A Brief Review of AFP's "Acute Kidney Injury: A Guide to Diagnosis and Management"

Acute Kidney Injury: A Guide to Diagnosis and Management
MAHBOOB RAHMAN, MD, MS, Case Western Reserve University School of Medicine, Cleveland, Ohio, FARIHA SHAD, MD, Kaiser Permanente, Cleveland, Ohio, MICHAEL C. SMITH, MD, Case Western Reserve University School of Medicine, Cleveland, Ohio
Am Fam Physician. 2012 Oct 1;86(7):631-639.
http://www.aafp.org/afp/2012/1001/p631.pdf

     Acute kidney injury is a common inpatient problem, occurring in 7% of hospitalized patients and 33% of ICU patients.  Patients with acute injury have a higher chance of developing chronic injury in the future. Risk factors include age greater than 75 years, diabetes, heart failure, liver failure, or sepsis.  The patient will have an elevated creatinine and reduced urine output within a 48 hour period  Dialysis may be necessary.  The three categories of acute kidney injury are prerenal, intrinsic, and postrenal.
      Prerenal injury is due to some type of volume loss. The patient will have decreased intravascular volume or decreased arterial pressure, which leads to a reduced GFR.  FENa will less than 1%. FEurea will be less than 35% if the patient is on diuretics. Causes include heart failure, sepsis, vomiting or diarrhea. Medications that can cause prerenal kidney injury include ACEIs, ARBs, and NSAIDs. A patient may have signs of volume loss such as orthostatic hypertension, poor skin turgor, ascites (decrease intravascular, but increased extravascular), increased thirst, decreased fluid intake, heart disease or liver disease.
     Postrenal injury is due to some type of blockage after the urine leaves the kidney. It can be by an enlarged prostate, a neurogenic bladder, mass or a stone causing an obstruction. The patient may complain of hematuria, urgency, hesitancy, or bladder distention. Ultrasound should be done in this case to find or rule out the cause. 
     Intrinsic injury has to due with part of the anatomy of the kidney. The FENa should be greater than 2%. Intrinsic injury can be broken down into four parts: tubular, glomerular, interstitial, or vascular. Acute tubular necrosis is either ischemic (hypotension) or nephrotoxic (drugs, contrast). It may also be from rhabdomyolysis (trauma). On UA, there may be renal tubular cells, tubular casts, or pigmented casts.  Glomerulonephritis is due to a systemic issue. Common causes are lupus, HCV, goodpasture's, HIV, and wegener's. It is a nephrotic syndrome so there will be heavy proteinuria, as well as RBC casts. Diagnosis of the specific cause may be done through biopsy, or other disease specific testing. Acute interstitial nephritis will produce WBC casts and eosinophils on UA. It is commonly caused by medication use, including antibiotics or PPIs. Patients may present with fever, rash or joint pain. Renal atheroembolic disease is the most common cause of vascular injury. The patient will be on anticoagulation. There may also be flank pain, recent trauma, recent vascular surgery, or recent vessel catheterization. 
     Hospitalized patients should have their volume status assessed and maintained on isotonic fluids, or diuretics if the patient is overloaded. Hypotensive patients may need vasopressors if it is severe. Hyperkalemic patients may need insulin and dextrose if it is above 6.5 mmol/L. Calcium gluconate may be added to reduce the risk of cardiac arrhythmias. Kayexalate has a role in hyperkalemia as well. Nephrotoxic medications should be discontinued, including metformin. Contrast media use should be avoided as well.  A conformational biopsy may be needed before treatment is started if the treatment itself is toxic. Patients may ultimately need dialysis if they have treatment refractory hyperkalemia, treatment refractory volume overload, uremic pericarditis, uremic pleuritis, encephalopathy, acidosis or intoxications form lithium or ethylene glycol.