Acute Kidney Injury

Abstract

Acute kidney injury (AKI) is defined as a loss of renal ­function measured by a decline in glomerular filtration rate that develops over hours to days, and is the preferred term over acute renal failure. A decline in GFR results in impairment of nitrogenous waste product excretion and loss of water, electrolyte regulation and acid-base regulation.

Appendices

Summary Points

Acute kidney injury (AKI) is defined as the loss of renal function measured by a decline in glomerular filtration rate (GFR) that develops over hours to days.

In children, AKI is usually secondary to systemic illness.

The etiology of AKI is best described by the renal anatomy most affected: pre-renal, renal, orpost-renal.

Progression of renal failure results in acute tubular necrosis (ATN).

A high BUN-Cr ratio is not as useful in infants and smaller children because their serum creatinine levels are so low.

In newborns, because of their decreased ability to resorb sodium, pre-renal disease is associated with FENa values of less than 2.5% and ATN is associated with values greater than 2.5–3.5%.

Initial management should be directed at halting the progression of AKI and minimizing complications.

Electrocardiographic findings associated with life-threatening hyperkalemia consist of initial peaking of T waves, followed by an increase in the PR interval, flattened P waves, widening of the QRS complex, bradycardia, and ventricular fibrillation.

There is no definitive evidence that the use of diuretics, vasodilators, dopamine or fenoldapam prevents or alters the course of AKI after cardiac surgery.

Aminoglycosides, amphotericin B, NSAIDs, and chemotherapy are frequently implicated in pediatric medication-associated AKI.

Hepato-renal syndrome is a form of functional renal failure that is characterized by severe vasoconstriction of the renal circulation.

Rhabdomyolysis is caused by muscle injury or extensive surgery; vigorous fluid resuscitation with normal saline can lessen kidney injury.

Radiocontrast nephropathy is very uncommon in children.

Seventy percent of patients with AKI in hospital not requiring dialysis survive.

Long-term results are excellent: over two-thirds of children with AKI go on to full recovery of renal function.

Editor’s Comment

Acute kidney injury occasionally occurs in healthy children after major surgery, usually from exposure to a nephrotoxic drug like gentamicin. Transient renal dysfunction can also occur after exposure to ketorolac or in patients who are allowed to become extremely dehydrated. Renal injury due to intravenous contrast material appears to be exceedingly rare in children. Since frequent routine daily blood draws have (appropriately) become a thing of the past, the clinician needs to be vigilant for the subtle signs of renal dysfunction, including nausea, ileus, and a generalized malaise. Urine output is usually normal, or consistent with the usual fluctuations observed in the postoperative period, and is therefore not a reliable sign. Basically, any patient whose postoperative progress seems to have stalled or taken a step back for no apparent reason (sepsis, obstruction, and hemorrhage have been ruled out) should raise the question of AKI. Electrolytes with BUN and creatinine should be drawn, fluid status should be assessed, and a urinalysis with specific gravity and urine sodium and creatinine (for calculation of ­fractional excretion of sodium) should be ordered. If AKI is confirmed, all potential nephrotoxins should be discontinued, fluid intake should be decreased, and, if the patient is oliguric, potassium should be removed from all intravenous solutions. The vast majority of these children will recover uneventfully without specific therapy or need for dialysis.

Infants and children with AKI will sometimes need to undergo dialysis or hemofiltration. The indication is usually either fluid overload, hyperkalemia, or, in the case of a prolonged recovery from ATN, azotemia. Options include peritoneal dialysis, standard hemodialysis, or continuous renal replacement therapy, usually in the form of continuous veno-venous hemofiltration (CVVH). Peritoneal dialysis is more often used in infants due to their limited vascular access for hemodialysis. Peritoneal dialysis catheters need to be placed under general anesthesia but in most cases dialysis is well tolerated. Hemodialysis is sometimes considered in older children and requires placement of a large-bore double-lumen hemodialysis catheter in the jugular vein. These can be percutaneous or tunneled, depending on the length of time dialysis is likely to be needed. CVVH is generally used only in patients admitted to the ICU who are critically ill. Hemofiltration differs from hemodialysis in that water and solutes from the blood are forced through a semipermeable membrane by hydrostatic pressure generated by a pump (convection), rather than across a gradient generated by the presence of dialysate on the other side of the membrane (­diffusion). It is slower than dialysis and requires daily sessions lasting 12–16 h. It has less of an effect on systemic blood pressure and may be better tolerated by patients who are hypotensive. Continuous arterio-venous hemofiltration, in which the patient’s blood pressure provides the hydrostatic pressure needed to create the ultrafiltrate, is sometimes used in adults but is rarely an option for children. The pediatric surgeon is often asked to provide the vascular access required by these various therapies and must therefore be familiar with the equipment available and the flow rates needed. Subclavian vein catheters should be avoided in children at risk for chronic renal failure – in the event they need to have a graft or arterio-venous fistula created in the future, it would be best not to have created a subclavian vein stenosis.

Differential Diagnosis

Pre-Renal

• Volume related

• Intravascular depletion

• Ineffective circulation

• Ischemic/thrombotic

• Abdominal compartment syndrome

• Renovascular

• Renal vein thrombosis

• Renal artery stenosis

• Neurohumoral signaling dysfunction

• Hepato-renal syndrome

• Medications

• Calcineurin inhibitors

• Radio-contrast agents

• ACEI and ARB

Intrinsic Renal

• Glomerular

  • Hemolytic uremic syndrome

  • Acute glomerulonephritis

  • Vasculitis

  • Lupus nephritis

  • Goodpasture syndrome

  • Wegener’s

  • ANCA-associated

• Vascular

  • Hemolytic uremic syndrome

  • Malignant hypertension

  • Tubular/interstitial

  • Uncorrected pre or post AKI

  • Asphyxia/hypoxia

• Medications

  • Aminoglycosides/vancomycin

  • Amphotericin B

  • Poisons

  • Crystals (acyclovir and methotrexate)

• Tumor lysis/urate nephropathy

• Rhabdo/hemolysis: pigment nephropathy

Post-Renal

• Urinary tract obstruction

• Posterior urethral valves

• Bilateral UPJ obstruction

• Bilateral nephrolithiasis

• Neoplasm

• Retroperitoneal fibrosis

• Trauma

Diagnostic Studies

• FENa and urine sodium concentration

• Urinalysis

• Renal ultrasound

Parental Preparation

Long-term results are excellent: over two-thirds of children with AKI go on to full recovery of renal function.

Technical Points

Volume overload is treated with fluid restriction (1/3 maintenance + urine output), diuretics (furosemide 0.5–1 mg/kg dose), or dialysis.

Hypertension is treated with diuretics (if volume overload) ± CCB (acute) or ACEI (chronic).

Electrolyte abnormalities are treated by minimizing intake (especially potassium and phosphorous), kayexalate for potassium, and oral calcium carbonate and severamer for phosphorus.

Metabolic acidosis should be corrected if the plasma bicarbonate concentration falls below 16 mEq/L or the arterial pH is less than 7.25, especially if the patient requires vasopressor therapy, as acidosis worsens myocardial dysfunction.