Guide — Renal
Chronic Kidney Disease (CKD)
CKD is the progressive, irreversible loss of kidney function over months to years. Management focuses on slowing progression, preventing complications, and preparing for renal replacement therapy when ESRD approaches.
13 min read · Renal
Educational use only. This content is intended for nursing students and exam preparation. Clinical decisions require licensed professional judgment and institutional protocols. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
CKD Definition
CKD is defined as abnormalities of kidney structure or function present for >3 months with health implications. Diagnosis requires either:
- ✦eGFR <60 mL/min/1.73m² for ≥3 months (stages G3–G5)
- ✦Markers of kidney damage for ≥3 months regardless of eGFR: albuminuria, urine sediment abnormalities, electrolyte disorders, structural abnormalities on imaging, or transplant history
CKD is irreversible — a critical distinction from AKI. End-stage renal disease (ESRD) = Stage 5 CKD (eGFR <15 mL/min) requiring dialysis or kidney transplant.
Causes
| Cause | Prevalence / Notes |
|---|---|
| Diabetic nephropathy | #1 cause of CKD in the US — affects ~40% of patients with diabetes; microalbuminuria is the earliest sign |
| Hypertensive nephrosclerosis | #2 cause — chronic hypertension damages glomerular capillaries; tight BP control slows progression |
| Glomerulonephritis | IgA nephropathy (most common worldwide), membranous nephropathy, FSGS, lupus nephritis |
| Polycystic kidney disease (PKD) | Most common inherited kidney disease; autosomal dominant; flank pain, hematuria, hypertension |
| Recurrent pyelonephritis | Chronic infection/scarring; more common in women and obstructive uropathy patients |
| Obstruction (chronic) | BPH, ureteral stricture, neurogenic bladder — hydronephrosis causes progressive damage |
| Nephrotoxin exposure | NSAIDs, aminoglycosides, contrast agents, heavy metals (lead, mercury), aristolochic acid |
CKD Staging Overview
| Stage | eGFR (mL/min) | Description | Focus |
|---|---|---|---|
| G1 | ≥90 | Normal or high eGFR with kidney damage markers | Treat underlying disease, reduce CVD risk |
| G2 | 60–89 | Mildly decreased | Slow progression, monitor annually |
| G3a | 45–59 | Mildly to moderately decreased | Treat complications (HTN, anemia) |
| G3b | 30–44 | Moderately to severely decreased | Nephrology referral, restrict protein/phosphorus |
| G4 | 15–29 | Severely decreased | Prepare for RRT — AV fistula creation, transplant evaluation |
| G5 | <15 | Kidney failure (ESRD) | Renal replacement therapy (dialysis or transplant) |
Clinical Manifestations
Early CKD (stages 1–3) is often asymptomatic. Symptoms develop as GFR falls below 15–20 mL/min (uremic syndrome).
Fluid/Electrolyte
- ✦Hypertension
- ✦Edema (peripheral, pulmonary)
- ✦Hyperkalemia
- ✦Hyperphosphatemia
- ✦Hypocalcemia
- ✦Metabolic acidosis
Hematologic
- ✦Normocytic, normochromic anemia (↓EPO)
- ✦Platelet dysfunction → bleeding risk
- ✦Immune suppression
Uremic Syndrome
- ✦Nausea, vomiting, anorexia
- ✦Uremic pruritus
- ✦Altered mental status, asterixis
- ✦Uremic frost (severe — rare)
- ✦Pericarditis
Musculoskeletal / Bone
- ✦Renal osteodystrophy
- ✦Secondary hyperparathyroidism
- ✦Calcifications in blood vessels/soft tissue
- ✦Bone pain, pathologic fractures
Complications
| Complication | Mechanism | Management |
|---|---|---|
| Anemia | ↓ EPO secretion by failing kidneys | Erythropoiesis-stimulating agents (ESAs), iron supplementation, blood transfusion if severe |
| Renal osteodystrophy | ↓ active vitamin D → ↓ Ca²⁺ → ↑ PTH → bone resorption; plus hyperphosphatemia | Phosphate binders (calcium acetate, sevelamer), active vitamin D (calcitriol), calcimimetics (cinacalcet) |
| Cardiovascular disease | HTN, fluid overload, uremic toxins, accelerated atherosclerosis | #1 cause of death in CKD — aggressive BP and lipid management |
| Metabolic acidosis | ↓ H⁺ excretion, ↓ ammonia synthesis, ↓ bicarbonate reclamation | Sodium bicarbonate supplementation; dietary acid restriction |
| Hyperkalemia | ↓ urinary potassium excretion | Dietary K⁺ restriction, patiromer or sodium zirconium cyclosilicate, dialysis in refractory cases |
| Infection risk | Impaired immune function, uremic toxin effect on WBCs | Vaccinations: pneumococcal, influenza, hepatitis B (give before dialysis) |
Treatment Overview
Blood pressure control (target <130/80 mmHg)
ACE inhibitors or ARBs are preferred for CKD patients — they reduce intraglomerular pressure and proteinuria. Monitor potassium and creatinine when starting (initial creatinine rise up to 30% is acceptable and expected).
Blood glucose control (if diabetic)
A1C target 7–8% in CKD. Metformin: contraindicated when eGFR <30 (lactic acidosis risk). SGLT2 inhibitors (empagliflozin, canagliflozin) have nephroprotective and cardioprotective benefits in CKD with T2DM.
Dietary modifications
Restrict: protein (0.6–0.8 g/kg/day in non-dialysis CKD), potassium, phosphorus, sodium. Adequate caloric intake to prevent malnutrition. Dialysis patients may need increased protein intake.
Manage anemia
Erythropoiesis-stimulating agents (ESAs — darbepoetin, epoetin alfa) to target Hgb 10–11.5 g/dL. Correct iron deficiency first. Avoid targeting normal Hgb (increased CVD/clot risk).
Prepare for renal replacement therapy (Stage 4–5)
AV fistula creation ideally 6–12 months before anticipated dialysis start. Evaluate for kidney transplant (living or deceased donor). Peritoneal dialysis training if preferred. Advance care planning discussions.
Nursing Considerations
Medication safety — renally cleared drugs
Metformin (hold if eGFR <30), NSAIDs (avoid entirely), ACE inhibitors/ARBs (monitor K⁺), digoxin (accumulates), opioids (active metabolites accumulate). Verify all doses with pharmacy.
Fluid and dietary teaching
CKD patients need individualized fluid allowances. Teach to read food labels for phosphorus, potassium, and sodium content. Phosphorus additives in processed foods are highly bioavailable.
Fistula and graft care
Never take BP, draw blood, or start IVs in the AV fistula arm. Assess bruit and thrill at each encounter — loss of bruit/thrill = occlusion, notify immediately.
Vaccination priority
Hepatitis B vaccine series before dialysis onset (immune response is better at higher eGFR). Annual influenza, pneumococcal vaccines.
Monitor electrolytes and weight
Daily weights (same time, same scale). Trend potassium — hyperkalemia is a common emergency. Report K⁺ >5.5 mEq/L.
NCLEX Pearls
- ✦CKD is IRREVERSIBLE. AKI is potentially reversible. This distinction is a frequent NCLEX question.
- ✦Top 2 causes: diabetic nephropathy (#1) and hypertensive nephrosclerosis (#2). Know these cold.
- ✦Cardiovascular disease is the #1 cause of death in CKD patients — not renal failure itself.
- ✦ACE inhibitors/ARBs are the preferred antihypertensives for CKD — they are renoprotective (reduce proteinuria).
- ✦Metformin is contraindicated when eGFR <30 (risk of lactic acidosis).
- ✦Anemia of CKD = normocytic, normochromic (unlike iron deficiency anemia = microcytic, hypochromic). Caused by decreased EPO.
- ✦AV fistula arm: NEVER use for BP, IV, or blood draw. Assess bruit and thrill each visit.
- ✦Give Hepatitis B vaccine BEFORE dialysis starts — immune response is blunted once on dialysis.
- ✦Renal osteodystrophy: low Ca²⁺ + high phosphorus + high PTH + low vitamin D = secondary hyperparathyroidism → bone disease.
- ✦Hyperkalemia is the most immediately life-threatening electrolyte abnormality in CKD — peaked T waves are the first ECG change.
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with KDIGO Clinical Practice Guidelines · National Kidney Foundation (NKF). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →