Chronic Renal Failure Nursing Care Plans

What is Chronic Renal Failure?

Chronic renal failure (CRF), or chronic kidney disease (CKD), is progressive structural and functional kidney damage from any of several causes. CKD is defined as an estimated glomerular filtration rate (eGFR) under 60 mL/min/1.73 m², or markers of kidney damage (albuminuria, hematuria, lab or imaging abnormalities), present for at least 3 months (KDIGO 2024). About 10% of adults worldwide have some form of CKD, accounting for 1 to 2 million deaths and 28 million years of life lost each year.

CKD drives cardiovascular disease and end-stage renal disease (ESRD), the final stage. Kidney disease is a leading cause of death in the United States, and the CDC estimates that more than 1 in 7 US adults, about 35.5 million people, have CKD, most of them undiagnosed (CDC).

The stages form a continuum:

• Stage 1: kidney damage with normal or increased GFR (>90 mL/min/1.73 m²)
• Stage 2: mild reduction (60 to 89 mL/min/1.73 m²)
• Stage 3a: moderate reduction (45 to 59 mL/min/1.73 m²)
• Stage 3b: moderate reduction (30 to 44 mL/min/1.73 m²)
• Stage 4: severe reduction (15 to 29 mL/min/1.73 m²)
• Stage 5: kidney failure (GFR <15 mL/min/1.73 m² or dialysis)

Risk factors for faster progression: proteinuria, hypertension, Black race, and hyperglycemia. Environmental contributors include lead exposure, smoking, metabolic syndrome, some analgesics, and obesity.

Stages 1 to 3 are usually asymptomatic. Endocrine, metabolic, water, and electrolyte derangements typically do not become clinically obvious until stages 4 to 5 (GFR <30 mL/min/1.73 m²), when compensatory mechanisms are spent.

Nursing Care Plans and Management

Care centers on managing fluid and electrolyte imbalances, preventing infection and uncontrolled hypertension, providing dietary counseling, coordinating the multidisciplinary team, and building self-care and adherence to slow progression. Because CKD is lifelong, patient education is not optional.

Nursing Problem Priorities

1. Fluid and electrolyte balance
2. Blood pressure control
3. Monitoring and managing renal function
4. Medication administration and adherence
5. Dietary modification and nutritional support
6. Assessing and managing complications (anemia, cardiovascular disease)
7. Education on self-care and lifestyle change
8. Managing comorbidities (diabetes, hypertension)

Nursing Assessment

Assess for these subjective and objective findings:

• Nausea, vomiting, loss of appetite
• Fatigue and weakness
• Sleep disturbances
• Polyuria or oliguria, nocturia
• Foamy urine, hematuria, pale or tea-colored urine
• Decreased mental sharpness
• Muscle twitches and cramps
• Swelling of feet and ankles
• Persistent pruritus
• Chest pain from uremic pericarditis
• Uncontrolled hypertension
• Shortness of breath from pulmonary edema

Assess factors tied to the underlying cause:

• Fluid shifts affecting circulating volume, myocardial workload, and systemic vascular resistance
• Rate, rhythm, and conduction changes from electrolyte imbalance and hypoxia
• Toxin accumulation (urea) and soft-tissue calcification (calcium phosphate deposition)
• Abnormal blood profile (suppressed erythropoietin, decreased RBC production and survival, altered clotting factors, increased capillary fragility)

Nursing Diagnosis

Diagnoses are framed from your assessment and clinical judgment against each patient's situation. Use them to organize care, not to box the patient in. The formal diagnostic label matters less than acting on what you find.

Nursing Goals

• Patient maintains cardiac output: BP and heart rate within their normal range, strong equal peripheral pulses, prompt capillary refill.
• Patient shows no signs of bleeding or hemorrhage.
• Patient maintains or improves lab values.
• Patient avoids injury, with normal BP, hemoglobin, and hematocrit maintained.
• Patient denies bone pain or sensory loss.
• Patient regains or maintains optimal mentation and compensates for memory deficits.
• Patient maintains intact skin and demonstrates breakdown-prevention behaviors.
• Patient maintains intact oral mucosa.
• Patient verbalizes understanding of the disease, treatment needs, and complications, and performs required procedures correctly.
• Patient and family identify positive coping mechanisms and begin the grief process.
• Patient maintains adequate urine output and works toward regular, complete bladder emptying.

Nursing Interventions and Actions

1. Managing Decreased Cardiac Output

Failure to excrete sodium and free water expands extracellular and total body volume. This becomes clinically obvious once GFR falls below 10 to 15 mL/min/1.73 m². Sodium retention then drives peripheral edema, pulmonary edema, and hypertension. A real drop in cardiac output redistributes blood volume to preserve kidney perfusion.

Auscultate heart and lung sounds; check for peripheral edema, vascular congestion, and dyspnea. S3 and S4 with muffled tones, tachycardia, irregular rhythm, tachypnea, crackles, wheezes, edema, and jugular distension point to heart failure. Low systemic pressure, venous congestion, and elevated intra-abdominal pressure all track with worsening renal function.

Assess for hypertension; monitor BP and note postural changes (sitting, lying, standing). Renin-angiotensin-aldosterone disturbance drives hypertension. Orthostatic hypotension can still occur from intravascular deficit, antihypertensives, or uremic pericardial tamponade. Hypertension is common in CKD but also common without it, so do not treat it as a standalone marker.

Investigate chest pain: location, radiation, severity (0 to 10 scale), and whether deep inspiration or supine position worsens it. About half of CRF patients on dialysis develop pericarditis, risking effusion or tamponade. Uremic pericarditis classically presents as pleuritic chest pain that eases when leaning forward.

Evaluate heart sounds (note friction rub), BP, peripheral pulses, capillary refill, vascular congestion, temperature, and mentation. Sudden hypotension, paradoxical pulse, narrow pulse pressure, diminished or absent pulses, marked jugular distension, pallor, and rapid mental decline signal tamponade, a medical emergency. A scratchy pericardial friction rub is best heard at the left sternal border with the patient leaning forward, holding their breath.

Assess activity tolerance. Weakness comes from heart failure and anemia. Normochromic normocytic anemia develops from decreased renal erythropoietin synthesis; it starts early and worsens as renal mass shrinks and GFR falls.

Monitor the ECG. Pericarditis shows diffuse ST and T-wave elevations. Unlike STEMI, these changes are diffuse and not confined to a coronary territory. Later, the ST normalizes with diffuse T-wave inversions.

Monitor electrolytes, chest x-ray, and echocardiogram. See Laboratory and Diagnostic Procedures.

Promote sodium restriction and adequate nutrition. Cutting salt slows progression of diabetic CKD, partly by lowering BP, with effects comparable to single-drug therapy.

Administer antihypertensives as indicated. See Pharmacologic Management.

Prepare for dialysis. Removing uremic toxins and correcting electrolytes and fluid overload limits cardiac complications. Uremic pericarditis responds rapidly to dialysis, with chest pain and effusion resolving in most cases; effective dialysis helps in over 50% of cases.

Assist with pericardiocentesis as indicated. Pericardial fluid can compromise filling and contractility, risking arrest. If dialysis fails, perform pericardiocentesis within 7 to 14 days; with tamponade, emergent pericardiocentesis is indicated.

Prepare for pericardiectomy. Surgical removal of the pericardium is not first-line and is reserved for recurrent pericarditis with effusions. Repeat echocardiograms every 3 to 5 days during an acute event to track resolution.

2. Infection Control and Reducing Infection Risk

Uremia blunts immune response: weaker antibody response to hepatitis B vaccine, higher infection risk as kidney function drops, and milder autoimmune disease once uremia sets in. CKD patients carry a 2 times higher risk of death after respiratory infections, and data show a 2 times increase in COVID-19 mortality with CKD.

Note increasing fatigue and weakness; watch for tachycardia, pallor, dyspnea, and chest pain. These reflect anemia and the cardiac effort to keep tissues oxygenated. CKD anemia, from reduced erythropoietin, shows as fatigue, reduced exercise capacity, and impaired cognition and immunity.

Monitor level of consciousness and behavior. Anemia causes cerebral hypoxia: changes in mentation, orientation, and behavior. Hypoxia is the strongest stimulus for renal erythropoietin production.

Evaluate activity tolerance and task ability; assist as needed and schedule rest. Anemia lowers tissue oxygenation and raises fatigue. Lower hemoglobin tracks with greater productivity loss and activity impairment.

Watch for oozing at venipuncture sites, ecchymosis after minor trauma, petechiae, joint swelling, bleeding gums, epistaxis, hematemesis, melena, and hazy or red urine. Capillary fragility and uremia-induced platelet dysfunction make bleeding easy and worsen anemia.

Hematest GI secretions and stool for blood. Uremic mucosal changes and platelet dysfunction cause gastric erosion and GI hemorrhage, a common and serious complication of renal failure.

Monitor CBC, clotting factors, and iron levels. See Laboratory and Diagnostic Procedures.

Limit vascular sampling and batch lab draws. Repeated sampling worsens anemia faster than marrow can replace the loss.

Use a soft toothbrush and electric razor; use the smallest needle possible and hold prolonged pressure after injections or punctures. This cuts bleeding and hematoma risk; larger needles damage vessels more.

Promote fruit and vegetable intake. In patients with eGFR 30 to 59 mL/min/1.73 m², plant-based diets may slow progression to ESRD and dialysis and may improve survival.

Encourage physical activity as tolerated. For dialysis patients, aerobic exercise has the strongest evidence for fitness, strength, and quality of life. Resistance training benefits earlier stages.

Administer erythropoiesis-stimulating agents (ESAs) as indicated. See Pharmacologic Management.

Administer antacids, stool softeners, anticoagulants, erythropoietin, and iron preparations as indicated. See Pharmacologic Management.

Provide vaccination teaching. Influenza and pneumococcal vaccination can indirectly prevent acute kidney injury and slow CKD progression. Hepatitis B and COVID-19 vaccines help prevent those infections.

Assess temperature and respiratory and urinary changes as disease progresses. This flags infection from progressive disease affecting every system.

Secure urine or sputum cultures. See Laboratory and Diagnostic Procedures.

Perform hand hygiene and medical or surgical asepsis during care; teach the patient and family handwashing and safe disposal of tissues and used articles. This blocks pathogen transmission. Staff in direct contact are a major route for nosocomial spread.

Administer antibiotics as ordered (specify drug, dose, route, times). See Pharmacologic Management.

Teach the patient and family to bathe daily, wipe front to back, and wear loose cotton underwear. Untreated UTI can worsen renal function and cause pyelonephritis, sepsis, septic shock, and death. Catch it early.

Teach avoidance of contact with people who have upper respiratory infections. CKD carries a 2 times increase in COVID-19 mortality. Asymptomatic carriers and long incubation make outbreaks hard to prevent even with screening.

Encourage telehealth for consultations. Remote care guides dietary and therapeutic decisions and reduces exposure. Patients can use video, text messaging, mobile apps, and peripheral devices such as scales, BP cuffs, and glucometers.

Provide information on vaccines appropriate for CKD. Early-stage CKD has minimal immune impairment and can be safely vaccinated. Live-attenuated vaccine (LAV) safety is not established in transplant recipients, who should receive inactivated forms. CKD patients can safely receive hepatitis B-recombinant, influenza-inactivated, diphtheria-tetanus, MMR, varicella, recombinant zoster, and zoster live vaccines.

Advocate early removal of urinary catheters, ventilators, and central venous catheters. These devices are major infection sources. Prompt removal cuts device-associated infection in a population already at high hospitalization risk.

3. Managing Cognitive Symptoms

CKD patients face substantially higher cognitive impairment than the general population, with prevalence of 10% to 40% depending on stage and assessment method. Low eGFR and albuminuria are both independent risk factors; prevalence is highest in dialysis-dependent patients.

Assess thinking, memory, orientation, and attention span. Uremic effects start with minor confusion and irritability and can progress to personality change or inability to take part in care. Deficits span memory, attention, language, visuospatial skills, and executive function.

Get the patient's baseline mentation from family or caregiver. This sets the comparison for tracking progression. Mild cognitive impairment (MCI) appears early; 5 to 10% of MCI patients eventually progress to dementia.

Assess specific cognitive domains. Test attention, memory, visuospatial ability, language, and executive function: naming a picture, copying a complex figure, or Trail Making Test A and B for processing speed.

Assess sleep. Central sleep apnea affects 22 to 27% of adult CKD patients. The nocturnal hypoxemia tracks with autonomic dysfunction, left ventricular hypertrophy, and high cardiovascular risk in ESRD.

Screen for depression. 45% of adults with CKD have depressive symptoms at dialysis initiation by self-report scales, though these scales overweight somatic symptoms (sleep disturbance, fatigue, anorexia) common to chronic disease.

Use validated tools for confusion or delirium. The 4AT screens quickly for delirium and moderate-to-severe impairment. The MoCA tests visuospatial skills, recall, and attention. The MMSE scores domains out of 30. The Confusion Assessment Method (CAM), four questions, is the gold standard for delirium and depends on you noticing subtle changes from baseline.

Monitor BUN, creatinine, serum electrolytes, glucose, and ABGs (PO2, pH). See Laboratory and Diagnostic Procedures.

Keep the patient and family informed of status. Mentation often improves as BUN, electrolytes, and serum pH normalize. Have the hard conversations (dialysis modality, conservative care) early, before significant decline.

Provide a quiet, calm environment with judicious TV, radio, and visitors. CKD patients show inattention and impaired inhibitory control; reducing overstimulation helps them focus.

Reorient to surroundings, person, and time; provide calendars, clocks, and outside windows. Hemodialysis patients recall lists of words and images worse than healthy people, and dialysis itself does not fix it.

Present reality concisely; do not challenge illogical thinking. Confrontation breeds defensiveness, mistrust, and deeper denial. Mix reality orientation with compassion, and back off if it causes distress. It suits mild to moderate impairment best.

Use simple, short sentences; ask direct yes-or-no questions; repeat as needed. This reduces confusion and improves recall. If the patient gets more upset, stop orienting and lead with compassion.

Set a regular schedule for expected activities. Routine supports orientation and reduces fear. KDIGO recommends regular exercise compatible with cardiovascular health, ideally at least 30 minutes 5 times per week. Maintain day and night routines.

Promote rest and undisturbed sleep. Sleep deprivation worsens cognition. CKD sleep disorders are common: reduced total sleep, insomnia, fragmentation, daytime somnolence, altered circadian rhythm, sleep apnea, and restless leg syndrome.

Avoid barbiturates and opiates. Renally cleared drugs have a longer half-life and cumulative effects that worsen confusion. Adjust doses and intervals to residual GFR; some drugs are contraindicated in moderate to severe impairment.

Encourage exercise as tolerated. Aerobic training improves cognition in populations like older adults with MCI and stroke. Refer to a qualified exercise professional for a tailored, supervised program.

Use validation therapy when appropriate. Validation works with the feelings behind the behavior rather than correcting facts, helping the patient process unresolved issues and find peace.

Apply the HELP interventions. The Hospital Elder Life Program bundles small actions to maintain cognitive and physical function during hospitalization, support discharge, and avoid readmission. It works only alongside regular, at least daily, medical review.

Administer erythropoietin as prescribed. Iron deficiency and anemia are common in CKD and worsen neuropsychological scores; erythropoietin appears to help cognition. See Pharmacologic Management.

Prepare for dialysis. Marked deterioration of thought may signal worsening azotemia needing prompt intervention. Hemodialysis is life-saving in ESRD and reverses acute uremic encephalopathy by removing small, brain-permeable molecules.

Provide information on cognitive rehabilitation. This individualized approach (problem-solving training, memory notebook training) improves everyday functioning rather than performance on isolated tasks.

4. Skin Care and Maintaining Skin Integrity

Stage 5 uremic skin changes come mainly from accumulated toxins. Metabolic acidosis can drive protein-energy malnutrition, lean mass loss, and weakness. Altered salt and water handling causes peripheral edema. Calciphylaxis (calcific uremic arteriolopathy) deposits calcium in deep dermal and subcutaneous arterioles, classically in ESRD patients on maintenance dialysis.

Inspect skin color, turgor, vascularity, redness, excoriation, ecchymosis, and purpura. These mark poor circulation or breakdown leading to decubitus and infection. Calciphylaxis presents as exquisitely painful retiform purpura or tender nodules, often on the abdomen and proximal lower extremities; resulting infection and sepsis are the leading cause of death in these patients.

Monitor fluid intake and skin and mucous membrane hydration. This catches dehydration or overhydration affecting circulation and tissue integrity. Higher water intake raises stratum corneum and dermal hydration, especially in low prior consumers.

Inspect dependent areas for edema; elevate legs as indicated. Edematous tissue breaks down faster. Elevation promotes venous return and limits stasis. Tubulointerstitial disease can also present first as polyuria and volume depletion, risking dehydration.

Investigate itching. The skin excretes waste like phosphate crystals (linked to ESRD hyperparathyroidism), causing itch. ESRD chronic itch shows excoriations, erosions, scars, nodules, and pigment change; 38% of patients report localized itch, mostly back, lower extremities, scalp, upper extremities, and abdomen.

Reposition frequently; move the patient carefully; pad bony prominences with sheepskin and heel or elbow protectors. This offloads pressure on edematous, poorly perfused tissue and reduces ischemia. Pair repositioning with appropriate mattresses and overlays.

Provide gentle skin care; limit soaps; apply ointments or creams. Baking soda and cornstarch baths reduce itch and dry less than soap. Use mild, non-alkaline cleansers and lukewarm water for no more than 20 minutes. Balneological therapy with polidocanol bath oil cleared itch completely in 87% of hemodialysis patients after 4 weeks.

Keep linens dry and wrinkle-free. Wrinkled or damp linens cause friction and a moist environment that breeds bacteria and fungi, leading to breakdown and infection.

Restrict dietary phosphate per the dietitian. Patients with calcium-phosphate imbalance need a dietitian versed in ESRD restrictions, with special attention to phosphate.

Use cool, moist compresses with pressure (not scratching) on itchy areas; keep fingernails short; use gloves during sleep if needed. Apply a cold, wet cloth or ice pack for 5 to 10 minutes until the itch eases. Cooling agents like menthol or calamine, or refrigerated moisturizer, add relief.

Suggest loose-fitting cotton garments. Cotton limits irritation and promotes moisture evaporation; wool and rough fabrics intensify itching.

Provide a foam or flotation mattress. Pressure redistribution surfaces (high-density foam, low air loss, viscoelastic foam, air-fluidized) protect existing injuries. Low-air-loss surfaces help diaphoretic or incontinent patients.

Promote water intake as tolerated. The National Kidney Foundation suggests a total daily water intake of 3 liters for men and 2.2 liters for women with CKD; French authorities recommend 1.5 liters, adjusted to thirst and excretion.

Administer topical therapy as indicated. See Pharmacologic Management.

Start phototherapy as prescribed. UV radiation reduces uremic pruritus through apoptosis of inflammatory cells, Langerhans cell inhibition, altered cytokine production, and antimicrobial effect, with reductions in pruritus score and skin phosphorus content.

Administer systemic medications (gabapentin, pregabalin, sodium thiosulfate) as prescribed. See Pharmacologic Management.

Provide information on acupressure for itching. Both acupressure and transcutaneous electrical acupoint stimulation relieved uremic pruritus better than control.

5. Promoting Oral Health

Oral health shapes outcomes in ESRD. These patients have more severe oral disease than the general population, and caries, periodontitis, and poor hygiene track with higher mortality through inflammation and malnutrition. An estimated 90% of CKD patients have oral symptoms.

Inspect the oral cavity: moistness, saliva, inflammation, ulceration, leukoplakia. This allows prompt intervention. The most common finding in a dialyzed patient is mucosal pallor from anemia.

Provide fluids across 24 hours within the prescribed limit. This prevents oral dryness from long periods without intake. The 2010 European Food Safety Authority guidelines recommend a total water intake of 2.5 liters/day for men and 2.2 liters/day for women. The National Kidney Foundation suggests 3 liters for men and 2.2 liters for women with CKD.

Offer frequent mouth care and rinsing with 10% hydrogen peroxide. Uremia and restricted intake leave the mouth dry, cracked, and unpleasant-tasting. A third of hemodialysis patients have "uremic fetor" and a metallic taste from high salivary urea. For uremic stomatitis, gargle with 10% hydrogen peroxide 4 times a day to promote healing.

Encourage dental hygiene after meals and at bedtime; avoid dental floss. Floss can cut gums and cause bleeding. Brush twice daily with fluoridated toothpaste.

Offer gum, hard candy, or breath mints between meals. Some CKD drugs cause dry mouth, raising caries and gum disease risk. Sugarless gum or candy boosts saliva.

Recommend stopping smoking; avoid lemon, glycerine products, and alcohol-containing mouthwash. These irritate and dry the mucosa. Tobacco raises oral mucosal lesions, periodontal disease, and caries, with strong links to leukoplakia and other lesions.

Provide artificial saliva (Ora-Lube) as needed. Salivary substitutes (carboxymethylcellulose or porcine gastric mucin based) and alcohol-free rinses prevent dryness, buffer acids, and add comfort.

Administer medications (cyproheptadine, pilocarpine, analgesics) as indicated. See Pharmacologic Management.

Promote an ideal toothbrush. Use even-length nylon bristles of medium hardness, small enough to reach all areas; angled or altered-filament brushes clean above and below the tooth without overbrushing.

6. Health Teaching and Patient Education

CKD affects an estimated 13% of the US population. Better management slows progression, prevents metabolic complications, and reduces cardiovascular outcomes. Patient awareness and engagement are central to better outcomes, as is provider knowledge of when to refer to nephrology.

Review disease process, prognosis, and future expectations. This gives the patient a base for informed choices. CKD awareness stays low, with self-awareness of 6% to 12% across populations and higher awareness in more severe disease.

Review dietary restrictions, including phosphorus (carbonated drinks, processed foods, poultry, corn, peanuts) and magnesium (whole grains, legumes). Phosphorus retention pulls calcium from bone (renal osteodystrophy); magnesium accumulation impairs neuromuscular function and mentation. Monthly phosphorus-focused education over 6 months significantly improved mean serum phosphate.

Enforce fluid and sodium restrictions when indicated. With fluid retention, the patient may need to restrict intake to 1100 cc or less and limit dietary sodium; diuretics or dialysis may be added. The general-population dietary sodium recommendation is less than 5 to 6 g daily.

Regulate protein intake to renal function (generally 0.6 to 0.7 g/kg/day of high-quality protein such as meat and eggs). Accumulating metabolites come almost entirely from protein catabolism, so protein drops as function declines, but too little causes malnutrition. Dialysis patients may not need to be as strict.

Encourage adequate calories, especially carbohydrate in nondiabetic patients. This spares protein, prevents muscle wasting, and supplies energy. Glucose polymer powders add calories without extra food or fluid. Increasing alkali-inducing fruits and vegetables (enough to halve dietary acid over 30 days) decreased urinary albumin.

Discuss drug therapy: calcium supplements, phosphate binders (aluminum hydroxide antacids), avoidance of magnesium antacids, and vitamin D. Binders reduce GI phosphate absorption and supply calcium to protect bone, but monitor aluminum products (osteodystrophy) and avoid magnesium products (hypermagnesemia). Vitamin D aids calcium absorption and lowers phosphate and PTH.

Stress reading all drug and food labels and clearing new medications with the provider. Exogenous intake makes electrolyte balance hard; routine calcium supplements plus fortified foods can cause hypercalcemia. Check dosing carefully in dialysis patients.

Review bleeding precautions: soft toothbrush, electric razor; avoid constipation, forceful nose blowing, strenuous exercise, and contact sports. This addresses altered clotting and low platelet count. In early CKD, non-vitamin K oral anticoagulants had a better benefit-risk profile than vitamin K antagonists.

Teach self-monitoring of BP: rest before measuring, same arm and position each time. Hypertension is common in CRF and needs close tracking of treatment effect. Patients with few symptoms resist self-management, so they need active support.

Caution against temperature extremes (heating pad, snow). Peripheral neuropathy, mainly in the lower limbs, impairs sensation and raises injury risk.

Establish a routine exercise program within ability, with adequate rest. This maintains muscle tone and joint flexibility and reduces immobility risks including bone demineralization. KDIGO recommends regular exercise ideally at least 30 minutes 5 times per week; aerobic exercise has the strongest evidence in dialysis patients.

Address sexual concerns. Uremia and antihypertensives impair desire and performance. Puberty is often delayed; women with advanced CKD develop menstrual irregularities, and ESRD typically causes amenorrhea and infertility. Pregnancy in advanced CKD carries markedly decreased fetal survival.

Identify resources and stress medical and lab followup. Close monitoring of renal function and electrolytes guides diet and treatment decisions. Refer to nephrology early and continue followup through dialysis and transplant, with a multidisciplinary team (nephrologist, primary care, renal dietitian, nurse, social worker).

Identify signs and symptoms needing immediate evaluation. See Potential Complications.

Review constipation prevention: stool softeners and bulk laxatives, avoiding magnesium products. Reduced fluid, dietary changes, and phosphate binders cause constipation; magnesium products raise hypermagnesemia risk.

Introduce reliable telehealth applications and resources. Telehealth reaches different learning styles and supports behavior change through engagement and self-reflection, using digital media, video conferencing, mobile apps, and store-and-forward technology.

Educate pregnant patients with CKD on disease implications. Fertility is reduced but pregnancy can occur at higher risk than in patients without renal disease. Many CKD drugs are teratogenic; patients on ACE inhibitors or certain immunosuppressants need clear counseling.

Encourage self-management skills. Patients need support to make decisions and sustain self-efficacy. Structured programs build autonomy, knowledge, and lasting self-management behavior.

7. Reducing Anxiety and Providing Emotional Support

Kidney disease patients can carry the same symptom burden, quality-of-life goals, and psychological distress as terminal cancer patients, with high mortality, end-of-life concerns, and potential hospice need. Patients, families, and staff all move through grief and loss along the disease course.

Assess the stage of grieving, difficulties, feelings about long-term illness, and potential loss. The longer the illness, the more the patient and family can move toward acceptance. CKD brings many losses (physical, cognitive, family and work roles), and depression is common in dialysis patients.

Screen for depression. 45% of adults with CKD have depressive symptoms at dialysis initiation, though self-report scales overweight somatic symptoms like sleep disturbance, fatigue, and anorexia.

Encourage the patient and family to express feelings and concerns. Feedback is essential to working through grief. Early intervention for distress can prevent or delay chronic mental disorders and protect adherence and outcomes.

Provide emotional and spiritual support in an accepting environment; avoid discussions that provoke guilt or anger. Families need support to adjust without added stressors. Peer and extended-family support helps them cope.

Help identify and use effective coping methods and accept what they cannot control. Long physical and emotional stress strains families. Deceased-donor transplant recipients may face complex emotions; some centers facilitate thank-you letters to donor families who opt in.

Teach family about grief stages and common grieving behaviors. Dialysis settings often avoid talking about death while emphasizing technology. Living and dying with CKD is a family experience, not just the patient's.

Help the patient and family build coping and problem-solving skills. This sustains coping over a prolonged illness. The disease strains relationships; encourage partners to make time for themselves and each other.

Refer to social work and counseling as indicated. This offers psychological and economic support. Social workers can create mourning rituals after a death and connect families to palliative teams.

Refer to clergy and local kidney disease support groups. These aid adaptation and acceptance and provide services and information.

Refer to palliative care. Early palliative care benefits patients with advanced CKD and their families, focusing on quality of life and relief of physical, psychosocial, and spiritual suffering.

Provide information on the disease, updates, and discharge care. Families want specific, customized information to reduce uncertainty, plus practical tips for daily medication routines.

Encourage families to ask for help with practical care. Informal care often falls to family or neighbors. Families may need help with transport, finances, and forms.

8. Promoting Safety and Preventing Injury

Renal bone disease is a common complication, with skeletal and extraskeletal effects. In children it occurs during growth, risking short stature, bone curvature, and poor mineralization. CKD-mineral and bone disorder reflects abnormalities in serum phosphorus, PTH, vitamin D, and alkaline phosphatase.

Assess blood pressure. This flags the hypertension typical of advanced renal disease, common in CKD but also seen without it.

Assess for sensory loss, confusion, and changes in consciousness. These reveal neurologic decline as uremic syndrome appears. Uremic encephalopathy shows as fatigue, weakness, headache, restless legs, asterixis, polyneuritis, mental status change, cramps, seizures, stupor, and coma. Amyloid deposits can cause median nerve neuropathy and carpal tunnel.

Assess I&O, electrolyte panel, and creatinine. These track renal function. Hyperkalemia usually does not develop until GFR falls below 20 to 25 mL/min/1.73 m². Plasma urea and creatinine rise measurably only after total GFR drops by 50%.

Assess bone pain and deformities affecting movement. These mark osteodystrophy from calcium-phosphorus imbalance: failure to synthesize vitamin D limits calcium absorption, acidosis dissolves bone alkaline salts, phosphate rises, and calcium falls. Hip fracture is more prevalent in dialysis patients across all ages.

Monitor RBC, hematocrit, and hemoglobin. See Laboratory and Diagnostic Procedures.

Assess ABG for acidosis by pH and bicarbonate loss. See Laboratory and Diagnostic Procedures.

Instruct on dietary needs: decrease sodium, potassium, phosphorus, calcium, and iron; limit protein and water as ordered; provide allowed-food lists and sample menus. Restrictions depend on the degree of failure. Phosphate restriction starts early but is insufficient alone for hyperphosphatemia.

Educate the patient and family on medications: actions, dose, frequency, and side effects to report. Adjust renally cleared drug doses and intervals to residual GFR; some are contraindicated in moderate to severe impairment.

Educate on dialysis procedure and frequency if appropriate, including biological, psychological, and social effects. Choice is based largely on creatinine and patient motivation. Peritoneal dialysis suits motivated patients needing schedule flexibility, possibly with cardiovascular disease. Hemodialysis needs functioning arteriovenous access and can be done at home or in a center.

Administer antihypertensives, diuretics, vitamin D, calcium salts, and alkalizing agents as ordered. See Pharmacologic Management.

Administer erythropoietin and hypoxia-inducible factor (HIF) agents as ordered. See Pharmacologic Management.

Educate on avoiding nephrotoxic medications. Avoid NSAIDs, nephrotoxic aminoglycosides, and other renal toxins. Many CKD patients are unaware of their disease and risk further injury from NSAIDs.

Promote smoking cessation. Smokers reach ESRD earlier than nonsmokers; cessation lowers the risk of future kidney failure, especially in men.

9. Managing Urinary Elimination

CKD prevalence is rising worldwide, estimated at 13% of the population. Diabetes and hypertension are the leading causes, but urological disorders also contribute: vesicoureteral reflux causing reflux nephropathy, recurrent UTIs causing pyelonephritis, urinary tract obstruction, and overactive bladder, especially in women.

Evaluate and maintain urinary catheters and drains. Many patients have a Foley, sometimes a suprapubic catheter, and pelvic drains. Pelvic drains and ureteral stents usually come out within 7 to 10 days; catheters stay longer.

Assess voiding pattern, frequency, and amount. This shows bladder emptying, renal function, and fluid balance. Patients with "positive" symptoms (polyuria, hematuria, edema) tend to present earlier.

Observe for changes in urine characteristics. For proteinuria, KDOQI recommends the spot urine albumin-to-creatinine ratio. RBCs and RBC casts suggest proliferative glomerulonephritis; pyuria or WBC casts suggest interstitial nephritis or UTI.

Observe for changes in mental status, behavior, or consciousness. Uremic wastes and electrolyte imbalance are toxic to the CNS. Uremia is marked by elevated blood urea with fluid, electrolyte, hormone, and metabolic derangement.

Monitor electrolytes, BUN, creatinine, albumin, and ABGs. Impaired function raises the risk of severe electrolyte and acid-base problems. Expect elevated BUN and creatinine, possible hyperkalemia or low bicarbonate, and possible hypoalbuminemia from protein loss or malnutrition.

Provide routine voiding measures: privacy, normal position, running water, warm water over the perineum. These relax perineal muscles and aid voiding. Extracellular volume overload appears once GFR falls below 10 to 15 mL/min/1.73 m².

Encourage fluid intake as prescribed. Adequate fluid maintains renal function and reduces bacterial adherence to the bladder wall. The National Kidney Foundation suggests 3 liters for men and 2.2 liters for women with CKD.

Provide and teach perineal care. Keep the area clean and dry to reduce irritation, breakdown, and ascending infection in an immune-compromised patient.

Insert a urinary catheter as indicated. An indwelling catheter prevents retention and measures output; intermittent catheterization reduces long-term catheter complications.

Encourage mobility and physical activity. Mobility promotes bladder emptying and lowers UTI risk. KDIGO recommends regular exercise ideally at least 30 minutes 5 times per week.

Maintain catheter patency; keep tubing free of kinks. Free drainage reduces stasis, retention, and ascending infection. Position tubing and bag for unimpeded flow.

10. Medications and Pharmacological Support

CKD drug management targets blood pressure (ACE inhibitors, ARBs) and complications like anemia (ESAs, iron).

Antihypertensives (prazosin, captopril, clonidine, hydralazine). These reduce systemic vascular resistance and renin release, cutting myocardial workload and preventing heart failure and MI. Aggressive BP control delays kidney function decline; guidelines target less than 130/80 mm Hg.

Serelaxin. Recombinant human relaxin-2 reduces rehospitalization and short-term mortality in acute heart failure, increases renal blood flow, and reduces filtration fraction without significantly changing GFR.

Beta-blockers. With symptomatically reduced ejection fraction, beta-blockers are first-line alongside renin-angiotensin-aldosterone inhibitors, reducing total mortality, sudden cardiac death, and heart failure progression in HFrEF.

Erythropoiesis-stimulating agents (ESAs). ESAs (epoetin alfa, darbepoetin alfa) are the preferred initial therapy for CKD anemia. The FDA advises considering ESA when hemoglobin is below 10 g/dL.

Erythropoietin preparations. These correct anemia by stimulating RBC production, reducing transfusion need. HIF-prolyl hydroxylase inhibitors stabilize HIF, improve iron mobilization, and produce lower but more consistent erythropoietin levels than ESAs.

Iron preparations. Oral iron helps non-dialysis CKD patients. Ferrous sulfate is inexpensive; ferric citrate also binds phosphate; iron polysaccharide complex offers high iron content with less GI irritation.

Cimetidine, ranitidine, and antacids. Given prophylactically to reduce gastric acid and GI hemorrhage risk.

Stool softeners and bulk laxatives. Straining against hard stool risks mucosal and rectal bleeding. Psyllium, dietary fiber, and methylcellulose retain fluid and increase stool weight; take with ample water.

Anticoagulants. CKD patients need anticoagulation for various indications. In early-stage CKD, non-vitamin K oral anticoagulants outperform vitamin K antagonists on benefit-risk.

Antihypertensives (ACEIs/ARBs). Use as tolerated with close monitoring for renal deterioration and hyperkalemia; check serum creatinine with every dose change. Bedtime dosing of at least one antihypertensive cut adjusted cardiovascular risk to about a third of morning-only dosing.

Diuretics. Loop diuretics are the mainstay for excess fluid; distal thiazide diuretics can reduce BP and extracellular volume even at lower eGFRs.

Supplemental vitamin D. Paricalcitol is FDA-approved for secondary hyperparathyroidism in stage 5 CKD and can safely reduce protein excretion in stages 2 to 5. Daily vitamin D decreased albuminuria in stage 3 to 4 patients with low vitamin D and high PTH.

Calcium salts. Phosphate binders bind GI phosphate to reduce hyperphosphatemia. Calcium acetate forms insoluble calcium phosphate excreted in feces; calcium carbonate normalizes phosphate and supplements calcium.

Alkalizing agents. Correcting metabolic acidosis may benefit protein and bone metabolism. Maintain serum bicarbonate above 22 mEq/L; sodium bicarbonate slowed CKD progression in the UBI trial.

Gabapentin. A GABA structural analog for epilepsy and neuropathic pain; markedly reduces itch intensity and pruritus score.

Pregabalin. Similar mechanism to gabapentin; 87% of patients had significant itch reduction, and the two were equally effective for neuropathic itch in ESRD.

Sodium thiosulfate. IV sodium thiosulfate markedly improves calciphylaxis as a potent antioxidant that increases solubility of calcium deposits, with symptomatic relief possible within 2 weeks.

Topical therapy. Emollients reduce stratum corneum water loss. An oil-in-water emulsion with glycerol 15% and paraffin 10% improved quality of life by day 56 in uremic xerosis. Cromolyn cream, gamma-linoleic acid 2.2% cream, sericin cream, and pramoxine 1% lotion also showed effect.

Cyproheptadine (Periactin). An H1 antagonist with 5-HT antagonism for itch relief. Side effects include sedation (sometimes desirable) and hypotension, usually responsive to IV fluids.

Pilocarpine (Salagen). Stimulates saliva production. Not suitable for all patients, but may be prescribed for dry mouth in CKD.

Analgesics. Paracetamol is the best choice; codeine can be used without dose modification. Ketoprofen, ibuprofen, and naproxen can cause hypertension and worsen bleeding. Aspirin is contraindicated: it increases platelet dysfunction, hemorrhage risk, and renal deterioration.

Antibiotics. For prevention or treatment of infection. Pseudomonas was highly sensitive to aminoglycosides, ceftazidime, cefoperazone-sulbactam, levofloxacin, and norfloxacin, with 100% susceptibility to piperacillin-tazobactam, carbapenems, polymyxin-B, and colistin. Gram-negative organisms including E. coli were highly sensitive to cefoperazone-sulbactam, piperacillin-tazobactam, carbapenems, fosfomycin, tigecycline, polymyxin-B, and colistin.

11. Monitoring for Complications and Diagnostics

Watch for fluid overload, electrolyte imbalance, hypertension, anemia, bone pain, neuropathy, and cardiovascular disease so you catch complications early.

Low-grade fever, chills, changes in urine and sputum, tissue swelling and drainage, oral ulceration. A depressed immune system, anemia, and malnutrition raise infection risk. Stage 5 acidosis can drive protein-energy malnutrition and lean mass loss.

Numbness and tingling of digits, abdominal and muscle cramps, carpopedal spasms. Uremia and decreased calcium absorption cause peripheral neuropathy, worsened by nutritional deficiency, hypocalcemia, and hypomagnesemia.

Joint swelling and tenderness, decreased ROM, reduced strength. Hyperphosphatemia with calcium shifts deposits calcium phosphate in joints and soft tissue. Hypocalcemia stems from low calcitriol and reduced intestinal absorption.

Headaches, blurred vision, periorbital and sacral edema, "red eyes." These suggest poorly controlled hypertension or calcium-related eye changes; scleral calcium deposition causes "red eye."

Laboratory and diagnostic monitoring in CKD includes serum creatinine, BUN, and eGFR, urine testing for proteinuria or hematuria, and renal ultrasound or CT for structure.

Electrolytes (potassium, sodium, calcium, magnesium), BUN, and creatinine. Imbalances alter conduction and cardiac function. Expect elevated BUN and creatinine, possible hyperkalemia or low bicarbonate. Hyperkalemia usually does not develop until GFR falls below 20 to 25 mL/min/1.73 m².

Chest x-ray and echocardiogram. These identify cardiac failure or soft-tissue calcification. Chest x-ray may show an increased cardiac silhouette from effusion; pericardial effusion is visible on echocardiogram in up to 50% of uremic pericarditis.

RBCs, hemoglobin, and hematocrit. Uremia depresses erythropoietin and RBC production and survival. Hemoglobin and hematocrit are usually low but tolerated; patients may stay asymptomatic until hemoglobin drops below 7.

Platelet count and clotting factors. Suppressed platelets and inadequate factors III and VIII impair clotting and risk bleeding, which can become intractable in ESRD. Major bleeding and all-cause death were 4 times higher in anemic patients.

Prothrombin time (PT). Abnormal prothrombin consumption lowers serum levels and impairs clotting. Clot lysis time is prolonged in hemodialysis and peritoneal dialysis, indicating a hypofibrinolytic state.

Iron levels and HbA1c. Check iron stores before starting erythropoietin; target iron saturation 30 to 50% and ferritin 200 to 500 ng/mL. In non-hemodialysis CKD, HbA1c above 9% tracks with worse outcomes.

ABG levels. These flag impending metabolic acidosis from failure to excrete metabolic acids; hydrogen ion is retained and bicarbonate lost. Acidosis contributes to renal osteodystrophy and interferes with vitamin D metabolism.

RBC, hematocrit, and hemoglobin. These confirm anemia from depleted erythropoietin and restricted iron intake. Anemia starts early and worsens as GFR falls, and is twice as prevalent in CKD as in the general population.

BUN, creatinine, serum electrolytes, glucose, and ABGs (PO2, pH). Correcting these can sharply affect cognition. High-flux, high-efficiency maintenance dialysis with monthly adequacy assessment has eliminated much severe cognitive impairment.

Urine or sputum cultures. These identify the organism and antibiotic sensitivities. Gram-negative organisms, especially E. coli, were the most common in CKD UTIs; the most common gram-positive isolate was Enterococcus, then Staphylococcus aureus.

Other Possible Nursing Care Plans

• Excess Fluid Volume: compromised regulatory mechanism.
• Fatigue: decreased metabolic energy production, dietary restriction, anemia, increased energy requirements (fever, inflammation, tissue regeneration).
• Ineffective Therapeutic Regimen Management: complex regimen, decisional conflict, powerlessness, economic difficulty, family conflict, lack of support systems.
• Hopelessness: deteriorating physiological condition, long-term stress, prolonged activity limitations.

Frequently Asked Questions

How is chronic kidney disease defined? CKD is an estimated glomerular filtration rate (eGFR) under 60 mL/min/1.73 m², or markers of kidney damage such as albuminuria, hematuria, or lab or imaging abnormalities, present for at least 3 months (KDIGO 2024). The 3-month requirement separates chronic disease from acute kidney injury.

What are the stages of CKD? Stages run on a continuum by eGFR: stage 1 (90 or above with kidney damage), stage 2 (60 to 89), stage 3a (45 to 59), stage 3b (30 to 44), stage 4 (15 to 29), and stage 5 (below 15 or on dialysis). Stages 1 to 3 are usually asymptomatic, and symptoms typically appear at stages 4 to 5.

What are the leading causes of CKD? Diabetes and high blood pressure are the leading causes, together accounting for about two-thirds of new cases of kidney failure (CDC). Faster progression is linked to proteinuria, uncontrolled hypertension, and hyperglycemia.

Why are CKD patients at high risk for cardiovascular complications? Sodium and fluid retention, renin-angiotensin-aldosterone disturbance, and anemia raise myocardial workload and blood pressure. Cardiovascular disease, not kidney failure itself, is the most common cause of death in people with CKD, so blood pressure control and fluid balance are nursing priorities.

What nursing assessments catch CKD complications early? Track fluid status (weight, edema, lung sounds, blood pressure), electrolytes (especially potassium, which usually rises only once GFR falls below 20 to 25 mL/min/1.73 m²), hemoglobin and hematocrit for anemia, and mental status for uremic encephalopathy. Watch for bleeding from uremic platelet dysfunction and for signs of infection.

Which medications should be avoided or adjusted in CKD? Avoid nephrotoxic drugs such as NSAIDs and aminoglycosides. Adjust renally cleared drug doses and intervals to residual GFR. Acetaminophen (paracetamol) is the preferred analgesic, while aspirin is contraindicated because it worsens platelet dysfunction and bleeding risk.