Acute Kidney Injury

 Acute kidney injury (AKI), formerly termed Acute Renal

failure, refers to an abrupt decrease in glomerular filtration
rate and tubular function.

 Hallmark; progressive rise in plasma creatinine and Blood

urea Nitrogen (BUN) due to accumulation of nitrogenous
waste products of metabolism
Classification
 Oliguric
- 1 mL/kg/h in neonates and infants
- <0.5 mL/kg/h in children
 Non-Oliguric
- urine output is normal or even polyuria
- electrolyte disturbances and uremia may become
significant.
Etiology
 May also be used to classify AKI
 Pre-renal, Intrinsic renal and post renal
Pre renal causes Intrinsic renal causes Post – renal causes
(Cytotoxic, Ischemic or
inflammatory insult)

•Dehydration •Acute tubular necrosis •Urethral obstruction

•Hemorrhage ( G.I and •Nephrotoxins (medications,
others) contrast, myoglobin)
•Septic shock •Infection (sepsis)
•Burns •Interstitial nephritis
•Heart failure •Glomerular injury (primary
glomerulonephritis, vasculitis, outlet
•Cirrhosis hemolytic uremic syndrome)
•Vascular (renal vein
thrombosis, arterial emboli,
malignant hypertension)
(stricture, posterior
urethral valves)
•Ureteral obstruction
•Ureterocele
•Extrinsic tumor
compressing bladder
•Neurogenic bladder
(myelomeningocele,
spinal cord injury)
Clinical Evaluation
Diagnosis
 Urinalysis
 Renal ultrasound scan
 Electrolyte studies
- Hyperkalemia
- Metabolic acidosis
- Hypocalcaemia
- Hyperphosphatemia
 MANAGEMENT OF AKD
GENERAL MEASURES
 Asses volume status; reduced urine, absent jvp, reduced BP,
raised pulse. Signs of fluid over load
 Aim for euvolemia , -avoid any potassium containing fluids
 Hypervolemia - 1 to 2 mg/kg of furosemide
 Stop nephrotoxic drugs (NSAIDs, ACEI, gentamicin,
amphotericin, metformin if creatinine is >150mmol/L)
 Monitoring; HDU, vitals, daily U&E, fluid balance and daily
weight charting
 Nutrition advise and monitoring
TREAT UNDERLYING CAUSE
 Pre renal ; correct fluids ,Rx sepsis ,consider ICU if signs of
shock
 Intrinsic renal; for over tubule-interstitial or glomerular or
systemic disease, multi-organ damage ,pulmonary-renal,
hepato-renal syndrome refer to nephrologist
 Post renal ; catheterise & consider CT of renal tract and
urology referral if obstruction, for obstruction and
hydronephrosis on CT/USS consider cystoscopy and
retrograde stents or nephrostomy insertion
 Manage complications
Hyperkalaemia, Pulmonary oedema, uraemia, acidemia
Renal replacement therapy
 Hyponatraemia correction <120mmol/L
 Hyperkalaemia correction
- 10% calcium gluconate 0.5–1 ml/kg by slow IV infusion
over 5–10 minutes to reduce the toxic effect of high
potassium on the heart
 Hypocalcaemia
- 10% calcium gluconate 0.5 ml/kg/hr
 Severe acidosis correction
- Alkali administration
 Correction of anemia and uremic platelet dysfunction
with transfusions
 Chronic Kidney Disease
 CKD is defined by the presence of kidney damage e.g. any
structural or functional abnormality involving pathological,
laboratory or imaging findings for >3 months based on
abnormal structure, function, or GFR <60mL/min/1.73m2
for >3 months.
 CKD is defined as abnormalities of kidney structure or
function, present for > 3 months, with implications for
health (KDIGO 2017).
 Etiology
< 5years old >5years old All Age groups
 Congenital anomalies  Acquired Metabolic disorders
- Renal hypoplasia - Glomerulonephritis - Cystinosis
- congenital Nephrotic - HIV
syndrome  Inherited  Inherited
- Polycystic kidney - Nephronophthisis - Polycystic kidney
disease - Alport’s syndrome disease
- cortical necrosis - Multisystem
autoimmune disorders
 Obstructive uropathy e.g. SLE
- PUV
- PUJ Others include
- Obstruction - Wilm’s tumor
- Renal vascular disease
 HUS
- EHEC 157:O7
- Shigella
Pathophysiology
 Hyper-filtration injury leads to glomerular destruction
 Remaining nephrons undergo structural/functional changes
to increase glomerular flow.
 Raised hydro static pressure damages capillary wall
 There is added toxic effect of proteins
 In proteinuria, traversing proteins through capillary walls
increase and exert direct toxic effect on tubular cells, recruit
monocytes and macrophages causing glomerular sclerosis
and interstitial fibrosis
 Hyperphosphatemia leads to disease progression by causing
excessive deposition on renal interstium and blood vessels
 Hypertension causes progressive vasoconstrictions
Progression of CKD

• The rate of progression to ESRD is influenced by the

underlying diagnosis and the baseline Creatinine
Clearance rate at presentation.
• Other factors include:- hypertension, proteinuria,
obesity, dyslipidemia, anemia, intra-renal
precipitation of calcium, phosphate and metabolic
acidosis.
• Genetic, familial, or ethnic predisposition may also
influence the rate of renal decline as seen by the
faster rate of progression among African-
Americans.
Stages of CKD

 Stage 1: Kidney damage with normal or Increased GFR (>90

mL/min /1.73 m2)

 Stage 2: Mild reduction in the GFR (60 - 89mL/min / 1.73 m2)

 Stage 3: Moderate reduction in the GFR (30 - 59 mL/min /1.73

m2 )

 Stage 4: Severe reduction in the GFR (15 - 29 mL/min / 1.73

m2 )

 Stage 5: Kidney failure (GFR <15 mL/min / 1.73 m2 or dialysis)

Clinical Presentation
 General symptoms
Nocturia, tiredness, pruritus, anorexia, weight loss, nausea and
vomiting, hiccups, deep respiration, Purpura, excoriations,
uremic tinge to skin, high BP, signs of fluid overload, and if
untreated progress to, muscular twitching, fits, drowsiness and
coma.
 Systemic symptoms
• Immune dysfunction - Cellular and humoral immunity is
impaired- infections due to protein loss.
• Hematological - Increased bleeding tendency (cutaneous
ecchymosis ) resulting from platelet dysfunction due to
uremia.
• Anemia - decreased erythropoietin, reduced red cell lifespan
(uremia)
• Muscle weakness ,bradycardia
• Neurological and muscle - Generalized due to poor
nutrition, hyperthyroidism, vitamin deficiency and
disorders of electrolyte metabolism, –muscle cramps,
restless leg syndrome, paresthesia and foot drop.

• CVS – HTN, cardiomegaly, left ventricular hypertrophy,

raised JVP, medial vascular calcification (high serum
phosphate)

• Metabolic bone disease –osteoporosis.

Physical Examination
 Serial measurements of growth parameters (height, weight,
and head circumference for patients under 3 years of age).
 BP measurement
 Pallor
 Signs of vasculitis
 Evidence of renal osteodystrophy: the site and type of
deformity of the extremities depends upon the age of the child
and the weight-bearing patterns in the limbs.
 Assessment for the presence and severity of peripheral edema.
 Assessment for any sign of hypervolemia by noting the
presence of edema, rales, hepatic enlargement and/or
tenderness and cardiac gallop.
 Cardiac auscultation to detect a pericardial rub due to
pericarditis or diminished heart sounds secondary to a
pericardial effusion.
 Glomerular diseases are more likely to present with
nephritic and/or Nephrotic syndrome (with edema,
hypertension, discolored urine and or oliguria)

 Polyuria kidneys have reduced ability to concentrate urine

e.g. dysplastic kidneys, nephronophthisis, and
tubulointerstitial.
Complications of CKD
 Anemia
 Renal osteodystrophy
 Hypertension
 Gastrointestinal (increased risk of PUD, constipation , elevation of
serum amylase due to defective platelet function)
 Metabolic (lipid metabolism abnormalities due to decreased
lipoprotein lipase activity )
 Nervous System (convulsions, coma, cardiac arrest, vomiting,
muscle cramps and pruritus are due to uremia)
 Hyperkalemia and metabolic acidosis due to reduced net acid
excretion by failing kidneys
 Growth retardation
 Neurological and muscle Disorders
 Metabolic bone disease
Diagnosis
 Serum Creatinine and GFR
 Urinalysis
 Nuclear scans
 Micturating cystourethrogram
 CBC
 Serum Electrolytes
Note: Ionic and non-ionic contrast agents nephrotoxic and can
cause acute renal dysfunction. Therefore, contrast agents
should be used with caution in patients with CKD
Management of CKD
 For anaemia, give erythropoietin 50-100mg /kg 3times
subcutaneously.
 For HTN, due to overload give thiazide diuretics. Also ACEIs and
ARBS if proteinuria
 Hyperkalaemia - dietary restriction, calcium gluconate, insulin,
sodium carbonate and kayexalate.
 Hyperphostaemia- phosphate binders, low phosphorus diets, non
calcium binders such as sevelamer
 Vitamin D therapy to improve level of activated vitamin
 Proteinuria and haematuria - antibiotics, steroids, furosemide and
antihypertensive for glomerulonephritis
 Renal transplant for ESRD
 Dialysis for end for end stage renal failure