Module 2 — Kidneys and Kidney Failure
Sources: Condensed study notes based on Core Curriculum for the Dialysis Technician, 7th ed. (MEI), plus free CDC/CMS/NIDDK resources.
Introduction — Why kidneys matter
Study guide
- The kidneys keep the internal environment within narrow limits (homeostasis): water, electrolytes, acid–base status, wastes, blood pressure, red-cell production, and bone/mineral balance all depend partly on renal function.
- Dialysis replaces selected filtration and fluid-removal work; it does not restore every excretory, endocrine, or regulatory function of healthy kidneys.
- The module’s map is: normal structure → normal function → acute/chronic loss → causes → body-wide effects.
Why answers are correct
- A patient can look well while losing substantial kidney function because the kidneys have a large nephron reserve. Symptoms and complications may appear late.
Limitations / traps
- Do not treat one lab value, one symptom, or a machine result as the whole clinical picture. Trends, symptoms, prescription, and the licensed team’s assessment matter.
Clinical pearl / safety
- A new or worsening symptom during treatment is a patient-safety finding: observe, protect the patient, notify the nurse, follow policy, and document—do not diagnose independently.
Kidney structure and urine pathway
Study guide
- The kidneys are paired, reddish-brown, bean-shaped organs behind the peritoneum near the back; the right is usually lower because of the liver. Fat, connective tissue, and ribs help protect them.
- Main gross parts and pathway:
- Capsule: tough outer covering.
- Cortex: outer tissue containing vessels and nephron structures; renal endocrine activity includes EPO production.
- Medulla: inner region organized into pyramids.
- Renal hilum: entry/exit area for renal artery, renal vein, ureter, nerves, and other vessels.
- Renal artery/vein: bring blood to the kidney and return filtered blood.
- Inside the kidney, pyramids end in papillae; papillae empty into cup-like calyces, then the renal pelvis, ureter, bladder, and urethra.
Why answers are correct
- Knowing the direction—blood into the kidney, filtrate through tubules, urine out through the collecting system—helps make access, fluid, and laboratory findings understandable.
Limitations / traps
- The ureter carries urine from kidney to bladder; the urethra carries urine out of the body. They are not interchangeable.
Exam cue
- Kidney → calyx → renal pelvis → ureter → bladder → urethra is the urine route.
Nephrons and filtration
Study guide
- A nephron is the functional unit. Each kidney has hundreds of thousands to a few million; new nephrons are not normally made after birth.
- Renal corpuscle: glomerulus plus Bowman’s capsule. The glomerulus is a capillary tuft whose pores pass water and small solutes while retaining cells and most proteins.
- Blood enters through the afferent arteriole and exits through the efferent arteriole—“afferent arrives; efferent exits.” Pressure drives water and small wastes into Bowman’s space as glomerular filtrate.
- Tubule sequence/functions:
- Proximal convoluted tubule: substantial reabsorption and secretion.
- Loop of Henle: reabsorbs water and salts.
- Distal convoluted tubule: adjusts water volume and mineral levels.
- Collecting duct: gathers urine and reabsorbs selected substances, including peptides.
- Healthy kidneys filter roughly 180 L of glomerular filtrate daily, but about 99% is reabsorbed; only the remainder becomes urine. The text also uses roughly 150 L/day as a broad estimate of blood filtration—these figures describe different quantities, not a contradiction.
- GFR measures filtration. Measured GFR is used chiefly in research; clinical practice commonly uses estimated GFR (eGFR), calculated from blood creatinine and other variables. The text notes that race-based adjustment was removed because it overestimated kidney function in Black patients and reinforced inequity.
Why answers are correct
- Protein or blood cells in urine suggest the filtration barrier is leaking or damaged; foamy urine can be a clue to proteinuria. Afferent/efferent and filtration/reabsorption/secretion/excretion are distinct steps.
Limitations / traps
- eGFR is an estimate, not a direct “health score.” Interpret it with albuminuria, symptoms, trend, age, body context, and clinician assessment.
- Do not confuse glomerular filtrate with final urine: most filtered water and useful solutes are reclaimed.
Clinical pearl / safety
- Report new foamy urine, swelling, reduced urine, or significant change in symptoms; do not reassure based only on appearance.
Exam cue
- Filtration: blood to Bowman’s space. Reabsorption: tubule back to blood. Secretion: blood to tubule. Excretion: body out as urine.
Kidney function: excretory, endocrine, and regulatory roles
Study guide
Healthy kidneys help to:
- Remove metabolic wastes and excess water.
- Keep sodium, potassium, calcium, magnesium, phosphorus, chloride, and bicarbonate within usable ranges.
- Adjust water balance and blood volume.
- Influence blood pressure through volume control and the renin–angiotensin–aldosterone system (RAAS).
- Produce or activate hormones involved in red-cell production and bone/mineral health.
- Maintain blood acid–base balance.
- Excretory work: removes metabolites, medication/vitamin by-products, nitrogen-containing waste, acids, minerals, and products of tissue breakdown. Urine becomes more concentrated when water is scarce and more dilute when excess fluid is available.
- Erythropoietin (EPO): low oxygen sensing by the kidney increases EPO signaling to bone marrow to make red cells.
- Calcitriol: active vitamin D supports intestinal calcium absorption and bone/mineral balance.
- Renin/RAAS: low renal perfusion, pressure, or sodium can stimulate renin; angiotensin II constricts vessels and promotes thirst and aldosterone release, while aldosterone promotes sodium and water retention.
- Electrolytes: dissolved salts form charged ions. Cations are positive; anions are negative. The kidney adjusts their excretion and retention.
- Blood pressure: more intravascular water generally raises pressure; less lowers it. Vessel resistance is also adjusted through RAAS.
- Acid–base: normal blood pH is tightly held around 7.35–7.45. Kidneys excrete acid and conserve or generate bicarbonate, a major buffer.
Why answers are correct
- Renal failure produces combined problems: volume overload, hypertension, anemia, acidosis, mineral/bone disease, and accumulation of uremic wastes. Dialysis can address some of these, but not with the continuous, full-range regulation of healthy kidneys.
Compare / contrast
| Function | Healthy kidney contribution | What failure may cause |
|---|---|---|
| Excretion | Removes urea, excess salts, water, and other wastes | Azotemia/uremia, fluid overload |
| Endocrine | EPO and calcitriol; renin signaling | Anemia, low active vitamin D, mineral/bone disorder, BP problems |
| Electrolyte/acid–base | Selective retention/excretion and bicarbonate handling | Potassium/phosphate problems and metabolic acidosis |
| Pressure/volume | Adjusts water and vascular resistance | Hypertension, hypotension or difficult fluid control |
Limitations / traps
- EPO is not a red blood cell. It is a hormone signal. Calcitriol is active vitamin D, not simply dietary vitamin D.
- A normal-looking pH does not prove normal kidney function; lungs, buffers, medications, and dialysis can also affect acid–base status.
Clinical pearl / safety
- Shortness of breath, new edema, chest pain, confusion, marked weakness, or palpitations can reflect dangerous fluid/electrolyte or cardiac problems. Escalate promptly.
Exam cue
- Remember the renal “six”: waste, electrolytes, water, pressure, hormones, acid–base.
Types and causes of kidney failure
Study guide
- AKI is a sudden, often severe loss of function and may be reversible; CKD is progressive nephron loss over months or years and may end in kidney failure.
- AKI categories:
- Prerenal: inadequate blood flow—dehydration, hemorrhage, burns, heart-pump failure, sepsis, anaphylaxis, or vasoactive drugs.
- Intrinsic: damage within the kidney, such as glomerular/tubular disease or nephrotoxic drugs.
- Postrenal: obstruction after the kidney—stones, tumors, clots, or kinked ureters—causing urine back-pressure.
- CKD can remain silent. Screening with urine testing, blood pressure, and creatinine can identify disease earlier; exercise, weight management, and control of contributing disease can slow progression.
- The text’s NKF framework uses five CKD stages by eGFR: stage 1 normal/high (≥90), stage 2 mild decrease (60–89), stage 3a (45–59), stage 3b (30–44), stage 4 (15–29), and stage 5 kidney failure (<15). Albuminuria increases progression risk. Dialysis or transplant is considered from the overall picture, not a number alone; the text describes ESKD on dialysis as stage 6.
Compare / contrast
| Feature | AKI | CKD |
|---|---|---|
| Time course | Sudden | Persistent/progressive |
| Potential recovery | Often possible if cause is corrected | Lost nephrons generally do not return |
| Typical reasoning | Ask “what reduced flow, injured kidney, or obstructed urine?” | Ask “what chronic disease is damaging nephrons and how fast?” |
| Technician focus | Rapid change, urine/fluid status, escalation | Trends, symptoms, adherence barriers, complications |
Causes of CKD/kidney failure
- Diabetes and hypertension are the leading causes emphasized by the module. High glucose damages delicate vessels; hypertension injures renal vessels and glomeruli.
- Diabetes type 1 is autoimmune beta-cell destruction; type 2 involves inadequate insulin and/or insulin resistance. Both can damage kidneys. Prevention messages include healthy weight, heart-healthy food, activity, smoking cessation, and individualized alcohol advice.
- Health differences are not proof of innate group biology. Access to fresh food, safe activity, language, health literacy, trust, income, discrimination, and other social conditions can shift risk and treatment.
- Glomerular diseases include glomerulonephritis (inflammation) and glomerulosclerosis (scarring/hardening); onset may be slow or fast.
- Polycystic kidney disease (PKD) is genetic cyst formation that can crowd out renal tissue; cysts may also occur in other organs. Other causes include lupus/autoimmune disease, congenital defects, cancer, medication or drug injury, recurrent stones, HIV/AIDS, infection, sickle-cell disease, and unknown causes.
Limitations / traps
- Do not label a missed treatment or high BP as “noncompliance” without looking for cost, side effects, food/transport access, language, work, or other barriers.
- Current staging, eGFR equations, and treatment thresholds can change; verify current clinical guidance.
Clinical pearl / safety
- A patient with AKI, infection, obstruction, or rapidly changing BP can deteriorate quickly. Report the change and relevant context rather than waiting for the next routine check.
Exam cue
- Prerenal = flow problem; intrinsic = kidney tissue problem; postrenal = outflow obstruction.
Problems caused by kidney failure
Azotemia and uremia
Study guide
- Azotemia: buildup of BUN and other nitrogenous wastes, sometimes with few symptoms.
- Uremia: azotemia accompanied by symptoms. Possible findings include edema, dyspnea, changing urine/nocturia, foamy urine, itching, ammonia breath/metal taste, nausea or food aversion, skin/eye changes, fatigue, sleep/sexual problems, neuropathy, and cognitive changes.
- Dialysis can lessen uremic symptoms, but standard in-center HD replaces only a fraction of normal kidney work. Full prescribed treatment time and frequency matter.
Why answers are correct
- Waste accumulation affects many systems, so symptoms are often vague and overlap with other illness. A person may look well yet be seriously ill.
Clinical pearl / safety
- Ask about symptoms the patient may not volunteer and report them to the nurse. Never assume itching, nausea, cramps, or fatigue is “just normal.”
Anemia
Study guide
- Failing kidneys make less EPO; dialysis-related blood loss, testing, inflammation, iron deficiency, GI bleeding, and menstruation may add to anemia.
- Watch for fatigue, weakness, cold intolerance, confusion, and pallor. Hgb measures the oxygen-carrying protein; hematocrit is another measure and is often roughly three times the Hgb value.
- Management may include iron, ESAs, newer HIF-activating drugs, and—when urgently needed—transfusion. ESAs and transfusions have important risks; transfusion can sensitize a transplant candidate.
- Technician role: return as much blood as safely possible, report bleeding/infection and anemia symptoms, use approved collection supplies, encourage complete treatments, and follow the clinic anemia plan.
Limitations / traps
- Do not adjust iron, ESA, or dialysis orders independently. Transfusion decisions are clinical and must respect informed patient preferences and beliefs.
Electrolyte imbalance
Study guide
- Sodium: mainly extracellular; affects water balance, pressure, and nerves. Low sodium may cause headache, confusion, nausea; high sodium can cause rapid breathing, restlessness, or sleep difficulty.
- Calcium: supports bone, clotting, enzymes, hormones, nerves, and muscle. Low calcium may cause tingling, cramps/tetany, confusion, seizures, and rhythm changes; high calcium may cause fatigue, appetite loss, weakness, constipation, and rhythm changes.
- Magnesium: mainly intracellular and involved in energy and neuromuscular function; low levels can be dangerous.
- Phosphorus: largely in bone/teeth and involved in energy metabolism. Low levels can cause irritability, seizures, rhythm changes, stones, and bone problems; high levels cause itching and contribute to calcium-phosphate deposition, vascular calcification, and fractures.
- Potassium: major intracellular ion and critical to cardiac/muscle cells. Both low and high potassium can cause weakness, cramps, paralysis, dangerous rhythms, or arrest; rapid HD-related swings can matter.
- Chloride: principal extracellular anion; supports acid–base and water distribution. Low chloride can accompany metabolic alkalosis; high chloride may be asymptomatic.
- Metabolic acidosis can cause headache, low energy, nausea/vomiting, rapid or deep breathing, fruity breath, confusion, and—when severe—coma or cardiac arrest.
Why answers are correct
- The danger is not simply “high” or “low”; each ion’s location and electrical role determines the symptoms and cardiac risk. Abnormal potassium, calcium, or magnesium deserves especially prompt attention.
Exam cue
- Hypo- means low, hyper- means high; -emia means in blood. Know the clinical danger of both hypo- and hyperkalemia.
Mineral and bone disorder (MBD)
Study guide
- CKD reduces active vitamin D and phosphate excretion. Low calcium stimulates PTH; PTH pulls calcium from bone. FGF-23, phosphate, PTH, calcium, and vitamin D then interact in a maladaptive cycle.
- MBD (renal osteodystrophy) can produce bone pain, weakness, fractures, itching, and calcium-phosphate deposits in vessels and soft tissue. Types include high-turnover disease, low-turnover/adynamic disease, and mixed disease; persistent secondary hyperparathyroidism can become tertiary when glands enlarge and remain autonomous.
- Treatments may include phosphate restriction, phosphate binders taken with meals, active vitamin D, calcimimetics, and parathyroidectomy when medication fails.
- Calciphylaxis is a rare, severe vascular/skin complication: painful purple wounds may not heal and can become infected/septic. Report new sores, swelling, or severe pain urgently.
Clinical pearl / safety
- Listen for bone/joint pain, itching, weakness, and skin changes; reinforce the prescribed meal/medication plan, but do not give independent dietary or medication changes.
Dialysis-related amyloidosis (DRA)
Study guide
- Beta-2-microglobulin normally clears through kidneys. With long dialysis vintage it can accumulate, form amyloid fibrils, and deposit in tissues.
- Typical problems include carpal tunnel, other nerve damage, joint destruction/pain, bone cysts, and fractures. More effective toxin removal and adequate treatment may reduce risk.
- Report pain, lumps, sores, or reduced function; support full prescribed treatments.
Cardiovascular complications
Left ventricular hypertrophy (LVH)
- Pressure/volume overload, anemia, uremic toxins, vascular calcification, and repeated rapid fluid shifts can enlarge and weaken the left ventricle. Fibrotic muscle occupies space that should hold blood and may not pump effectively.
- Ejection fraction is the percentage ejected per beat; a healthy LV is roughly 50–70%. Heart failure can occur even when EF appears preserved.
- Report shortness of breath or chest pain. Set the machine exactly as prescribed; gentle ultrafiltration and prescribed cool dialysate may reduce rapid-shift “stunning.”
Pericarditis
- Pericarditis is inflammation of the sac around the heart. Uremic pericarditis occurs before dialysis or early after starting; dialysis-associated pericarditis occurs later and has a less clear cause.
- Sudden sharp central chest pain, worse with breathing/coughing/lying down and sometimes better leaning forward, is urgent. A friction rub may occur.
- Do not start a treatment for a patient with pre-treatment chest pain until the nurse assesses them; report any intratreatment chest pain immediately.
Neuropathy, pruritus, and sleep problems
Study guide
- Uremic wastes, glucose injury, and electrolyte abnormalities can damage peripheral and optic nerves. Symptoms include burning pain, numbness/tingling, restless legs, weakness/atrophy, erectile dysfunction, and balance/walking problems.
- Neuropathy plus poor blood flow can hide foot injuries and increase limb-loss risk. Encourage protective footwear and daily foot inspection; report wounds.
- Uremic pruritus may reflect retained wastes, MBD, anemia/iron deficiency, inflammation, dry skin, or dialyzer/drug allergy. Do not scratch broken skin; report hives during treatment promptly.
- Insomnia, sleep apnea, and restless legs are common. Ask about sleep, snoring/pauses, daytime sleep, and RLS; report rather than minimizing.
Limitations / traps
- Itching or neuropathy is not automatically an allergy, and a rash/hives limited to treatment is not automatically “uremia.” Timing and appearance must be reported for assessment.
Clinical pearl / safety
- Protect feet, skin, and fall safety. New weakness, loss of sensation, hives, breathing trouble, or chest symptoms warrants immediate escalation.
Important tests and adequacy overview
Study guide
- The module’s test table groups monitoring as follows:
- CBC/anemia: hemoglobin, hematocrit, platelets, WBCs.
- Iron: ferritin and transferrin saturation (TSAT).
- Chemistry: albumin, BUN, calcium, carbon dioxide/bicarbonate, chloride, creatinine, glucose, sodium, phosphorus, potassium.
- Parathyroid: intact PTH.
- Viral screening: hepatitis B surface antibody, hepatitis B surface antigen, and core antibody according to clinic protocol.
- Adequacy: single-pool Kt/V and standard Kt/V; the table gives common minimum/target values for HD, but current facility standards govern.
- Treat a lab as a clue in context. The technician observes symptoms, obtains accurate measurements, protects specimens, and reports—not independently interprets or changes therapy.
Why answers are correct
- Labs connect directly to renal functions: Hgb/EPO to anemia; albumin/nutrition; BUN/creatinine to waste; potassium and bicarbonate to electrical/acid–base risk; calcium/phosphorus/PTH to MBD; Kt/V to delivered dialysis dose.
Compare / contrast
| Finding | Renal link | Safe technician response |
|---|---|---|
| Low Hgb/fatigue/pallor | Low EPO, blood loss, iron/inflammation | Report symptoms/bleeding; follow anemia plan |
| High K/weakness/palpitations | Reduced K excretion or shift | Immediate nurse notification per policy |
| High phosphorus/itching/sores | MBD and deposition | Report; reinforce prescribed plan |
| High BUN/uremic symptoms | Waste accumulation or inadequate dose | Report symptoms and missed/shortened treatment |
| Low delivered Kt/V | Dose/access/flow or shortened time issue | Escalate; do not alter prescription alone |
Vocabulary
Uncommon words from this chapter. Plain definitions + a short dialysis-related example.
- homeostasis
- The body's steady inner balance of water, salts, wastes, and other internals.
- Example. Healthy kidneys keep homeostasis within a narrow range; dialysis only partly replaces that work.
- nephron
- The kidney's working filter unit; each kidney has hundreds of thousands of them.
- Example. Lost nephrons generally do not grow back, which is why CKD can progress.
- glomerulus
- A tiny capillary tuft that starts filtration of water and small wastes.
- Example. Protein in urine can mean the glomerulus is leaking.
- afferent
- Coming in; the vessel that arrives at a part.
- Example. The afferent arteriole brings blood into the glomerulus.
- efferent
- Going out; the vessel that leaves a part.
- Example. The efferent arteriole carries blood out of the glomerulus.
- filtrate
- The watery fluid pushed out of blood at the start of urine making.
- Example. Most glomerular filtrate is reabsorbed; only a small part becomes urine.
- reabsorption
- Taking useful water and solutes from the tubule back into blood.
- Example. Reabsorption keeps needed salts from being lost in urine.
- secretion
- Moving selected substances from blood into the tubule for removal.
- Example. Secretion helps the kidney clear some wastes and medicines.
- GFR
- Glomerular filtration rate: how much blood the kidneys filter over time.
- Example. eGFR is an estimate of GFR from blood creatinine and other variables.
- erythropoietin
- A kidney hormone that signals bone marrow to make red blood cells.
- Example. Low erythropoietin is a main reason people with kidney failure become anemic.
- calcitriol
- The active form of vitamin D made or activated by the kidney.
- Example. Low calcitriol impairs calcium absorption and bone-mineral balance.
- renin
- A kidney signal that starts the RAAS pathway and can raise blood pressure.
- Example. Low kidney blood flow can trigger renin release.
- azotemia
- Buildup of BUN and other nitrogen wastes, sometimes with few symptoms.
- Example. Azotemia can be present before a person feels uremic.
- uremia
- Waste buildup plus symptoms such as nausea, itching, or confusion.
- Example. Uremia can look vague, so report new itching, nausea, or fatigue.
- prerenal
- A kidney-function problem caused by not enough blood flow to the kidney.
- Example. Severe dehydration can cause prerenal AKI.
- acidosis
- Blood that is too acidic because acid is retained or bicarbonate is lost.
- Example. Kidney failure often causes metabolic acidosis.
- calciphylaxis
- A rare, severe vessel and skin problem with painful wounds that may not heal.
- Example. Report new sores or severe pain promptly because calciphylaxis can become septic.
- pericarditis
- Inflammation of the sac around the heart.
- Example. Sharp chest pain that eases when leaning forward can be pericarditis and is urgent.
- neuropathy
- Nerve damage that can cause pain, numbness, tingling, or weakness.
- Example. Uremic neuropathy plus poor blood flow can hide foot injuries.
- pruritus
- Itching.
- Example. Uremic pruritus may reflect retained wastes, mineral imbalance, or dry skin.
- amyloidosis
- Buildup of amyloid protein deposits in tissues over long dialysis vintage.
- Example. Dialysis-related amyloidosis can cause carpal-tunnel pain and joint damage.
- adequacy
- Whether the delivered dialysis dose is enough for the patient's needs.
- Example. Kt/V is one lab clue to adequacy, not a complete picture by itself.
Must-know
- List the six renal jobs: waste, electrolytes, water, pressure, hormones, acid–base.
- Trace urine: kidney structures → calyx → renal pelvis → ureter → bladder → urethra.
- What is a nephron, and what do the glomerulus, proximal tubule, loop of Henle, distal tubule, and collecting duct do?
- Distinguish afferent from efferent and filtration from reabsorption, secretion, and excretion.
- Why can eGFR be misleading if read without albuminuria, symptoms, and trends?
- Distinguish AKI from CKD and classify prerenal, intrinsic, and postrenal AKI.
- Name the leading chronic causes emphasized: diabetes and hypertension; explain how each damages nephrons.
- Define azotemia versus uremia and list symptoms that must be reported.
- Explain renal EPO, calcitriol, renin, and RAAS roles.
- Why can kidney failure cause anemia, acidosis, fluid overload, hypertension, and MBD?
- Which electrolyte abnormalities are especially urgent because of cardiac/muscle risk? Potassium, calcium, and magnesium are key examples.
- Describe MBD, secondary/tertiary hyperparathyroidism, phosphate binders, and calciphylaxis.
- What technician findings suggest anemia, uremic neuropathy, DRA, LVH/heart failure, pericarditis, pruritus, or sleep apnea?
- Compare uremic chest pain/pericarditis warning signs with ordinary discomfort: treat new chest pain as urgent and escalate.
- Why do neuropathy and poor perfusion make foot checks and protective footwear important?
- What tests belong to CBC/anemia, chemistry/electrolyte, PTH, viral-screening, and adequacy monitoring?
- What does Kt/V broadly assess, and why do shortened or missed treatments matter?
- In every vignette: identify the renal function affected, recognize the symptom/lab risk, stay within scope, notify the right team member, follow policy, and document accurately.