Acute on Chronic Kidney Disease

Authored by , Reviewed by Prof Cathy Jackson | Last edited | Meets Patient’s editorial guidelines

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This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Acute Kidney Injury article more useful, or one of our other health articles.

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Any sudden decline in renal function in patients with known chronic kidney disease (CKD) requires rapid assessment, diagnosis and appropriate management to prevent an accelerated and possibly irreversible decline in renal function. CKD predisposes to episodes of acute kidney injury (AKI) and optimal care of CKD is essential to reduce the risk of AKI[1].

The patient may be known to have CKD or may be presenting for the first time, having been previously not known to have CKD. There is also an association between AKI with incomplete recovery or lack of recovery and CKD[2].

Management is directed towards identification and treatment of the underlying cause of the acute deterioration of renal function, and treatment for AKI. In addition to the morbidity and mortality associated with AKI, there is increasing evidence that AKI accelerates the progression of CKD[3].

The most common causes are:

  • Systemic infection - eg, urinary tract infection (UTI), chest infection, central line.
  • Drugs - eg, diuretics, angiotensin-converting enzyme (ACE) inhibitors, aminoglycosides.
  • Dehydration.
  • Urinary tract obstruction or urinary retention - eg, due to spinal cord compression or neurogenic bladder, or renal vein thrombosis (particularly in patients with nephrotic syndrome).

Other likely causes include:

  • Renal hypoperfusion secondary to dehydration from diarrhoea, diuretics, surgery or cardiac failure, pericardial tamponade, aortic dissection or renal vascular disease.
  • Metabolic and toxic causes - eg, diabetic ketoacidosis, hyperosmolar coma.
  • Hypercalcaemia.
  • Hyperuricaemia.
  • Progression of underlying diseases - eg, relapse of glomerulonephritis.
  • Development of accelerated-phase hypertension.
  • Pregnancy: at the end of the pregnancy or after delivery (eg, in patients with reflux nephropathy), pre-eclampsia, eclampsia.

Possible underlying causes of urinary retention and/or infection include:

  • Papillary necrosis and sloughing.
  • Stones.
  • Pelvic malignancy.
  • Bladder cancer.
  • Polycystic cysts.
  • Clot in the ureter.
  • Contrast media (especially in diabetes).

The patient may present with the cause of the exacerbation (eg, local infection), features of chronic failure or may present with AKI.

Clinical assessment should include:

  • Identifying possible causes of acute exacerbation - eg, drug history, signs of infection or evidence of prostatic hypertrophy.
  • Identifying any degree of urinary tract obstruction.
  • Assessment of pre-existing renal function and whether an episode represents acute on chronic kidney disease or acute kidney injury in a patient with previously normal renal function (see separate Chronic Kidney Disease and Acute Kidney Injury articles).
  • Assessment of blood pressure and general cardiovascular status.


  • Serial assessment of renal function: estimated GFR (eGFR), serum urea, creatinine and electrolytes.
  • Urine: urinalysis, microscopy, electrolytes and protein excretion.
  • FBC.
  • Infection swabs and cultures as appropriate.
  • ECG: evidence of hyperkalaemia, myocardial infarction.
  • Ultrasound scan of the urinary tract and lower abdomen to identify urinary tract obstruction or urinary tract abnormalities.
  • Further investigations and management will depend on the well-being of the patient, likely cause of the exacerbation and current renal function.
  • A full assessment, as described in the separate Acute Kidney Injury article, may be required[4, 5].
  • Renal biopsy may also be required.

Other causes of raised urea and creatinine:

  • Raised urea can also be caused by intravascular volume depletion, diuretics, congestive heart failure, gastrointestinal bleeding, corticosteroids and tetracyclines.
  • Creatinine levels can be increased by muscle damage (rhabdomyolysis) and decreased tubular secretion - eg, cimetidine, trimethoprim.
  • Ingestion of cooked meat and severe exercise cause a rapid but temporary rise in serum creatinine.
  • Management involves treatment of the underlying cause and management of acute injury.
  • Depending on the nature and certainty of the cause, clinical well-being and underlying renal function, patients often require referral to hospital for full assessment and appropriate management.
  • However, some patients with an obvious cause and who are clinically stable, may be safely managed at home.
  • Regular monitoring and early effective treatment of any potential cause of acute deterioration of renal function.
  • Many commonly used drugs and procedures can potentially cause AKI, and patients with decreased GFR have an increased risk of drug-induced injury. Non-steroidal anti-inflammatory drugs, phosphorus-based enemas and iodinated contrast should particularly be avoided if possible[6].

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Further reading and references

  1. Fraser SD, Blakeman T; Chronic kidney disease: identification and management in primary care. Pragmat Obs Res. 2016 Aug 177:21-32. eCollection 2016.

  2. Heung M, Chawla LS; Acute kidney injury: gateway to chronic kidney disease. Nephron Clin Pract. 2014127(1-4):30-4. doi: 10.1159/000363675. Epub 2014 Sep 24.

  3. Hsu RK, Hsu CY; The Role of Acute Kidney Injury in Chronic Kidney Disease. Semin Nephrol. 2016 Jul36(4):283-92. doi: 10.1016/j.semnephrol.2016.05.005.

  4. Acute Kidney Injury; Renal Association (2011)

  5. Lameire N, Van Biesen W, Vanholder R; Acute kidney injury. Lancet. 2008 Nov 29372(9653):1863-5.

  6. Levey AS, Coresh J; Chronic kidney disease. Lancet. 2012 Jan 14379(9811):165-80. Epub 2011 Aug 15.