Acute Renal Injury and Failure

Acute renal injury, or acute renal failure, is the abrupt drop in GFR sufficient to lead to retention of creatinine, urea, and other wastes, and the perturbation of extracellular fluid volume, electrolyte, and acid-base homeostasis. It occurs over a period of hours to days.

 

Up to 60% of people with ARF presents in community. The 40% of patients who develop ARF in hospital (5-7% of all hospitalized patients and in up to 30% of people admitted to the ICU) are more likely to have acute tubular necrosis.

 

The RIFLE designation describes degrees of kidney dysfunction:

RIFLE is useful for correlating suggesting prognosis and risk for renal failure, but is problematic in that GFR determinations are valid in steady state only.

 

 

Causes and Risk Factors

Acute kidney injury can result from diseases or conditions above, in, or below the kidney. Prerenal azotemia is the most important cause in hospitalized patients, while acute tubular necrosis is the most common intrinsic renal disease leading to the condition. It is characterized by an abrupt and sustained decline in GFR following an ischemic or nephrotoxic event.

prerenal

  • decreased effective blood volume (hemorrhage, burns, GI losses, renal losses, fluid pooling)
  • dec ECV (CHF, cirrhosis, sepsis)
  • arterial occlusion
  • meds: NSAIDs, ACE, ARB

 

renal

Glomerular

Tubular


Interstitial

vascular

  • cholesterol emboli
  • vasculitis
  •  systemic disease, vasomotor (cyclosporine, NSAIDs, hypercalcmia)

postrenal

Specific agents which are known to lead to acute tubular necrosis include radiographic contrast agents, aminoglycosides, vancomycin, amphoteracin B, cyclosporine, statins, acyclovir, methotrexate, NSAIDs, COX-2 inhibitors, cisplatin, ethylene glycol, and ACE inhibitors.

 

 

 

Signs, Symptoms, and Diagnosis

Current diagnostic criteria for AKI include:

  • history
  • physical exam
  • labs
  • imaging

History

Chart review is important in people with acute kidney injury, with special attention to recent changes in GFR. Other important clues include infection, nephrotoxic drugs, contrast studies, and anaesthesia.

 

Prerenal features include thirst.

 

Obstructive symptoms can include

 

comorbid conditions, procedures

Past Medical History

  • Kidney stones
  • UTI/pyelonephritis

 

Physical Exam

Reduced body weight, postural changes in blood pressure and pulse, and decreased JVP all suggest reduced extracellular fluid volume.

 

Fever and rash suggest acute interstitial nephritis.

Abdominal examination may reveal distended bladder of lower urinary tract obstruction.

A Foley catheter should be done to rule out bladder or below obstruction.

Labs

 

Urinalyisis

 

should be carried out, along with thorough sediment examination. In prerenal failure, a number of hyaline and finely granular casts may be evident, while in acute tubular necrosis, dirty brown casts and renal tubular cells are present in a majority of patients.

 

Urinary indices can reveal a lowered FeNa and an increased U/PCr in prerenal azotemia, while the opposite in acutue tubular necrosis. However, many factors can influence these guidelines.

 

Blood Tests

* ASOT, hep B and C screen, HIV screen
* ANA, anti ds-DNA, C3, C4, ANCA, anti-GBM
* serum protein electrophoresis
* calcium, albumin, bilirubin

Red cell casts are ~10 cells thick

 

 

Imaging

Renal ultrasound should be done to rule out stones or other causes of obstruction. Assess for  

renal pyelogram

renal scan

renal biopsy

 

 

 

Pathophysiology

It appears that acute tubular necrosis is actually apoptosis, with mitochondrial dysfunction, ATP depletion, elevation in cytosolic calcium, and production of free radicals all potentially being involved.

 

 

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Treatments

Prophylaxis is the best treatment; people and situations susceptible to acute tubular necrosis (ie cardiac surgery) need to be approached with caution, and fluid deficiencies should be corrected beforehand. Nephrotoxic drugs should be used only when essential and with careful monitoring.

Contrast nephrotoxicity can be avoiding through adequate hydration and bicarbonate

 

Specific therapy (prerenal: fluids; postrenal: catheter, nephrostomy tube)

Correct pre- and post-renal factors as identified.

Stop offending drugs and avoid drugs of the same class.

Treat complications (K+, pH, BP, pulmonary edema.

Consider hemodynamic monitoring.

Provide nutrition support.

 

Dialysis should be considered where indications exist.

 

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Consequences and Course

Infection is a serious cause of death in people with acute kidney injury requiring dialysis. For those who survive, renal function returns essentially to normal.

 

Uremia can cause cardiac, neurologic, hematoligic, gastrointestinal, and skin signs and symptoms.

Hyperkalemia can be a life-threatening complication of AKI.

Moderate acidosis is generally well tolerated and does not need treatment, unless accompanied by the need to control acidosis.

 

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The Patient

 

 

 

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References