Lesson
Surveillance and Systems Thinking
CKD complications emerge at different rates and interact. Surveillance should become more frequent as filtration falls, abnormalities appear, therapies change, or symptoms evolve.
- Risk-based monitoring
- Trend interpretation
- Competing causes
- Medication contribution
- Escalation triggers
Repeat unexpected results and verify context
Kidney function, illness, nutrition, volume, and medicines
Symptoms, trajectory, treatment threshold, or referral
Monitor by risk and consequence
Advanced GFR category, faster progression, albuminuria, prior abnormalities, comorbidity, and treatment determine monitoring frequency. A useful panel may include complete blood count, ferritin, TSAT, calcium, phosphate, bicarbonate, potassium, albumin, PTH, alkaline phosphatase, and disease-specific tests, but not every test belongs at every visit.
Treat patterns, not isolated values
Confirm unexpected results and interpret trends. Hemoglobin, ferritin, TSAT, phosphate, calcium, PTH, bicarbonate, potassium, weight, and albumin change with inflammation, illness, nutrition, bleeding, volume, and treatment. A single abnormal value rarely identifies mechanism by itself.
Look beyond CKD
CKD increases the probability of anemia, mineral and bone disorder, electrolyte disturbance, and symptoms, but it does not exclude gastrointestinal bleeding, malignancy, marrow disease, endocrine disease, medication toxicity, infection, liver disease, or another diagnosis. Avoid diagnostic closure.
Connect complications
Iron deficiency can worsen ESA response. Acidosis can accelerate muscle loss. Hyperkalemia can limit RAAS therapy. Volume overload can dilute hemoglobin and worsen pressure. Phosphate, PTH, bone turnover, and vascular calcification interact. Design one integrated plan with sequencing and follow-up.
Quick check
Checking for saved practice…
Lesson
Anemia and Iron Management
Anemia in CKD reflects reduced erythropoietin signaling, iron restriction, inflammation, blood loss, shortened red-cell survival, nutrition, medications, and other disease. Treatment begins with cause and iron availability.
- Anemia workup
- Ferritin and TSAT
- Oral and IV iron
- ESA and HIF-PHI
- Transfusion strategy
Blood loss, iron restriction, inflammation, nutrition, and marrow
Ferritin and TSAT interpreted together
Individual goals, lowest effective exposure, and current label
Evaluate before attributing
Confirm hemoglobin, indices, reticulocyte response, ferritin, TSAT, B12, folate, blood loss, hemolysis, inflammation, infection, medications, nutrition, thyroid disease, and marrow clues as indicated. Erythropoietin deficiency is important, but unexplained rapid or disproportionate anemia requires another cause.
Use ferritin and TSAT together
Ferritin reflects stores but rises with inflammation, while TSAT estimates circulating iron available for erythropoiesis. KDIGO 2026 suggests iron initiation in nonhemodialysis CKD when ferritin is below 100 ng/mL with TSAT below 40%, or ferritin is 100 to 300 ng/mL with TSAT below 25%. Individualize and withhold routine iron when ferritin exceeds 700 ng/mL or TSAT is at least 40%.
Choose route and monitor response
Oral or IV iron can be used in CKD not receiving hemodialysis according to severity, tolerance, efficacy, access, and preference. In G5 hemodialysis, KDIGO 2026 suggests initiating iron when ferritin is 500 ng/mL or lower and TSAT is 30% or lower, and generally favors IV iron. Monitor hemoglobin, ferritin, TSAT, symptoms, hypersensitivity, infection context, and treatment response rather than repeating iron indefinitely.
Use erythropoiesis therapy carefully
ESA initiation is individualized by symptoms, transfusion risk, hemoglobin trajectory, transplant candidacy, cardiovascular and thrombotic risk, malignancy, and treatment setting. Use the lowest dose that meets the goal and avoid targeting a normal hemoglobin. HIF-PHIs have specific eligibility and safety boundaries, and in the United States daprodustat is labeled for adults receiving dialysis for at least four months.
Quick check
Checking for saved practice…
Lesson
Mineral, Bone, and Vascular Disorder
CKD-MBD is a systemic disorder of phosphate, calcium, vitamin D, PTH, bone turnover, fracture risk, and soft-tissue or vascular calcification. Management follows serial relationships, not one target.
- Phosphate retention
- Secondary hyperparathyroidism
- Bone turnover
- Vascular calcification
- Phosphate-lowering therapy
A changing endocrine response to falling filtration
Use serial calcium, phosphate, PTH, and alkaline phosphatase
Limit avoidable calcium and phosphate burden
Follow the physiology
Declining phosphate excretion increases FGF23 and PTH, reduces active vitamin D, alters calcium balance, and changes bone remodeling. Begin calcium, phosphate, PTH, and alkaline phosphatase monitoring by CKD G3a, then adjust frequency to abnormality and progression.
Use serial values together
Base treatment on trends in phosphate, calcium, and PTH considered together. In nondialysis CKD, an elevated PTH should prompt review of phosphate intake, hyperphosphatemia, hypocalcemia, vitamin D deficiency, and progression before routine active vitamin D treatment. The optimal PTH is not known.
Treat overt phosphate excess
Lower persistently or progressively elevated phosphate rather than treating a normal value preemptively. Combine source-aware dietary counseling, dialysis clearance when relevant, and binders when indicated. Limit excess calcium-based binder exposure when hypercalcemia, arterial calcification, adynamic bone concern, or high calcium load shifts risk.
Assess bone and vascular risk
DXA can predict fracture in CKD and is reasonable when the result will change treatment. Bone biopsy remains the gold standard for renal osteodystrophy when turnover type will alter a high-stakes decision. Lateral abdominal radiograph, echocardiography, or CT can identify calcification, but testing should change care.
Quick check
Checking for saved practice…
Lesson
Potassium and Acid-Base Disorders
Reduced potassium and acid excretion interact with diabetes, RAAS therapy, diet, constipation, tissue breakdown, and medicines. Chronic management should preserve outcome-improving therapy when it can be done safely.
- Hyperkalemia confirmation
- Medication drivers
- Dietary source
- Potassium binders
- Metabolic acidosis
Find actual sources and salt substitutes
Acute physiology changes extracellular potassium
Preserve beneficial therapy when control is safe
Separate acute danger from chronic control
Repeat a hemolyzed or unexpected potassium while responding immediately to severe or symptomatic hyperkalemia. ECG change, rapid rise, muscle weakness, acidosis, tissue breakdown, and impaired excretion increase urgency. Chronic control cannot substitute for acute cardiac stabilization and shifting when danger is present.
Correct reversible drivers
Review RAAS and MRA therapy, NSAIDs, trimethoprim, potassium supplements and salt substitutes, constipation, glucose and insulin deficiency, acidosis, dehydration, tissue breakdown, and laboratory artifact. Preserve disease-modifying therapy when dose adjustment, diuresis, acidosis treatment, dietary modification, or a binder can control risk.
Use dietary counseling with precision
Assess actual sources, portions, processing, salt substitutes, cultural pattern, constipation, and nutritional quality. Plant foods differ in bioavailability and benefit. Avoid broad restriction that replaces healthy foods with highly processed low-potassium products or worsens fiber intake.
Treat clinically important acidosis
Confirm metabolic acidosis and its cause. KDIGO 2024 suggests considering pharmacologic treatment to prevent clinically important acidosis, particularly when bicarbonate is below about 18 mmol/L, while monitoring pressure, potassium, fluid, and treatment effects. Nutrition and oral alkali choices require individualized sodium and volume assessment.
Quick check
Checking for saved practice…
Lesson
Volume, Nutrition, and Metabolic Health
Sodium and water excess can coexist with poor intake, sarcopenia, and protein-energy wasting. Weight, edema, albumin, and appetite must be interpreted as a system.
- Sodium and volume
- Diuretic response
- Protein-energy wasting
- Sarcopenia
- Nutrition assessment
Symptoms, JVP, weight, pressure, and response
Intake, inflammation, restrictions, and losses
Strength, mobility, appetite, and quality of life
Diagnose the volume phenotype
Combine symptoms, orthopnea, edema, JVP, pressure, weight trend, lung findings, cardiac status, sodium intake, urine, and diuretic exposure. Edema can coexist with low effective arterial volume, and a normal examination does not exclude early congestion.
Use diuretics as a monitored strategy
Loop diuretics are central for sodium and volume excess, often requiring higher doses as kidney function falls. Assess adherence, sodium intake, absorption, timing, urine response, weight, pressure, electrolytes, and combination nephron blockade before labeling resistance.
Recognize protein-energy wasting
Poor appetite, inflammation, acidosis, dialysis losses, restrictions, depression, dental disease, and socioeconomic barriers can produce weight loss, low intake, muscle loss, and frailty. Serum albumin is strongly affected by inflammation and volume and is not a stand-alone nutrition diagnosis.
Preserve function
Use dietitian assessment, adequate energy, individualized protein, resistance and aerobic activity as tolerated, oral nutrition support when needed, symptom treatment, and correction of acidosis or inflammation. Avoid a restrictive plan that lowers laboratory values while accelerating frailty.
Quick check
Checking for saved practice…
Lesson
Cardiovascular and Cutaneous Burden
Cardiovascular disease, pruritus, and calcific skin injury are not peripheral concerns in advanced CKD. They can dominate survival, sleep, function, and quality of life.
- Cardiovascular burden
- Lipid strategy
- CKD-associated pruritus
- Calciphylaxis
- Treatment safety
Coordinate pressure, volume, lipids, diabetes, and rhythm care
Skin, dialysis, mineral, neurologic, and systemic contributors
Urgent evaluation for retiform or necrotic lesions
Treat cardiovascular risk as a primary outcome
People with CKD face high risks of atherosclerotic disease, heart failure, arrhythmia, stroke, and sudden death. Control pressure, diabetes, tobacco exposure, volume, anemia, mineral metabolism, and lipids as one cardiorenal plan. Do not assume every chest symptom or troponin change is simply renal.
Use lipid therapy by treatment setting
Statin-based therapy reduces atherosclerotic events in many adults with nondialysis CKD. Starting a statin solely for primary prevention after a patient is already dialysis dependent is generally not recommended, while established therapy may often continue. Secondary prevention and other clear indications remain individualized.
Phenotype CKD-associated pruritus
Ask about distribution, timing, sleep, excoriations, dialysis relationship, skin disease, neuropathy, liver or thyroid disease, iron status, phosphate control, and medication causes. Optimize emollients and dialysis care, then choose symptom therapy with renal dosing and fall, cognition, and sedation risk in mind. Difelikefalin is a labeled option for moderate to severe CKD-associated pruritus in adults receiving hemodialysis.
Recognize calciphylaxis as an emergency
Severe pain that precedes retiform purpura, plaques, or necrotic ulcers in a person with advanced CKD should trigger urgent multidisciplinary evaluation. Address wound and infection care, pain, calcium and phosphate exposure, warfarin and other contributors, and kidney replacement factors. No single laboratory value excludes the diagnosis.
Quick check
Checking for saved practice…
Lesson
Uremia, Symptoms, and Advanced Care
Advanced CKD creates symptom, medication, decision, and preparation needs before an emergency indication appears. Kidney replacement therapy and comprehensive conservative care are both active care pathways.
- Uremic syndrome
- Pruritus and restless legs
- Cognitive and functional burden
- Kidney failure planning
- Supportive care
Track symptoms and failed homeostasis
Transplant, access, home therapies, and support
Dialysis or comprehensive conservative care
Recognize uremia clinically
Uremia is a syndrome, not a BUN threshold. Progressive anorexia, nausea, weight loss, pruritus, sleep disturbance, restless legs, cognitive change, neuropathy, bleeding, pericarditis, and declining function require evaluation for reversible causes and may signal kidney replacement need.
Treat symptom mechanisms
Review skin care, phosphate control, iron, neuropathy, sleep, depression, medications, and dialysis adequacy when relevant. Use renally adjusted symptom therapies carefully because gabapentinoids, opioids, sedatives, and antihistamines can accumulate and worsen cognition, falls, or respiratory risk.
Prepare before crisis
Use trajectory, symptoms, KFRE, comorbidity, transplant candidacy, access anatomy, home context, support, and patient values to begin education early. Dialysis start is based on symptoms, failed homeostasis, nutrition, or volume control rather than an eGFR number alone.
Offer comprehensive conservative care
Conservative kidney management includes active treatment of symptoms, anemia, volume, pressure, acidosis, medications, nutrition, psychosocial needs, advance care planning, and caregiver support without dialysis. Shared decisions should be revisited as health and priorities change.
Quick check
Checking for saved practice…
Module practice
Check the connections.
Each attempt draws 10 questions from the complete 120 question bank.
Each attempt draws a fresh set and rearranges the answer choices.
References
Current clinical foundation.
Core source material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.