(AKI)

Mandy
Function of Kidney
➢ The kidney participates in whole-body homeostasis, regulating
acid-base balance, electrolyte concentrations, extracellular fluid
volume, and blood pressure.

➢ The kidneys excrete a variety of waste products produced by

metabolism into the urine including creatinine, and the nitrogenous
wastes urea (from protein catabolism), and uric acid (from nucleic
acid metabolism).
Definition of AKI
➢ An abrupt decrease in kidney function, resulting in the retention
of urea and other nitrogenous waste products and in the
dysregulation of extracellular volume and electrolytes.
Cause of AKI
Urine Output Definition
Oliguria < 500 mls/day
< 17-21 mls/hr
< 0.24-0.3 mls/kg/hr
< 0.5 mls/kg/hr
Anuria < 100 mls/day

Polyuria > 2.3-2 L/day

 Complication of AKI
➢ Metabolic: HyperK, hypoNa, hypoCa, hyperPO4, hyperMg,
hyperuricemia, metabolic acidosis.
➢ Cardiovascular: Pulmonary oedema, arrhythmia, pericarditis,
pericardial effusion, PE, HTN, MI.
➢ GI: Nausea, vomiting, malnutrition, hemorrhage.
➢ Neurologic: Irritability, tremor, seizures, AMS
➢ Haematology: anemia, bleeding
➢ Infections: pneumonia, septicemia, UTI
➢ Others: Elevated PTH, low T3 & T4
 AKI- Indication for Dialysis
Acidosis – metabolic acidosis with a pH <7.1

Electrolytes – refractory hyperkalemia with a serum

potassium >6.5 mEq/L or rapidly rising potassium levels

Intoxications – use the mnemonic SLIME to remember

the drugs and toxins that can be removed with dialysis:
Salicylates, Lithium, Isopropanol, Methanol, Ethylene
Glycol

Overload – volume overload refractory to diuresis

Uremia – elevated BUN with signs or symptoms of uremia,

including pericarditis, neuropathy, uremic bleeding, or an
otherwise unexplained decline in mental status (uremic
encephalopathy)
Case study 1
S: A 50 year old alcoholic male presents with urosepsis. He is treated with IV
antibiotics.

B: IHD, previous pneumonia, hypercholesterolaemia and hypertension.

Medications include: furosemide, enalapril, aspirin, clopidogrel, co-amoxiclav
(current) and simvastatin.

A: Clinically he is mildly dry, with a BP 135/83, HR 90, U/O 35 ml/hr.

Lab result: Sodium 132, Potassium 5.0, Urea 24 (from 8), Creatinine 390
(from 60).

What is your management option?

Case study 1
➢ stop furosemide, stop enalapril, adequate fluids to maintain urine output, daily
bloods.

This patient has risk factors for AKI (hypertension and dehydration) and is on various
renotoxic medications including aspirin, enalapril (ACE-I) and furosemide (loop diuretic).

The key is to maintain hydration to keep urine output reasonable (>0.5ml/kg/hr) while
stopping as many renotoxic medications as possible.

Fluids should be given and furosemide and enalapril stopped. He has a history of IHD so
stopping aspirin is not ideal. Daily bloods to monitor response is advised.
 Case study 2
S: A thin, frail 64-year-old female presenting for acute abdominal pain, nausea, and vomiting x 2 days.
CT scan with IV contrast show no acute bleeding, but a possible small bowel obstruction.

B: Nil PMH

A: Parameters: HR 96, RR 22, BP 147/80, SpO2 93%, Pain 3/10. The patient voids 200mL of dark,

concentrated urine 12 hours after admission. Doctor orders a IV Normal Saline (0.9%) 500 mL bolus

over 1 hour and a renal function panel. After 6 hours, she still has had no further urine output. A

bladder scan shows approximately 60 mL of urine in the bladder. Assessment now reveals crackles in

her lungs and her SpO2 is 89%.

Renal panel: Cr 350, Na 132, Ca 2.6, Phos 0.85, K 5.5, Mg 0.8, GFR 47 mL/min/m2
Case study 2
➢ IV Furosemide
➢ O2 therapy
➢ adequate fluids hydration
➢ Trend renal panel
➢ Monitor and treat primary issues
Thank You