Acute Renal Failure Diagnosis

Diagnosis of Acute Renal Failure
Although acute renal failure (ARF) is relatively uncommon, its mortality rate is potentially so high that it is important to recognize this condition in children. Rapid deterioration of renal function is caused by numerous insults and results in typical findings, including extracellular volume expansion, hyperkalemia, hypertension, metabolic acidosis, and azotemia. It usually is reversible, with the majority of patients recovering completely. However, ARF can lead to residual impairment of renal function and progress to end-stage renal disease and death. Conservative medical treatment often is life-saving.

Definition
ARF represents the rapidly progressive (within several hours or days) cessation of renal function, which results in the inability of the kidney to control body homeostasis, manifesting in retention of nitrogenous waste products (azotemia) and fluid and electrolyte imbalance. On the basis of pathophysiologic process, ARF has been divided broadly into three diagnostic categories: prerenal, intrarenal (organic-intrinsic), and postrenal failure (Table 1). Prerenal and early postrenal failures are renal functional disorders and responses of a structurally intact kidney to extrarenal processes. These forms of renal dysfunction recover rapidly as soon as the cause is reversed. However, if these two disorders are not recognized in time, persist too long, or are treated inadequately, they can result in intrinsic renal failure. Intrinsic or organic renal failure is caused by structural changes within the kidney. It is potentially reversible but requires an extended period of recovery.

Etiology
Prerenal failure is the most common form of ARF in children. The main process in the development of prerenal failure is hypoperfusion of the kidney, secondary to reduced effective plasma volume or heart failure. Numerous underlying conditions can lead to prerenal failure (Table 1). In children, the most common causes are hypovolemia secondary to gastrointestinal losses, the state of shock, and postoperative conditions. For example, ARF may occur after heart surgery when the aorta is cross-clamped or following prolonged cardiopulmonary bypass time.
A variety of renal disorders and insulting events can contribute to the development of intrinsic renal failure (Table 1). Among these are acute glomerulonephritis and vasculitis of childhood, acute tubular necrosis, and acute interstitial nephritis.
Acute tubular necrosis (ATN) is the most common cause of intrinsic renal failure. It is associated with necrosis of the tubular epithelium following hypoxic or nephrotoxic injury. Various substances, including ethylene glycol, heavy metals, hydrocarbons, and certain antibiotics, including cephalosporins, aminoglycosides, sulfonamides, methicillin, and colistin, are potent nephrotoxins. Aminoglycoside-induced acute renal failure occurs typically 5 days after drug administration and represents a dose-dependent phenomenon.
Radiologic contrast material of the ionic type can cause ARF, usually within 24 hours after exposure, especially in individuals who are dehydrated, have diabetes mellitus, or have preexisting renal insufficiency. Primary diseases of the glomeruli and small blood vessels of the kidney may present with rapidly progressive ARF (Table 1). Large vessel diseases (renal artery thrombosis or embolism, renal vein thrombosis) are uncommon. Acute interstitial nephritis usually results from immune-mediated drug sensitivity or infection.
Postrenal failure is a less frequent cause of ARF in children. It presents as an abrupt decline in glomerular filtration rate (GFR) secondary to lower tract obstruction or bilateral upper tract obstructions, unless the patient has a single kidney. Obstruction can be secondary to structural, congenital, or acquired anomalies of the urinary tract, including posterior urethral valve, ectopic ureter, aberrant vessels, or stones, or may result from functional abnormalities such as neurogenic bladder. Uric acid, the end product of purine metabolism, is insoluble at high concentrations in an acidic medium; during rapid cellular lysis before or after chemotherapy it often will precipitate in a distal nephron and cause renal obstruction. Depending on localization, obstruction can be extrinsic or intrinsic, at the level of the collecting duct, pelvis, ureter, bladder, urethra, or meatus (Table 1).

Pathophysiology
Prerenal dysfunction can lead to development of renal failure and is characterized by a decline in renal blood flow (RBF), GFR, and urine flow. After an acute reduction in effective intravascular volume, compensatory mechanisms of both the organism and the kidney will operate to counteract the volume loss and restore renal perfusion. Central activation of several neural and humoral responses occurs, including increased activity of the sympathetic system and the renin-angiotensin II-aldosterone system and enhanced release of antidiuretic hormone. Hemodynamic alterations within the kidney develop. An initial, short response of maximum dilatation of afferent arteriole is replaced by vasoconstriction. Blood flow is redistributed away from the renal cortex to juxtamedullary nephrons, which results in extensive tubular reabsorption of sodium, water, and urea.
With intense vasoconstriction, the kidney, acting as a blood reservoir, will shunt additional volumes of blood to the most vital organs (brain and heart); this response actually may be lifesaving in states of shock, blood loss, or severe dehydration. When the kidney has used these compensatory mechanisms fully, and the delivery of oxygen to the kidney remains critically impaired, acute necrosis of tubular cells occurs.
Injury due to ischemia or toxins is manifested by alterations in cellular metabolism. Cell detachment, desquamation, necrosis, and generation of intratubular debris and cast formations develop. The backward leak of tubular fluid across the injured tubular membrane and tubular obstruction results in further hemodynamic changes.
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