Acute Kidney Injury

Previously called acute kidney failure. AKI is characterized by increased creatinine and decreased urine volume.

• Specifically: an increase in creatinine (Cr) higher than 0.3 mg/dl (26.5 umol/L) in 48 hours, a rise of creatine greater than 1.5 times the baseline ((occurring within the last seven days) and a decrease of urine volume of equal to or lesser than 0.5 ml/kg/h (2012 Kidney Disease: Improving Global Outcomes)).

KDIGO Staging Guidelines Note that there may be no immediate change in creatinine and the only sign may be reduce urine output. AKI onset is sudden, and injury is often reversible when underlying causes are addressed. Azotemia is increased blood urea nitrogen (BUN), creatinine, and other nitrogenous waste products in the blood (azot = nitrogen, emia = blood). Azotemia occurs in both acute and chronic kidney injury, which are characterized by reduced renal filtering. Uremia: Azotemia can lead to uremia, which is a clinical syndrome characterized by a cluster of signs/symptoms in various body systems, including the cardiac and nervous systems. Uremia can occur in acute kidney injury but is more common in chronic injury. Sudden onset of oliguria, edema, fluid retention (weight gain), lethargy, nausea, loss of appetite. Note that ATN and prerenal disease are most common causes. "Pre-renal" etiologies affect renal perfusion at the renal artery (which is a "pre-renal" vessel, anatomically). "Intrinsic" or 'intrarenal" etiologies affect the renal medulla, which includes the vasculature, interstitium, or the nephrons, themselves. "Post-renal" etiologies affect the ureter or bladder, which are distal to the kidney (anatomically "post-renal"). Pre-Renal AKI Pre-renal etiologies are those that induce changes to renal hemodynamics and perfusion. Because renal blood flow is reduced, so is the glomerular filtration rate. As a result, less fluid and solutes are filtered from the blood. Thus, some indicators of pre-renal AKI include reduced sodium urine levels, less than 20 mEq/L, and less than 1% fractional excretion of sodium. Also note that, upon fluid administration, patients with pre-renal AKI will show reduction in serum creatinine. Etiologies are numerous, since any event that alters systemic circulation or renal perfusion can impact GFR, including: Intravascular volume depletion and hypotension, bilateral renal stenosis, heart failure, and use of ACE inhibitors or Angiotensin II receptor blockers (ARBs). Recall that, in healthy individuals, GFR is maintained by autoregulatory mechanisms, but those mechanisms are overwhelmed in renal disease. Intrinsic/intrarenal AKI Intrinsic acute kidney injury is associated with urine sodium above 40 mEq/L, and fractional excretion of sodium greater than 2 percent. This form of AKI can be further divided into four groups, based on the renal structures primarily involved: Vascular causes, which include vasculitis, Hemolytic uremic syndrome (HUS), malignant hypertension, and thrombotic thrombocytopenia purpura (TTP). Glomerular damage, which can be further divided into Nephrotic or Nephritic disorders, based on which solutes erroneously pass through the membrane.

• Nephrotic syndrome occurs when proteins leak out of the capillaries and into the ultrafiltrate; this occurs in focal segmental glomerulosclerosis, membranous nephropathy, and minimal change disease.

• Nephrotic syndrome (aka nephrosis) is characterized by a group of signs/symptoms resulting from the loss of protein in the urine: proteinuria, hypoalbuminemia, edema, hyperlipidemia, with puffy eyelids and edema, foamy urine, fatigue, and loss of appetite.

• Nephritic syndrome occurs when blood cells leak into the ultrafiltrate, and is associated with infection associated glomerulonephritis, IgA nephropathy, and anti-glomerular basement membrane antibody disease.
• Signs and symptoms of nephritic syndrome include hematuria, hypertension, edema, and oliguria, with red blood cells and their casts and WBC in urine; proteinuria is not uncommon, but to a lesser degree than in nephrotic syndrome.

Tubular damage, which is usually caused by acute tubular necrosis (ATN), and is the most common cause of AKI overall (especially in hospitalized patients). This is associated with high morbidity and mortality.

• Acute tubular necrosis is characterized by patchy injury to the nephron tubule, often caused by ischemia (so etiologies of pre-renal AKI can also cause acute tubular necrosis) or toxic substances (medicines, hemoglobin/myoglobin, lead, etc.).

• Renal tubular cell damage and death impair tubular function, and the debris that obstructs tubules with backflow leads to reduced GFR. Urine analysis shows muddy brown casts, and tubular cells.

Acute interstitial nephritis (AIN), which is usually caused by medicines, esp. antibiotics and NSAIDs, but can also be caused by autoimmune disorders and infections.

• Notable signs and symptoms include skin rash, fever, and eosinophilia, with white blood cells and their casts in urine.

Post-renal AKI is the result of urine obstruction. Bladder outlet obstruction is the most common cause of post-renal AKI. In these patients, urine is trapped in the bladder and can backflow into the ureters, which increases pressure in the renal system and results in lowered GFR.

• Important obstructive causes include tumors (including prostrate tumors), kidney stones, infections that cause swelling or compression, and congenital anomalies (such as renal dysplasia).

• Note that unilateral renal obstruction is less often associated with AKI because the non-obstructed structure can typically compensate.

Address underlying cause; remove triggers (i.e., drugs). Treat hypovoemia, electrolyte imbalances, and acidosis. Emergency dialysis should be performed in patients with hypervolemia and pulmonary edema, hyperkalemia, and life-threatening uremic symptoms. Review Renal Failure