Lowering BP slows the rate of renal fx decline in CKD.

● Lowering the risk of hypertensive heart failure, stroke and peripheral

vascular disease+ reduce the proteinuria.
● TARGETED BP:
● 130/80 mmHg for uncomplicated CKD.
● 125/75 mmHg for CKD + proteinuria.

● May need multiple anti HTN mx to achieve the target BP.

Reduction of proteinuria (ACEI/ARB)
● reducing proteinuria  reduces the risk of progression of CKD.
● ACEI and ARBs 
1.reduce proteinuria and retard the progression of CKD.
2. reduce the risk of CVS events and all-cause mortality in CKD.
● S/E: May A/W immediate reduction in GFR when Rx is initiated, due to a
reduction in glomerular perfusion pressure
NOTE: Rx can be continued as long as the reduction in GFR is < 20% and is
not progressive.
● ACEI or ARBs should be prescribed to all patients with diabetic
nephropathy and/or proteinuria, irrespective of whether or not
hypertension is present, providing that hyperkalaemia does not occur
Dietary and lifestyle interventions
● All patients with stage 4 and 5 CKD should be given dietetic advice aimed at:
● 1. preventing excessive consumption of protein,
● 2. ensuring adequate calorific intake.
● 3. limiting K and ph intake.
● 4. stop smoking
● 5. Exercise and Wt loss.
Lipid-lowering therapy
● Hypercholesterolaemia is almost universal in patients with significant
proteinuria.
● Lipid lowering  reduce vascular events in non-dialysis CKD patients
● It may slow the rate of progression of renal disease.
Treatment of anaemia
● Recombinant human erythropoietin is effective in correcting the
anaemia of CKD and improving the associated morbidity.
● S/E: hypertension and thrombosis (including thrombosis of AVF).
● Target Hb is 10–12 g/dL.
● Erythropoietin is less effective in the presence of iron deficiency, active
inflammation or malignancy, and in patients with aluminium overload.
● Iron/Vit B12.
Maintaining fluid and electrolyte balance
● Deacrease dietary Na intake (100 mmol/day).
● loop diuretics (early when pt still have good urine output).

● hyperK:
1.drug therapy should be reviewed.
2. limiting K intake to about 70 mmol/day.
3. Use of Potassium-binding resins.e.g: calcium resonium (short term).

● Acidosis: plasma bicarbonate should be maintained above 22 mmol/L by

giving sodium bicarbonate supplements.
Renal bone disease
● active Vit D metabolites (either 1-α-hydroxyvitamin D or 1,25-
dihydroxyvitamin D) in pt with hypocalcaemia or serum PTH levels more than
twice the upper limit of normal.
● Aim: PTH levels 2 - 4 times ULN to avoid over-suppression of bone turnover
and adynamic bone disease.
● Hyperphosphataemia (1.dietary restriction.2. phosphate-binding drugs e.g
caco3, aluminium hydroxide,lanthanum carbonate and polymer-based
phosphate binders such as sevelamer.
● Aim: serum phosphate < 1.8 mmol/L