Renal Failure & Dialysis Guide

AKI Definition (KDIGO 2012)

AKI is defined as any one of the following:
• Serum creatinine rise ≥26.5 μmol/L within 48 hours
• Serum creatinine rise ≥1.5× baseline within 7 days
• Urine output <0.5 mL/kg/h for ≥6 consecutive hours

Baseline creatinine = lowest creatinine in the preceding 3 months (or estimated from MDRD if unknown).

KDIGO AKI Staging — Interactive Calculator

Baseline Creatinine (μmol/L)

Current Creatinine (μmol/L)

Urine Output Scenario

Stage	Creatinine Criteria	Urine Output Criteria
Stage 1	1.5–1.9× baseline or rise ≥26.5 μmol/L	<0.5 mL/kg/h for 6–12h
Stage 2	2.0–2.9× baseline	<0.5 mL/kg/h for ≥12h
Stage 3	≥3.0× baseline or ≥353.6 μmol/L or RRT	<0.3 mL/kg/h for ≥24h or anuria ≥12h

AKI Causes — Pre-renal / Intrinsic / Post-renal

Category	Common Causes	Clinical Clues
Pre-renal	Dehydration, sepsis, heart failure, haemorrhage, NSAIDs, ACEi/ARBs	Low BP, high HR, dry mucous membranes, BUN:Cr ratio >20, FeNa <1%, urine Na <20 mmol/L, responds to fluids
Intrinsic	ATN (aminoglycosides, contrast, ischaemia), glomerulonephritis, interstitial nephritis, rhabdomyolysis	No response to fluids, muddy-brown granular casts on urine microscopy, FeNa >2%, urine Na >40 mmol/L
Post-renal	BPH, renal calculi, pelvic/retroperitoneal malignancy, bilateral ureteric obstruction	Palpable bladder, haematuria, flank pain, history of prostate disease, hydronephrosis on USS

Urinalysis Interpretation

Urine Casts

Cast Type	Suggests
Granular (muddy-brown)	Acute tubular necrosis (ATN)
RBC casts	Glomerulonephritis
WBC casts	Pyelonephritis / interstitial nephritis
Waxy / broad casts	Chronic kidney disease
Hyaline casts	Normal / dehydration

FeNa Calculation

FeNa (%) = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100

<1% — Pre-renal (kidneys avidly retaining Na)
>2% — Intrinsic renal (tubular damage)
Note: unreliable if diuretics used. Use FeUrea instead (<35% = pre-renal).

Cockcroft-Gault CrCl Calculator

Age (years)

Weight (kg)

Serum Creatinine (μmol/L)

Sex

CKD Staging by eGFR

Stage	eGFR (mL/min/1.73m²)	Description	Key Action
G1	≥90	Normal kidney function	Monitor if markers of kidney damage present
G2	60–89	Mildly decreased	Manage risk factors, monitor annually
G3a	45–59	Mildly to moderately decreased	Hold metformin cautiously, review NSAID use
G3b	30–44	Moderately to severely decreased	Nephrology referral, avoid nephrotoxins, avoid contrast
G4	15–29	Severely decreased	Prepare for RRT, AV fistula creation
G5 / ESRD	<15	Kidney failure	Dialysis or transplantation

Hyperkalaemia Severity Tool

Enter K+ Level (mmol/L)

Mild Hyperkalaemia — K+ 5.5–6.0 mmol/L

Dietary K+ restriction: avoid bananas, citrus, potatoes, tomatoes, dried fruit
Review and withhold contributing medications: ACEi/ARBs K-sparing diuretics NSAIDs Trimethoprim
Sodium polystyrene sulphonate (Kayexalate) 15–30 g orally — binds K+ in gut
Repeat U&E in 24 hours
Ensure adequate urine output

Moderate Hyperkalaemia — K+ 6.0–6.5 mmol/L

Continuous cardiac monitoring — obtain 12-lead ECG
Calcium resonium 15–30 g oral or rectal (removes K+ from body)
Consider IV frusemide 40–80 mg if adequate renal function / fluid overloaded
Ensure IV access and senior review
Repeat BMP (U&E) in 4–6 hours
Restrict dietary K+, withhold contributing medications

SEVERE Hyperkalaemia — K+ >6.5 mmol/L OR ECG Changes — EMERGENCY

1
Calcium Gluconate 10 mL of 10% IV over 5–10 min
Stabilises cardiac membrane. Onset within 1–3 min. Duration 30–60 min. Repeat if no ECG improvement. Does NOT lower K+.
2
Insulin 10 units + 50 mL 50% Dextrose IV
Drives K+ into cells. Onset 15–30 min, duration 4–6h. Monitor BSL every 30 min ×2h. If glucose >14 mmol/L, give insulin without dextrose.
3
Salbutamol 10–20 mg nebulised
Beta-2 agonist drives K+ intracellularly via Na/K-ATPase. Onset 15–30 min. Additive effect with insulin. May cause tachycardia.
4
Sodium Bicarbonate 100 mL 8.4% IV (if metabolic acidosis)
Slow onset. Works by correcting acidosis which drives K+ out of cells. Avoid in fluid overload.
5
Kayexalate / Calcium Resonium (oral or rectal)
Removes K+ from the body over hours via GI tract. Onset 1–2h. Long-term K+ elimination.
6
Emergency Dialysis if refractory
Contact nephrology immediately. Haemodialysis is the most effective and rapid method for K+ removal. Consider if K+ >7.0, ECG changes, or no response to medical management.

Ongoing monitoring: K+ hourly, continuous cardiac monitoring, repeat 12-lead ECG after each intervention, BSL monitoring after insulin-dextrose.

ECG Progression in Hyperkalaemia

▲

Peaked T Waves

K+ ~5.5–6.5

→

↦

PR Prolongation

K+ ~6.5–7.0

→

⸻

Wide QRS

K+ ~7.0–7.5

→

Sine Wave

K+ >7.5

→

⚠

Asystole / VF

K+ >8.0

ECG changes may not follow strict K+ levels — treat ECG changes as emergency regardless of K+ value. Rate of rise matters as much as absolute level.

HD Principles

Haemodialysis removes waste products and excess fluid by passing blood across a semipermeable membrane against dialysate flowing in the opposite direction (countercurrent). Solutes move by diffusion (small molecules: urea, creatinine, K+) and ultrafiltration (fluid removal by transmembrane pressure).

Parameter	Typical Range	Notes
Blood flow rate (Qb)	200–400 mL/min	Higher = better clearance
Dialysate flow rate (Qd)	500–800 mL/min	Usually fixed
Session duration	3–5 hours	Standard 3×/week for ESRD
Ultrafiltration rate	Individualised	Target: dry weight achieved by end of session
Anticoagulation	Heparin infusion	Citrate locking between sessions; systemic heparin during

Vascular Access Types

AVF — Gold Standard
Arteriovenous fistula (usually radial/cephalic or brachial). Requires 6–8 weeks to mature before use. Longest patency, lowest infection risk. Never take BP or blood from fistula arm.

AVG — Arteriovenous Graft
Synthetic (PTFE) conduit between artery and vein. Usable in 2–4 weeks. Higher thrombosis rate than AVF. Good for patients with poor vessels.

Vascath — Temporary CVC
Tunnelled or non-tunnelled. Sites: right internal jugular (preferred), femoral, subclavian (avoid — causes stenosis). High infection risk. Used acutely or as bridge.

Tunnelled CVC (Permcath)
Long-term catheter for those unsuitable for AVF/AVG. Dacron cuff reduces infection. Still inferior to AVF.

Intradialytic Complications

Complication	Cause	Management
Hypotension Most common (~25%)	Fluid removal too rapid, dry weight set too low, antihypertensives taken pre-HD	Reduce UF rate, Trendelenburg position, 100–200 mL NS bolus, reassess dry weight
Muscle Cramps	Rapid fluid removal, low sodium dialysate, electrolyte shifts	Reduce UF rate, warm saline, sodium profiling, reassess dry weight
Arrhythmias	Rapid electrolyte shifts (K+, Ca²+), underlying cardiac disease	Check ECG, electrolytes, reduce blood flow, notify physician
Air Embolism	Air entering circuit via disconnection or empty saline bag	Clamp venous line immediately, left lateral Trendelenburg position, 100% O&sub2;, emergency call
Disequilibrium Syndrome	Rapid urea removal → cerebral oedema (first HD sessions)	Short initial sessions (2h), slow blood flow, mannitol; usually self-limiting
Haemolysis	Hypotonic dialysate, kinked tubing, overheated dialysate	Stop HD, clamp blood lines (do NOT return blood), emergency labs, notify physician

Post-Dialysis Care & AVF Nursing

Post-HD Checklist

Weigh patient — compare to pre-HD weight and target dry weight
Blood pressure — administer held antihypertensives now if BP elevated
Access site haemostasis: AVF needle sites — pressure for 5–10 min
Vascath locking: instil heparin or citrate lock per protocol
Post-dialysis labs if ordered (K+, pH)
Document session: UF achieved, access pressures, complications

AVF Nursing Rules

Protect the Fistula Arm:
• NO blood pressure cuff
• NO venepuncture or IV cannulation
• NO tight jewellery or watch
• NO sleeping on fistula arm
• Palpate thrill & auscultate bruit every shift
• Absent thrill/bruit → urgent vascular review

Peritoneal Dialysis (PD) Overview

PD uses the peritoneal membrane as a natural dialysis filter. Dextrose-containing dialysate is instilled into the peritoneal cavity; waste products and fluid move across the membrane by osmosis and diffusion. Primarily a home-based modality — promotes patient independence.

CAPD (Continuous Ambulatory PD)
4 exchanges per day manually. Each exchange: 2 L dialysate, dwell 4–6h. Patient performs exchanges independently. No machine required.

APD (Automated PD)
Overnight automated cycling machine (cycler). 8–10 exchanges during sleep. Patient free during day. Better for working patients.

PD Peritonitis — Recognition & Management

Peritonitis is the most serious complication of PD. Untreated, it leads to catheter loss, membrane failure, and death.

Feature	Detail
Classic Triad	Cloudy effluent • Abdominal pain • Fever
Diagnosis	Effluent cell count >100 WBC/mm³ (>50% neutrophils). Send effluent for MC&S urgently.
Common Organisms	Staph. epidermidis (CoNS) most common. Staph. aureus — exit site/tunnel. Gram negatives — bowel source.
Empirical Treatment	Intraperitoneal (IP) antibiotics: vancomycin + ceftazidime/gentamicin. Local hospital protocol applies.
Catheter Removal	If refractory at 5 days, fungal, relapsing, or tunnel infection. Restart PD after 4–6 weeks.

PD Catheter Care

Clean exit site daily with chlorhexidine or as per local protocol
Apply mupirocin or gentamicin cream to exit site (reduces Staph. aureus colonisation)
Immobilise catheter with adhesive dressing — prevent trauma
Avoid submersion in baths or swimming pools (showering acceptable with waterproof cover)
Prevent constipation — reduces intra-abdominal pressure, reduces catheter malfunction
Inspect for redness, discharge, or tunnel tenderness at each contact
Teach patient to inspect exchanges: effluent should be clear

CRRT — Continuous Renal Replacement Therapy (ICU)

CRRT is indicated for haemodynamically unstable patients (septic shock, ARDS, multi-organ failure) who cannot tolerate rapid fluid shifts of conventional HD. Slow, continuous therapy over 24+ hours.

CRRT Modes

Mode	Mechanism
CVVH	Convection only (ultrafiltration + replacement fluid)
CVVHD	Diffusion only (dialysate) — like slow HD
CVVHDF	Convection + diffusion — most common ICU mode

Anticoagulation Options

Systemic Heparin: Traditional, cheap, risk of HIT and bleeding.

Regional Citrate (RCA): Increasingly preferred in GCC ICUs (SQUH, HMC). Citrate chelates Ca²+ in circuit; calcium infused into patient separately. Lower bleeding risk. Monitor ionised Ca²+ in circuit and patient every 4–6h.

CRRT Nursing Monitoring

Parameter	Frequency	Action Threshold
Fluid balance (net removal)	Hourly	Adjust effluent rate per physician order
Circuit pressures (access, return, filter)	Continuous alarm monitoring	Rising filter pressure → filter clotting → change circuit
K+, phosphate, Mg²+, Ca²+	Every 4–6 hours	CRRT removes electrolytes — replace per protocol
Temperature	Hourly	Blood cooling through circuit — warming blankets, warmed replacement fluid
Filter life	Log start time	Typical 24–72h; citrate anticoagulation extends life
Ionised Ca²+ (if citrate RCA)	Every 4–6h (circuit & patient)	Circuit iCa <0.35 mmol/L; patient iCa 1.0–1.2 mmol/L

Drug dosing during CRRT: Many medications are cleared by CRRT (vancomycin, piperacillin-tazobactam). Contact pharmacy for adjusted dosing — standard renal dose tables do NOT apply.

Drug / Class	Mechanism of Nephrotoxicity	Nursing Action
NSAIDs	Inhibit prostaglandins → afferent arteriolar constriction → reduced GFR. Risk highest in dehydration, heart failure, CKD.	Avoid in AKI/CKD. Educate patients. Check creatinine if used >5 days.
Aminoglycosides (gentamicin, amikacin)	Proximal tubular cell accumulation → direct tubular necrosis. Potentiated by dehydration, loop diuretics, repeated doses.	Once-daily dosing preferred. Monitor peak & trough levels. Daily creatinine. Limit course to <5–7 days.
Iodinated Contrast	Direct tubular toxicity + vasoconstriction. Risk highest in CKD G3b+, DM, dehydration, multiple myeloma.	Pre-hydration: 1 mL/kg/h normal saline for 6h before and 6h after. Avoid in eGFR <30. Use lowest volume. Consider iso-osmolar contrast.
ACEi / ARBs	Block angiotensin II → efferent arteriolar dilation → drop in GFR. Protective in CKD long-term (reduce proteinuria) but can precipitate AKI acutely.	Beneficial in stable CKD with proteinuria. Hold temporarily in AKI, sepsis, dehydration, or pre-contrast. Monitor K+ and creatinine at initiation and dose changes.
Metformin	Not nephrotoxic itself, but accumulates in renal impairment → risk of lactic acidosis.	Hold if eGFR <45 mL/min/1.73m². Stop 48h before contrast. Restart only when creatinine stable post-contrast.
Vancomycin	Proximal tubular toxicity — especially with concomitant aminoglycosides or in AKI.	Target AUC-guided dosing. Trough <15–20 mg/L. Daily creatinine if on vancomycin >3 days.
Calcineurin Inhibitors (tacrolimus, ciclosporin)	Renal vasoconstriction → chronic nephrotoxicity. Common in transplant patients.	Regular drug levels, creatinine, BP monitoring. Avoid nephrotoxin combinations.

KDIGO AKI Staging (Creatinine)
Stage 1	1.5–1.9× baseline or +26.5 μmol/L
Stage 2	2.0–2.9× baseline
Stage 3	≥3.0× or ≥353.6 μmol/L or RRT

CKD eGFR Thresholds
G1	≥90 mL/min/1.73m²
G2	60–89
G3a	45–59
G3b	30–44
G4	15–29
G5	<15 (ESRD)