Chart — Renal
CKD Complications Overview Chart
The six major systemic complications of chronic kidney disease — anemia, metabolic bone disease, hyperkalemia, metabolic acidosis, hypertension/fluid overload, and cardiovascular disease. Each with mechanism, lab findings, symptoms, treatment, and nursing priorities.
Chart · Renal
Educational use only. CKD management requires a multidisciplinary team (nephrology, cardiology, endocrinology, renal dietitian). Target values and treatment thresholds vary by clinical context. 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.
Anemia of Chronic Kidney Disease
| Mechanism | Failing kidneys produce INSUFFICIENT ERYTHROPOIETIN (EPO) — the hormone that stimulates RBC production in bone marrow. Also: decreased RBC lifespan (uremic toxins), iron deficiency (poor absorption, dialysis-related blood loss), folate deficiency, chronic inflammation suppressing erythropoiesis. |
| Key Labs | Low Hgb (target 10–11.5 g/dL in CKD), low reticulocyte count, low EPO level, iron studies (often iron-deficient: low ferritin, low TSAT), normocytic or microcytic anemia |
| Symptoms | Fatigue, weakness, dyspnea on exertion, pallor, decreased exercise tolerance, tachycardia, left ventricular hypertrophy (compensatory), worsening cognitive function |
| Treatment | Erythropoiesis-stimulating agents (ESAs): darbepoetin alfa (Aranesp) or epoetin alfa (Procrit/Epogen). IV iron supplementation (ferric gluconate, iron sucrose — PO poorly absorbed in uremia). Address iron deficiency before starting ESA. Transfusion only if Hgb severely low or symptomatic. |
| Nursing Priority | Monitor Hgb — target 10–11.5 g/dL (higher targets increase stroke/MI risk). Administer ESAs subcutaneously. Ensure adequate iron before ESA. IV iron: monitor for hypersensitivity reactions. Teach energy conservation techniques. Assess functional status and activity tolerance. |
| NCLEX Pearl | EPO is produced by the kidney — CKD causes EPO deficiency → anemia. IV iron preferred over PO in dialysis patients (poor PO absorption). ESA target Hgb 10–11.5 g/dL; exceeding 12 g/dL increases cardiovascular events. |
Renal Osteodystrophy (CKD-MBD) — Metabolic Bone Disease
| Mechanism | Complex cascade: (1) Decreased kidney activation of vitamin D (kidneys convert 25-OH D → 1,25-OH₂ D) → decreased calcium absorption from gut → hypocalcemia. (2) Decreased phosphorus excretion → hyperphosphatemia. (3) Low calcium + high phosphate → stimulates PTH secretion → secondary hyperparathyroidism. (4) PTH: leaches calcium from BONE to raise serum calcium → bone demineralization, osteitis fibrosa cystica. (5) High Ca × Phosphate product → vascular and soft tissue calcification. |
| Key Labs | Low calcium (or normal with high PTH), elevated phosphorus, elevated PTH (secondary hyperparathyroidism), low 25-OH vitamin D, elevated FGF-23 (early marker), elevated alkaline phosphatase (bone turnover) |
| Symptoms | Bone pain and tenderness, pathological fractures, bone deformities, pruritis (calcium-phosphate deposits in skin), 'rubber jaw' (mandibular resorption), muscle weakness, joint calcifications |
| Treatment | Phosphate binders (taken with meals: calcium carbonate, sevelamer, lanthanum). Active vitamin D analogs: calcitriol (Rocaltrol) or calcimimetics (cinacalcet — reduces PTH secretion). Dietary phosphorus restriction. Parathyroidectomy if severe/refractory secondary hyperparathyroidism. |
| Nursing Priority | Administer phosphate binders WITH meals (not before or after). Monitor calcium, phosphorus, PTH levels. Fall prevention (bone fragility). Pruritis management: tepid baths, emollients, antihistamines (phosphate reduction resolves long-term). Avoid calcium-containing binders if hypercalcemia or vascular calcification present — use sevelamer. |
| NCLEX Pearl | CKD → low vitamin D → low calcium → HIGH PTH (secondary hyperparathyroidism) → bone breakdown. Phosphate binders MUST be taken WITH food. PTH pulls calcium from bones → bone pain, fractures. |
Hyperkalemia
| Mechanism | Kidneys normally excrete 90% of dietary potassium. In CKD: (1) Reduced tubular potassium excretion. (2) Metabolic acidosis shifts K⁺ out of cells (H⁺ in, K⁺ out — each 0.1 decrease in pH = ~0.5–0.7 mEq/L rise in serum K⁺). (3) Reduced aldosterone responsiveness. (4) ACE inhibitors/ARBs (reduce aldosterone-driven K⁺ excretion). (5) Dietary: CKD patients often unaware of high-K⁺ foods, salt substitutes (KCl). |
| Key Labs | Serum K⁺ > 5.5 mEq/L (concerning); > 6.0 mEq/L (dangerous); > 7 mEq/L (life-threatening). ECG changes: peaked T waves (earliest) → prolonged PR → wide QRS → sine wave → VF/asystole. |
| Symptoms | Muscle weakness, fatigue, paresthesias, bradycardia, palpitations. Severe: cardiac dysrhythmias (VF, PEA, asystole), respiratory muscle weakness, ascending paralysis. Often ASYMPTOMATIC until ECG changes. |
| Treatment | Mild/asymptomatic: dietary restriction, hold ACE/ARB, sodium polystyrene sulfonate (Kayexalate) or patiromer (Veltassa) to bind K⁺ in GI tract. Moderate-Severe (> 6.0 or ECG changes): IV calcium gluconate (cardiac membrane stabilization — immediate), glucose + insulin (drives K⁺ into cells — within 30 min), albuterol (shifts K⁺ intracellular). Definitive removal: sodium bicarbonate (metabolic acidosis), dialysis (most effective). Loop diuretics if urine output preserved. |
| Nursing Priority | CONTINUOUS cardiac monitoring if K⁺ > 6.0 mEq/L. Have calcium gluconate at bedside for emergency. Dietary teaching: high-K⁺ foods, salt substitutes. Do NOT crush Kayexalate tablet into food/liquids that contain K⁺. Assess for muscle weakness (early sign). Report peaked T waves on telemetry immediately. |
| NCLEX Pearl | Peaked T waves = earliest ECG sign of hyperkalemia. Calcium gluconate = cardiac membrane STABILIZATION (does NOT lower K⁺). Glucose + insulin = shift K⁺ into cells (temporary). Dialysis = only definitive treatment for severe hyperkalemia in ESRD. Salt substitutes (KCl) = dangerous in CKD. |
Metabolic Acidosis
| Mechanism | Kidneys normally excrete H⁺ (acid) and regenerate HCO₃⁻ (bicarbonate). In CKD: (1) Decreased ammoniagenesis (proximal tubules cannot make NH₄⁺ for H⁺ buffering). (2) Decreased H⁺ secretion in collecting duct. (3) Net acid retention → metabolic acidosis. (4) Chronic acidosis: bone buffering (Ca²⁺ phosphate released from bone to buffer H⁺ → contributes to bone disease). (5) Muscle catabolism and protein breakdown (ammonia as acid buffer). |
| Key Labs | Low HCO₃⁻ (< 22 mEq/L in CKD; often 12–20 mEq/L). Low pH (< 7.35). Normal anion gap (hyperchloremic) early; high anion gap (accumulation of uremic acids like sulfate, phosphate, hippurate) in advanced CKD. Arterial blood gas: metabolic acidosis with respiratory compensation (decreased pCO₂). |
| Symptoms | Kussmaul respirations (deep rapid breathing — compensatory), fatigue, weakness, anorexia, nausea. Chronic: bone demineralization (contributes to renal osteodystrophy), muscle wasting, insulin resistance, stimulates protein catabolism. |
| Treatment | Oral sodium bicarbonate supplementation (target HCO₃⁻ > 22 mEq/L). Sodium citrate (Bicitra) as alternative. Dialysis provides bicarbonate via dialysate. Dietary protein restriction reduces acid production. |
| Nursing Priority | Monitor bicarbonate levels and acid-base status. Assess respiratory pattern (Kussmaul breathing = compensation for metabolic acidosis). Sodium bicarbonate has sodium content — monitor BP and edema. Metabolic acidosis worsens hyperkalemia (each 0.1 pH drop = +0.5–0.7 K⁺). Correct acidosis to help control potassium. |
| NCLEX Pearl | CKD metabolic acidosis = normal anion gap early, high anion gap late (uremic acids accumulate). Kussmaul respirations = deep rapid breathing to compensate (blow off CO₂). Acidosis worsens hyperkalemia. Correct acidosis = helps lower K⁺. |
Hypertension & Fluid Overload
| Mechanism | Multiple mechanisms: (1) Sodium and water retention → volume expansion. (2) Renin hypersecretion (ischemic kidneys → RAAS activation → vasoconstriction and aldosterone-driven sodium retention). (3) Sympathetic nervous system activation. (4) Impaired vasodilatory prostaglandin production. (5) Endothelin excess. Hypertension accelerates CKD progression — vicious cycle. Also: fluid overload from reduced UO → pulmonary edema, peripheral edema. |
| Key Labs | Elevated BUN/Cr (worsening with hypertension-driven injury). Elevated aldosterone. Urinary protein (hypertensive nephropathy). Chest X-ray: pulmonary vascular congestion, cardiomegaly. Echocardiogram: LVH. |
| Symptoms | Hypertension (often severe and resistant to standard therapy), peripheral edema, dyspnea (pulmonary edema), orthopnea, headache, left ventricular hypertrophy → heart failure. Uncontrolled: hypertensive urgency/emergency. |
| Treatment | Target BP < 130/80 mmHg in CKD. ACE inhibitors or ARBs: first-line (also reduce proteinuria — renoproctive). Diuretics: loop diuretics (furosemide — especially with reduced GFR; thiazides less effective at GFR < 30). Fluid and sodium restriction. Dialysis removes excess fluid in ESRD. |
| Nursing Priority | Regular BP monitoring (both sitting and standing — orthostatic hypotension from overdiuresis). Daily weights. Fluid restriction compliance. Sodium restriction education. Monitor for ACE/ARB side effects (hyperkalemia, dry cough → switch to ARB). Loop diuretic administration: assess for electrolyte depletion (hypokalemia, hyponatremia, hypomagnesemia). Fluid restriction education: count all fluids including ice chips. |
| NCLEX Pearl | ACE inhibitors/ARBs are PREFERRED antihypertensives in CKD (also reduce proteinuria). Thiazide diuretics lose effectiveness at eGFR < 30 — use loop diuretics. ACE inhibitor side effect: dry cough → switch to ARB (not a reason to stop treatment). |
Cardiovascular Disease (CVD)
| Mechanism | CKD is an independent, powerful cardiovascular risk factor. Mechanisms: (1) Traditional: hypertension, diabetes, dyslipidemia. (2) CKD-specific: uremic toxins damage endothelium, hyperphosphatemia and calcium-phosphate precipitation cause vascular and coronary artery calcification, anemia increases cardiac workload → LVH → cardiomyopathy, fluid overload → HF. CKD patients are more likely to die of CVD than progress to ESRD. |
| Key Labs | Elevated troponin (commonly elevated in CKD even without ACS — reduced clearance; trend is more useful than single value). Elevated BNP/NT-proBNP (heart failure marker — higher cutoff used in CKD). Elevated phosphorus, elevated PTH → vascular calcification. Lipid panel: often dyslipidemia. Elevated CRP, homocysteine. |
| Symptoms | Angina, MI, HF symptoms (dyspnea, orthopnea, edema), atrial fibrillation, sudden cardiac death. Uremic pericarditis: friction rub, chest pain (indication for urgent dialysis). |
| Treatment | Aggressive CVD risk factor management: BP control (< 130/80), glycemic control in DM (target A1c), lipid management (statins). Anemia management (ESAs + iron). Phosphorus and PTH control (reduces vascular calcification). Dialysis adequacy. Cardiology co-management. Uremic pericarditis: dialysis. |
| Nursing Priority | Continuous cardiac monitoring for dysrhythmias. Report new chest pain immediately (troponin interpretation altered in CKD — provider must know). Weigh daily — rapid weight gain indicates fluid overload and potential decompensated heart failure. Assess for friction rub (uremic pericarditis = urgency). Medication adherence to all cardiovascular medications. Dialysis compliance — skipping sessions leads to fluid overload and cardiac events. |
| NCLEX Pearl | Leading cause of death in CKD patients = CARDIOVASCULAR disease (NOT kidney failure). Uremic pericarditis = friction rub + chest pain in CKD → requires urgent dialysis. Troponin elevated in CKD even without ACS — trend matters more than single value. |
CKD Complications — Quick Summary
Anemia: EPO deficiency → ESA + IV iron. Target Hgb 10–11.5 g/dL.
Bone disease: Low vitamin D → low Ca → high PTH → bone breakdown. Phosphate binders WITH meals. Active vitamin D (calcitriol).
Hyperkalemia: Peaked T waves → calcium gluconate (stabilizes heart, does NOT lower K⁺). Glucose + insulin shifts K⁺ into cells. Dialysis removes it.
Metabolic acidosis: Kussmaul breathing (compensation). Oral bicarb supplementation. Acidosis worsens hyperkalemia.
HTN + fluid overload: ACE/ARBs first-line. Loop diuretics (thiazides ineffective at eGFR < 30). Daily weights. Fluid restriction.
CVD = leading cause of death in CKD (not kidney failure). Uremic pericarditis = urgent dialysis indication.
Related Resources
Chronic Kidney Disease GuideCKD staging, progression, full management, and complication prevention
Open →CKD Dietary Restrictions ReferencePotassium, phosphorus, protein, sodium, and fluid management by stage
Open →AKI Types Comparison ChartPrerenal vs intrarenal vs postrenal AKI — labs and management
Open →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 →