Acute Renal Failure: Definition, Incidence, Diagnosis, Management, Treatment

Acute Renal Failure

Acute renal failure (ARF) is a common and serious problem in clinical medicine. It is characterized by an abrupt reduction (usually within a 48-h period) in kidney function. This results in an accumulation of nitrogenous waste products and other toxins. Many patients become oliguria (low urine output) with subsequent salt and water retention. In patients with pre-existing renal impairment, a rapid decline in renal function is termed ‘acute on chronic renal failure’. The nomenclature of ARF is evolving and the term acute kidney injury (AKI) is being increasingly used in clinical practice.

Acute Renal Failure

Acute Renal Failure


Classification and Causes of Acute Renal Failure

AKI is not a single disease state with a uniform etiology, but a consequence of a range of different diseases and conditions. The most useful practical classification comprises three main groupings: (i) prerenal, (ii) renal, or (iii) postrenal. More than one category may be present in an individual patient.

Prerenal Acute Kidney Injury

This is caused by impaired perfusion of the kidneys with blood, and is usually a consequence of decreased intravascular volumes (hypovolemia) and/or decreased intravascular pressures.

  • Hypovolemia: This results from any condition that causes intravascular fluid depletion, either directly by hemorrhage or indirectly to compensate for the extravascular loss.
  • Hypotension: In addition to hypovolemia, hypotension can result from pump (cardiac) failure, of which there are a number of causes, the most common of which is ischaemic heart disease.
  • Intra-renal acute kidney injury: This is caused by a variety of causes most commonly (in >80% of cases) acute tubular necrosis (ATN).
  • Acute tubular necrosis: ATN is a diagnosis made by renal biopsy; the findings can include damage to the proximal tubule and the ascending limb of the loop of Henle, interstitial edema, and sparse infiltrating inflammatory cells. Common causes of acute tubular necrosis: Immune and inflammatory renal disease, Rapidly progressive glomerulonephritis, Interstitial nephritis,

Signs and Symptoms of Acute Renal Failure

The signs and symptoms of AKI are often nonspecific and the diagnosis can be confounded by coexisting clinical conditions. The patient may exhibit signs and symptoms of volume depletion or overload, depend upon the precipitating conditions, a course of the disease and prior treatment.

History

  • Thirst
  • Weight increase
  • Excessive fluid loss (vomiting or diarrhea)Orthopnoea/nocturnal
  • Dyspnoea
  • Oliguria

Physical Examination

  • Dry mucosal
  • Decrease Skin elasticity
  • Ankle swelling
  • Oedema
  • Tachycardia
  • Jugular venous distension
  • Decrease Blood pressure
  • Pulmonary crackles
  • Decrease Jugular venous pressure
  • Pleural effusion

Diagnosis and Clinical Evaluation of Acute Renal Failure

In hospitalized patients, AKI is usually diagnosed incidentally by the detection of increasing serum creatinine and/or a reduction in urine output.

Monitoring Fluid Balance in Acute Kidney Disease

Maintaining appropriate fluid balance in AKI is a critical component of the clinical management of the patient.

Intravascular monitoring Central Venous Pressure (CVP)

can be measured following insertion of a central venous catheter, and is a measure of the pressure in the large systemic veins and the right atrium produced by venous return.

Monitoring key Parameters in Acute Kidney Disease

Serum electrolytes including potassium, bicarbonate, calcium, phosphate and acid–base balance should be measured on a daily basis.

Management

  • The aim of the medical management of a patient with AKI is to prolong life in order to allow recovery of kidney function.
  • Effective management of AKI depends upon a rapid diagnosis. If the underlying acute deterioration in renal function is detected early enough, it is often possible to prevent progression.
  • If the condition is advanced, however, management consists mainly of supportive strategies, with close monitoring and appropriate correction of metabolic, fluid and electrolyte disturbances.
  • Patients with severe AKI usually require renal replacement therapy with dialysis. Specific therapies that promote recovery of ischaemic renal damage remain under investigation.
  • Patients with immune-mediated causes of AKI should be treated with appropriate immunosuppressant regimens to treat the underlying cause of the AKI.
  • Non-dialysis treatment of established acute kidney injury
  • Uraemia and intravascular volume overload In renal failure, the symptoms of uremia include nausea, vomiting and anorexia, and result principally from the accumulation of toxic products of protein metabolism including urea.

Hyperkalemia:

Dietary potassium should be restricted to less than 40 mmol/ day and potassium supplements and potassium-sparing diuretics removed from the treatment schedule.

Acidosis:

It may be treated orally with sodium bicarbonate 1–6g/day in divided doses, or 50–100 mmol of bicarbonate ions (preferably as isotonic sodium bicarbonate 1.4% or 1.26%, 250–500mL over 15–60 min) intravenously may be used.

Renal Replacement Therapy

It is indicated in a patient with AKI when kidney function is so poor that life is at risk. However, it is desirable to introduce renal replacement therapy early in AKI, as complications and mortality are reduced if the serum urea level is kept below 35 mmol/L.

Forms of Renal Replacement Therapy

The common types of renal replacement therapy used in clinical practice are:

  • hemodialysis
  • haemofiltration
  • hemodiafiltration
  • peritoneal dialysis

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