| Stage | eGFR (ml/min/1.73m²) | Description |
|---|---|---|
| G1 | ≥90 | Normal or high — kidney damage marker present |
| G2 | 60–89 | Mildly decreased |
| G3a | 45–59 | Mildly to moderately decreased |
| G3b | 30–44 | Moderately to severely decreased |
| G4 | 15–29 | Severely decreased — prepare for RRT |
| G5 | <15 | Kidney failure (ESRD) |
| Stage | ACR (mg/mmol) | Description |
|---|---|---|
| A1 | <3 | Normal to mildly increased |
| A2 | 3–30 | Moderately increased (microalbuminuria) |
| A3 | >30 | Severely increased (macroalbuminuria) |
KDIGO heatmap principle: Both G-stage and A-stage together define progression risk — G3b+A3 = very high risk. Increasing albuminuria independently predicts faster progression.
EPO deficiency is the primary cause of anaemia in CKD — failing kidneys produce insufficient erythropoietin. Always exclude iron deficiency before starting ESA. ESA without adequate iron stores is ineffective (functional iron deficiency).
ESA hyporesponsiveness: Consider iron deficiency, infection/inflammation, vitamin B12/folate deficiency, aluminium toxicity, hyperparathyroidism, haemolysis, malignancy.
CKD reduces phosphate excretion and impairs vitamin D activation — low Ca, high PO₄, and low calcitriol all drive PTH secretion. Untreated = renal osteodystrophy, vascular calcification, fracture risk.
Vascular calcification: High Ca×PO₄ product (>4.4 mmol²/L²) increases coronary and vascular calcification risk — leading cause of CVD mortality in dialysis patients.
| Complication | Typical Stage | Mechanism | Nursing Management |
|---|---|---|---|
| Anaemia | G3+ | Reduced EPO production | ESA + IV iron, Hb monitoring monthly |
| Metabolic Acidosis | G3b+ | Impaired acid excretion, reduced HCO₃⁻ reabsorption | Oral sodium bicarbonate, monitor bicarb, dietary protein moderation |
| Hyperkalaemia | G3b+ | Reduced K⁺ excretion | Potassium-restricted diet, avoid NSAIDs/ACEi if K⁺ >5.5, patiromer/SPS resins |
| Fluid Overload | G4+ | Reduced urine output, Na retention | Daily weights, fluid restriction, loop diuretics, dietary Na <2g/day |
| Uraemia | G5 | Retention of nitrogenous waste products | Initiate RRT, monitor nausea, pruritus, encephalopathy signs |
| 2° Hyperparathyroidism | G3+ | PO₄ retention, low Ca, low Vit D | Phosphate binders with meals, active Vit D, monitor PTH/Ca/PO₄ |
Diabetic nephropathy is the leading cause of ESRD in the GCC region, mirroring extremely high Type 2 DM prevalence (Saudi Arabia 18–20%, UAE ~19%, Kuwait ~21%). Aggressive DM control is the single most effective intervention to slow CKD progression.
Education should begin at CKD G4 (eGFR <30). Patients discuss HD vs PD vs transplant, understand access options.
Counter-current flow of blood and dialysate maintains maximal concentration gradient throughout the dialyser membrane, optimising small-molecule clearance (urea, creatinine, potassium).
Definition: SBP drop ≥20 mmHg or SBP <90 mmHg during HD with symptoms.
Causes: excessive UF rate, low dry weight estimate, autonomic dysfunction (diabetics), low dialysate sodium, cardiac dysfunction, anti-hypertensives taken pre-HD.
Mechanism: Rapid removal of urea from blood creates osmotic gradient — water shifts into brain cells (cerebral oedema) before urea equilibrates.
Presentation: Headache, nausea, confusion, seizures (severe) — typically first 1–3 HD sessions or in very uraemic patients.
Cramps: Caused by excessive UF, low dialysate sodium, hypovolaemia. Manage with reduced UF, warm towels, quinine sulphate prophylaxis.
AVF infiltration: Haematoma formation from missed/dislodged needles. Apply firm pressure, cold compress first 24h, warm compress after. Document and review needling technique.
AVF infection: Redness, warmth, exudate, systemic fever. Swab for culture, IV antibiotics (gram-positive cover). TCVC exit-site infections — risk of bacteraemia (Staph aureus).
Kt/V explained: K = dialyser clearance of urea, t = treatment time, V = volume of distribution of urea (body water). Higher Kt/V = better clearance. Inadequate dialysis leads to uraemic symptoms, hospitalisation, and mortality.
Blood samples for URR/Kt/V: pre-dialysis blood (slow pump rate before drawing), and post-dialysis sample (at reduced flow rate 15 seconds before stopping — to avoid recirculation).
CRRT advantage: Slow continuous therapy allows better haemodynamic stability, controlled fluid removal, and continuous solute clearance 24 hours/day.
| Modality | Mechanism | Notes |
|---|---|---|
| CVVH | Convection only (haemofiltration) | Large-molecule clearance; replacement fluid required |
| CVVHD | Diffusion only (haemodialysis) | Small-molecule clearance; dialysate used |
| CVVHDF | Both — most common in ICU | Combines benefits of convection + diffusion |
Mechanism: Citrate infused pre-filter chelates ionised calcium (Ca²⁺) — calcium is essential cofactor for clotting cascade. Filter anticoagulated without systemic anticoagulation.
Calcium replacement: Separate calcium infusion post-filter/central line to restore systemic ionised calcium.
Pre-filter heparin infusion — systemic anticoagulation. Monitor APTT (target 45–60 seconds). Use when citrate contraindicated (liver failure — impaired citrate metabolism) or not available.
Contraindicated in HIT (heparin-induced thrombocytopaenia) — use argatroban or fondaparinux instead.
Hypothermia risk: Blood passing through external circuit loses heat. Use in-line blood warmer and maintain warm environment. Target core temp ≥36.5°C.
Peritoneum acts as semi-permeable membrane — dialysate instilled into peritoneal cavity removes toxins via diffusion and fluid via osmosis (glucose gradient). Glucose concentration drives ultrafiltration.
Continuous Ambulatory PD: 4 exchanges/day (2L each), manually performed by patient. Free overnight. Suitable for motivated, mobile patients.
Automated PD: Cycler machine performs 8–10 overnight exchanges while patient sleeps. Free during day. Better compliance for working patients.
| Feature | Exit-Site Infection | Peritonitis |
|---|---|---|
| Effluent | Clear | Cloudy |
| Abdominal pain | Absent | Present |
| Fever | Low-grade/absent | Common |
| WBC in effluent | Normal | >100 cells/μL (>50% PMN) |
| Management | Topical/oral antibiotics | IP antibiotics ± catheter removal |
Diagnostic criteria (2 of 3): (1) Clinical features — abdominal pain, cloudy effluent, fever; (2) Effluent WBC >100 cells/μL with >50% neutrophils; (3) Positive culture of effluent
Allograft placed in iliac fossa (retroperitoneal) — native kidneys remain in situ unless causing problems (e.g., polycystic kidneys).
Definition: Need for dialysis in first week post-transplant. Common in deceased-donor transplants (ischaemia-reperfusion injury).
Key nursing message: DGF does NOT mean graft failure. Most grafts recover with supportive management. Reassure patient and family.
Manage expectantly — continue dialysis (HD or PD), maintain graft perfusion, avoid nephrotoxins, monitor creatinine for recovery trend.
Signs: Sudden rise in serum creatinine, fall in urine output, low-grade fever, graft tenderness. Often asymptomatic — detected on routine monitoring.
Diagnosis: Renal biopsy — gold standard (Banff classification).
Treatment: IV methylprednisolone 500mg daily for 3 days (pulse steroids). Antibody-mediated rejection — IV immunoglobulin, plasmapheresis.
Living related donor transplant is common in GCC. Islamic scholars have clarified that organ donation is permissible (halal) and can be an act of sadaqa jariya. Saudi national transplant programme (SCOT — Saudi Centre for Organ Transplantation) coordinates deceased-donor transplantation. Cultural sensitivity around brain death declaration remains important in family counselling.
| G-Stage | eGFR (ml/min/1.73m²) | Description | Key Actions |
|---|---|---|---|
| G1 | ≥90 | Normal eGFR — CKD only if other damage marker | BP control, treat cause (DM/HTN) |
| G2 | 60–89 | Mildly reduced | Risk factor optimisation |
| G3a | 45–59 | Mildly to moderately reduced | Anaemia screen, start CKD-MBD monitoring |
| G3b | 30–44 | Moderately to severely reduced | Nephrology referral, acidosis management |
| G4 | 15–29 | Severely reduced | Pre-dialysis education, AVF referral |
| G5 | <15 | Kidney failure — ESRD | Initiate RRT or conservative management |
| Feature | Haemodialysis | Peritoneal Dialysis | CRRT |
|---|---|---|---|
| Setting | HD unit (3×/week) | Home | ICU only |
| Mechanism | Diffusion + convection | Diffusion + osmosis | Convection ± diffusion (continuous) |
| Haemodynamic stability | Less stable | Most stable | Most stable (slow, continuous) |
| Clearance speed | Rapid | Slow/continuous | Slow/continuous |
| Vascular access | AVF / graft / TCVC | Peritoneal catheter | Large-bore CVC |
| Infection risk | Moderate (access) | Peritonitis risk | High (CVC) |
| Anticoagulation | Heparin / LMWH | Not required | Heparin / citrate |
| Protein loss | Minimal | Significant (albumin) | Moderate |
| Independence | Clinic-dependent | High independence | ICU-dependent |
ISPD Criteria: 2 of the following 3 must be present:
Cloudy PD effluent + abdominal pain ± fever. Cloudy effluent alone should trigger investigation.
Effluent WBC >100 cells/μL (after at least 2h dwell) with >50% polymorphonuclear neutrophils (PMN). PMN predominance indicates bacterial peritonitis.
Culture-negative peritonitis still treated empirically if criteria 1+2 met. Most common organisms: Staphylococcus epidermidis (touch contamination), Staph aureus, gram-negatives.
| Finding | Normal / Action |
|---|---|
| Thrill (palpate) | Continuous vibration = patent. Absent = urgent Doppler |
| Bruit (auscultate) | Low-pitched whoosh = patent. High-pitched = stenosis. Absent = thrombosis |
| Arm swelling | Venous hypertension — suspect central stenosis |
| Aneurysm | Skin thinning / pulsatile swelling — avoid needling aneurysm; surgical review |
| Erythema / warmth | Infection — swab, IV antibiotics, surgical review |
| Ischaemic hand | Steal syndrome — pain/pallor/pulselessness distal — urgent vascular referral |
Answer: Diabetic nephropathy. Given extremely high DM2 prevalence across Gulf states, diabetic nephropathy accounts for the majority of new ESRD cases. Hypertensive nephropathy is second.
Answer: ≥1.2 per session (single-pool Kt/V). URR target >65%. Measured monthly. Inadequate dialysis = uraemic symptoms, hospitalisation, increased mortality.
Answer: 2 of 3 — (1) Clinical: cloudy effluent + abdominal pain/fever; (2) Effluent WBC >100/μL (>50% PMN); (3) Positive culture. First signs often noticed by patient as cloudy bag — educate patients to report immediately.
Answer: Suspected thrombosis (occlusion). Requires urgent assessment with Doppler ultrasound. Do NOT attempt to needlise a thrombosed fistula. Contact vascular access team immediately. Salvage rates decline rapidly with time.
Answer: Cerebral oedema from rapid urea removal creating osmotic gradient across blood-brain barrier. Water shifts into brain cells. Most at risk: new HD patients, very high pre-HD urea. Prevention: first session short (2h), low blood flow (150–200 ml/min), incremental approach.
Answer: Systemic ionised calcium target = 1.1–1.3 mmol/L. Post-filter circuit ionised calcium = 0.25–0.35 mmol/L (intentionally low — inhibits clotting). If systemic ionised Ca falls below 1.1 = increase calcium replacement infusion rate.
Answer: DGF = need for dialysis in first week post-renal transplant. Common in deceased-donor kidneys (ischaemia-reperfusion injury). Does NOT mean transplant failure. Most grafts recover. Manage expectantly — continue dialysis, avoid nephrotoxins, monitor creatinine trend for recovery.
Answer: Target Hb 100–120 g/L. Do NOT exceed 130 g/L — studies (CHOIR, CREATE, TREAT) showed Hb >130 g/L with ESA is associated with increased thrombotic events, stroke, and cardiovascular death. Reduce ESA dose if Hb approaches ceiling.