CKD Advanced Nursing Guide | GCC Nursing Platform

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KDIGO CKD Definition

KDIGO 2012 Definition

CKD is defined as abnormalities of kidney structure or function, present for >3 months, with implications for health. Requires either: kidney damage markers (albuminuria ≥30 mg/g, haematuria, structural abnormality, biopsy findings, transplant history) OR GFR <60 mL/min/1.73m².

CGA Staging System

CKD is staged using three parameters: Cause + GFR category + Albuminuria category. All three must be documented for complete staging.

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GFR Staging (G1–G5)

Stage	GFR (mL/min/1.73m²)	Description	Monitoring
G1	≥90	Normal/high — only CKD if damage markers present	Annual, treat underlying cause
G2	60–89	Mildly decreased — only CKD if damage markers present	Annual, optimise CVD risk
G3a	45–59	Mildly to moderately decreased	Every 6 months
G3b	30–44	Moderately to severely decreased	Every 3–6 months
G4	15–29	Severely decreased — prepare for RRT	Every 3 months, refer nephrology
G5	<15	Kidney failure — RRT or conservative pathway	Monthly, or per dialysis schedule

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Albuminuria Categories (A1–A3)

Category	ACR (mg/g)	ACR (mg/mmol)	Description
A1	<30	<3	Normal to mildly increased
A2	30–300	3–30	Moderately increased (microalbuminuria)
A3	>300	>30	Severely increased (macroalbuminuria/proteinuria)

Clinical Significance

A3 albuminuria independently predicts CKD progression, cardiovascular events, and mortality. First morning spot urine ACR is preferred over 24-hour urine collection.

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KDIGO Risk Heat Map

Combined GFR and Albuminuria prognosis for CKD progression and mortality:

A1
<30 mg/g

A2
30–300 mg/g

A3
>300 mg/g

G1 (≥90)

Low

Moderate

High

G2 (60–89)

Low

Moderate

High

G3a (45–59)

Moderate

High

Very High

G3b (30–44)

High

Very High

G4 (15–29)

Very High

G5 (<15)

Very High

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Main Causes of CKD

Diabetic nephropathy: 40–50% of CKD — leading cause in GCC due to T2DM epidemic
Hypertensive nephrosclerosis: 25–30%; uncontrolled BP causes glomerulosclerosis
Glomerulonephritis: IgA nephropathy commonest in adults worldwide; FSGS, membranous
Polycystic kidney disease (PKD): ADPKD most common inherited kidney disease
Obstructive uropathy: BPH, renal calculi, retroperitoneal fibrosis
Lupus nephritis: class III/IV require aggressive immunosuppression
Renovascular disease: renal artery stenosis — atherosclerosis or FMD

GCC Context

Saudi Arabia, UAE and Kuwait have among the world's highest diabetes prevalence (20–25%). This directly translates to very high CKD and ESRD rates in the region.

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Pathophysiology of CKD Progression

Key Mechanisms

Glomerular hyperfiltration: initial compensation by remaining nephrons → intraglomerular hypertension
Proteinuria: protein leak activates tubular inflammation and fibrosis signalling (TGF-β pathway)
Tubulointerstitial fibrosis: progressive scarring replaces functional nephron mass
RAAS activation: angiotensin II drives hypertension, inflammation, fibrosis
Endothelial dysfunction: accelerates cardiovascular risk and glomerular damage
Nephron loss: progressive decline in GFR → uraemic syndrome

Acute-on-Chronic Risk

Dehydration — commonest acute insult in GCC climate
NSAIDs, contrast nephropathy, aminoglycosides
Urinary tract obstruction
Intercurrent infection / sepsis

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Anaemia of CKD

Pathophysiology

EPO deficiency: reduced production by peritubular fibroblasts as GFR declines
Iron deficiency: absolute (poor intake/blood loss) or functional (hepcidin-mediated)
Shortened RBC survival: uraemic toxin-mediated haemolysis
Marrow suppression: uraemic inhibitors impair erythropoiesis

Targets & Thresholds

Start EPO work-up when Hb <100 g/L (KDIGO)
Target Hb: 100–120 g/L (avoid >130 — increased thrombosis/CVD risk)
Iron: ferritin >200 µg/L + TSAT >20% before starting ESA
Dialysis patients: ferritin target 200–500 µg/L

Treatment

IV iron: preferred in dialysis (ferric carboxymaltose, iron sucrose, ferric derisomaltose)
ESA: darbepoetin alfa (weekly/fortnightly SC) or epoetin alfa/beta (3×/week SC)
HIF-PHI: roxadustat — newer oral agent stimulates EPO production
Blood transfusion: avoid if possible (sensitisation risk pre-transplant)

ESA Hypertension Risk

Monitor BP closely when initiating ESA — can worsen hypertension. Reduce ESA dose or add antihypertensive. Avoid rapid Hb rise (>20 g/L over 4 weeks).

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Renal Bone Disease (CKD-MBD)

Pathophysiology Sequence

Reduced GFR → phosphate retention → hyperphosphataemia
Reduced 1,25(OH)₂D (active Vit D) production by kidney
Low calcium + high phosphate → PTH ↑ (secondary hyperparathyroidism)
PTH mobilises Ca²⁺ from bone → renal osteodystrophy
Vascular calcification from Ca×P product elevation

Laboratory Monitoring

Phosphate: target 0.8–1.5 mmol/L
Calcium: target normal range (2.1–2.5 mmol/L)
PTH: target 2–9× upper limit normal in G5D
25-OH Vitamin D: maintain >50 nmol/L

Management

Dietary phosphate restriction: avoid processed foods, cola drinks, fast food
Phosphate binders (take with meals):
— Calcium carbonate (avoid if hypercalcaemia)
— Sevelamer hydrochloride (non-calcium, preferred)
— Lanthanum carbonate (chew with meals)
Active Vitamin D: alfacalcidol or calcitriol — monitor Ca to avoid hypercalcaemia
Cinacalcet (calcimimetic): lowers PTH by sensitising CaSR — causes hypocalcaemia, nausea
Parathyroidectomy: for refractory secondary/tertiary HPT

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Hyperkalaemia Management

EMERGENCY: Hyperkalaemia (K⁺ >6.5 mmol/L or ECG changes)

Calcium gluconate 10% 10 mL IV: membrane stabilisation — acts in minutes (NOT corrects K⁺)
Insulin 10 units + 50% Dextrose 50 mL IV: shifts K⁺ into cells (onset 20 min)
Salbutamol 10–20 mg nebuliser: β₂ agonist shifts K⁺ intracellularly
Sodium bicarbonate: if severe acidosis — some K⁺ shift
Dialysis: definitive treatment for refractory hyperkalaemia

Dietary Restriction (High-K⁺ Foods to Avoid)

Bananas, oranges, dates, dried fruits, avocado
Potatoes (leach by peeling, dicing, boiling in large water)
Tomatoes, tomato paste, tomato juice
Nuts, chocolate, legumes, bran cereals
Salt substitutes (contain KCl)

Chronic Management

Patiromer (Veltassa): K⁺ binder in colon — take 6 hours from other medications
Sodium zirconium cyclosilicate (Lokelma): rapid onset K⁺ binder
Resonium A (sodium polystyrene sulphonate): older agent, less preferred
Review nephrotoxic medications (ACE-I/ARB doses, K⁺-sparing diuretics)
Treat constipation (↓ faecal K⁺ excretion)

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Fluid Management & Oedema

Sodium restriction: <2g/day (5g salt) — most important intervention
Fluid restriction: based on urine output + 500 mL/day insensible losses
Furosemide: higher doses needed in CKD (up to 500 mg/day); loses efficacy in ESRD
Metolazone: add to furosemide for synergistic diuresis (monitor K⁺, Na⁺)
Daily weight monitoring — report >2 kg gain in 24–48 hours
Oedema grading: document site, severity, pitting (1+ to 4+)

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Cardiovascular Risk & Metabolic Acidosis

CVD Risk in CKD

CKD patients have 5–10× higher CVD risk than general population
BP target: <130/80 mmHg (KDIGO 2021)
ACE inhibitor/ARB: first-line — reduce proteinuria and slow CKD progression; monitor K⁺/creatinine at 1–2 weeks post initiation
SGLT2 inhibitors: dapagliflozin/empagliflozin — additional CV and kidney protection
Statin therapy: recommended in CKD G1–G5 (not initiated on dialysis per SHARP trial)
Antiplatelet: aspirin in established CVD

Metabolic Acidosis

Target bicarbonate: ≥22 mmol/L
Sodium bicarbonate supplementation: 500 mg–1 g TDS orally
Acidosis accelerates muscle wasting, bone disease, and CKD progression

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Haemodialysis (HD)

HD Prescription

Schedule: 3× per week, 4 hours per session (minimum)
Adequacy: Kt/V target >1.2 per session (spKt/V)
URR (urea reduction ratio) target: >65%
Blood flow rate: 250–400 mL/min
Dialysate flow: 500–800 mL/min
Ultrafiltration rate: based on interdialytic weight gain (max 10–13 mL/kg/hr)

HD Session Nursing Procedure

Machine setup: priming circuit (500 mL NS), check membranes, dialysate conductivity/temperature
Pre-HD: weigh patient, check BP/HR, inspect access
Connect patient: sterile technique, 2-needle cannulation (arterial + venous)
Set UF rate to remove interdialytic weight gain
Monitoring during session: BP every 30 min, HR, UF progress, alarms
Heparin anticoagulation (loading dose + maintenance) or citrate lock
Post-HD: disconnect, pressure haemostasis, weigh, BP, document

Vascular Access Hierarchy

1st: AV Fistula (AVF) — radio-cephalic or brachio-cephalic; 6+ weeks maturation; gold standard
2nd: AV Graft (AVG) — synthetic (PTFE); earlier needling; higher infection/thrombosis risk
3rd: Tunnelled Cuffed Catheter (TCC) — internal jugular preferred; highest infection/recirculation risk
Temporary catheter (non-tunnelled): emergency only

AVF Assessment

Thrill: palpate over anastomosis — continuous vibration (normal)
Bruit: auscultate — low-pitched, continuous (normal)
Loss of thrill/bruit = EMERGENCY — thrombosis or stenosis → urgent referral
No BP cuff, venepuncture, or IV access on fistula arm
Avoid tight clothing/watch on fistula arm
Elevate arm for swelling; gentle exercises to mature fistula

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HD Complications & Troubleshooting

Intradialytic Hypotension (IDH) — Most Common

Definition: SBP drop >20 mmHg or symptomatic
Causes: over-ultrafiltration, autonomic neuropathy, low albumin
Action: reduce UF to 0, Trendelenburg position, 100–200 mL NS bolus, reduce blood flow temporarily

Air Embolism

Signs: chest pain, dyspnoea, cough, neurological changes
Action: CLAMP venous line immediately, left lateral decubitus + Trendelenburg (air to apex RV), 100% O₂, urgent medical review

Access Recirculation

Treated blood re-enters dialyser — reduces efficiency
Causes: reversed needle positions, stenosis, inadequate flow
Check by urea recirculation test or access surveillance

Muscle Cramps

Due to rapid fluid removal and Na⁺ shifts
Action: reduce UF, saline bolus 100 mL, stretch
Prevention: avoid excessive interdialytic weight gain

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Peritoneal Dialysis (PD)

PD Modalities

CAPD (Continuous Ambulatory PD): 4 manual exchanges/day, ~2 L/dwell, dwell time 4–6 hours (night dwell 8–10 h); no machine needed
APD (Automated PD): overnight cycler machine (8–10 hrs), 5–8 rapid exchanges; daytime freedom; better for working patients
High-transport membrane: better with APD (short dwells); low-transport: better with CAPD (long dwells)

PD Advantages vs HD

Home therapy — independence, better QoL
Better preservation of residual renal function
Haemodynamic stability — no rapid fluid shifts
Dietary freedom — less restriction needed
Higher protein requirements: ~1.2 g/kg/day (protein losses in dialysate)

PD Catheter & Exit Site Care

Tenckhoff catheter — inserted surgically or laparoscopically, 2-week healing before use
Daily exit site cleaning with saline or chlorhexidine
No occlusive dressings; keep dry during shower (waterproof cover)
Topical mupirocin or gentamicin if S. aureus carrier
Inspect for: redness, swelling, crust, discharge, tunnel tenderness

PD Peritonitis — EMERGENCY

Signs: cloudy effluent, abdominal pain, fever, nausea
Action: drain effluent, send for MC&S (cell count, culture), start IP antibiotics empirically (vancomycin + aminoglycoside or ceftazidime)
Commonest organisms: Gram-positive cocci (S. epidermidis)
Catheter removal if: fungal peritonitis, refractory >5 days, tunnel infection
Encapsulating peritoneal sclerosis (EPS): rare but life-threatening long-term complication — abdominal cocoon

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Pre-dialysis Planning & Low-Clearance Clinic

Low-Clearance Clinic Referral

Initiate when eGFR 10–15 mL/min/1.73m² (G4–G5 transition)
Multidisciplinary: nephrologist, nurse specialist, dietitian, social worker
Topics: modality education (HD/PD/transplant/conservative), access planning, symptom management

Vascular Access Planning

Refer to vascular surgeon when eGFR <20–25 to plan AVF creation
AVF requires ≥6 months to mature before dialysis use
Preserve forearm veins: avoid cannulation, phlebotomy in non-dominant arm
Document vein mapping (duplex USS)

Dialysis Initiation Criteria

Uraemic symptoms: nausea, pericarditis, encephalopathy
Refractory fluid overload/hypertension
Hyperkalaemia refractory to medical management
Metabolic acidosis refractory to treatment
eGFR <6–8 mL/min (even if asymptomatic)

Conservative Management Pathway

Suitable for: elderly, frail, multiple comorbidities where dialysis may not improve QoL/survival
Focus: symptom control (oedema, pruritus, nausea, pain, restless legs), advance care planning, DNAR discussions
Median survival on conservative pathway in elderly: 6–24 months
Community palliative care and hospice liaison

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Kidney Transplantation

Recipient Assessment (Work-Up)

ABO blood group and HLA typing
Panel Reactive Antibody (PRA): measures sensitisation — high PRA (>80%) = difficult to find compatible donor
Donor Specific Antibodies (DSA): HLA antibodies against specific donor — contraindication or desensitisation protocol
Cardiac assessment: stress echo/angiography (high CVD risk)
Exclude active infection, malignancy, non-compliance
Ideally listed before starting dialysis (pre-emptive transplant)

Live vs Deceased Donor

Living donor: better outcomes, shorter waiting time, elective surgery
Deceased donor: DBD (donation after brain death) or DCD (donation after circulatory death)
HLA matching: better match → less rejection risk

Immunosuppression (Triple Therapy)

Tacrolimus (Tac): CNI — target levels (trough) 8–12 ng/mL early, 5–8 long-term; nephrotoxic at high levels; monitor drug levels, glucose (diabetogenic)
Mycophenolate mofetil (MMF): antimetabolite — causes GI side effects, bone marrow suppression; teratogenic
Prednisolone: taper from 20 mg to 5 mg over months; cushingoid, hypertension, hyperglycaemia
Induction: basiliximab (IL-2R antagonist) or ATG (high-risk recipients)

Rejection Types

Hyperacute: preformed antibodies — minutes to hours; irreversible
Acute cellular (ACR): T-cell mediated; rising creatinine d7–d90; treated with methylprednisolone pulses
Antibody-mediated (AMR): donor-specific antibodies; treated with IVIG + plasmapheresis + rituximab; worse prognosis
Surveillance biopsies: 3 months, 12 months post-transplant

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Post-Transplant Complications & Nursing

Opportunistic Infections

CMV: commonest opportunistic infection; prophylaxis with valganciclovir 3–6 months; monitor CMV PCR
BK virus nephropathy: BK polyomavirus — monitor BKV PCR blood/urine; treatment = immunosuppression reduction
PCP (Pneumocystis jirovecii): prophylaxis with co-trimoxazole for 12 months
Fungal prophylaxis: nystatin for 1 month; fluconazole if high risk
Avoid live vaccines post-transplant (MMR, yellow fever, BCG)

Post-Operative Nursing (First 48–72 Hours)

Urine output: monitor hourly — target >100 mL/hr initially; replace ml-for-ml if low
Fluid replacement: normal saline or Hartmann's — guided by urine output
Wound care: drain output, dressing — graft in iliac fossa (RIF or LIF)
Monitor creatinine daily — fall indicates graft function
Delayed graft function (DGF): dialysis may be needed post-op; reassess daily
Tacrolimus trough level: check day 1–2 and daily until stable

Long-Term Monitoring

Monthly: creatinine, FK levels, FBC, glucose, BP
Skin cancer screening: annual dermatology review (markedly increased SCC risk)
PTDM (post-transplant diabetes): monitor fasting glucose especially with tacrolimus

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Daily Clinical Monitoring in CKD

<130/80

BP Target in CKD (KDIGO 2021)

<53 mmol/mol

HbA1c Target (T2DM + CKD)

<0.8 g/kg/day

Protein Intake (non-dialysis CKD)

Fluid Balance Monitoring

Daily weights at same time, same scale, same clothing
Fluid restriction: urine output (previous 24h) + 500 mL insensible losses
Fluid intake diary — include all oral intake (foods with high water content)
Document oedema: pitting scale 1–4+, site (bilateral pedal, sacral, ascites)

Blood Glucose Monitoring

Tight glucose control slows diabetic nephropathy progression
Hypoglycaemia risk increases in CKD (impaired gluconeogenesis, prolonged insulin action)
Beware hypoglycaemia unawareness in dialysis patients

Medication Review (Renal Dose Adjustment)

Metformin: review at eGFR <45, stop at eGFR <30 (lactic acidosis risk)
NSAIDs: CONTRAINDICATED in CKD (reduce GFR, fluid retention, hyperkalaemia)
Iodinated contrast: pre-hydrate with IV saline; KDIGO states contrast not contraindicated but caution in G3b+
Aminoglycosides: single daily dosing, extend interval per eGFR, level monitoring essential
DOACs: dose reduction in CKD — rivaroxaban/apixaban reduced at eGFR <50; avoid at eGFR <15
LMWH: enoxaparin accumulates — halve dose or use UFH when eGFR <30
Gabapentin/pregabalin: significant dose reduction needed; accumulates causing sedation

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Renal Dietary Counselling

Important: CKD Diet Differs from Dialysis Diet

Pre-dialysis CKD patients require protein restriction (0.8 g/kg/day). Haemodialysis patients require HIGHER protein (1.2 g/kg/day) due to dialysis-related losses. Always clarify the patient's current stage before dietary advice.

Low Potassium Advice

Avoid: bananas, oranges, dried fruits, avocado, tomatoes, potatoes, nuts, chocolate
Leaching vegetables: peel, dice, boil in large amount of water, discard water
Avoid salt substitutes (contain KCl)
Restrict fruit juice and smoothies

Low Phosphate Advice

Avoid: processed foods, fast food, cola drinks, dark sodas, dairy excess, bran cereals
Organic phosphate (meat/fish) absorbed less than inorganic (additives)
Read food labels: avoid phosphate additives (E452, E338)

Protein

Non-dialysis CKD: 0.8 g/kg/day — avoid high protein diets
HD patients: 1.2 g/kg/day — ensure adequate intake
PD patients: 1.2–1.5 g/kg/day — protein losses in dialysate

Fluid & Sodium

Sodium: <2 g/day (5 g salt) — most important modification
Fluid: urine output + 500 mL (pre-dialysis); 500–800 mL/day (anuric HD)

Caloric Adequacy

Target 30–35 kcal/kg/day — malnutrition is common in CKD
Malnutrition-inflammation complex syndrome (MICS) — linked to CVD mortality
Renal dietitian referral essential

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Symptom Management & Quality of Life

Uraemic Pruritus

Affects 40–70% of dialysis patients — most distressing symptom
Emollients: aqueous cream, E45 — apply twice daily after bathing
Antihistamines: chlorphenamine at night (limited evidence)
Gabapentin: 100–300 mg post-dialysis — effective but accumulates (sedation risk)
Difelikefalin (kappa-opioid agonist): licensed specifically for dialysis pruritus
Improve dialysis adequacy + phosphate control

Restless Legs Syndrome (RLS)

Prevalence: 20–30% in dialysis patients
Worsens at rest/evening — disrupts sleep severely
Treatment: gabapentin, pramipexole (dopamine agonist), iron supplementation

Fatigue — Most Reported Symptom

Multifactorial: anaemia, uraemia, poor sleep, depression, dialysis schedule
Intradialytic exercise: cycling on recumbent bike during HD session
Strength training: improves muscle mass, fatigue, QoL

Psychological & Social Support

Depression prevalence: 25–40% in CKD/dialysis
Regular PHQ-9 screening; refer psychology/psychiatry
Employment: support return-to-work; nocturnal/home dialysis facilitates
Driving: assess fitness; daytime HD fatigue may impair driving
Travel/holiday dialysis: plan 3–6 months ahead; EDTNA/ERCA resources

Skin Care

Avoid prolonged sun exposure (post-transplant skin cancer risk)
Calcineurin inhibitor cream (tacrolimus) — avoidance on thinning skin
Dry skin: regular emollient application

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GCC Renal Context

Epidemiology

Saudi Arabia: highest dialysis prevalence per million population in the MENA region; rapid growth year-on-year
UAE, Qatar, Kuwait: rapidly expanding dialysis programmes; increasing living donor transplants
King Salman Medical City (Riyadh): major tertiary dialysis centre
King Faisal Specialist Hospital: leading transplant centre in KSA
GCC T2DM prevalence: 20–25% (among highest globally) — driving ESRD epidemic
Saudi Center for Organ Transplantation (SCOT): deceased donor programme coordination

Nursing Licensing (GCC)

SCFHS (Saudi Arabia): classification exam includes renal nursing topics at staff nurse/advanced practice level
DHA (Dubai): nursing licence exam — CKD management, dialysis nursing common question areas
DOH (Abu Dhabi): similar curriculum focus on chronic disease management
HAAD/DOH — haemodialysis technician pathway distinct from nursing

SGLT2 Inhibitors in CKD — Landmark Trials

CREDENCE Trial (2019) — Canagliflozin

Reduced relative risk of ESRD/doubling creatinine/renal death by 34% in patients with T2DM + CKD (eGFR 30–90 + ACR >300). First agent to show renal protection beyond RAAS blockade.

DAPA-CKD Trial (2020) — Dapagliflozin

30% reduction in composite kidney/CV outcome regardless of diabetes status. Led to indication expansion: dapagliflozin (Farxiga) indicated for CKD regardless of T2DM, eGFR 25–75.

EMPA-KIDNEY Trial (2022) — Empagliflozin

Broadest CKD population studied (eGFR 20–45 OR eGFR 45–90 + ACR ≥200). Significant reduction in kidney disease progression and CV death.

Mechanism: SGLT2 inhibitors reduce intraglomerular pressure via tubuloglomerular feedback, reduce albuminuria, and have anti-fibrotic/anti-inflammatory properties beyond glycaemic control.

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CKD Stage & Risk Calculator

📊 CKD Stage, KDIGO Risk & Management Planner

eGFR (mL/min/1.73m²)

Urine ACR Units

Urine ACR Value

Diabetes (T2DM/T1DM) Hypertension

GFR Stage

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Albuminuria

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CKD Stage

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KDIGO Risk

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Key Management Priorities

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Practice MCQs — DHA / DOH / SCFHS Exam Style

1. According to KDIGO 2012, CKD is defined as kidney damage or GFR <60 mL/min/1.73m² for at least:

A. 1 month
B. 6 weeks
C. 3 months
D. 6 months

The KDIGO 2012 definition requires the abnormality to be present for >3 months to distinguish CKD from acute kidney injury. The duration threshold is important for clinical classification.

2. A patient on haemodialysis has a thrill that has disappeared from their AV fistula. What is the MOST appropriate immediate nursing action?

A. Apply warm compression and monitor for 2 hours
B. Elevate the arm and reassess next dialysis session
C. Urgently refer to vascular surgery/interventional radiology
D. Increase blood flow rate during next session

Loss of thrill (and bruit) from an AVF indicates acute thrombosis or severe stenosis. This is a vascular emergency requiring urgent assessment within hours — delay risks permanent access loss. Time-sensitive thrombectomy or thrombolysis is most effective within 24–48 hours.

3. Which phosphate binder is preferred in a CKD patient with hypercalcaemia and secondary hyperparathyroidism?

A. Calcium carbonate
B. Calcium acetate
C. Sevelamer hydrochloride
D. Aluminium hydroxide

Sevelamer is a non-calcium, non-aluminium phosphate binder — preferred when calcium is already elevated (to avoid worsening hypercalcaemia and vascular calcification). Aluminium hydroxide is avoided long-term due to aluminium toxicity risk.

4. A PD patient presents with cloudy dialysate effluent and mild abdominal discomfort. Temperature is 37.8°C. What is the FIRST action?

A. Admit for IV antibiotics and await culture results
B. Increase exchange frequency and reassess in 24 hours
C. Drain effluent, send for cell count and MC&S, start empirical intraperitoneal antibiotics
D. Remove the PD catheter immediately

Cloudy effluent = peritonitis until proven otherwise. Protocol: drain effluent, send urgent cell count (WCC >100/mm³ with >50% neutrophils is diagnostic) and MC&S, then start empirical IP antibiotics (vancomycin + aminoglycoside or ceftazidime) without waiting for culture results. Catheter removal is reserved for refractory cases.

5. A dialysis patient's ECG shows peaked T-waves and widened QRS complex. Serum K⁺ is 7.1 mmol/L. Which medication should be given FIRST?

A. Sodium bicarbonate IV
B. Insulin + dextrose IV
C. Calcium gluconate 10% IV
D. Salbutamol nebuliser

With ECG changes, the priority is cardiac membrane stabilisation with calcium gluconate — it does NOT lower K⁺ but protects the myocardium within 1–3 minutes. Subsequent K⁺-lowering agents (insulin/dextrose, salbutamol) are then used. Dialysis is the definitive treatment in ESRD.

6. According to DAPA-CKD trial, dapagliflozin is now indicated for CKD in patients:

A. With T2DM only, eGFR >60
B. On dialysis with residual urine output
C. Regardless of diabetes status, with eGFR 25–75 and elevated ACR
D. With eGFR <25 and heavy proteinuria only

DAPA-CKD demonstrated benefit irrespective of diabetes status. Current indication: eGFR 25–75 mL/min/1.73m² with ACR ≥22.6 mg/mmol (200 mg/g). This is a paradigm shift from glucose-lowering to direct kidney-protective therapy.

7. Which haemoglobin target is recommended for CKD patients receiving erythropoiesis-stimulating agents (ESA)?

A. 70–90 g/L
C. 100–120 g/L
D. 130–140 g/L

KDIGO guidelines recommend targeting Hb 100–120 g/L with ESA therapy. Targeting Hb >130 g/L was associated with increased cardiovascular events (stroke, MI) in CHOIR and CREATE trials and should be avoided.

8. Which drug is CONTRAINDICATED in a patient with eGFR of 25 mL/min/1.73m²?

A. Amlodipine
B. Bisoprolol
C. Ibuprofen (NSAID)
D. Omeprazole

NSAIDs are contraindicated in CKD as they reduce renal prostaglandin synthesis, causing afferent arteriolar constriction and further GFR reduction. They also cause fluid retention, hypertension, and hyperkalaemia. Amlodipine and bisoprolol are safe. Omeprazole does not require dose adjustment.

9. A kidney transplant recipient develops a rising creatinine on day 10 post-transplant. Tacrolimus level is therapeutic. Ultrasound shows no obstruction. Biopsy shows CD8+ T-lymphocyte infiltration. This is:

A. Antibody-mediated rejection (AMR)
B. Hyperacute rejection
C. Acute cellular rejection (ACR)
D. BK nephropathy

CD8+ T-lymphocyte tubulitis/interstitial infiltration on biopsy = Banff acute T-cell mediated (cellular) rejection. ACR occurs days to weeks post-transplant. Treatment: IV methylprednisolone 500 mg daily for 3 days. AMR shows peritubular capillaritis + C4d staining + DSA.

10. When creating an AV fistula, what is the minimum recommended maturation time before first use for haemodialysis?

A. 2 weeks
B. 4 weeks
C. 6 weeks (minimum), 3–6 months preferred
D. 12 months

AVF requires time for arterialization (enlargement and wall thickening). Minimum 6 weeks but 3–6 months is preferred for optimal maturation. Early cannulation risks haematoma, pseudoaneurysm, and fistula failure. This is why access planning must begin at least 6+ months before anticipated dialysis start.