Chronic Kidney Disease: A BSN Course Module

Course Overview

Chronic kidney disease (CKD) is a global public health challenge affecting approximately 10–15% of the adult population worldwide and more than 37 million Americans. It is defined as abnormalities of kidney structure or function — including a glomerular filtration rate (GFR) below 60 mL/min/1.73 m² or markers of kidney damage (such as albuminuria) — present for more than three months. CKD is progressive in many patients, ultimately leading to kidney failure, cardiovascular disease, and premature death if not identified and managed aggressively.

Nurses across all settings — primary care, outpatient clinics, medical-surgical units, intensive care, dialysis centers, and hospice — encounter patients with CKD at every stage of illness. This course equips BSN graduates with the foundational knowledge, clinical reasoning skills, and evidence-based practice competencies required to assess, manage, educate, and advocate for patients living with CKD. Emphasis is placed on early detection, interdisciplinary collaboration, patient-centered goal-setting, and culturally competent care throughout the disease trajectory.

Learning Objectives

By the end of this course module, students will be able to:

Describe the anatomy and physiology of the kidney and explain how progressive nephron loss produces the clinical syndrome of CKD. (Bloom’s: Understand)
Classify CKD by GFR category and albuminuria category using the KDIGO staging system and explain the clinical implications of each stage. (Bloom’s: Apply)
Identify the most common etiologies of CKD — including diabetic nephropathy, hypertensive nephrosclerosis, and glomerulonephritis — and explain the underlying pathophysiological mechanisms. (Bloom’s: Understand)
Perform a systematic nursing assessment of the patient with CKD including physical examination findings, laboratory data interpretation, and diagnostic study review. (Bloom’s: Apply)
Analyze laboratory findings characteristic of CKD, including changes in BUN, creatinine, GFR, electrolytes, CBC, and acid-base status. (Bloom’s: Analyze)
Apply evidence-based pharmacological management strategies for CKD and its comorbidities, including antihypertensives, erythropoiesis-stimulating agents, phosphate binders, and vitamin D analogs. (Bloom’s: Apply)
Implement individualized nutritional plans for patients with CKD addressing protein, potassium, phosphorus, sodium, and fluid restrictions. (Bloom’s: Apply)
Compare hemodialysis, peritoneal dialysis, and kidney transplantation as renal replacement therapies, including indications, access management, and nursing responsibilities. (Bloom’s: Analyze)
Identify and manage acute and chronic complications of CKD, including hyperkalemia, metabolic acidosis, CKD-mineral and bone disorder (CKD-MBD), cardiovascular disease, and uremic syndrome. (Bloom’s: Analyze)
Develop culturally sensitive patient and family education plans supporting self-management, medication adherence, dietary compliance, and vascular/peritoneal access site care. (Bloom’s: Create)
Apply palliative and end-of-life care principles for patients who choose conservative management or who discontinue dialysis. (Bloom’s: Apply)

Course Structure

Module	Title	Key Focus
1	Renal Anatomy, Physiology, and Pathophysiology of CKD	Nephron function, GFR, compensatory mechanisms, progression
2	CKD Staging and Etiology	KDIGO staging, diabetic nephropathy, hypertension, GN
3	Clinical Assessment of the Patient with CKD	History, physical exam, laboratory analysis, imaging
4	Pharmacological Management	Antihypertensives, ESAs, phosphate binders, vitamin D, diuretics
5	Nutritional Therapy in CKD	Protein, potassium, phosphorus, sodium, fluid restrictions
6	Renal Replacement Therapy: Hemodialysis	Indications, vascular access, procedure, nursing care
7	Renal Replacement Therapy: Peritoneal Dialysis	CAPD/APD, catheter care, peritonitis prevention
8	Kidney Transplantation	Evaluation, immunosuppression, rejection, post-transplant care
9	Complications of CKD	Hyperkalemia, acidosis, CKD-MBD, anemia, cardiovascular risk
10	Patient Education and Self-Management	Medication adherence, diet, access care, care transitions
11	Palliative Care and Conservative Management	Symptom management, goals of care, end-of-life planning

Module 1: Renal Anatomy, Physiology, and Pathophysiology of CKD

Overview

An understanding of normal renal structure and function is prerequisite to understanding how its loss produces the multisystem manifestations of CKD. The kidneys are paired retroperitoneal organs responsible for filtration, fluid and electrolyte homeostasis, acid-base regulation, blood pressure control, erythropoiesis stimulation, and vitamin D activation. The functional unit of the kidney is the nephron; each kidney contains approximately one million nephrons.

Key Concepts

Glomerular filtration rate (GFR): The volume of filtrate produced per minute across all glomeruli; normal is approximately 90–120 mL/min/1.73 m². GFR declines with age and progressively in CKD.
Renal autoregulation: Intrinsic mechanisms (myogenic reflex, tubuloglomerular feedback) maintain relatively constant GFR across a wide range of blood pressures.
Hyperfiltration: In early CKD or after nephron loss, remaining nephrons increase individual GFR to compensate. Over time, this adaptive response accelerates glomerulosclerosis and further nephron loss.
Proteinuria: Damage to the glomerular filtration barrier allows protein (primarily albumin) to pass into the filtrate. Proteinuria is both a marker and a mediator of CKD progression — filtered proteins activate tubular cells to release pro-inflammatory and pro-fibrotic mediators.
Renin-angiotensin-aldosterone system (RAAS): Activated by reduced renal perfusion, RAAS drives sodium retention, vasoconstriction, and hypertension — all of which accelerate CKD progression.
Erythropoietin (EPO): Produced by peritubular fibroblasts in response to hypoxia; stimulates red blood cell production. EPO deficiency in CKD leads to normocytic, normochromic anemia.
1,25-dihydroxyvitamin D (calcitriol): Activated in the proximal tubule; promotes intestinal calcium absorption. Impaired activation in CKD leads to hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism.

Pathophysiology of CKD Progression

CKD is characterized by an irreversible loss of functional nephrons. Regardless of the initial injury (diabetes, hypertension, immune-mediated, or obstructive), a common final pathway of glomerulosclerosis and tubulointerstitial fibrosis leads to progressive kidney failure. Key mediators of this progression include:

Intraglomerular hypertension and hyperfiltration
Proteinuria-induced tubular inflammation
Activation of the RAAS and transforming growth factor-beta (TGF-β)
Oxidative stress and chronic inflammation
Accumulation of uremic toxins

Discussion Questions

Why does proteinuria worsen CKD progression, and what interventions target this mechanism?
Explain why a patient with CKD develops anemia. What laboratory values would confirm this, and what is the underlying mechanism?
How does RAAS activation contribute to both hypertension and glomerulosclerosis in CKD?

Readings and Resources

Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. (2024). KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International, 105(4S).
National Kidney Foundation. (2023). About chronic kidney disease. https://www.kidney.org/atoz/content/about-chronic-kidney-disease
Levey, A. S., & Coresh, J. (2012). Chronic kidney disease. The Lancet, 379(9811), 165–180.

Module 2: CKD Staging and Etiology

Overview

Accurate staging of CKD guides prognosis, monitoring frequency, and therapeutic decision-making. The Kidney Disease: Improving Global Outcomes (KDIGO) framework classifies CKD using a combination of GFR category and albuminuria category, producing a risk matrix that informs clinical management at every stage.

KDIGO GFR Categories

GFR Category	GFR (mL/min/1.73 m²)	Description
G1	≥ 90	Normal or high (with markers of kidney damage)
G2	60–89	Mildly decreased (with markers of kidney damage)
G3a	45–59	Mildly to moderately decreased
G3b	30–44	Moderately to severely decreased
G4	15–29	Severely decreased
G5	< 15	Kidney failure (dialysis or transplant required if untreated)

KDIGO Albuminuria Categories

Albuminuria Category	AER (mg/24 h) or ACR (mg/g)	Description
A1	< 30	Normal to mildly increased
A2	30–300	Moderately increased (microalbuminuria)
A3	> 300	Severely increased (macroalbuminuria)

Major Etiologies of CKD

Diabetic nephropathy is the leading cause of CKD and kidney failure in the United States, accounting for approximately 44% of new cases of kidney failure annually. Persistent hyperglycemia causes glomerular basement membrane thickening, mesangial expansion, and efferent arteriolar vasoconstriction, leading to intraglomerular hypertension and progressive glomerulosclerosis. The earliest clinical marker is microalbuminuria (AER 30–300 mg/24 h), which precedes overt proteinuria by years.

Hypertensive nephrosclerosis is the second most common cause, particularly among African American patients. Sustained systemic hypertension damages the afferent arterioles, causing ischemic glomerulosclerosis and tubulointerstitial fibrosis. Target blood pressure in patients with CKD and proteinuria is < 130/80 mmHg per current guidelines.

Glomerulonephritis (GN) encompasses a heterogeneous group of immune-mediated disorders — including IgA nephropathy, lupus nephritis, focal segmental glomerulosclerosis (FSGS), and membranous nephropathy — that cause glomerular inflammation and progressive scarring. Presentation varies from microscopic hematuria and proteinuria to acute nephritic syndrome.

Other common etiologies include polycystic kidney disease (PKD), obstructive uropathy, renovascular disease, and nephrotoxin exposure (e.g., chronic NSAID use, contrast-induced nephropathy, certain chemotherapy agents).

Key Concepts

Uremia: The clinical syndrome resulting from accumulation of uremic toxins when GFR falls below approximately 10–15 mL/min; manifests as nausea, vomiting, encephalopathy, pericarditis, and pruritus.
Kidney failure (ESKD): End-stage kidney disease requiring renal replacement therapy (RRT) or conservative management for survival.
Acute kidney injury (AKI) on CKD: AKI superimposed on CKD accelerates progression; common precipitants include nephrotoxins, volume depletion, and infections.

Clinical Application

Scenario: A 58-year-old man with a 20-year history of type 2 diabetes mellitus and poorly controlled hypertension presents with fatigue and ankle swelling. His serum creatinine is 2.8 mg/dL, eGFR is 26 mL/min/1.73 m², and urine albumin-to-creatinine ratio (ACR) is 450 mg/g.

GFR category: G4 (severely decreased)
Albuminuria category: A3 (severely increased)
KDIGO risk category: Very high risk for CKD progression and cardiovascular events
Most likely etiology: Diabetic nephropathy (given duration of diabetes, degree of albuminuria, and concurrent hypertension)
Priority nursing actions: Blood pressure optimization, RAAS blockade evaluation, glycemic control review, nephrology referral, and patient education about stage G4 CKD and preparation for RRT

Discussion Questions

Why is early identification of microalbuminuria critical in patients with type 2 diabetes, and what nursing interventions promote early detection?
How does the KDIGO risk matrix (GFR × albuminuria) guide monitoring frequency?
Compare and contrast the pathophysiology of diabetic nephropathy and hypertensive nephrosclerosis.

Readings and Resources

KDIGO CKD Work Group. (2024). KDIGO 2024 Clinical Practice Guideline for CKD. Kidney International.
National Kidney Foundation. (2022). Causes of chronic kidney disease. https://www.kidney.org
Tuttle, K. R., et al. (2022). Diabetic kidney disease: A report from an ADA Consensus Conference. Diabetes Care, 45(12), 3075–3090.

Module 3: Clinical Assessment of the Patient with CKD

Overview

Systematic nursing assessment is essential for detecting CKD complications early, monitoring disease progression, evaluating treatment response, and identifying reversible precipitants of AKI on CKD. Assessment integrates a thorough health history, targeted physical examination, laboratory data analysis, and review of diagnostic studies.

Health History

A thorough history includes:

Past medical history: Diabetes, hypertension, cardiovascular disease, autoimmune disorders, recurrent UTIs, kidney stones, obstructive uropathy
Family history: Polycystic kidney disease, hereditary nephritis (Alport syndrome), diabetes, hypertension
Medication review: NSAIDs, aminoglycosides, contrast agents, lithium, calcineurin inhibitors, proton pump inhibitors, herbal supplements — all potential nephrotoxins
Social history: Tobacco use (associated with faster CKD progression), alcohol intake, dietary habits, access to care, health literacy
Symptom review: Fatigue, dyspnea, edema, changes in urine output or color, nocturia, pruritus, muscle cramps, altered mentation, nausea/vomiting, bone pain

Physical Examination Findings in CKD

System	Common Findings
Cardiovascular	Hypertension; peripheral edema; pericardial friction rub (uremic pericarditis in ESKD)
Respiratory	Kussmaul respirations (metabolic acidosis); pulmonary edema (fluid overload)
Neurological	Fatigue, difficulty concentrating, asterixis (uremic encephalopathy), peripheral neuropathy
Integumentary	Pallor (anemia), sallow/yellowish hue (urochrome deposition), uremic frost (ESKD), excoriation (pruritus), ecchymoses (platelet dysfunction)
Musculoskeletal	Bone pain, muscle weakness, pathological fractures (CKD-MBD)
Gastrointestinal	Nausea, vomiting, metallic taste, anorexia, hiccups (uremia)
Access sites	AV fistula/graft thrill/bruit assessment; peritoneal catheter exit-site inspection

Laboratory Assessment

Nurses must be proficient in interpreting the following laboratory values in the context of CKD:

Laboratory Value	Expected Change in CKD	Clinical Significance
Serum creatinine	Elevated (inversely proportional to GFR)	Primary marker; affected by muscle mass, age, sex
eGFR (CKD-EPI equation)	Decreased	Standardized measure of kidney function; guides staging
BUN (blood urea nitrogen)	Elevated	Uremia marker; also affected by protein intake and volume status
Serum potassium	Elevated (hyperkalemia) in moderate-to-advanced CKD	Risk for fatal dysrhythmias; requires dietary restriction and/or medication
Serum bicarbonate	Decreased (metabolic acidosis)	Accelerates CKD progression, catabolism, and bone disease
Serum phosphorus	Elevated in advanced CKD	Drives secondary hyperparathyroidism and CKD-MBD
Serum calcium	Decreased (early); variable with treatment	Hypocalcemia triggers PTH secretion
PTH (intact)	Elevated (secondary hyperparathyroidism)	Marker and driver of CKD-MBD
Hemoglobin/hematocrit	Decreased (normocytic, normochromic anemia)	EPO deficiency; requires ESA therapy and iron supplementation
Serum ferritin / TSAT	Variable; assess iron stores before ESA therapy	Iron deficiency is common and limits ESA response
Urine albumin-to-creatinine ratio (ACR)	Elevated in diabetic and hypertensive nephropathy	Prognostic marker; target of RAAS blockade therapy
25-hydroxyvitamin D	Decreased	Nutritional vitamin D deficiency is common; assess before prescribing calcitriol

Discussion Questions

A patient with CKD G4 has a serum potassium of 6.2 mEq/L and is asymptomatic. What are your priority nursing interventions and why?
How would you differentiate fluid volume overload from fluid volume deficit in a patient receiving hemodialysis?
Why is the BUN:creatinine ratio clinically useful, and what does an elevated ratio (>20:1) suggest?

Readings and Resources

Inker, L. A., et al. (2021). New creatinine- and cystatin C-based equations to estimate GFR without race. New England Journal of Medicine, 385(19), 1737–1749.
Lewis, S. L., Bucher, L., Heitkemper, M. M., & Harding, M. M. (2023). Medical-surgical nursing: Assessment and management of clinical problems (11th ed.). Elsevier.
National Kidney Foundation. (2023). Understanding lab values. https://www.kidney.org

Module 4: Pharmacological Management

Overview

Pharmacological management in CKD serves two primary goals: (1) slowing progression of kidney disease by addressing modifiable risk factors, and (2) managing the complications that arise as kidney function declines. Nurses must understand the indications, mechanisms, dosing adjustments required by reduced GFR, and monitoring parameters for each drug class.

Renin-Angiotensin-Aldosterone System (RAAS) Blockade

ACE inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) are first-line agents for patients with CKD and proteinuria. They reduce intraglomerular pressure by dilating the efferent arteriole, thereby decreasing proteinuria and slowing progression independent of their blood pressure-lowering effect. Key nursing considerations include:

Monitor serum creatinine and potassium 1–2 weeks after initiation or dose titration (an increase in creatinine of up to 30% from baseline is acceptable and expected).
Contraindicated in bilateral renal artery stenosis and pregnancy.
Do not combine ACEi with ARB (dual RAAS blockade increases AKI and hyperkalemia risk without added benefit).
SGLT2 inhibitors (e.g., dapagliflozin, empagliflozin) have demonstrated significant reno-protective and cardiovascular benefits in patients with CKD and type 2 diabetes and are now recommended as first-line adjuncts per KDIGO 2024.

Antihypertensive Therapy

Target blood pressure in CKD with proteinuria is < 130/80 mmHg. Additional antihypertensive agents commonly used include:

Dihydropyridine calcium channel blockers (CCBs): Amlodipine — effective and generally well-tolerated; used when ACEi/ARB alone is insufficient.
Diuretics: Loop diuretics (furosemide, bumetanide) are preferred in patients with GFR < 30 mL/min because thiazides lose efficacy; monitor fluid status, electrolytes, and creatinine.
Beta-blockers: Used in patients with concurrent heart failure or coronary artery disease; dose adjustments required for renally cleared agents (e.g., atenolol, metoprolol).

Erythropoiesis-Stimulating Agents (ESAs)

ESAs (epoetin alfa, darbepoetin alfa) stimulate red blood cell production and are indicated when hemoglobin falls below 10 g/dL and iron stores are replete. Nursing considerations include:

Check iron stores (ferritin, TSAT) before initiating ESA; iron deficiency must be corrected first.
Target hemoglobin 10–11.5 g/dL — avoid normalization (Hgb > 13 g/dL), which increases stroke and cardiovascular event risk.
Administered subcutaneously or intravenously; rotate injection sites.
Monitor blood pressure (ESAs can cause or worsen hypertension).
Intravenous iron (ferric gluconate, iron sucrose, ferumoxytol) is preferred over oral iron in dialysis-dependent patients due to superior bioavailability.

Phosphate Binders

Hyperphosphatemia in CKD stimulates PTH secretion and contributes to vascular calcification and mortality. Phosphate binders are taken with meals and snacks to block dietary phosphate absorption:

Agent	Type	Key Considerations
Calcium carbonate	Calcium-based	Inexpensive; risk of hypercalcemia and vascular calcification
Sevelamer (Renagel, Renvela)	Non-calcium, non-aluminum	Preferred in dialysis patients; also lowers LDL
Lanthanum carbonate (Fosrenol)	Non-calcium, non-aluminum	Chewable; effective; long-term safety profile established
Ferric citrate	Iron-based	Dual benefit: phosphate binding and iron supplementation

Vitamin D Analogs and Calcimimetics

Calcitriol (active vitamin D) or analogs (paricalcitol, doxercalciferol) suppress PTH secretion. Monitor calcium and phosphorus to avoid hypercalcemia.
Cinacalcet (Sensipar): A calcimimetic agent that sensitizes the calcium-sensing receptor to circulating calcium, reducing PTH secretion. Used in secondary hyperparathyroidism; can cause nausea and hypocalcemia.

Medication Dosing in CKD

Many renally cleared medications require dose adjustment or are contraindicated in CKD. Key examples include:

Metformin: Contraindicated when eGFR < 30 mL/min; use with caution at 30–45 mL/min.
Gabapentin: Dose reduce significantly; accumulation causes sedation and encephalopathy.
Morphine: Active metabolite accumulates; prefer hydromorphone or fentanyl in advanced CKD.
Direct oral anticoagulants (DOACs): Dose adjustment required; rivaroxaban and apixaban preferred over dabigatran.
NSAIDs: Avoid in all stages of CKD — cause renal vasoconstriction and worsen kidney function.

Discussion Questions

A patient with CKD G3b is started on lisinopril. Two weeks later, her creatinine has increased from 1.9 to 2.4 mg/dL and potassium is 5.4 mEq/L. How do you interpret these findings, and what actions are indicated?
Why is iron deficiency the most common reason for ESA hyporesponsiveness in CKD patients, and how is it assessed?
Your patient with ESKD is prescribed sevelamer carbonate 800 mg three times daily with meals. She asks why she needs a “phosphate pill.” How would you explain this?

Readings and Resources

KDIGO CKD Work Group. (2024). KDIGO 2024 CKD Guideline. Kidney International.
Kidney Disease: Improving Global Outcomes (KDIGO). (2012). KDIGO Clinical Practice Guideline for Anemia in CKD. Kidney International Supplements, 2(4), 279–335.
Agarwal, R., et al. (2023). FIDELIO-DKD and FIGARO-DKD: Finerenone in CKD and type 2 diabetes. NEJM Evidence.

Module 5: Nutritional Therapy in CKD

Overview

Nutritional management is a cornerstone of CKD care. As kidney function declines, the ability to excrete dietary nitrogen, potassium, phosphorus, and fluid is compromised. At the same time, patients with CKD are at high risk for protein-energy wasting (PEW) — a state of decreased body protein and energy stores associated with increased morbidity and mortality. Individualized dietary counseling by a renal dietitian, guided by the nurse’s ongoing assessment, is essential at every stage.

Protein

In non-dialysis CKD (G3–G5), a low-protein diet (0.6–0.8 g/kg/day) has been shown to slow progression by reducing hyperfiltration, proteinuria, and uremic toxin generation. However, excessive restriction increases the risk of PEW. In dialysis-dependent patients, protein requirements increase (1.2 g/kg/day for HD; 1.2–1.3 g/kg/day for PD) because dialysis removes amino acids. Plant-based protein sources are preferred for their favorable effect on acid-base balance and phosphorus bioavailability.

Potassium

Hyperkalemia is a life-threatening complication of advanced CKD that can cause fatal cardiac dysrhythmias. Dietary potassium restriction is typically implemented when serum potassium exceeds 5.5 mEq/L or GFR falls below 15–30 mL/min. Foods high in potassium to limit include:

Bananas, oranges, melons, dried fruits
Potatoes, tomatoes, winter squash, avocado
Legumes, nuts, chocolate, salt substitutes (often contain potassium chloride)

Leaching (soaking and boiling vegetables) reduces potassium content by up to 30–50%. Potassium binders (patiromer, sodium zirconium cyclosilicate) are now available as pharmacological adjuncts to dietary restriction.

Phosphorus

Dietary phosphorus restriction (800–1,000 mg/day) is typically initiated in G3b–G4 CKD or earlier if serum phosphorus is elevated. Foods high in phosphorus that require restriction include:

Dairy products (milk, cheese, yogurt)
Dark colas and processed foods (contain inorganic phosphate additives with nearly 100% absorption)
Organ meats, nuts, seeds, whole grains
Note: Plant-based phosphorus (phytate-bound) has lower bioavailability than animal-based or additive phosphorus

Patients must be taught to read food labels and recognize phosphate-containing food additives (e.g., dicalcium phosphate, phosphoric acid).

Sodium and Fluid

Sodium restriction (< 2,000–2,300 mg/day) reduces fluid retention, blood pressure, and left ventricular hypertrophy. In patients receiving hemodialysis with minimal residual kidney function, fluid restriction is typically 1,000–1,500 mL/day to limit interdialytic weight gain (IDWG) to < 4–4.5% of dry body weight. Excessive IDWG is associated with fluid overload, hypertension, and cardiovascular mortality.

Key Concepts

Dry weight (target weight): The weight at which the patient is euvolemic — free from edema and not hypotensive after dialysis; adjusted periodically by the nephrology team.
Protein-energy wasting (PEW): A syndrome of decreased protein and energy stores caused by inadequate intake, increased catabolism, or dialysis-associated losses; assessed by serum albumin, prealbumin, and anthropometric measurements.
Renal diet teaching: Should be individualized, culturally sensitive, and adapted for health literacy; involve a renal dietitian and use teach-back methodology to confirm understanding.

Discussion Questions

A patient on hemodialysis three times per week tells you he gained 5 kg since his last session (four days ago). What are your priority assessments, and what dietary counseling is indicated?
Why must salt substitutes be avoided in CKD patients with hyperkalemia? What teaching strategy would you use to help a patient make safe seasoning choices?
Explain why patients on peritoneal dialysis may have different protein requirements than those on hemodialysis.

Readings and Resources

KDIGO CKD Work Group. (2024). KDIGO 2024 CKD Guideline. Kidney International.
Kalantar-Zadeh, K., et al. (2017). Protein-energy wasting. Journal of Renal Nutrition, 27(5), 291–300.
National Kidney Foundation. (2023). Kidney kitchen: Recipes and nutrition guidance. https://www.kidneykitchen.org

Module 6: Renal Replacement Therapy — Hemodialysis

Overview

Hemodialysis (HD) is the most widely used form of renal replacement therapy worldwide. In HD, blood is removed from the patient via a vascular access device, circulated through an extracorporeal circuit where solutes and fluid are removed by diffusion and convection across a semipermeable membrane (dialyzer), and returned to the patient. Conventional HD is typically performed three times per week for three to five hours per session, though more frequent or home-based options exist.

Vascular Access

Vascular access is the lifeline of hemodialysis. The three types — in order of preference per the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines — are:

Arteriovenous fistula (AVF): Surgical anastomosis of a native artery and vein; gold standard due to superior patency and lowest infection risk; requires 6–12 weeks to mature before use.
Arteriovenous graft (AVG): Synthetic conduit between artery and vein; can be used sooner than AVF (2–3 weeks); higher risk of thrombosis and infection than AVF.
Central venous catheter (CVC): Tunneled (preferred) or non-tunneled; used as a bridge to permanent access or when other access is not feasible; highest infection risk (bacteremia, endocarditis); last resort for long-term use.

Nursing Assessment and Care of AVF/AVG

Assess for thrill (palpable vibration) and bruit (audible whooshing sound) at every shift — absence indicates thrombosis requiring immediate reporting.
Protect the access arm: No blood draws, IV insertions, blood pressure measurements, or tight clothing on the access extremity.
Educate patients to inspect the site daily for warmth, redness, swelling, or drainage indicating infection.
Instruct patients to apply gentle pressure to needle sites post-dialysis and report prolonged bleeding.

The Hemodialysis Procedure

During HD, the dialysate solution — containing electrolytes calibrated to normalize serum levels — flows countercurrent to the blood. Uremic solutes (urea, creatinine, potassium, phosphorus) diffuse from the blood down a concentration gradient into the dialysate. Excess fluid is removed by ultrafiltration (UF), controlled by adjusting transmembrane pressure.

Nursing Monitoring During Hemodialysis

Nurses monitor patients continuously during HD for:

Intradialytic hypotension (IDH): The most common complication; caused by rapid fluid removal; manage by reducing UF rate, placing patient supine, administering 0.9% NaCl bolus per protocol.
Muscle cramps: Common with aggressive ultrafiltration; managed by reducing UF rate, NaCl bolus, or warm packs.
Dysrhythmias: Particularly associated with rapid electrolyte shifts; continuous ECG monitoring for high-risk patients.
Air embolism: Rare but life-threatening; present with sudden chest pain, dyspnea, cyanosis; place patient on left lateral decubitus position, administer 100% O₂, notify provider immediately.
Clotted dialyzer or lines: Monitor for increased venous pressure alarms, dark blood in the circuit.

Discussion Questions

A patient’s AV fistula has no palpable thrill or audible bruit on your assessment. What is your priority action, and why is time-sensitive?
Compare the advantages and disadvantages of AVF, AVG, and tunneled CVC as long-term hemodialysis access.
A patient experiences symptomatic hypotension (BP 78/44) during hemodialysis. Outline your stepwise nursing response.

Readings and Resources

National Kidney Foundation KDOQI. (2019). Clinical practice guidelines for vascular access. American Journal of Kidney Diseases.
Counts, C. S. (Ed.). (2022). Core curriculum for nephrology nursing (7th ed.). ANNA/Pitman.
Daugirdas, J. T., Blake, P. G., & Ing, T. S. (Eds.). (2015). Handbook of dialysis (5th ed.). Wolters Kluwer.

Module 7: Renal Replacement Therapy — Peritoneal Dialysis

Overview

Peritoneal dialysis (PD) uses the patient’s own peritoneum as a semipermeable membrane. Dialysate is infused into the peritoneal cavity via a permanent catheter, dwells for a prescribed period during which solutes and fluid equilibrate across the peritoneal membrane, and is then drained. PD can be performed at home, offering greater patient autonomy and preservation of residual kidney function compared to HD.

Types of Peritoneal Dialysis

Continuous ambulatory peritoneal dialysis (CAPD): Manual exchanges performed 3–5 times per day; patient is ambulatory between exchanges.
Automated peritoneal dialysis (APD) / continuous cycling peritoneal dialysis (CCPD): A cycler machine performs exchanges during sleep; patient is free during the day.
Incremental PD: Less frequent exchanges in patients with significant residual kidney function; preserves residual function longer.

Peritoneal Catheter Care

The Tenckhoff catheter is the most commonly used PD catheter. Proper exit-site care is critical to preventing infection:

Cleanse the exit site daily with prescribed antiseptic solution (per center protocol, often chlorhexidine or mupirocin for Staphylococcus aureus prophylaxis).
Keep the exit site dry and covered with sterile dressing.
Inspect for signs of exit-site infection: erythema, induration, purulent drainage, pain.
Never immerse the catheter in water (no baths, swimming pools); showering with waterproof cover is acceptable per provider guidance.

Peritonitis: Recognition and Response

Peritonitis is the most serious complication of PD and a leading cause of technique failure. Nurses and patients must recognize:

Signs and symptoms: Abdominal pain, cloudy effluent (turbid drainage), fever, nausea/vomiting.
Diagnosis: Peritoneal effluent cell count (WBC > 100 cells/µL with > 50% neutrophils), Gram stain, and culture of effluent.
Management: Intraperitoneal (IP) antibiotics initiated empirically while cultures are pending; common regimens include IP vancomycin plus a gram-negative agent (e.g., ceftazidime or gentamicin).
Prevention: Strict aseptic technique during all exchanges; handwashing; prophylactic antibiotics before invasive procedures.

Advantages and Disadvantages of PD

Advantage	Disadvantage
Home-based; preserves independence	Daily technique required; patient/caregiver burden
Continuous, gentle solute clearance	Risk of peritonitis; potential for catheter dysfunction
Better preservation of residual kidney function	Glucose absorption from dialysate → hyperglycemia, weight gain
Preferred in patients with cardiovascular instability	Contraindicated with prior abdominal surgeries/adhesions
No vascular access required	Protein losses in effluent → increased dietary requirements

Discussion Questions

A patient calls the dialysis clinic reporting that her PD effluent looks “milky” and she has had abdominal pain since this morning. What is the most likely complication, and what instructions do you provide?
How does continuous peritoneal dialysis achieve solute clearance more gently than intermittent hemodialysis, and why might this benefit the cardiovascular system?
What factors should be considered when helping a patient and family choose between hemodialysis and peritoneal dialysis?

Readings and Resources

Li, P. K. T., et al. (2022). ISPD Peritonitis Guideline Recommendations: 2022 Update. Peritoneal Dialysis International, 42(2), 110–153.
Counts, C. S. (Ed.). (2022). Core curriculum for nephrology nursing (7th ed.). ANNA/Pitman.
National Kidney Foundation. (2023). Peritoneal dialysis. https://www.kidney.org

Module 8: Kidney Transplantation

Overview

Kidney transplantation offers the best quality of life and survival outcomes for eligible patients with kidney failure. It remains the only curative option for ESKD. However, organ shortage, immunological barriers, and the need for lifelong immunosuppression make transplantation available to only a subset of patients with ESKD. Nurses play key roles in patient evaluation, post-transplant monitoring, medication teaching, and long-term follow-up.

Transplant Evaluation

Potential recipients undergo extensive evaluation including:

Cardiovascular assessment (stress testing, echocardiography)
Cancer screening (colonoscopy, mammography, Pap smear, PSA as appropriate)
Infectious disease evaluation (HIV, hepatitis B/C, TB, CMV, EBV status)
Psychosocial and social support assessment
Surgical anatomy evaluation (vascular, urological)

Contraindications include active malignancy, active infection, uncontrolled cardiovascular disease, current substance use disorder, and inability to adhere to immunosuppressive regimen.

Immunosuppressive Therapy

Lifelong immunosuppression is required to prevent rejection. Standard maintenance regimens typically include:

Calcineurin inhibitors (CNIs): Tacrolimus (preferred) or cyclosporine — prevent T-cell activation; monitor trough levels; nephrotoxic.
Antimetabolites: Mycophenolate mofetil (MMF) or azathioprine — inhibit lymphocyte proliferation.
Corticosteroids: Prednisone — anti-inflammatory; often weaned over time; risk of diabetes, osteoporosis, infection.
mTOR inhibitors: Sirolimus, everolimus — used in some protocols; delayed wound healing, proteinuria.

Types of Rejection

Rejection Type	Timing	Mechanism	Management
Hyperacute	Minutes to hours	Preformed antibodies; rare with cross-match	Immediate nephrectomy; no effective treatment
Acute cellular	Days to weeks	T-cell mediated	High-dose IV corticosteroids; anti-thymocyte globulin (ATG)
Antibody-mediated (AMR)	Days to years	Donor-specific antibodies	Plasmapheresis, IVIG, rituximab
Chronic	Months to years	Cumulative immune and non-immune injury	Optimize immunosuppression; blood pressure control

Post-Transplant Nursing Care

Immediate post-operative nursing priorities include:

Monitor urine output hourly — oliguria or anuria may indicate delayed graft function (DGF), thrombosis, or rejection.
Strict fluid management — replace urine output mL-for-mL as ordered.
Monitor immunosuppressant trough levels daily initially.
Assess transplant site for pain, swelling, or hematoma.
Monitor for signs of infection (neutropenic fever protocol as applicable).
Educate patient to self-monitor daily weight, blood pressure, urine output, and signs of rejection (pain over graft, decreased urine output, fever, elevated creatinine).

Discussion Questions

A post-transplant patient reports decreased urine output (< 30 mL/hr for 2 hours), low-grade fever, and tenderness over the transplant site. What are your priority nursing actions?
Why is a patient who received a kidney transplant at higher lifetime risk for skin cancer and post-transplant lymphoproliferative disorder (PTLD)?
What medication adherence strategies would you incorporate into the discharge teaching plan for a transplant recipient?

Readings and Resources

Kidney Disease: Improving Global Outcomes (KDIGO). (2022). KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients. American Journal of Transplantation.
Danovitch, G. M. (Ed.). (2023). Handbook of kidney transplantation (6th ed.). Wolters Kluwer.
United Network for Organ Sharing (UNOS). (2024). Transplant data and resources. https://www.unos.org

Module 9: Complications of CKD

Overview

CKD affects virtually every organ system. Nurses must be competent in recognizing and managing the complex, overlapping complications that arise as kidney function declines. The most clinically significant include hyperkalemia, metabolic acidosis, CKD-mineral and bone disorder, anemia, and accelerated cardiovascular disease.

Hyperkalemia

Hyperkalemia (serum K⁺ > 5.5 mEq/L) is a potentially lethal complication of CKD. Its management is stratified by severity and ECG findings:

Severity	K⁺ (mEq/L)	ECG Changes	Management
Mild	5.5–6.0	None or peaked T waves	Dietary restriction; potassium binder (patiromer or SZC); medication review
Moderate	6.0–6.5	Peaked T waves; prolonged PR	Above + loop diuretic; nephrology notification
Severe	> 6.5 or symptomatic	Wide QRS; sine wave; VF risk	Immediate: Calcium gluconate IV (membrane stabilization) → Insulin + dextrose → Sodium bicarbonate → Kayexalate or kayexalate (if tolerated) → Emergent dialysis

Priority nursing action: Continuous cardiac monitoring; ensure IV access; notify provider immediately for any K⁺ > 6.0 mEq/L or ECG changes.

Metabolic Acidosis

Reduced hydrogen ion excretion and bicarbonate regeneration in CKD lead to metabolic acidosis (serum HCO₃⁻ < 22 mEq/L). Chronic acidosis:

Accelerates CKD progression through tubular injury
Increases muscle catabolism and protein-energy wasting
Exacerbates bone disease (acidosis dissolves hydroxyapatite mineral)
Impairs insulin signaling

Management: Oral sodium bicarbonate supplementation to maintain serum HCO₃⁻ ≥ 22 mEq/L; protein restriction reduces acid load. Target HCO₃⁻ 22–26 mEq/L.

CKD-Mineral and Bone Disorder (CKD-MBD)

CKD-MBD is a systemic disorder linking abnormal mineral metabolism (phosphorus, calcium, PTH, vitamin D) to cardiovascular calcification and bone disease. The cascade begins early in CKD:

Reduced GFR → phosphate retention → hyperphosphatemia
Hyperphosphatemia + reduced calcitriol production → hypocalcemia
Hypocalcemia + hyperphosphatemia → secondary hyperparathyroidism (elevated PTH)
Elevated PTH → renal osteodystrophy (bone resorption) and vascular/soft tissue calcification
FGF-23 (phosphatonin) rises early in CKD as an adaptive response but is independently associated with cardiovascular mortality

Manifestations: Bone pain, fractures, calciphylaxis, vascular calcification, left ventricular hypertrophy.

Management: Dietary phosphorus restriction, phosphate binders, active vitamin D analogs, calcimimetics, and bisphosphonates (with caution in advanced CKD).

Anemia of CKD

CKD anemia is primarily normocytic and normochromic, resulting from:

Absolute EPO deficiency (most common)
Iron deficiency (most common cause of ESA hyporesponsiveness)
Shortened red blood cell survival (uremic milieu)
Chronic inflammation and hepcidin elevation (functional iron deficiency)

Management follows a stepwise approach: assess and replete iron stores → initiate ESA when Hgb < 10 g/dL → titrate ESA to target Hgb 10–11.5 g/dL. Blood transfusion is reserved for symptomatic anemia unresponsive to ESA and may sensitize transplant candidates.

Cardiovascular Disease

CKD is an independent risk factor for cardiovascular disease (CVD). Patients with CKD G3b or worse have a higher risk of dying from CVD than reaching kidney failure. Mechanisms include:

Traditional risk factors (diabetes, hypertension, dyslipidemia)
Non-traditional risk factors (volume overload, anemia, LVH, arterial stiffness, inflammation, oxidative stress, uremic toxins)

Management: Blood pressure control, RAAS blockade, lipid management (statins initiated in non-dialysis CKD; evidence less clear in dialysis patients), smoking cessation, and glycemic optimization.

Uremic Syndrome

Advanced uremia (GFR < 10–15 mL/min) produces a constellation of symptoms that collectively constitute the uremic syndrome:

Neurological: Uremic encephalopathy, peripheral neuropathy, restless leg syndrome
Cardiovascular: Uremic pericarditis (friction rub; risk of tamponade)
Hematological: Platelet dysfunction (uremic bleeding)
Gastrointestinal: Nausea, vomiting, anorexia, metallic taste, hiccups, GI bleeding
Dermatological: Uremic pruritus, uremic frost (rare)

Recognition of uremic syndrome signals the need for urgent initiation of RRT or, in patients who decline, palliative management of symptoms.

Discussion Questions

Explain the pathophysiological cascade that links declining GFR to secondary hyperparathyroidism in CKD-MBD.
A patient’s ECG shows wide, bizarre QRS complexes and a serum potassium of 7.2 mEq/L. What is the first medication you administer and why?
Why is a patient with CKD G4 at greater absolute risk of dying from a cardiovascular event than from progressing to kidney failure?

Readings and Resources

Kalantar-Zadeh, K., Jafar, T. H., Nitsch, D., Neuen, B. L., & Perkovic, V. (2021). Chronic kidney disease. The Lancet, 398(10302), 786–802.
KDIGO. (2017). KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder. Kidney International Supplements.
Sarnak, M. J., et al. (2019). Kidney disease as a risk factor for development of cardiovascular disease. Circulation, 108(17), 2154–2169.

Module 10: Patient Education and Self-Management

Overview

Effective patient education is among the most powerful interventions in CKD care. Self-management skills — including dietary compliance, medication adherence, access site care, recognition of warning signs, and active participation in treatment decisions — directly influence disease progression, hospitalization rates, and quality of life. Nurses are the primary educators in nephrology care and must tailor teaching to the individual patient’s literacy level, cultural background, language, learning preferences, and readiness to change.

Core Self-Management Competencies for CKD Patients

Patients and caregivers should demonstrate understanding and skills in:

Medication management: Purpose, dose, timing, and side effects of all prescribed medications; importance of not taking OTC NSAIDs; safe use of herbal supplements.
Dietary adherence: Protein, potassium, phosphorus, sodium, and fluid restrictions appropriate to CKD stage; reading food labels; identifying hidden phosphate additives; safe food preparation techniques.
Blood pressure self-monitoring: Correct technique; target values; when to call the provider.
Weight monitoring: Daily weights at the same time each day; recognizing and reporting sudden weight gain (> 2 kg in 24 hours).
Access site care (dialysis patients): AVF/AVG thrill/bruit assessment; exit-site care for PD catheters; when to seek emergency evaluation.
Signs and symptoms to report promptly: Fever, decreased urine output, sudden swelling, chest pain, bleeding from access site, signs of peritonitis or access infection.
Avoiding nephrotoxins: NSAIDs, certain antibiotics, contrast dye (hydration protocol); informing all healthcare providers of CKD diagnosis before procedures.

Health Literacy and Teach-Back

Approximately one in three Americans has limited health literacy, and health literacy is independently associated with CKD outcomes. Strategies to optimize CKD education include:

Use plain language (6th-grade reading level or below for written materials).
Avoid medical jargon; explain terms when they must be used.
Present information in small chunks (3–4 key points per session).
Use visual aids, models, and demonstration for procedural skills.
Use the teach-back method: Ask patients to explain instructions in their own words (“Can you tell me what you will do if your effluent looks cloudy?”) rather than asking “Do you understand?”
Involve caregivers and designated support persons in all teaching sessions.
Reassess and reinforce at every encounter — CKD education is a continuous process, not a one-time event.

Culturally Sensitive Dietary Teaching

Food choices are deeply embedded in culture, family, and identity. Renal dietary restrictions may conflict with culturally traditional foods. Effective teaching:

Acknowledges the importance of cultural food practices without judgment.
Works with the patient and a renal dietitian to identify culturally acceptable substitutions and cooking modifications.
Focuses on portions and preparation methods rather than blanket prohibition of cultural foods.
Engages family members who prepare meals in dietary education sessions.

Care Transitions and Advance Care Planning

As CKD progresses, transitions between care settings (clinic to hospital, hospital to dialysis center, dialysis to hospice) create high-risk periods for medication errors, missed dialysis treatments, and loss of continuity. Nurses facilitate safe transitions by:

Providing a comprehensive and updated medication reconciliation at every transition.
Communicating with receiving care teams regarding access sites, dialysis schedule, and diet orders.
Initiating advance care planning discussions early (G3b–G4) before uremia impairs decision-making capacity.
Exploring patient values, preferences, and goals of care regarding RRT modalities and conservative management.

Discussion Questions

Your patient with ESKD says, “My doctor told me to limit fluids, but I’m always thirsty. I don’t think I can do this.” How do you respond, and what strategies might help?
How would you adapt a kidney diet teaching session for a patient from a Caribbean cultural background whose staple foods include rice and peas, plantains, and salt fish?
Describe the teach-back method and explain why “Do you understand?” is an ineffective assessment of patient learning.

Readings and Resources

National Kidney Foundation. (2023). Patient education resources. https://www.kidney.org/patients
Osborn, C. Y., et al. (2011). Health literacy explains racial disparities in diabetes medication adherence. Journal of Health Communication, 16(S3), 268–278.
Havas, K., et al. (2018). Patient-centered approaches to nursing management of chronic kidney disease. Clinical Nursing Research, 27(6), 661–676.

Module 11: Palliative Care and Conservative Management

Overview

Not all patients with CKD and kidney failure elect or are eligible for dialysis or transplantation. Conservative management (also called comprehensive conservative care or maximal medical management) is a legitimate, patient-centered approach for individuals who choose to forgo dialysis, focusing on symptom management, quality of life, and dignified death. Palliative care principles are appropriate at every stage of CKD — they complement rather than replace disease-directed treatment.

Integrating Palliative Care Across the CKD Trajectory

Palliative care in CKD includes:

Advance care planning (ACP): Facilitated conversations about values, goals, and preferences for end-of-life care; completion of advance directives (living will, health care proxy/power of attorney).
Prognosis communication: Sharing individualized prognosis information with patients and families in a sensitive, culturally appropriate manner.
Symptom management: Uremic pruritus (topical emollients, gabapentin with dose adjustment, UV phototherapy); pain (opioids with renal-safe selection); nausea (antiemetics); dyspnea (opioids, positioning, fan therapy); restless leg syndrome (gabapentin, dopamine agonists with caution).
Psychosocial support: Depression and anxiety are highly prevalent in CKD — screen routinely; facilitate referral to social work, chaplaincy, and mental health services.
Family support and caregiver education: Explain the dying process in renal failure (uremic coma, Cheyne-Stokes respiration); provide grief support resources.

Withdrawing Dialysis

Dialysis withdrawal is the second most common cause of death in U.S. ESKD patients after cardiovascular disease. Key nursing considerations include:

Decisions to withdraw dialysis should reflect informed, voluntary, and capable patient choice (or surrogate decision-making if patient lacks capacity).
Withdrawal is ethically and legally distinct from suicide or euthanasia.
After withdrawal, death typically occurs within days to two weeks, depending on residual kidney function.
Intensive symptom management (comfort-focused care) should begin immediately; hospice referral is recommended.
Support interdisciplinary team members who may experience moral distress around dialysis withdrawal decisions.

Signs of Approaching Death in ESKD

Nurses caring for patients who have withdrawn from dialysis or chosen conservative management should recognize:

Increasing uremic encephalopathy (somnolence, confusion, agitation)
Cheyne-Stokes respirations
Mottling and peripheral cooling
Decreased urine output to anuria
Changes in cardiac rhythm

Family education about these expected physiological changes reduces distress and promotes a peaceful death.

Discussion Questions

An 82-year-old patient with ESKD tells her family she does not want to start dialysis. Her son disagrees and insists she “must fight.” How do you as the nurse respond and what ethical principles guide your practice?
Why is it important to introduce palliative care principles at KDIGO stage G3b rather than waiting until kidney failure?
A patient withdrawing from dialysis asks if he will be in pain when he dies. What information do you provide, and how do you ensure comfort during the dying process?

Readings and Resources

Davison, S. N., et al. (2019). Executive summary of the KDIGO controversies conference on supportive care in CKD. Kidney International, 95(6), 1280–1301.
Brown, M. A., & Crail, S. M. (2022). Palliative care and conservative management in ESKD. Nephrology Dialysis Transplantation.
Renal Physicians Association. (2010). Shared decision-making in the appropriate initiation of and withdrawal from dialysis. RPA.

Standards Alignment Summary

Standard	Domains / Competencies Addressed
AACN Essentials (2021)	D1 (Knowledge), D2 (Person-Centered Care), D3 (Population Health), D4 (Scholarship/EBP), D6 (Interprofessional Collaboration), D9 (Professionalism), D10 (Personal/Professional Development)
NCLEX-NG CJMM	Recognize Cues (RC), Analyze Cues (AC), Prioritize Hypotheses (PH), Generate Solutions (GS), Take Action (TA), Evaluate Outcomes (EO)
QSEN	Patient-Centered Care (PCC), Teamwork and Collaboration (TC), Evidence-Based Practice (EBP), Quality Improvement (QI), Safety (S), Informatics (I)
CCNE Standards	Standard I (Mission and Governance), II (Institutional Resources and Support), III (Curriculum and Teaching-Learning Practices), IV (Aggregate Faculty and Student Outcomes)
ACEN Standards	Standard 3 (Students), 4 (Curriculum), 5 (Resources)