Enfermedad renal aguda sobre crónica

What is acute on chronic kidney disease?¹

Patients with enfermedad renal crónica, especially in more advanced stages (eGFR less than 30 mL/min per 1·73 m²) often do not exhibit linear progression of disease, which might be related to superimposed episodes of lesión renal aguda or other factors. Some studies suggest that each acute kidney injury event might accelerate progression of chronic kidney disease.

Therefore, preventing acute kidney injury is an important part of the management of chronic kidney disease. This prevention involves avoiding acute kidney injury-associated drug combinations (eg, ACE inhibitors or angiotensin receptor blockers in conjunction with loop diuretics and non-steroidal anti-inflammatory drugs) and preventing infections that can precipitate hypotension or septic shock and requiring the use of potentially nephrotoxic antimicrobials.

Other potential contributors to acute kidney injury include cardiovascular events, particularly decompensated heart failure leading to venous congestion and impaired kidney blood flow, or coronary artery bypass and other major surgeries with possible intraoperative hypotensive episodes.

Therefore, 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.²

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.³

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.⁴

Causas comunes

• Systemic infection - eg, urinary tract infection (UTI), chest infection, central line.

• Drugs - eg, diuretics, angiotensin-converting enzyme (ACE) inhibitors, aminoglycosides.

• Deshidratación.

• 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

• 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, cetoacidosis diabética, hyperosmolar coma.

• Hipercalcemia.

• Hyperuricaemia.

• Progression of underlying diseases - eg, relapse of glomerulonefritis.

• 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.

• Malignidad pélvica.

• 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 the separate Enfermedad renal crónica y Acute Kidney Injury articles).

• Assessment of blood pressure and general cardiovascular status.

Investigaciones

• 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.⁶

• 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.⁷