Acute Renal Failure Nursing Care and Management: Study Guide

When the kidneys stop clearing waste and regulating fluid, every system pays for it fast. Your job at the bedside is to catch the drop early, track urine output and labs hourly, and protect what kidney function is left. A healthy adult on a normal diet needs at least 400 mL of urine a day to clear metabolic waste; less than that means the GFR is falling.

What is Acute Renal Failure?

Acute renal failure (ARF), now more often called acute kidney injury (AKI), is a rapid loss of renal function from damage to the kidneys. It shows up in hospitalized patients and in outpatient settings.

Pathophysiology

The trigger is usually a specific underlying problem: hypovolemia, hypotension, reduced cardiac output, heart failure, or obstruction. Any of these cuts blood flow to the kidneys, blood flow drops, kidney function drops with it. Left untreated, the insult becomes permanent damage.

Statistics and Incidences

ARF affects about 1% of patients on admission, 2% to 5% during the hospital stay, 4% to 15% after cardiopulmonary bypass surgery, and in 10% of cases it occurs in isolation (single organ failure). In the United States the annual incidence is 100 cases for every million people. It is diagnosed in 1% of hospital admissions. Hospital-acquired ARF occurs in 4% of all admitted patients and 20% of patients admitted to critical care units.

Categories

ARF has four well-defined stages: onset, oliguric or anuric, diuretic, and convalescent. Treatment depends on the stage and severity. By site, ARF splits into three major classifications.

Prerenal. Caused by interference with renal perfusion (blood volume depletion, volume shifts such as third-space sequestration, or excessive or too-rapid volume expansion), shown by a decreased glomerular filtration rate (GFR). Disorders that lead here include cardiogenic shock, heart failure (HF), myocardial infarction (MI), burns, trauma, hemorrhage, septic or anaphylactic shock, and renal artery obstruction.

Renal (intrarenal). Parenchymal changes from ischemia or nephrotoxic substances. Acute tubular necrosis (ATN) accounts for 90% of cases of acute oliguria. Tubular epithelial cells are destroyed by (1) ischemia or hypoperfusion (like prerenal hypoperfusion, except correcting the cause may still be followed by oliguria for up to 30 days) and/or (2) direct damage from nephrotoxins.

Postrenal. Obstruction anywhere from the tubules to the urethral meatus. Most often stones in the ureters, bladder, or urethra, but trauma, infection-related edema, prostate enlargement, and strictures also cause it.

Phases

Four phases: initiation, oliguria, diuresis, and recovery.

• Initiation. Begins with the initial insult, ends when oliguria develops.
• Oliguria. Serum levels of substances normally excreted by the kidneys climb.
• Diuresis. Urine output rises gradually, signaling that glomerular filtration is recovering.
• Recovery. Renal function improves and may take 3 to 12 months.

Causes

By category: prerenal causes are volume depletion, impaired cardiac efficiency, and vasodilation. Intrarenal causes are prolonged renal ischemia, nephrotoxic agents, and infectious processes. Postrenal cause is urinary tract obstruction.

Clinical Manifestations

Almost every system feels the loss of renal regulation. Waste accumulates, so expect lethargy. Skin and mucous membranes are dry from dehydration. CNS signs include drowsiness, headache, muscle twitching, and seizures. Creatinine rises in all phases of ARF.

Prevention

• Hydration. Keep patients at risk for dehydration adequately hydrated.
• Shock. Treat shock promptly with blood and fluid replacement.
• Close monitoring. Track central venous and arterial pressures and hourly urine output in critically ill patients to catch the onset early.
• Blood administration. Confirm the right blood goes to the right patient to avoid severe transfusion reactions.
• Infections. Treat promptly; infection causes progressive renal damage.
• Toxic drug effects. Watch dosage, duration, and blood levels of every drug metabolized or excreted by the kidneys.

Complications

Depending on duration and severity, ARF carries a range of life-threatening complications. Waste the kidneys cannot eliminate drives metabolic acidosis. Fluid and electrolyte imbalances follow from hemorrhage, renal losses, and gastrointestinal losses.

Assessment and Diagnostic Findings

Assessment centers on changes in the urine, imaging of kidney contour, and lab values.

Urine

• Volume: Usually less than 100 mL/24 hr (anuric phase) or 400 mL/24 hr (oliguric phase), occurring within 24 to 48 hr after the renal insult. Nonoliguric failure (more than 400 mL/24 hr) also occurs when nephrotoxic agents (contrast media, antibiotics) cause the damage.
• Color: Dirty, brown sediment indicates RBCs, hemoglobin, myoglobin, porphyrins.
• Specific gravity: Less than 1.020 reflects kidney disease (glomerulonephritis, pyelonephritis with loss of concentrating ability); fixed at 1.010 reflects severe renal damage.
• pH: Greater than 7 in urinary tract infections (UTIs), renal tubular necrosis, and chronic renal failure (CRF).
• Osmolality: Less than 350 mOsm/kg indicates tubular damage; urine/serum ratio is often 1:1.
• Creatinine (Cr) clearance: Renal function may be significantly decreased before BUN and serum Cr rise noticeably.
• Sodium: Usually increased if ATN is the cause, more than 40 mEq/L when the kidney cannot resorb sodium, though it may be decreased in other prerenal causes.
• Fractional sodium (FeNa): Less than 1% indicates prerenal problems; higher than 1% reflects intrarenal disorders.
• Bicarbonate: Elevated if metabolic acidosis is present.
• Red blood cells (RBCs): May be present from infection, stones, trauma, tumor, or altered glomerular filtration.
• Protein: High-grade proteinuria (3 to 4+) strongly indicates glomerular damage when RBCs and casts are also present. Low-grade proteinuria (1 to 2+) with WBCs suggests infection or interstitial nephritis. In ATN, proteinuria is usually minimal.
• Casts: Signal renal disease or infection. Cellular casts with brownish pigments and many renal tubular epithelial cells are diagnostic of ATN. Red casts suggest acute glomerular nephritis.

Blood

• BUN/Cr: Elevated, usually rising in proportion with a ratio of 10:1 or higher.
• CBC: Hemoglobin (Hb) decreased with anemia. RBCs often decreased from increased fragility and shortened survival.
• ABGs: Metabolic acidosis (pH less than 7.2) develops as the kidney loses the ability to excrete hydrogen and metabolic end products. Bicarbonate decreased.
• Sodium: Usually increased, but may vary.
• Potassium: Elevated from retention, cellular shifts (acidosis), or tissue release (red cell hemolysis).
• Chloride, phosphorus, and magnesium: Usually elevated.
• Calcium: Decreased.
• Serum osmolality: More than 285 mOsm/kg, often equal to urine.
• Protein: Decreased serum level may reflect urine loss, fluid shifts, decreased intake, or reduced synthesis from lack of essential amino acids.
• Radionuclide imaging: May reveal calicectasis, hydronephrosis, narrowing, and delayed filling or emptying.
• KUB x-ray: Shows size of kidneys, ureters, bladder, cysts, tumors, and displacement or obstruction (stones).
• Retrograde pyelogram: Outlines abnormalities of the renal pelvis and ureters.
• Renal arteriogram: Assesses renal circulation, identifies extravascularities and masses.
• Voiding cystoureterogram: Shows bladder size, reflux into ureters, retention.
• Renal ultrasound: Determines kidney size and presence of masses, cysts, or upper urinary tract obstruction.
• Nonnuclear CT scan: Cross-sectional view of kidney and urinary tract to detect disease extent.
• MRI: Information about soft tissue damage.
• Excretory urography (IV urogram or pyelogram): Radiopaque contrast concentrates in urine to visualize the KUB.
• Endourology: Direct visualization of urethra, bladder, ureters, and kidney to diagnose, biopsy, and remove small lesions or calculi.
• ECG: May be abnormal, reflecting electrolyte and acid-base imbalances.

Urine tests

• Urinalysis: Gives major insight into kidney function.
• 24-hour urine test: Collect all urine for 24 consecutive hours, analyzed for protein and waste products (urea nitrogen and creatinine). Protein in the urine indicates kidney damage. Creatinine and urea excreted are used to calculate kidney function and GFR.
• Glomerular filtration rate (GFR): The standard measure of overall kidney function; it falls as kidney disease progresses. Normal GFR is about 100 to 140 mL/min in men and 85 to 115 mL/min in women, and decreases with age. It is calculated from waste products in the 24-hour urine or with IV markers. Patients fall into five stages of chronic kidney disease based on GFR.
• Urine specific gravity: Measures how concentrated the sample is. A concentrated sample reads over 1.030 or 1.040.

Blood tests

• Creatinine and urea (BUN): The most common blood tests to screen for and monitor renal disease. Creatinine is a product of normal muscle breakdown; urea is the product of protein breakdown. Both rise in the blood as kidney function worsens.
• Electrolytes and acid-base balance: Kidney dysfunction throws off potassium, phosphorus, and calcium. High potassium (hyperkalemia) is a particular concern. Acid-base balance is usually disrupted as well.
• Vitamin D and phosphorus: Decreased production of the active form of vitamin D lowers blood calcium. Failing kidneys cannot excrete phosphorus, so its blood level rises.
• Blood cell counts: Kidney disease disrupts blood cell production and shortens red cell survival, so RBC count and hemoglobin may be low (anemia). Some patients also have iron deficiency from GI blood loss, and other nutritional deficiencies impair red cell production.

Other tests

• Ultrasound: A noninvasive standby in kidney diagnosis. Kidneys are usually shrunken in chronic kidney disease, though they may be normal or large in adult polycystic kidney disease, diabetic nephropathy, and amyloidosis.
• Biopsy: A kidney tissue sample, sometimes needed when the cause is unclear. Usually collected under local anesthesia by passing a needle through the skin into the kidney.

Medical Management

The goal is to restore chemical balance and prevent complications until renal tissue repairs and function returns.

• Pharmacologic therapy. Cation-exchange resins (Kayexalate) reduce elevated potassium; IV dextrose 50%, insulin, and calcium replacement shift potassium back into cells; diuretics control fluid volume.
• Nutritional therapy. Individualize dietary protein to minimize uremic symptoms. Meet caloric needs with high-carbohydrate meals (carbohydrates spare protein). Restrict foods and fluids with potassium or phosphorus. After the diuretic phase, move the patient to a high-protein, high-calorie diet.

Nursing Management

Nursing Assessment

Assessment focuses on the urine. Output ranges from scanty to normal. Hematuria may be present. Lab results rise, fall, or stabilize and mark each phase of ARF.

Nursing Diagnosis

• Electrolyte imbalance related to increased potassium levels.
• Risk for deficient volume related to increased urine output.

Nursing Care Planning & Goals

Goals for the patient with ARF: improve nutritional intake, restore fluid balance, reduce metabolic rate, promote pulmonary function, and prevent infection.

Nursing Interventions

Interventions aim to restore renal function and cut potential causes of further injury.

• Monitor fluid and electrolyte balance. Track fluid and electrolyte levels and physical signs of complications through all phases.
• Reduce metabolic rate. Encourage bed rest; prevent or treat fever and infection promptly.
• Promote pulmonary function. Have the patient turn, cough, and take deep breaths often to prevent atelectasis and respiratory infection.
• Prevent infection. Use strict asepsis with invasive lines and catheters.
• Provide skin care. Bathe with cool water, turn frequently, keep skin clean and moisturized, and trim fingernails to prevent excoriation and skin breakdown.
• Provide safety measures. Patients with CNS involvement may be dizzy or confused.

Evaluation

A successful plan shows improved nutritional intake, restored fluid balance, reduced metabolic rate, promoted pulmonary function, and prevented infection.

Discharge and Home Care Guidelines

Teach the patient and family. Refer to a nutritionist for the dietary changes required. Make sure they know which problems to report to the provider. Stress followup exams and treatment, since physical status and renal function keep changing.

Documentation Guidelines

Document vital signs; muscle strength and reflexes; lab and diagnostic results; degree of deficit and current sources of fluid intake; I&O and fluid balance; plan of care; teaching plan; the client's responses to treatment, teaching, and actions performed; attainment of or progress toward desired outcomes; modifications to the plan of care; and long-term needs.