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NLE Renal & Urinary Nursing — Acute & Chronic Kidney DiseaseCheat Sheet

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One-page cheat sheet for NLE Renal & Urinary Nursing — Acute & Chronic Kidney Disease. Every formula, definition, and key fact you need for this chapter, condensed to a single printable page. Designed for the final review session before the NLE 2026.

Exam context

For the Philippine Nurse Licensure Examination (PNLE), Professional Regulation Commission (PRC) — Board of Nursing tests Renal & Urinary Nursing under a "Core" label, with Acute & Chronic Kidney Disease in the 3rd slot across 3 chapters. NLE candidates must clear the 75% weighted average with no sub-test below 60% cut on the 2026 paper, which draws about 50 Renal & Urinary Nursing questions. Date to watch: Bi-annual.

Acute & Chronic Kidney Disease - Cheat Sheet

Your final 30-minute companion for renal & urinary nursing exams. Master the causes, phases, complications, and critical interventions for AKI and CKD—with a sharp focus on hyperkalemia, fluid overload, and dialysis management.

Sections

Formulas

Formula

BUN:Creatinine Ratio

Meaning

High ratio (>20:1) = prerenal; Low ratio (<10:1) or normal = intrarenal; Help differentiate cause

Watch Out

Prerenal patients often have dehydration with elevated BUN out of proportion to creatinine; intrarenal (ATN) maintains a lower ratio

When To Use

Interpreting labs in acute kidney dysfunction to identify if problem is perfusion vs. tissue damage

Common Values

Value

<400 mL/day

Symbol

Quantity

Oliguria threshold

Value

3.5–5.0 mEq/L

Symbol

K+

Quantity

Normal serum potassium

Value

0.7–1.3 mg/dL

Symbol

Scr

Quantity

Normal serum creatinine (adult)

Section Title

Acute Kidney Injury (AKI) — Causes & Classification

Important Facts

Prerenal = most common cause of AKI (~55–60%); intrarenal ~30%; postrenal ~10%.
Oliguric phase (<400 mL/day) lasts ~1–3 weeks and is THE MOST DANGEROUS phase—hyperkalemia + fluid overload risk.
Diuretic phase = urine output rises (3–5 L/day) but kidneys cannot yet concentrate—risk of dehydration & electrolyte loss.
If prerenal AKI is NOT fixed quickly, prolonged ischemia triggers ATN (becomes intrarenal).
STAGING: KDIGO uses changes in serum creatinine & urine output; Stage 3 is when GFR falls <30 mL/min.
Contrast-induced nephropathy (CIN) is common postrenal/intrarenal trigger—always hydrate before contrast studies.
Recovery phase can take months; some renal damage may be permanent if insult was severe.

Key Definitions

Term

Acute Kidney Injury (AKI)

Example

A patient on aminoglycosides develops ATN; serum creatinine rises from 1.0 to 3.2 mg/dL in 48 hours.

Definition

Sudden, often reversible decline in renal function with rising BUN/creatinine and usually decreased urine output (<400 mL/day in oliguric phase).

Term

Acute Tubular Necrosis (ATN)

Example

Post-contrast dye imaging—acute rise in creatinine despite adequate hydration.

Definition

Intrinsic kidney damage from nephrotoxic drugs (aminoglycosides, contrast dye, NSAIDs) or prolonged ischemia; most common cause of intrarenal AKI.

Term

Prerenal AKI

Example

Hemorrhage, severe dehydration, shock, or heart failure → decreased blood flow to kidneys.

Definition

Decreased renal perfusion with intact kidney tissue; reversed if perfusion is restored in time.

Term

Postrenal AKI

Example

Kidney stones, BPH, urethral strictures, or tumors obstructing urethra/ureter.

Definition

Obstruction of urine flow distal to the kidney; causes back-pressure and tubular dysfunction.

Diagrams To Know

AKI cause classification tree (prerenal → perfusion, intrarenal → tissue, postrenal → obstruction)
The four phases of AKI plotted over time with urine output, creatinine, potassium trends

Common Values

Value

1–3 weeks (avg)

Symbol

Timeline

Quantity

Oliguric phase duration

Section Title

AKI Phases — Timeline & Clinical Focus

Important Facts

Oliguric phase = 1–3 weeks on average; absence of oliguria has better prognosis.
NOT all AKI becomes oliguric ('non-oliguric' AKI); non-oliguric has lower mortality.
During diuretic phase, REPLACE losses (IV fluid + electrolytes); patient may need as much fluid as during oliguric phase.
In recovery phase, check for BASELINE renal function—some patients never fully recover (CKD).
Diuretic phase can be mistaken for recovery; still monitor potassium and sodium closely.
Mortality in oliguric AKI is ~50%; in non-oliguric AKI ~5–10% (early recognition key).

Key Definitions

Term

Onset (Initiating) Phase

Example

Patient given aminoglycoside; no symptoms yet, but tubular injury is beginning.

Definition

From the insult (hypotension, nephrotoxin, obstruction) until clinical signs appear (hours to days).

Term

Oliguric Phase

Example

A burn victim 2 days post-injury: UO 200 mL/day, K+ 6.2, Cr rising, crackles on exam.

Definition

Peak of kidney dysfunction; urine <400 mL/day; rising BUN/Cr; MOST DANGEROUS—hyperkalemia, metabolic acidosis, fluid overload.

Term

Diuretic Phase

Example

Post-oliguric phase, patient urinates 4 L/day but labs show K+ 3.0, Na+ 128—net losses from polyuria.

Definition

Urine output rises as tubules recover but cannot concentrate; risk of dehydration, hypokalemia, hyponatremia from loss.

Term

Recovery (Convalescent) Phase

Example

Baseline Cr recovers to 1.5 (slightly elevated from pre-AKI of 1.0) after 8 weeks.

Definition

Gradual return of renal function over weeks to months; some permanent deficit may remain.

Diagrams To Know

Time-course graph of urine output, serum creatinine, and serum potassium across all four phases
Clinical priorities checklist for each phase (what to monitor/intervene for)

Common Values

Value

3.5–5.0 mEq/L

Symbol

K+

Quantity

Normal serum K+

Value

>5.5 mEq/L

Symbol

K+

Quantity

Hyperkalemia threshold

Value

>7.0 mEq/L

Symbol

K+

Quantity

CRITICAL hyperkalemia

Section Title

HYPERKALEMIA in AKI — The #1 Life Threat

Important Facts

PEAKED T WAVES are the earliest sign of hyperkalemia on ECG—classic NLE item.
Severity is not always proportional to K+ level; patient symptomatic at K+ 6.0+ or asymptomatic at 7.0+.
Acidosis WORSENS hyperkalemia (H+ shifts out of cell, K+ shifts in to maintain electroneutrality).
Hyperkalemia develops rapidly in oliguric phase—MONITOR K+ DAILY or every 4–6 hours if high risk.
Rhabdomyolysis (crush, statin, statins) → release of cellular K+ → severe hyperkalemia.
ANY peaked T wave on ECG = TREAT immediately, do not wait for repeat labs.

Key Definitions

Term

Hyperkalemia in AKI

Example

Crush injury → myoglobinuria → ATN + rapid K+ rise to 7.0 → peaked T waves on ECG → risk of cardiac arrest.

Definition

Serum potassium >5.5 mEq/L due to loss of renal excretion + tissue breakdown + acidosis shifting K+ out of cells; causes fatal cardiac arrhythmias.

Term

ECG Changes in Hyperkalemia

Example

K+ 6.5: peaked T; K+ 7.5: widened QRS; K+ >8: sine wave pattern—immediate life threat.

Definition

Progressive: peaked T waves → prolonged PR interval → widened QRS → sine wave → cardiac arrest.

Diagrams To Know

ECG progression with rising potassium levels (peaked T → widened QRS → sine wave)
Hyperkalemia management algorithm (IV calcium → insulin/glucose → bicarb → Kayexalate → dialysis)

Formulas

Formula

Daily Fluid Restriction in Oliguric AKI

Meaning

Previous day's urine output + ~500 mL for insensible loss (respirations, skin, feces)

Watch Out

Do NOT restrict so tightly that patient becomes hypovolemic; reassess if weight drops or orthostatic hypotension develops

When To Use

Calculating safe daily fluid intake in oliguric phase to prevent overload

Common Values

Value

~400–800 mL/day (skin, lungs, feces)

Symbol

IFL

Quantity

Insensible fluid loss per day

Value

0.6–1.0 g/kg/day

Symbol

Protein

Quantity

Protein intake in AKI pre-dialysis

Section Title

AKI Interventions — Nursing Priority Management

Important Facts

HYPERKALEMIA emergency management: (1) IV calcium gluconate (FIRST—protects myocardium, does NOT lower K+ level), (2) insulin 10 U IV + dextrose 25 g (shifts K+ INTO cells), (3) sodium bicarbonate 50–100 mEq IV (same effect in acidosis), (4) beta-agonists inhaled (shift K+ in), (5) sodium polystyrene sulfonate (Kayexalate) PO/PR (removes K+ via GI), (6) DIALYSIS for refractory hyperkalemia.
IV calcium gluconate takes effect in 1–3 minutes; effects last 30–60 minutes; repeat as needed if peaked T waves persist.
Insulin + dextrose onset 10–20 min; peak ~30–60 min; duration 4–6 hours.
Kayexalate (sodium polystyrene) takes 2–12 hours to work; combined with lactulose or sorbitol for GI action.
DAILY WEIGHT is mandatory—gain >1 kg/day suggests fluid retention; monitor for crackles, JVD, edema.
DIET: restrict K+, Na+, Phos; adequate calories; controlled protein to reduce uremic load (usually 0.6–1 g/kg/day until dialysis starts).
Hold/adjust all nephrotoxic drugs (NSAIDs, ACE-I, ARBs initially, aminoglycosides, radiocontrast dye).
Prepare for DIALYSIS if: refractory hyperkalemia, fluid overload with pulmonary edema, severe acidosis (pH <7.1), or uremia.
Monitor for AKI-to-CKD progression if baseline Cr not recovered after 3 months.

Key Definitions

Term

Renal Dosing

Example

Gentamicin: normal dose Q8H, but in AKI with GFR 10 mL/min → Q24–48H to prevent accumulation & toxicity.

Definition

Adjustment of drug dose/interval based on GFR; required for aminoglycosides, NSAIDs, ACE-I, many antibiotics in renal failure.

Term

Strict I&O Monitoring

Example

Patient with AKI: IN 500 mL (IV fluids) → OUT 150 mL (urine) = +350 mL positive balance that day.

Definition

Hourly or every 4-hour intake & output recording in oliguric AKI to guide fluid replacement and detect oliguria worsening.

Diagrams To Know

Hyperkalemia emergency treatment flowchart (time-sensitive steps)
Oliguric phase I&O monitoring template

Formulas

Formula

GFR-based CKD Staging (KDIGO)

Meaning

Stage 1: ≥90 mL/min/1.73m² (normal/high); Stage 2: 60–89 (mildly decreased); Stage 3a: 45–59; Stage 3b: 30–44; Stage 4: 15–29; Stage 5 (ESRD): <15

Watch Out

GFR calculation varies by formula (MDRD, CKD-EPI); always clarify which formula used; do NOT rely on serum Cr alone

When To Use

Classifying severity of CKD and determining need for renal replacement therapy (dialysis at Stage 5 or when symptomatic)

Common Values

Value

90–120 mL/min/1.73m²

Symbol

GFR

Quantity

Normal GFR (adult)

Value

<15 mL/min/1.73m²

Symbol

GFR

Quantity

ESRD threshold (Stage 5)

Value

2.5–4.5 mg/dL

Symbol

Phos

Quantity

Normal serum phosphate

Value

8.5–10.5 mg/dL

Symbol

Quantity

Normal serum calcium

Value

10–65 pg/mL

Symbol

PTH

Quantity

Normal PTH

Section Title

Chronic Kidney Disease (CKD) — Stages & Pathophysiology

Important Facts

DIABETES + HYPERTENSION = leading causes of CKD (~75% of new ESRD cases).
CKD is progressive and IRREVERSIBLE (unlike AKI); focus is slowing progression.
As GFR declines, kidneys lose ability to: excrete K+, regulate blood pressure, produce erythropoietin, activate vitamin D, balance acid-base.
Proteinuria (albuminuria) is BOTH a sign of kidney damage AND a driver of progression—reduce with ACE-I/ARB.
Secondary hyperparathyroidism begins early (Stage 2–3 CKD) due to low calcitriol + high phosphate.
Anemia in CKD is multifactorial: ↓ erythropoietin (primary), ↓ RBC lifespan, ↑ blood loss (dialysis), uremia.
Cardiovascular disease is the LEADING CAUSE OF DEATH in ESRD (hypertension, LVH, MI, stroke, pericarditis).
CKD patients are at HIGH RISK for: hyperkalemia, metabolic acidosis, fluid overload, bone disease, and infections.
Transition to ESRD is often at Stage 4 (GFR 15–29); prepare patient for dialysis/transplant counseling.

Key Definitions

Term

Chronic Kidney Disease (CKD)

Example

Diabetic patient with HTN: baseline Cr 1.0 → over 5 years climbs to 2.5 → Stage 4 CKD.

Definition

Progressive, IRREVERSIBLE loss of nephrons over months to years; defined by GFR <60 mL/min/1.73m² for ≥3 months or albuminuria.

Term

End-Stage Renal Disease (ESRD / Stage 5 CKD)

Example

Patient with GFR 12 mL/min; symptoms of uremia; on thrice-weekly hemodialysis.

Definition

GFR <15 mL/min/1.73m²; requires renal replacement therapy (dialysis or transplant) to sustain life.

Term

Uremia

Example

ESRD patient: fatigue, metallic taste, nausea, pruritus, confusion, pericardial friction rub.

Definition

The systemic toxic syndrome of retained nitrogenous wastes and electrolyte abnormalities from kidney failure; manifests in neuro, GI, cardiac, hematologic, and dermatologic systems.

Term

Renal Osteodystrophy

Example

CKD Stage 4 patient: low 1,25-vitamin D, high phosphate (5.5), high PTH (300), and X-ray shows loss of bone density.

Definition

Bone disease in CKD from lack of active vitamin D (calcitriol) + high phosphate + secondary hyperparathyroidism; leads to demineralization and fractures.

Diagrams To Know

GFR-based CKD stages with clinical milestones (when to start phosphate binders, epoetin, dialysis)
Multisystem manifestations of uremia mapped to organ systems

Section Title

CKD Manifestations — Uremia Syndrome

Important Facts

CARDIOVASCULAR: hypertension (fluid + renin-angiotensin), LVH, heart failure, MI, pericarditis (uremic), pericardial effusion/tamponade.
HEMATOLOGIC: anemia (low EPO + ↓ RBC lifespan + blood loss), bleeding tendency (platelet dysfunction from uremic toxins).
BONE/MINERAL: ↓ active vitamin D → ↓ calcium absorption, ↑ phosphate retention → secondary hyperparathyroidism, renal osteodystrophy, bone pain, fractures.
NEURO: fatigue, confusion, difficulty concentrating, peripheral neuropathy, restless legs syndrome, seizures (severe uremia), uremic encephalopathy.
SKIN: sallow/gray-yellow appearance, severe pruritus (phosphate, parathyroid hormone, dry skin), uremic frost (crystals) in severe cases.
GI: anorexia, nausea, vomiting, metallic taste, uremic fetor (ammonia breath), constipation, GI bleeding.
IMMUNE: increased infection risk from uremic toxins suppressing WBC function; dialysis patients at high risk.
METABOLIC: metabolic acidosis, hyperkalemia, hyperphosphatemia with hypocalcemia, hypoalbuminemia (protein-energy malnutrition).

Key Definitions

Term

Uremic Frost

Example

ESRD patient not on dialysis; white crystals visible on forehead and arms.

Definition

White, powdery urea crystals on skin in severe uremia; indicates critical kidney failure.

Term

Uremic Fetor

Example

Nurse notes 'ammonia smell' on breath of ESRD patient—indicates need for dialysis intensification.

Definition

Characteristic ammonia-like breath odor from high urea in saliva and lungs; sign of advanced uremia.

Term

Metabolic Acidosis in CKD

Example

CKD Stage 4: pH 7.28, HCO3− 16 mEq/L → mild metabolic acidosis, contributes to fatigue.

Definition

Loss of renal ability to excrete acid → low HCO3− and low pH; contributes to bone disease and uremic symptoms.

Diagrams To Know

Multisystem organ involvement in CKD/ESRD (each system affected by uremia)
Calcium-phosphate-PTH-vitamin D interrelationship in renal bone disease

Common Values

Value

2.5–4.5 mg/dL

Symbol

Phos

Quantity

Target serum phosphate in CKD

Value

8.5–10.5 mg/dL (corrected)

Symbol

Quantity

Target serum calcium in CKD

Value

35–70 pg/mL (varies by stage)

Symbol

PTH

Quantity

Target PTH in Stage 3–4 CKD

Value

10–11 g/dL

Symbol

Hgb

Quantity

Target Hgb on ESA

Value

<2000 mg/day

Symbol

Na+

Quantity

Sodium restriction

Value

2000–3000 mg/day

Symbol

K+

Quantity

Potassium restriction (Stage 3–4)

Section Title

CKD Management — Pharmacology & Dietary Control

Important Facts

PHOSPHATE BINDERS: (1) Calcium-based (cheap, effective) but risk hypercalcemia if combined with high-dose vitamin D; (2) Non-calcium (sevelamer, lanthanum) for hypercalcemic patients.
TIMING: phosphate binders MUST be taken WITH MEALS (breakfast, lunch, dinner) to bind dietary phosphate in GI tract; taking between meals is INEFFECTIVE.
AVOID: magnesium-containing antacids (Mg accumulates in renal failure), NSAIDs (worsen renal function), and all nephrotoxic drugs; always RENAL DOSE medications.
VITAMIN D: Active vitamin D (calcitriol, 1,25-OH vitamin D3) is given in CKD to raise calcium and suppress PTH; vitamin D2 or D3 supplements are NOT activated by failing kidneys.
ESAs: given IV (preferred in dialysis) or SQ; target Hgb is typically 10–11 g/dL (not higher—increased thrombotic risk); check iron stores (ferritin, TSAT) before starting.
ACE-I/ARB: REDUCE PROTEINURIA & slow CKD progression; start low-dose, titrate up; MONITOR K+ and Cr closely (acute Cr rise of 30% in first week is expected, >30% indicates renal artery stenosis).
DIETARY: Na+ <2 g/day (control HTN, fluid), K+ 2000–3000 mg/day (Stage 3–4), Phos <1000 mg/day (Stage 3–4), Protein 0.8–1.0 g/kg/day pre-dialysis (restrict nitrogenous waste).
FLUID: generally unrestricted in early CKD; restrict when oliguric or fluid overloaded (advise spacing fluids, suck on ice chips, hard candy).
MONITORING: Hgb Q1–3 months (on ESA), K+ and Cr every 3–6 months (more if on ACE-I/ARB or diabetic), phosphate/calcium/PTH every 3–6 months.
Statins for cardiovascular protection; antihypertensives titrated to target BP <130/80 mmHg (KDIGO guideline).

Key Definitions

Term

Phosphate Binders

Example

Patient takes calcium carbonate 1000 mg TID with meals; binds phosphate, preventing hyperphosphatemia.

Definition

Medications (calcium carbonate, calcium acetate, sevelamer, lanthanum) that bind dietary phosphate in the GI tract to reduce absorption; taken WITH meals.

Term

Erythropoietin-Stimulating Agents (ESAs)

Example

ESRD patient with Hgb 7.5 started on epoetin 4000 U IV 3x/week; Hgb rises to 10 by week 4.

Definition

Drugs (epoetin alfa, darbepoetin alfa) that stimulate RBC production to correct anemia of CKD; given IV or SQ, dose titrated to Hgb target ~10–11 g/dL.

Term

ACE Inhibitors / ARBs in CKD

Example

CKD Stage 3 patient with diabetes and proteinuria started on lisinopril 10 mg daily; proteinuria decreases from 2.5 g to 0.5 g over 3 months.

Definition

Medications that reduce glomerular hypertension, decrease proteinuria, and slow CKD progression; require careful K+ monitoring (can cause hyperkalemia).

Diagrams To Know

CKD medication timeline (what to start at which Stage)
Phosphate binder comparison chart (calcium vs. non-calcium)

Formulas

Formula

Fluid Removed by Dialysis (Weight Change)

Meaning

Pre-dialysis weight − Post-dialysis weight = Ultrafiltration (volume of fluid removed)

Watch Out

Excessive ultrafiltration (>1 kg/hour) risks intradialytic hypotension; monitor BP, symptoms of dizziness/cramping during HD

When To Use

Assessing HD effectiveness and determining safe ultrafiltration rate for next session

Common Values

Value

3–4 hours

Symbol

Quantity

Standard HD duration

Value

3 times/week

Symbol

Freq

Quantity

Standard HD frequency

Value

≥1.2

Symbol

Kt/V

Quantity

Target Kt/V

Value

<1 kg/hour

Symbol

UFR

Quantity

Safe ultrafiltration rate

Value

6–12 weeks

Symbol

Maturation

Quantity

AVF maturation time

Section Title

Hemodialysis (HD) — Access, Procedure, Complications

Important Facts

STANDARD HD: 3–4 hours, 3 times per week (total ~12 hours/week); goal Kt/V ≥1.2 (adequacy measure).
AVF is BEST access: fistula uses native vessels, lasts years, lowest infection rate (~0.8 infections/1000 patient-days); arteriovenous graft (synthetic) is second choice; central catheter is temporary.
AV FISTULA CARE: (1) Palpate THRILL (buzz) daily at home, (2) auscultate for BRUIT, (3) NO BP measurement on access arm, (4) NO blood draws/IV on access arm, (5) NO tight clothing/jewelry on access arm, (6) do NOT sleep on the access arm, (7) keep skin clean, (8) report absent thrill/bruit immediately = clotting.
CLOTTING: fistula thrombosis is EMERGENCY; present with loss of thrill/bruit + swelling + pain; requires immediate thrombolysis or revision.
INFECTION: most common complication of HD catheters; signs = fever, chills, redness at site; use sterile technique at all connections.
Heparin is used during HD to prevent clotting; BLEED RISK postdialysis—monitor for bleeding from access site, GI bleed, or hematoma.
DISEQUILIBRIUM SYNDROME: risk highest with first treatment or large BUN/Cr; prevent by using lower blood flow rates, shorter first session, shorter dialyzer; treat with IV mannitol or hypertonic saline.
HYPOTENSION: prevent by calculating safe ultrafiltration rate (<1 kg/hour), checking dry weight, ensuring adequate dialysate sodium, giving IV fluids if needed during HD.
DIALYZABLE DRUGS (removed by HD, so dose AFTER dialysis): many antihypertensives, antibiotics, NSAIDs, some anticonvulsants—always check if drug is dialyzable.
Pre-HD: measure weight, vital signs, check access patency (thrill/bruit), verify dialysis prescription. Post-HD: weigh, check BP, assess access site, hold BP meds until post-HD levels available.

Key Definitions

Term

Arteriovenous (AV) Fistula

Example

AVF created in left arm; patient waits 8 weeks, then undergoes 'cannulation' for HD needles.

Definition

Surgically created direct connection between artery and vein (usually radial artery to cephalic vein); preferred HD access due to low infection/clot risk and longevity; needs 6–12 weeks to mature.

Term

Thrill

Example

Nurse palpates left forearm AVF with thumb; feels characteristic thrill—indicates patency.

Definition

Palpable 'buzzing' vibration felt over a patent AV fistula; indicates blood flow through fistula.

Term

Bruit

Example

Stethoscope over AVF reveals a loud bruit—fistula is functioning.

Definition

Audible 'swooshing' sound heard on auscultation over a patent AV fistula; indicates turbulent blood flow.

Term

Dialysis Disequilibrium Syndrome

Example

First HD session in ESRD patient; mid-session develops severe headache, nausea, confusion; treated by slowing dialyzer and giving IV mannitol.

Definition

Acute neurologic symptoms (headache, nausea, confusion, seizures) during or after HD; caused by rapid removal of urea creating osmotic gradient (urea clears faster from blood than from CNS).

Term

Intradialytic Hypotension

Example

Patient loses 3 kg in 2 hours; BP drops from 150/90 to 110/60; feels dizzy and has leg cramps.

Definition

Drop in BP during HD due to rapid ultrafiltration exceeding cardiovascular compensation; causes dizziness, cramping, syncope.

Diagrams To Know

AV fistula anatomy and needle cannulation sites
HD circuit flow (blood pump → dialyzer → heparin administration → venous drip chamber)
Intradialytic hypotension management flowchart

Formulas

Formula

Net Fluid Removal (PD Balance)

Meaning

Volume drained − Volume instilled = Net ultrafiltration (positive = net fluid removed; negative = fluid retained)

Watch Out

Always clarify if reporting 'drained volume' or 'net balance'; confusing the two leads to incorrect fluid management

When To Use

Calculating true fluid balance in PD to assess adequacy and prevent fluid overload

Common Values

Value

1.5–2.5 L

Symbol

V_ex

Quantity

Standard dialysate volume per exchange

Value

4–5

Symbol

N_CAPD

Quantity

CAPD exchanges per day

Value

4–8 hours

Symbol

t_dwell

Quantity

Dwell time (CAPD)

Value

36.5°C (body temp)

Symbol

Quantity

Dialysate temperature

Section Title

Peritoneal Dialysis (PD) — Procedure, Technique, Complications

Important Facts

PD uses peritoneal membrane as 'dialyzer'—much larger surface area than HD dialyzer, but exchange is slower.
FILL–DWELL–DRAIN cycle: instill 1.5–2.5 L warm dialysate → dwell 4–8 hours (CAPD) or 1–2 hours (APD) → drain completely into bag.
WARM dialysate to body temperature (36.5°C) BEFORE instilling; cold fluid causes cramping and vasoconstriction, reducing efficiency.
NORMAL outflow: clear and pale yellow; ABNORMAL outflow: cloudy, bloody, or brown = peritonitis, hemoperitoneum, or bowel perforation.
STRICT ASEPTIC TECHNIQUE at every connection (cat-clamp disconnect method or Y-set); hand hygiene, mask, clean environment are essential.
PERITONITIS risk factors: poor technique, constipation (fecal contamination), prolonged catheter dwell, depression of immune system.
PERITONITIS signs: cloudy effluent, fever, peritoneal signs (pain, tenderness, rebound), sometimes diarrhea or vomiting; is life-threatening if untreated.
PERITONITIS treatment: empiric IV/intraperitoneal antibiotics (vanc + gent); send effluent culture; usually treat 2–3 weeks; some patients lose peritoneal function after multiple peritonitis episodes.
POOR DRAINAGE (outflow slower than inflow): suspect obstruction; reposition/turn patient, ensure catheter is not kinked, check that bag is below abdomen, confirm patient not constipated.
POSITIVE BALANCE (output <input over 24 hours): indicates inadequate ultrafiltration; assess dialysate dextrose concentration, increase dwell time, or switch to higher glucose dialysate.
INFECTION prevention: daily catheter exit site care (sterile dressing, betadine or chlorhexidine), inspect for signs of tunnel infection (redness, discharge, pain along catheter tract).
PD ADVANTAGES: gentler, more continuous (less hypervolemia/hypotension), can be done at home, fewer dietary/fluid restrictions, patient autonomy; DISADVANTAGES: slower clearance than HD, peritonitis risk, patient compliance critical, protein loss in dialysate.

Key Definitions

Term

Peritoneal Dialysis (PD)

Example

CAPD patient: instills 2 L dextrose dialysate at 6 AM, dwells 4–5 hours, drains at 10 AM; repeats 4 times daily.

Definition

Renal replacement therapy using the peritoneal membrane as a filter; dialysate is instilled into peritoneal cavity via catheter, dwells while diffusion/osmosis occur, then is drained (fill–dwell–drain cycle).

Term

CAPD (Continuous Ambulatory PD)

Example

Patient exchanges dialysate before breakfast, lunch, dinner, and bedtime; continues this schedule indefinitely.

Definition

Manual PD; patient performs 4–5 fill–dwell–drain cycles daily (day + night) over ~30–40 min per cycle; does NOT require machine.

Term

Automated PD (APD / CCPD)

Example

APD patient runs cycler from 10 PM–8 AM with 4–5 exchanges; does 1 manual exchange during the day.

Definition

Machine-assisted PD; cycler performs multiple exchanges overnight (8–10 hours); patient does 1 daytime dwell exchange.

Term

Peritonitis (PD complication)

Example

PD patient reports cloudy drained dialysate, fever (38.5°C), and abdominal pain; peritonitis suspected; sends dialysate for culture; starts empiric antibiotics (typically vancomycin + gentamicin).

Definition

Infection of peritoneal cavity; presents with cloudy dialysate outflow, fever, abdominal pain, and tenderness; most common serious complication of PD.

Diagrams To Know

CAPD/APD fill–dwell–drain cycle with time intervals
PD catheter anatomy (silicone catheter tunneled through abdomen into pelvis)
Peritonitis prevention and management flowchart

Common Values

Value

>100 mL/hour (initially); >1.5–2 L/day by day 3–5

Symbol

Quantity

Urine output goal post-transplant

Value

0.8–1.5 mg/dL (depends on baseline donor function)

Symbol

Quantity

Target serum creatinine post-transplant

Value

Lifelong

Symbol

Duration

Quantity

Immunosuppression duration

Section Title

Kidney Transplant — Perioperative & Immunosuppression

Important Facts

Transplant is DEFINITIVE treatment for ESRD; best outcomes if done within 5 years of dialysis onset.
Donor sources: living related (best outcomes), living unrelated, cadaver brain-dead, donation-after-cardiac-death (DCD).
SURGICAL PLACEMENT: iliac fossa (usually right); native kidneys left in place UNLESS they have active infection or malignancy.
POST-OP PRIORITY #1: monitor URINE OUTPUT HOURLY—immediate urine production indicates graft function; no urine = hyperacute rejection, thrombosis, or poor anastomosis.
POST-OP MONITORING: Hgb/Hct (perioperative blood loss), electrolytes (especially K+ if no urine early), Cr/BUN, fluid balance, access to dialysis if primary non-function.
IMMUNOSUPPRESSION is LIFELONG and CRITICAL—failure to take meds = rejection = graft loss.
Triple immunosuppression regimen typically: (1) Corticosteroid (prednisone), (2) Calcineurin inhibitor (cyclosporine or tacrolimus), (3) Antimetabolite (mycophenolate or azathioprine).
Calcineurin inhibitors (tacrolimus, cyclosporine) = most effective but nephrotoxic; require drug level monitoring; narrow therapeutic window.
SIDE EFFECTS of immunosuppression: infection (bacterial, viral, fungal, PCP), malignancy (skin cancer, lymphoma, post-transplant lymphoproliferative disorder—PTLD), hypertension, diabetes, dyslipidemia, gingival hyperplasia (cyclosporine), hirsutism (cyclosporine).
INFECTION is the #1 cause of death in transplant recipients (especially CMV, BK virus, fungal); teach signs: fever, cough, dysuria, sores.
ACUTE REJECTION signs: ↓UO, fever, graft tenderness/swelling, rising Cr, HTN, oliguria; MUST be treated ASAP with pulse steroids ± OKT3/ATG.
CHRONIC REJECTION: no cure; inevitable slow decline; only way to extend graft life is excellent immune suppression adherence and management of HTN/proteinuria.
DRUG INTERACTIONS: many medications interact with calcineurin inhibitors (grapefruit juice increases levels!); renal dosing still applies if graft function declining.
COUNSELING: never skip immunosuppressants, report infection signs immediately, keep all appointments, monitor BP at home, avoid crowds and sick contacts, use sun protection (malignancy risk).

Key Definitions

Term

Kidney Transplant (Renal Allograft)

Example

Cadaver donor kidney placed in right iliac fossa; anastomosed to right iliac vessels; ureter to bladder; patient immediately produces urine post-op.

Definition

Surgical placement of a donor kidney (usually in the iliac fossa; native kidneys left in place) into an ESRD recipient; definitive treatment for ESRD with best long-term outcomes.

Term

Hyperacute Rejection

Example

Incompatible cross-match missed; graft never produces urine despite excellent surgical placement; loss within 1 hour.

Definition

Immediate (minutes to hours post-transplant) loss of graft function due to pre-existing donor-specific antibodies; graft becomes non-functional immediately; rare with modern cross-matching.

Term

Acute Rejection

Example

Post-transplant day 10: patient develops fever 38.3°C, swelling/pain over graft, urine drops to 800 mL/day, Cr rises to 3.2; acute rejection suspected.

Definition

Cell-mediated (T-cell) or antibody-mediated immune attack on graft; occurs days to months post-transplant; presents with ↓urine output, fever, pain over graft, rising Cr; treatable with high-dose steroids/antilymphocyte agents.

Term

Chronic Rejection

Example

Transplant patient 5 years post-op; Cr gradually climbs from 1.4 to 2.8 over 2 years; biopsy shows chronic interstitial fibrosis.

Definition

Slow, progressive graft dysfunction over months to years; insidious loss of graft function despite adequate immunosuppression; mainly from chronic antibody attack; no treatment stops progression.

Diagrams To Know

Renal transplant surgical anatomy (vascular anastomosis to iliac vessels, ureter to bladder)
Timeline of rejection types (hyperacute, acute, chronic) with clinical presentation

Common Values

Value

<100 mL

Symbol

PVR

Quantity

Normal post-void residual (PVR)

Value

>100 mL

Symbol

PVR

Quantity

Post-void residual (significant)

Value

~20 g

Symbol

Prostate

Quantity

Prostate size (normal)

Value

>1–2 voids per night

Symbol

Nocturia

Quantity

Nocturia (abnormal threshold)

Section Title

Benign Prostatic Hyperplasia (BPH) — Pathophysiology & Management

Important Facts

BPH prevalence rises with age: ~50% of men age 50–60, ~80% age 70+; BUT only ~50% develop symptoms.
PATHOPHYSIOLOGY: androgen-driven epithelial hyperplasia + alpha-smooth-muscle tone increase → urethral compression → BOO.
LUTS STORAGE symptoms: frequency (>8 voids/day), urgency (sudden need to void), nocturia (>1 void at night—abnormal >2).
LUTS VOIDING symptoms: hesitancy (delay in starting stream), weak/intermittent stream, terminal dribbling, incomplete emptying.
ACUTE URINARY RETENTION (AUR): sudden inability to void; precipitated by cold medicines (anticholinergics), anesthesia, bed rest, large alcohol intake, or progression of BPH; is a medical emergency.
DIAGNOSIS: digital rectal exam (smooth, firm, enlarged prostate vs. nodular = cancer concern), IPSS symptom score, PSA (elevated in BPH but not diagnostic for cancer), post-void residual (PVR >100 mL abnormal), uroflowmetry (weak flow rate).
ALPHA-1 BLOCKERS (-osin drugs: tamsulosin, terazosin, doxazosin, alfuzosin): relax smooth muscle in prostate/bladder neck; RAPID symptom relief (1–2 weeks); SIDE EFFECT = orthostatic hypotension (teach rise slowly, avoid sudden position changes).
5-ALPHA-REDUCTASE INHIBITORS (finasteride, dutasteride): block testosterone → DHT conversion; SHRINK prostate over 3–6 months; slower relief than alpha-blockers; side effects = sexual dysfunction, decreased PSA; TERATOGENIC (pregnant women must not handle crushed tablets or absorb topically).
COMBINATION THERAPY: alpha-blocker + 5-alpha inhibitor for men with large prostate (>40 g) or elevated PSA.
SURGICAL OPTION—Transurethral Resection of Prostate (TURP): gold standard if medical therapy fails or acute retention; removed 90% of prostate tissue via transurethral approach.
POST-TURP NURSING: maintain continuous bladder irrigation (CBI) with sterile normal saline to prevent clot obstruction and keep urine output flowing; monitor irrigation fluid vs. drained volume.
POST-TURP DRAINAGE: expect pink/light-red urine initially (from hemorrhage); should CLEAR over first 24–48 hours; bright-red, ketchup-thick output with large clots = hemorrhage (increase CBI rate, report).
POST-TURP COMPLICATIONS: TUR syndrome (fluid absorption → dilutional hyponatremia with confusion, seizures, cerebral edema), infection, bleeding, urethral stricture, erectile dysfunction.
TUR SYNDROME prevention: use hypotonic irrigation fluid (glycine, sorbitol) in minimal volume, keep resection time <60–90 min; if symptoms (confusion, headache, BP changes), check Na+ and slow/stop irrigation.
POST-TURP CATHETER CARE: maintain continuous irrigation, monitor output color and quantity, keep CBI running until output clears, catheter removed when output is clear and urine flows freely.

Key Definitions

Term

Benign Prostatic Hyperplasia (BPH)

Example

65-year-old man with progressive frequency, urgency, nocturia (×5 night), weak stream; DRE shows smooth, firm, enlarged prostate; PSA normal.

Definition

Non-malignant enlargement of the prostate gland in aging men; compresses the urethra causing bladder outlet obstruction (BOO) and lower urinary tract symptoms (LUTS).

Term

Lower Urinary Tract Symptoms (LUTS) in BPH

Example

Patient with BPH has nocturia ×4, frequency ×8, weak stream, and post-void residual of 150 mL.

Definition

Storage symptoms (frequency, urgency, nocturia) and voiding symptoms (hesitancy, weak stream, incomplete emptying, dribbling); severity assessed by IPSS score.

Term

Postrenal Obstruction from BPH

Example

Untreated BPH patient develops acute urinary retention (bladder distension to 1200 mL) → elevated post-void residual → hydronephrosis on ultrasound → rising Cr.

Definition

Chronically elevated bladder pressure → hydronephrosis and back-pressure on kidneys; can cause prerenal AKI if severe (retrograde pressure reduces GFR).

Diagrams To Know

Prostate anatomy and relationship to urethra (normal vs. enlarged BPH)
BPH management algorithm (medical vs. surgical decision tree)
Post-TURP continuous bladder irrigation setup and monitoring

Must Remember

HYPERKALEMIA is the #1 life threat in AKI/CKD—peaked T waves on ECG are diagnostic; treat immediately with IV calcium gluconate (protects heart FIRST), then insulin/dextrose, bicarb, Kayexalate, and dialysis.
AKI causes by location: PRE-renal = poor perfusion (most common, BUN:Cr >20:1), INTRA-renal = ATN/nephrotoxins (BUN:Cr <10:1), POST-renal = obstruction (BPH, stones, tumors).
AKI oliguric phase (<400 mL/day) is THE MOST DANGEROUS—lasts 1–3 weeks; manage with strict I&O, fluid restriction (previous day's output + 500 mL), K+/Na+/Phos restriction, and prepare for dialysis.
CKD is progressive and IRREVERSIBLE; diabetes + hypertension are top causes; focus is slowing progression with ACE-I/ARB + HTN control + phosphate binders + EPO for anemia.
Phosphate binders MUST be given WITH MEALS to bind dietary phosphate; calcium-based binders (cheap) vs. non-calcium (sevelamer) for hypercalcemic patients; AVOID magnesium antacids.
AV fistula is the best HD access—palpate for THRILL (buzz), auscultate for BRUIT; NO blood draws/BP/IV on access arm; loss of thrill = clotting = emergency.
Post-TURP continuous bladder irrigation: pink drainage is expected and clears in 24–48 hours; bright-red with clots = hemorrhage; calculate true urine output by subtracting irrigation fluid instilled from total drained.
PD cloudy outflow = PERITONITIS (emergency); use strict aseptic technique, warm dialysate to body temp before instilling, and monitor for poor drainage (reposition, check kinks, check bag below abdomen).
Kidney transplant requires lifelong immunosuppression; acute rejection signs = ↓UO, fever, graft pain, ↑Cr; monitor urine output HOURLY post-op; infection is the #1 cause of death in transplant recipients.
BPH causes postrenal obstruction (bladder outlet obstruction); alpha-blockers give rapid relief but cause orthostatic hypotension; finasteride is teratogenic—pregnant women must not handle tablets; post-TURP requires continuous bladder irrigation.

Last Minute Tips

On exam, if you see 'peaked T waves' + kidney failure, think HYPERKALEMIA EMERGENCY—the answer is always IV calcium gluconate FIRST, then shift K+ into cells (insulin + dextrose). Do NOT give potassium-lowering diuretics in renal failure.
Distinguish AKI from CKD by acuity: AKI = sudden rise in Cr over hours–days with oliguria (often reversible if cause fixed); CKD = months-to-years progressive decline, bilateral small kidneys on ultrasound, anemia present, bone disease present (irreversible). Always ask 'baseline Cr?'
In dialysis questions, HD is FAST & EXTRACORPOREAL (external filter) but causes hemodynamic stress (hypotension, disequilibrium); PD is SLOW & CONTINUOUS (patient's own membrane) but risks PERITONITIS if asepsis broken. Match modality to patient's stability & lifestyle.
Post-transplant: urine output = graft function; no urine = rejection, thrombosis, or poor anastomosis. If acute rejection suspected (fever + ↓UO + graft tenderness + ↑Cr), treat IMMEDIATELY with pulse steroids or antilymphocyte agents—time is kidney.
BPH exam questions often test access care (fistula) or post-TURP irrigation: remember THRILL (fistula patency), pink drainage (normal post-TURP), and CBI (continuous irrigation to prevent clots). If bright-red ketchup-thick output = hemorrhage, SPEED UP irrigation and report NOW.

Comparison Tables

Rows

Values

Sudden (hours to days)
Gradual (months to years)

Property

Onset

Values

Often reversible if cause removed
Progressive and IRREVERSIBLE

Property

Reversibility

Values

Normal size (initially)
Bilateral small and scarred

Property

Kidney size on imaging

Values

Prerenal (perfusion), intrarenal (tissue), postrenal (obstruction)
Diabetes (~35%), hypertension (~30%), glomerulonephritis, polycystic kidney

Property

Causes

Values

NOT typically present acutely
Present (low EPO); often severe

Property

Anemia

Values

Not present
Renal osteodystrophy common

Property

Bone disease

Values

Acute (confusion, seizures only if severe)
Chronic, progressive (fatigue, pruritus, fetor, frost)

Property

Uremic manifestations

Values

Treat cause; manage hyperkalemia, fluid overload; supportive care
Slow progression (ACE-I/ARB); manage complications (anemia, bone, HTN); prepare for dialysis/transplant

Property

Management focus

Values

Often temporary (weeks); needed if anuric/severe
Permanent (lifelong) when GFR <15 (Stage 5)

Property

Dialysis need

Columns

Feature
Acute Kidney Injury (AKI)
Chronic Kidney Disease (CKD)

Table Title

AKI vs. CKD — Key Differences

Rows

Values

↓ Perfusion (hypovolemia, shock, HF)
Direct kidney tissue damage (drugs, ischemia)
Obstruction of urine flow (stones, BPH, tumor)

Property

Cause

Values

>20:1 (HIGH)
<10:1 (LOW/normal)
Variable

Property

BUN:Cr ratio

Values

>500 mOsm/kg (CONCENTRATED)
<300 mOsm/kg (dilute)
Variable

Property

Urine osmolality

Values

<20 mEq/L (avid retention)
>40 mEq/L (wasted in urine)
Variable

Property

Urine sodium (UNa)

Values

<1% (kidneys reabsorbing Na to conserve volume)
>2% (kidneys cannot reabsorb)
Variable

Property

FENa (Fractional excretion of Na)

Values

Intact
Damaged (necrotic tubules)
Intact (obstruction is mechanical)

Property

Kidney tissue

Values

RAPID if perfusion restored within hours–days
Slower recovery; may be irreversible if prolonged
RAPID if obstruction relieved promptly

Property

Reversibility

Values

Hours to days
Days to weeks (oliguria 1–3 weeks)
Hours to days if decompressed promptly

Property

Time to reverse

Values

Normal kidney size
Normal or swollen kidney
Hydronephrosis on ultrasound

Property

Imaging

Columns

Characteristic
Prerenal
Intrarenal (ATN)
Postrenal

Table Title

Prerenal vs. Intrarenal vs. Postrenal AKI

Rows

Values

External artificial dialyzer
Peritoneal membrane (patient's own membrane)

Property

Filter mechanism

Values

3x/week, 3–4 hours each = ~12 hours/week
CAPD: 4–5 exchanges/day (~30 min each); APD: 8–10 hr overnight

Property

Frequency & duration

Values

RAPID (high efficiency); large solute removal
SLOW (gradual); gentler on body

Property

Clearance

Values

AV fistula, graft, or central catheter (required)
Peritoneal catheter (tunneled into abdomen)

Property

Vascular access

Values

STRICT (K+, Na+, Phos, fluid between sessions)
LESS strict (more fluid/nutrient flexibility)

Property

Dietary restrictions

Values

Rapid fluid shifts → hypotension, arrhythmias
Gradual fluid removal → less hemodynamic stress

Property

Cardiovascular stress

Values

Access-related (bacteremia, sepsis); ~0.8–1.5 infections/1000 patient-days
Peritonitis (~0.5 episodes/patient/year); catheter tunnel infection

Property

Infection risk

Values

Hypotension, disequilibrium, vascular access thrombosis
Peritonitis (life-threatening if untreated)

Property

Major complication

Values

Mostly in-center (3x/week clinic); home HD also available
Home-based (CAPD or APD); patient autonomous

Property

Home vs. In-center

Values

Can continue indefinitely (if vascular access maintained)
Peritoneal membrane can fail after years (avg 5–10 years before peritonitis loss)

Property

Longevity of modality

Values

Rapid clearance need; large patients; high-K+ diet; compliance issues
Residual renal function; cardiovascular instability; patient preference; younger/active

Property

Best for

Columns

Feature
Hemodialysis (HD)
Peritoneal Dialysis (PD)

Table Title

Hemodialysis vs. Peritoneal Dialysis

Rows

Values

Stabilizes myocardial membrane; does NOT lower K+
1–3 minutes
30–60 minutes
GIVE FIRST if peaked T waves; repeat if ECG still abnormal; check for extravasation (tissue necrosis)

Property

IV Calcium Gluconate

Values

Shifts K+ INTO cells (anabolic effect)
10–20 minutes
4–6 hours
Always pair insulin with dextrose to prevent hypoglycemia; monitor glucose

Property

Insulin 10 U IV + Dextrose 25 g

Values

In acidosis, shifts K+ into cells; alkalosis increases K+ renal excretion
30 minutes–1 hour
4–6 hours
Most effective in metabolic acidosis; less effective in normal pH

Property

Sodium Bicarbonate 50–100 mEq IV

Values

Shifts K+ into cells via beta-2 stimulation
30 minutes
4–6 hours
Inhaled or IV; can cause tachycardia; avoid in CAD

Property

Beta-2-Agonists (albuterol)

Values

K+-binding resin; removes K+ via GI tract
2–12 hours (slow)
Long-term (hours–days)
Mix with sorbitol for GI action; takes time; NOT for acute emergency alone

Property

Sodium Polystyrene Sulfonate (Kayexalate)

Values

Direct removal of K+ (most effective)
During dialysis
Minutes–hours
Most definitive; use if refractory or life-threatening; HD preferred over PD for speed

Property

DIALYSIS

Columns

Intervention
Mechanism
Onset
Duration
Key points

Table Title

Hyperkalemia Emergency Management — Interventions & Time-to-Effect

Rows

Values

Minutes–hours post-transplant
Pre-existing donor-specific antibodies (IgG/IgM)
Graft swollen, dusky, no urine output; immediate non-function
NOT reversible; graft loss immediate; prevention via cross-match

Property

Hyperacute

Values

Days to months (peak ~2–3 weeks)
T-cell (cellular) or antibody-mediated immune attack
↓UO, fever, graft pain/swelling, ↑Cr; may have hypertension, weight gain
Reversible if treated promptly with high-dose steroids ± OKT3/ATG

Property

Acute

Values

Months to years (insidious)
Chronic antibody-mediated injury; immune complex deposition; fibrosis
Gradual ↑Cr over weeks–months; progressive renal insufficiency; hypertension, proteinuria
Largely irreversible; focus on maximizing immunosuppression to slow decline

Property

Chronic

Columns

Rejection Type
Timing
Mechanism
Presentation
Reversibility

Table Title

Types of Kidney Rejection — Timeline & Presentation

Rows

Values

Relax smooth muscle in prostate/bladder neck
Block testosterone → DHT conversion; shrink prostate

Property

Mechanism

Values

RAPID (1–2 weeks)
SLOW (3–6 months)

Property

Onset of symptom relief

Values

No reduction (but symptoms improve)
Significant reduction (20–30%)

Property

Prostate size reduction

Values

Men with LUTS regardless of prostate size
Men with LARGE prostate (>40 g) + elevated PSA

Property

Best for

Values

Orthostatic hypotension (dizziness, syncope on standing), headache, fatigue, nasal congestion
Sexual dysfunction (ED, ↓libido), gynecomastia, decreased ejaculatory volume

Property

Side effects

Values

Rise slowly from bed/chair; avoid driving if dizzy
NOT for pregnant women (teratogenic); never let pregnant woman handle crushed tablets or absorb topically

Property

Key side effect to teach

Values

Yes, often combined with 5-alpha inhibitor for synergy
Yes, often combined with alpha-blocker for rapid + sustained relief

Property

Combination therapy?

Columns

Feature
Alpha-Blockers (-osin)
5-Alpha-Reductase Inhibitors (-astride, -uteride)

Table Title

Alpha-Blockers vs. 5-Alpha-Reductase Inhibitors in BPH

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