Acute kidney injury

Acute kidney injury is characterized by a rapid decrease in renal functioning with an increased accumulation of waste products such as urea and creatinine in the blood. There is a decreased glomerular filtration rate.

Azotaemia: high levels of nitrogenous compounds (urea and creatinine) in the blood due to insufficient filtering  in the kidneys

Uraemia: urine in the blood- is a syndrome which develops from continual kidney function decline and affects the functioning of multiple body systems.

AKI usually develops over hours to days and causes elevated urea, creatinine and potassium and oliguria (less than 400ml urine output per day)

AKI can be divided into 3 categories: prerenal, intrarenal, and postrenal


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Prerenal causes

  • Hypovolaemia: haemorrhage, dehydration, GI losses, burns
  • Decreased cardiac output: arrhythmia, heart failure, MI, cardiogenic shock
  • Decreased vascular resistance: anaphylaxis, neuro injury, septic shock
  • Decreased renovascular blood flow: embolism, renal artery thrombosis

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Intrarenal causes

  • Prolonged prerenal ischaemia
  • Nephrotoxic injury: drugs, crush injury, chemical exposure, radio-contrast agents
  • Interstitial nephritis: allergies, infections
  • Malignant hypertension
  • Systemic lupus erythematosus
  • Acute tubular necrosis

Acute tubular necrosis is caused by prolonged ischaemia or nephrotoxins. It is the cause for 90% of intrarenal injury. Necrotic tubular epithelial cells slough off and block the tubules. The basement membrane becomes disrupted and causes holes in which the filtrate leaks back into plasma, further decreasing intratubular flow.


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Postrenal causes

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Manifestations of AKI


  • decreased output
  • proteinurua
  • casts
  • increased sodium


  • Volume overload
  • Heart failure
  • Hypertension (oliguric phase)
  • Hypotension  (diuretic phase)
  • Arrhythmias
  • pericarditis


  • Kassmaul breathing
  • Pleural effusions
  • Pulmonary oedema


  • Nausea and vomiting
  • Anorexia
  • Bleeding
  • Diarrhoea/constipation


  • Anaemia
  • Increased risk of infection
  • Abnormal platelet functioning


  • Increased urea
  • Increased potassium
  • Increased creatinine
  • Decreased sodium
  • Increased hydrogen (acidosis)
  • Decreased bicarb
  • Decreased calcium


  • Lethargy
  • Seizures
  • Asterixis
  • Memory impairment

Phases of AKI

There are three main phases: oliguric, diuretic, and recovery

Oliguric phase

Only 50% of patients with AKI will display signs of oliguria. It usually occurs within 7 days of the initial injury. The phase generally last for 10-14 days. Poor outcomes are associated with longer length oliguric phases.

Prerenal oliguria vs oliguria of  intrarenal AKI

It is important to distinguish the two as prerenal oliguria is caused from low circulating volume with no kidney tissue damage whereas oliguria of intrarenal AKI  is a result from damaged tubules which are unable to maintain regulatory functions. RBC and WBC are present in the urine from the necrotic tubular epithelial cells.

Urinary changes

Urine output will decrease to below 400ml per day. Proteinuria resulting from glomerular membrane dysfunction may occur.

Fluid volume excess

With the activation of the renin-angiotensin-aldosterone system and decreased urinary output, fluid retention can occur. If the cause of AKI is not due to a decrease in total circulating volume, fluid overload can result in hypertension and oedema. This can ultimately lead to CHF, pulmonary oedema, or pleural effusion (excess fluid in the pleural space).

Metabolic acidosis

Hydrogen ions build up as the ammonia required for hydrogen excretion  can not be synthesized in the kidneys. Sodium bicarb gets used to buffer the increased acidity, decreasing available bicarb. Kassmaul breathing will occur in an attempt to remove CO2 and regulate pH.

Sodium depletion

Hyponatraemia occurs as sodium can not be reabsorbed in damaged tubules. Despite this, excessive intake of sodium should be avoided.

Potassium excess

Normally, the kidneys excrete up to 90% of potassium but limited renal function results in an accumulation of K. K can further increase if tissues are damaged as cells release it into the extracellular compartment. Acidosis compounds hyperkalaemia as potassium leaves the cells as hydrogen ions enter them. Levels above 6mmol/L required urgent treatment. ECG changes should be monitored for peak T waves as this is an indication of increasing T waves.

Haemotological disorders

impaired erythropoietin (hormone produced by the kidney is needed for the development of RBC in bone marrow) can cause anaemia (decreased RBC). Platelet function is altered due to uraemia and can lead to excessive bleeding.


Damaged kidneys are unable to activate vitamin D which is essential in the absorption of calcium from the GI tract. In response to decreased calcium levels, the thyroid releases PTH to cause bone demineralization.

Waste product accumulation 

Urea and creatinine levels increase as the kidneys are ineffective in excreting the waste products. Normal urea levels are 3.0-8.0 mmol/L and creatinine 0.05-0.12 mmol/L.

Diuretic Phase

This phase may last up to three weeks. An increase of urine production of up to 5L per day can occur in this phase. The increased urine output is due to the high content of urea and creatinine in the filtrate, causing fluid from plasma to shift into the filtrate in an attempt to reach equilibrium. This is known as osmotic diuresis. During this phase, the kidneys are able to excrete waste but are not functioning enough to be able to concentrate the urine.  Uraemia may still be present during the diuretic phase.

Recovery phase

An increased GFR signals the recovery phase. Urea and creatinine levels decrease. It may take up to 12 months for full function to return to the kidneys. Depending on the overall health of the patient, complications associated with AKI will very. Older adults and those with co-morbidities can develop chronic kidney failure as a result of acute kidney injury.

This video discusses the important aspects of AKI:

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Nursing considerations

  • Fluid replacement therapy
  • Daily weight of patient
  • Monitor for hypervolaemia in oliguric phase and hypovolaemia in diuretic phase
  • Monitor potassium levels and ECG
  • Monitor GSC as waste product accumulation can affect mental status
  • Restrict potassium and sodium
  • Calcium supplements
  • Adequate protein intake
  • monitor closely for signs of infection as this is a common cause of death with AKI
  • Encourage respiratory exercises

Nursing care plans for patients with AKI can be found here:




Bellomo, R., Kellum, J. A., & Ronco, C. (2012). Acute kidney injury. The Lancet, 380(9843), 756–766. doi: 10.1016/S0140-6736(11)61454-2

Hryciw, D. (2015). The structure and function of the urinary system. In J. Craft & C. Gordon (Eds.), Understanding pathophysiology (2nd ed., pp. 820–842). Sydney, Australia: Mosby Elsevier.

Hryciw, D., & Bonner, A. (2015). Alterations of renal and urinary tract function across the life span. In J. Craft & C. Gordon (Eds.), Understanding pathophysiology (2nd ed., pp. 871–908). Sydney, Australia: Mosby Elsevier.

Kellum, J. A. (2008). Acute kidney injury. Critical Care Medicine, 36, S141–S145. doi: 10.1097/CCM.0b013e318168c4a4

Mathers, T., & Bonner, A. (2008). Nursing management: Acute renal failure and chronic kidney disease. In D. Brown & H. Edwards (Eds.), Lewis’s medical-surgical nursing: Assessment and management of clinical problems (2nd ed., pp. 1286–1327). Sydney, Australia: Mosby Elsevier.