RENAL FAILURE

 

INTRODUCTION:  Renal failure results when the kidneys are unable to remove metabolic waste and perform their regulatory functions. Acute renal failure (ARF) is a rapid loss of renal function due to damage to the kidneys. Three major categories of ARF are prerenal (hypoperfusion, as from volume depletion disorders, extreme vasodilation, or impaired cardiac performance); intrarenal (parenchymal damage to the glomeruli or kidney tubules, as from burns, crush injuries, infections, transfusion reaction, or nephrotoxicity, which may lead to acute tubular necrosis [ATN]); and postrenal (urinary tract obstruction, as from calculi, tumor, strictures, prostatic hyperplasia, or blood clots).

CLINICAL STAGES:  Initiation period: initial insult and oliguria.  Oliguric period (urine volume less than 400 mL/day): Uremic symptoms first appear and hyperkalemia may develop.  

Diuresis period: gradual increase in urine output signaling beginning of glomerular filtration’s recovery. Laboratory values stabilize and start to decrease.

Recovery period: improving renal function (may take 3 to 12 months).

CLINICAL MANIFESTATIONS:  Critical illness and lethargy with persistent nausea, vomiting, and diarrhea.  Skin and mucous membranes are dry.  Central nervous system manifestations: drowsiness, headache, muscle twitching, seizures.  Urine output scanty to normal; urine may be bloody with low specific gravity.  Steady rise in blood urea nitrogen (BUN) may occur depending on degree of catabolism; serum creatinine values increase with disease progression.  Hyperkalemia may lead to dysrhythmias and cardiac arrest.  Progressive acidosis, increase in serum phosphate concentrations, and low serum calcium levels may be noted.  Anemia from blood loss due to uremic GI lesions, reduced red blood cell life-span, and reduced erythropoietin production.

ASSESSMENT AND DIAGNOSTIC METHODS: Urine output measurements.  Renal ultrasonography, CT and magnetic resonance imaging (MRI) scans.  BUN, creatinine, electrolyte analyses.

MEDICAL MANAGEMENT:  Treatment objectives are to restore normal chemical balance and prevent complications until renal tissues are repaired and renal function is restored. Possible causes of damage are identified and treated.  Fluid balance is managed on the basis of daily weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and clinical status. Fluid excesses are treated with mannitol, furosemide, or ethacrynic acid to initiate diuresis and prevent or minimize subsequent renal failure.  Blood flow is restored to the kidneys with the use of intravenous (IV) fluids, albumin, or blood product transfusions.  Dialysis (hemodialysis, hemofiltration, or peritoneal dialysis) is started to prevent complications, including hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema.  Cation-exchange resins (orally or by retention enema).  IV dextrose 50%, insulin, and calcium replacement for the patient who is hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia).  Shock and infection are treated if present.  Arterial blood gases are monitored when severe acidosis is present.  Sodium bicarbonate to elevate plasma pH.  If respiratory problems develop, ventilatory measures are started.  Phosphate-binding agents to control elevated serum phosphate concentrations.  Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms.  Caloric requirements are met with high-carbohydrate feedings; parenteral nutrition (PN).  Foods and fluids containing potassium and phosphorus are restricted.  Blood chemistries are evaluated to determine amount of sodium, potassium, and water replacement during oliguric phase.  After the diuretic phase, high-protein, high-calorie diet is given with gradual resumption of activities.

 

RELATED;

1.  GENITAL URINARY TRACT CONDITIONS AND INFECTIONS

2.  EXCRETION OF DRUGS

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