Acute and Chronic Renal Failure

Published on 06/06/2015 by admin

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Last modified 06/06/2015

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65 Acute and Chronic Renal Failure

Acute Renal Failure

Acute kidney injury (AKI), previously referred to as acute renal failure (ARF), is defined as an abrupt reduction in kidney function measured by a rapid decline in glomerular filtration rate (GFR). AKI implies that an acute decline in kidney function is secondary to an injury that leads to functional or structural changes in the kidney. AKI is characterized by a disturbance of renal physiologic functions, including impairment of nitrogenous waste product excretion and inability to regulate water, electrolyte, and acid–base homeostasis. The precise incidence and prevalence of AKI in children is difficult to ascertain. The overall incidence of AKI appears to be rising because of advances in pediatric medical technology including bone marrow, hepatic, and cardiac transplantation, in surgery for congenital heart disease, and in the care of very low birth weight infants.

Etiology and Pathogenesis

The causes of AKI can be related to any process that interferes with the structure or function of the renal vasculature, glomeruli, renal tubules, interstitium, or urinary tract. The causes of AKI can be categorized as prerenal, renal (intrinsic renal disorder), or postrenal.

Renal

AKI (intrinsic renal disease) is the result of disorders that involve the renal vascular, glomerular, or tubular–interstitial pathology. Acute tubular necrosis (ATN) results from ischemia caused by decreased renal perfusion or injury from tubular nephrotoxins (Figure 65-1). All causes of prerenal AKI can progress to ATN if renal perfusion is not restored or nephrotoxins are not withdrawn. Nephrotoxic AKI is mostly caused by toxic tubular injury by medications, including aminoglycosides, contrast agents, amphotericin B, chemotherapeutic agents (ifosfamide, cisplatin), and acyclovir. Toxic tubular injury can also be induced by the release of heme pigments, as it occurs from myoglobinuria caused by rhabdomyolysis and hemoglobinuria caused by intravascular hemolysis. Uric acid nephropathy and tumor lysis syndrome are causes of AKI in children with leukemia. During chemotherapy, a rapid breakdown of tumor cells causes increased release and subsequent excretion of uric acid, resulting in precipitation of uric acid crystals in the tubules and renal microvasculature. Hyperphosphatemia in tumor lysis syndrome results in precipitation of calcium phosphate crystals in the tubules. Acute interstitial nephritis most commonly results from hypersensitivity reactions to drugs, including penicillin analogs (e.g., methicillin), cimetidine, sulfonamides, rifampin, nonsteroidal antiinflammatory drugs, and proton pump inhibitors, but can also be idiopathic. Glomerulonephritis of any etiology (including those caused by vasculitis, systemic lupus erythematosus, or Goodpasture’s syndrome) may present with AKI, with postinfectious glomerulonephritis being the most common cause of AKI in this group. Rapidly progressive glomerulonephritis presents as the most severe degree of any form of glomerulonephritis and presents with AKI. Vascular causes of AKI include cortical necrosis (mostly caused by hypoxic or ischemic injury in newborns), renal artery or vein thrombosis, and hemolytic-uremic syndrome (HUS).

Clinical Presentation

A careful history and physical examination can frequently identify disease processes that underlie AKI and suggest an underlying diagnosis.

Evaluation and Diagnosis

In addition to a careful history and physical examination, the initial evaluation includes additional laboratory studies.

Prevention and Management

The basic principles of the general management of AKI are shown in Box 65-1.

General measures to help prevent AKI include close monitoring of serum levels of nephrotoxic drugs, adequate fluid repletion in patients with hypovolemia, and aggressive hydration and alkalinization of the urine before chemotherapy. Unless contraindicated, a child with a history of fluid loss (vomiting and diarrhea), a physical examination consistent with hypovolemia (hypotension and tachycardia), or oliguria requires immediate intravenous (IV) fluid therapy in an attempt to restore renal function and perhaps prevent ischemic renal injury. Commonly used fluids are crystalloid solutions, such as normal saline (20 mL/kg) administered over 20 to 30 minutes, which may be repeated. If urine output does not increase and renal function fails to improve, invasive monitoring may be required to adequately assess the child’s fluid status and help guide further therapy.

Hyperkalemia is a life-threatening complication of AKI that may result in fatal cardiac arrhythmia. Hyperkalemia is treated by shifting potassium from the intravascular to the intracellular space using IV glucose and insulin, β-agonists (albuterol inhalation), and bicarbonate and by using enteric exchange resins such as polystyrene sulfonate. IV infusion of calcium is used to stabilize cell membranes and decrease the risk of cardiac arrhythmias. Dialysis may be required to remove potassium.

Acid (H+)