GC034 Chronic Kidney Disease And Its Complications
Chronic kidney disease is a progressive, irreversible decline in kidney function (GFR < 60 mL/min/1.73 m² for ≥3 months or evidence of kidney damage) leading to complications such as anemia, mineral-bone disorder, cardiovascular disease, electrolyte imbalances, and ultimately end-stage renal failure.
Chronic Kidney Disease and its Complications
This lecture, delivered by Dr Pearl Pai (April 2025), is one of the highest-yield nephrology topics for HKUMed summative exams. CKD is a systemic disease — not simply "kidney failure" — and the lecture deliberately takes you through a complete clinical journey: from understanding what the nephron does, to how we measure kidney function, to why CKD causes cardiovascular death more often than it causes dialysis. The exam tests your ability to integrate pathophysiology with clinical staging, investigations, complications, and management — especially the pharmacology of newer agents (SGLT2i, GLP-1RA, finerenone, HIF-PHi).
Learning Objectives (from the lecture slide):
- Understanding kidney function
- eGFR and CKD stages
- Major CKD causes
- Global burden of CKD
- Clinical features of CKD
- Making the diagnosis
- Complications of CKD
- Management of CKD and its complications [1]
"The function of a nephron: Filtration, Absorption, Transport, Secretion, Concentration gradient, Receptors/channels, enzymes (Na/K ATPase) — across Bowman capsule, Tubules, Loop of Henle, Collecting ducts." [1]
Each kidney contains ~1 million nephrons. The nephron is the functional unit; when nephrons are lost, the remaining ones hypertrophy and hyperfiltrate to compensate — which paradoxically accelerates their own destruction (maladaptive hyperfiltration). This is the central self-perpetuating mechanism of CKD progression.
The Glomerular Filtration Barrier — Reading the Electron Micrograph
The lecture's electron micrograph should be read from blood to urine:
- Fenestrated capillary endothelium — excludes blood cells but permits water and small solutes.
- Glomerular basement membrane (GBM) — the shared extracellular matrix scaffold and a major size/charge-selective layer.
- Podocyte foot processes and slit diaphragms — the final filtration interface before Bowman's urinary space.
The platelet in the capillary lumen is a useful scale marker; the urinary space lies beyond the interdigitating podocyte foot processes. Damage at different layers produces different clues: endothelial injury may accompany thrombotic microangiopathy, GBM disease may cause haematuria, and podocyte/slit-diaphragm injury typically produces albuminuria. [1]
Six core functions of the nephron: [1]
- Get rid of nitrogenous waste products (urea, creatinine)
- Conserve Na and water (maintain volume status)
- Maintain electrolyte balance (K⁺, Na⁺, Cl⁻, Mg²⁺)
- Maintain acid-base balance (HCO₃⁻ reabsorption, H⁺/NH₄⁺ excretion)
- Erythropoiesis (EPO production by peritubular interstitial cells)
- Mineral Bone Disorder (1α-hydroxylation of 25-OH vitamin D → active calcitriol)
Why this matters for CKD: Every complication of CKD maps directly back to one of these six functions failing. Acidosis = failure #4. Anaemia = failure #5. CKD-MBD = failure #6. This is the scaffold for understanding everything that follows.
2. Measuring Kidney Function: eGFR and Albuminuria
Methods for estimating GFR: [1]
- CKD-EPI creatinine (per 1.73 m²) — now the recommended equation
- CKD-EPI creatinine-cystatin C (per 1.73 m²) — more accurate when creatinine alone is unreliable
- MDRD (per 1.73 m²) — commonly used in HA laboratories but underestimates eGFR > 60 [3]
- Cockcroft-Gault = [(140 − age) × weight (kg) × 1.23] / serum creatinine (µmol/L) — weight-based, useful for drug dosing
- 24-hour creatinine clearance (CrCl) (UV/P) — sometimes used when an estimate is inadequate, but collection error is common
Key Concept: Serum Creatinine Alone is Insensitive
Serum creatinine does not rise above the normal range until GFR has already dropped by ~40-50%. This is because creatinine is inversely proportional to GFR on a hyperbolic curve — a small rise from 70 to 130 µmol/L represents a massive loss of function. Always convert to eGFR.
| Equation | Pros | Cons |
|---|---|---|
| CKD-EPI Cr | Most accurate overall, recommended by KDIGO 2024 | Less accurate at extremes of body size |
| MDRD | Most commonly used in HA labs | Underestimates eGFR > 60 → overdiagnoses CKD [3] |
| Cockcroft-Gault | Useful for drug dosing (uses weight) | Weight data often unavailable to lab |
| CKD-EPI Cr-CysC | Best accuracy; reduces bias from muscle mass | Cystatin C not routinely measured |
| 24h CrCl (UV/P) | Uses timed urine rather than an estimating equation | Not a gold-standard GFR measurement: collection error is common and tubular creatinine secretion can overestimate true GFR |
When an accurate value will change an important decision, measured GFR using an exogenous filtration marker (for example iohexol or iothalamate clearance) is the reference approach. A timed CrCl is not equivalent to measured GFR. [8]
eGFR calculator available on the National Kidney Foundation website. [1]
GFR declines with age: [1]
| Age (years) | Average eGFR |
|---|---|
| 20-29 | 116 |
| 30-39 | 107 |
| 40-49 | 99 |
| 50-59 | 93 |
| 60-69 | 85 |
| 70+ | 75 |
Why this matters: GFR falls on average with age, but CKD is still defined by the same persistence and damage criteria. A 75-year-old with eGFR 68 and no other marker of kidney damage does not meet the CKD definition; albuminuria or another persistent damage marker would establish CKD. Do not dismiss a low eGFR as “just ageing,” because risk rises continuously as eGFR falls. [8]
Proteinuria up to 150 mg/day can be normal. [1] The slide calls ACR > 3 mg/mmol in diabetes “microalbuminuria” and links it to ACE inhibitor or ARB therapy. [1] ACR 3-30 mg/mmol for > 3 months indicates CKD. [1]
| Category | ACR (mg/mmol) | Significance |
|---|---|---|
| A1 (Normal-mildly increased) | < 3 | Normal |
| A2 (Moderately increased) | 3-30 | Early marker of kidney damage; RAS inhibition is recommended in diabetes with CKD G1-G4 |
| A3 (Severely increased) | > 30 | High-risk albuminuria; RAS inhibition is recommended in CKD G1-G4 unless contraindicated |
“Microalbuminuria” and “macroalbuminuria” are older labels; A2 and A3 are preferred because the urine contains ordinary albumin, not a smaller molecule. Confirm a random ACR ≥3 mg/mmol with a subsequent first-morning midstream sample and establish chronicity; exercise, fever, UTI, menstruation and marked hyperglycaemia can transiently raise it. Current KDIGO guidance supports ACEi/ARB for CKD G1-G4 with A2-A3 albuminuria in diabetes, for A3 without diabetes, and suggests it for A2 without diabetes—not merely because one isolated ACR exceeds 3 mg/mmol. [8]
Other causes of albuminuria: Hypertension, High protein diet, Exercise, fever, UTI. [1]
Exam Trap
A positive urine dipstick for protein in a febrile patient with UTI does NOT automatically mean CKD. Always repeat the test after the acute illness resolves. Transient causes must be excluded before labelling someone with CKD.
3. Definition and Staging of CKD
Chronic Kidney Disease = > 3 months of either: [1]
- GFR less than 60 ml/min/1.73 m²
- ACR > 3 mg/mmol or other markers of kidney damage
"Other markers of kidney damage" include: haematuria of glomerular origin, structural abnormalities on imaging (e.g. small kidneys, polycystic kidneys), pathological abnormalities on biopsy, history of kidney transplant, or electrolyte abnormalities due to tubular disorders.
The staging is a two-dimensional grid of GFR (G1-G5) and albuminuria (A1-A3). The combination determines prognosis ("heat map"):
| Stage | GFR (ml/min/1.73m²) | Description |
|---|---|---|
| G1 | ≥90 | Normal or high (need markers of damage to qualify as CKD) |
| G2 | 60-89 | Mildly decreased (also need markers of damage) |
| G3a | 45-59 | Mild-moderately decreased |
| G3b | 30-44 | Moderate-severely decreased |
| G4 | 15-29 | Severely decreased |
| G5 | < 15 | Kidney failure |
Note: G1 and G2 require another kidney abnormality (e.g. albuminuria, haematuria, structural abnormality) to qualify as CKD; GFR alone at these levels is not sufficient. The two-dimensional classification grid (eGFR × albuminuria) shows that risk increases both downward (G1→G5) and rightward (A1→A3). [1]
| eGFR \ ACR | A1 (< 3) | A2 (3-30) | A3 (> 30) |
|---|---|---|---|
| G1 ≥ 90 | No CKD | G1 A2 | G1 A3 |
| G2 60-89 | No CKD | G2 A2 | G2 A3 |
| G3a 45-59 | G3a A1 | G3a A2 | G3a A3 |
| G3b 30-44 | G3b A1 | G3b A2 | G3b A3 |
| G4 15-29 | G4 A1 | G4 A2 | G4 A3 |
| G5 < 15 | G5 A1 | G5 A2 | G5 A3 |
Risk increases → (higher albuminuria) and ↓ (lower eGFR). [1]
High Yield
You need BOTH a GFR criterion OR a damage marker AND chronicity (> 3 months) to diagnose CKD. A single abnormal creatinine result is NOT CKD — it could be AKI. Always check previous creatinine values and imaging.
| Feature | Favours AKI | Favours CKD |
|---|---|---|
| Previous RFT | Normal ≤3 months ago (diagnostic) | Abnormal > 3 months ago (diagnostic) |
| Kidney size on US | Normal | Small, shrunken, ↓ corticomedullary differentiation |
| Bone changes on imaging | None | Renal osteodystrophy |
| Urine output | Often oliguria | Usually maintained until late |
| Rate of creatinine rise | Rapid daily increase | Slow progressive increase |
| Anaemia | Not always (but can occur in AKI) | NcNc anaemia (EPO deficiency) |
4. Causes of CKD
Causes of CKD: [1]
- Diabetes (most common worldwide and in HK)
- Hypertension / vascular
- Chronic glomerulonephritis (e.g. IgA GN)
- Chronic pyelonephritis
- Polycystic kidney disease
- Drug induced, TIN, TCM
- Myeloma (CRAB), Monoclonal gammopathy
- Vasculitis, SLE, other autoimmune diseases
- Obstruction, kidney stones
- Alport's or other hereditary/rare diseases
- Obesity
From the Hong Kong Renal Registry (HKMJ 2024), diabetic nephropathy is the leading cause of ESRD in HK. [1]
The two world maps answer different questions. The 2021 map depicts incidence of treated kidney failure (dialysis/transplant), which is shaped by registry coverage and access to KRT as well as disease burden; a pale or missing country is not proof of little CKD. The years-of-life-lost map instead shows where CKD ranked among causes of premature mortality. Read the maps as burden/access signals, not as directly comparable CKD-prevalence maps. [1]
HK Renal Registry 2022 — Incidence by diagnosis: [1]
| Diagnosis | % of incident ESRD (2022) |
|---|---|
| Diabetes | 51.53% |
| Glomerulonephritis | 18.69% |
| Hypertension | 11.69% |
| Unknown causes | 7.75% |
| Cystic kidney & other hereditary | 3.81% |
| Other causes | 3.54% |
| Other urologic | 2.99% |
Overall incidence of kidney failure with replacement therapy in HK rose from ~95 per million population (pmp) in 1996 to 197.48 pmp in 2022, with PD accounting for the majority (162.57 pmp) reflecting the HA "PD-first" policy. [1]
Risk factors: Diabetes, High blood pressure, Overweight/obesity, Over the age of 60, Polypharmacy, Family history of CKD or kidney failure. Usually, CKD is the result of a combination of physical, environmental, and social factors. [1]
Drug-induced kidney disease can be: [1]
- Acute (< 7 days), Subacute (7-90 days), Chronic (> 90 days)
- Mechanisms: Vasoconstriction, Glomerular disease, Tubular toxicity, Tubulointerstitial nephritis, Nephrolithiasis, Crystalluria
Examples: [1]
| Drug | Mechanism / Injury Pattern |
|---|---|
| Aminoglycosides | AKI (direct tubular toxicity) |
| Calcineurin inhibitor | Vasoconstriction → AKI → CKD |
| Cisplatin | Tubular toxicity |
| NSAID | Vasoconstriction, ATIN, nephrotic syndrome, papillary necrosis |
| PPI | Acute and Chronic TIN → CKD |
| PD-1 inhibitor | AKI (ATIN) |
NSAID Nephrotoxicity — Common Exam Question
NSAIDs inhibit prostaglandin synthesis → prostaglandins normally maintain afferent arteriolar vasodilation. In CKD or volume-depleted patients, removing this protective vasodilation causes acute haemodynamic AKI. Additionally, NSAIDs cause ATIN (hypersensitivity), membranous-like nephropathy (nephrotic syndrome), and renal papillary necrosis. This is a discriminator question — know ALL four mechanisms.
Cardiovascular-kidney-metabolic (CKM) syndrome is a health disorder due to connections among heart disease, kidney disease, diabetes, and obesity leading to poor health outcomes. [1]
This concept reflects the bidirectional damage loop: DM → CKD → CVD → worsening of all three. It is the modern framing replacing older "cardiorenal syndrome" terminology.
5. Clinical Features of CKD
Few symptoms and signs: [1]
- Fatigue
- Nocturia (early — loss of concentrating ability)
- Thirst
- Fluid retention
- Itch (uraemic pruritus, a/w hyperphosphataemia)
- Poor appetite
Why symptoms are late: Compensatory hyperfiltration maintains near-normal waste clearance until GFR drops below ~20-30. Nocturia is actually an early sign because concentrating ability (Loop of Henle and collecting duct function) is lost before filtration fails significantly.
Features of CKD: [1]
- Hyperkalaemia
- Acidosis
- Hypertension, LVH, Congestive cardiac failure
- Anaemia: normochromic, normocytic, due to a lack of erythropoietin
- CKD-MBD: high or low PTH, bone biochemistry abnormality, vascular calcification
Each of these is discussed in depth below.
A 50-year-old man was referred to medical OPC because BP 142/90 mmHg, serum creatinine 130 µmol/L (normal range 60-115 µmol/L) after a GP check up. What other info do you need? [1]
Required information: [1]
- History, PMH, DH
- Weight, height (to calculate eGFR, BMI)
- Past serum creatinine (to determine acute or chronic)
- Urine (dipstick, ACR, microscopy)
- Determine acute or chronic
- Cause?
- Stable or progressive?
This scenario is the template for SAQ stems: you are given a creatinine and asked "what next?" The answer is always: (1) calculate eGFR, (2) check urine ACR, (3) compare with previous creatinine, (4) ultrasound kidneys, (5) establish aetiology.
What the Nephrologist Does
The nephrologist's approach: [1]
- Tell AKI or CKD. Find the cause.
- How to treat or reverse or stabilize kidney failure?
- Advice on lifestyle modification
- Specific measure
- Cardiovascular protection
- Management of CKD complications
- Preparation for RRT
7. Investigations
Investigation tools: [1]
- Blood: RFT (creatinine, eGFR, urea, electrolytes, bicarbonate), CBP (anaemia), Ca/PO4/ALP/PTH, iron studies, lipids, glucose/HbA1c
- Urine: Dipstick, ACR, microscopy, 24h protein/CrCl
- Imaging: Renal ultrasound
- Special: CT renal artery, renal biopsy (when indicated), autoimmune screen
Normal size 10-12 cm and symmetrical. [1]
- 'Small' kidney(s) may be dysplastic, scarred, or shrunken due to chronic kidney disease.
- 'Large' kidneys may be due to polycystic kidney disease (PKD), infiltration e.g. amyloid, or obstruction.
| Finding | Significance |
|---|---|
| Small bilateral kidneys | CKD (chronic scarring/fibrosis) |
| Asymmetric kidneys | Renovascular disease, reflux nephropathy, congenital |
| Large bilateral kidneys | PKD, amyloid, diabetic nephropathy (early), obstruction |
| Hydronephrosis | Obstructive uropathy |
| Loss of corticomedullary differentiation | Chronic parenchymal disease |
CT Renal Artery — used to assess for renal artery stenosis (a reversible cause of CKD/refractory hypertension). [1]
- Hydronephrosis: the ultrasound/CT example shows branching, fluid-filled dilatation of the renal pelvis and calyces. This is a pattern of collecting-system obstruction, not a diagnosis by itself; correlate with the ureter/bladder, symptoms and urgency because obstruction may be reversible.
- Renal artery CT angiography: a narrowed renal arterial lumen can support renovascular disease, but imaging is pursued when the clinical probability is meaningful (for example resistant hypertension, recurrent flash pulmonary oedema or an otherwise unexplained large fall in GFR after RAS blockade).
- Renal biopsy: the slide pairs the biopsy needle/core with glomerular histology. Biopsy is used when tissue is likely to change diagnosis, prognosis or treatment—such as unexplained rapidly progressive kidney dysfunction, active urine sediment, nephrotic-range proteinuria or suspected systemic/glomerular disease. Small scarred kidneys often have lower diagnostic yield and greater procedural difficulty. [1]
Even mild CKD and albuminuria increases the risk of cardiovascular death. Finding and treating the cause, delaying the progression, long term follow up and cardiovascular protection are all important. [1]
This is a critical teaching point: patients with CKD stage 3 are more likely to die of cardiovascular disease than to ever reach dialysis. The exam loves this concept.
Rate determined by: [1]
- Causes (e.g. diabetic nephropathy progresses faster than IgA nephropathy)
- Baseline serum creatinine and Proteinuria (higher baseline Cr and proteinuria = faster decline)
- Severity of Hypertension
- Renal fibrosis and Aging
- Rate ranged from 1 ml/min to 7 ml/min/year
Risk Prognostication Tools: [1]
- Kidney Failure Risk Equation (KFRE) — gives 2- and 5-year risk of kidney failure in CKD patients
- CKD-PC risk models with heatmaps (www.ckdpc.org)
The quoted 1-7 ml/min/year range is descriptive lecture material, not a universal expected slope. Follow the patient's serial eGFR and ACR: a subsequent > 20% change in eGFR or doubling of ACR exceeds expected variability and warrants evaluation. In CKD G3-G5, a validated kidney-failure risk equation is more useful than eGFR alone for decisions such as specialist referral, multidisciplinary care and KRT planning. [8]
High Yield
Proteinuria is the single strongest modifiable predictor of CKD progression. Reducing proteinuria with RAAS blockade (ACEi/ARB), SGLT2i, and now ns-MRA (finerenone) directly slows progression. This is why every management plan starts with antiproteinuric therapy.
10. Complications of CKD — Deep Dive
The slide summarizes the hypertension target as “< 120/80.” [1]
The precise KDIGO 2021 recommendation is a target SBP < 120 mmHg, when tolerated, using standardized office BP measurement in adults with high BP and non-dialysis CKD. It does not specify a DBP target of < 80, and the < 120 target should not be transplanted onto a casual routine-clinic measurement. Treatment should be individualized when orthostasis, frailty, advanced CKD or other harms outweigh benefit. [9]
Antihypertensive choices in CKD: [1]
| Drug Class | Key Consideration |
|---|---|
| ACEI or ARB | Albuminuria — first-line if proteinuria present. Monitor U&E (can cause ↑K⁺ and ↑Cr via efferent arteriolar dilation) |
| Beta blocker | Cardio-protection. Risk of accumulation in renal failure (some are renally cleared) |
| Calcium channel blocker | Watch for swollen feet (peripheral oedema) |
| Diuretics | Can cause worsening renal function (volume depletion) |
| Alpha blocker | Useful if prostate co-morbidity |
ACEI/ARB Monitoring — Exam Classic
After starting or uptitrating ACEI/ARB, check BP, creatinine and K⁺ within 2-4 weeks (earlier when baseline eGFR/K⁺ makes risk higher). A creatinine rise up to about 30% within 4 weeks can reflect the expected haemodynamic effect. If the rise is > 30%, evaluate volume depletion, AKI, NSAIDs/diuretics and possible renal artery stenosis; do not automatically stop a kidney-protective drug without assessing reversible causes. Dose reduction/cessation is considered if the problem persists, or with symptomatic hypotension or hyperkalaemia uncontrolled despite treatment. Never combine ACEI + ARB. [8]
10.2 Renal Anaemia
Anaemia in CKD: normochromic, normocytic, due to a lack of erythropoietin. [1]
Pathophysiology from first principles:
- EPO is produced by peritubular interstitial fibroblasts in response to hypoxia
- As nephrons are lost → fewer EPO-producing cells → ↓ EPO → ↓ erythropoiesis
- Additionally: uraemic toxins suppress bone marrow, and hepcidin (an acute phase reactant elevated in CKD due to chronic inflammation) blocks iron absorption and mobilization — now termed iron-restricted erythropoiesis
The lecture's hepcidin diagram ties these mechanisms together: inflammation (especially IL-6) drives hepatic hepcidin production; hepcidin degrades ferroportin, so less iron crosses the enterocyte into blood and less stored iron leaves macrophages. Ferritin may therefore be normal/high while TSAT is low. At the same time, reduced renal EPO and direct cytokine inhibition suppress marrow erythropoiesis. [1][10]
The lecture uses an ESA target Hb of 10-12 g/dL (< 12 g/dL), based on TREAT and CHOIR. [1]
Current KDIGO 2026 guidance is slightly more conservative: for adults receiving an ESA, keep the maintenance target at or below 11.5 g/dL, typically 10-11.5 g/dL, and individualize. Do not normalize Hb: higher ESA targets increase hypertension and vascular-event risk. ESA initiation is also individualized after correctable causes are treated rather than triggered by one Hb value alone. [10]
The lecture quotes TSAT > 20% and ferritin 100-500 µg/L as practical iron goals. [1]
Iron preparations: [1]
- Oral iron
- IV iron dextran
- IV iron sucrose (Venofer)
- IV iron carboxymaltose (Ferinject)
Route and thresholds depend on dialysis status. KDIGO 2026 suggests IV iron for haemodialysis; in non-haemodialysis CKD or PD, either oral or IV iron can be selected according to severity, response, tolerability, access and preference. Suggested initiation thresholds also differ by setting, so ferritin 100-500 is not a universal treatment target. [10]
ESA examples: [1]
- Epoetin alfa (Procrit, Epogen)
- Epoetin beta (NeoRecormon)
- Epoetin zeta (Silapo, Retacrit)
- Darbepoetin alfa (Aranesp) — longer half-life
- Methoxy polyethylene glycol-epoetin beta (Mircera) — very long acting, monthly dosing
HIF-PH inhibitors work by stabilizing the HIF complex and stimulate endogenous EPO production even in ESKD patients; Given orally TIW. It also improves iron mobilization to the bone. [1]
Mechanism from first principles: Under normoxia, HIF-α is hydroxylated by prolyl hydroxylase (PHD) → tagged for proteasomal degradation. HIF-PHi blocks PHD → HIF-α accumulates → enters the nucleus and dimerizes with HIF-β → upregulates EPO signalling and lowers hepcidin, improving iron mobilization. [1]
The oral route is convenient, but HIF-PHIs are not simply “better oral ESAs.” KDIGO 2026 suggests an ESA rather than a HIF-PHI as first-line therapy after correctable causes are addressed; a HIF-PHI may be considered when ESA response/intolerance or practical barriers justify it, after discussing uncertain long-term safety and vascular risks. Do not combine the two classes. [10]
Causes of ESA resistance: [1]
- Inflammation, neckline infection, failed allograft
- HD versus PD
- Functional iron deficiency (hypochromic reticulocytes)
- Chemotherapy and immunotherapy
- Bleeding
- Marrow failure
- Aluminium toxicity
- Severe hyperparathyroidism
- Pure red cell aplasia (PRCA) — rare but important; anti-EPO antibodies
PRCA — Rare but Examinable
PRCA occurs when patients develop neutralizing antibodies against exogenous EPO. It presents as severe anaemia with absent reticulocytes and absent erythroid precursors on marrow biopsy. All ESAs must be stopped. Treatment: immunosuppression. This is a classic viva/MCQ topic.
10.3 Hyperkalaemia
Why CKD causes hyperkalaemia: Potassium is 90% renally excreted (distal tubule/collecting duct under aldosterone influence). As GFR drops, K⁺ excretion capacity diminishes. Additionally, CKD patients often take RAAS blockers (further ↓ K⁺ excretion) and may have Type 4 RTA (hyporeninemic hypoaldosteronism, especially in diabetic nephropathy). [1][3]
Management includes ISN RAASi toolkit: [1]
- Nuts and bolts of RAASi therapy
- Management of hyperkalemia
- Dietary approaches to hyperkalemia
- Monitoring and managing acute changes in renal function related to RAASi
Acute management: severity depends on the potassium value, rate of rise, symptoms, renal function and ECG—not a single cutoff alone. Confirm/exclude pseudohyperkalaemia when clinically safe, stop exogenous K⁺ and obtain an ECG, but do not delay treatment in an unstable patient or with convincing ECG toxicity.
- Protect the myocardium: IV calcium according to the local emergency protocol when ECG changes/toxicity are present (it does not lower K⁺).
- Shift K⁺ into cells: IV insulin-dextrose with glucose monitoring; nebulized salbutamol is an adjunct. IV bicarbonate is mainly useful when clinically important metabolic acidosis is present, not as routine monotherapy.
- Remove K⁺ from the body: a suitable potassium binder, loop diuretic if urine output/volume status permit, and urgent haemodialysis for severe or refractory hyperkalaemia. Patiromer and SPS have delayed effects and do not replace immediate membrane stabilization/shift therapy. [1][8]
Chronic management:
- Individualized dietary review, prioritizing foods with highly bioavailable potassium (potassium additives in processed foods, potassium-chloride salt substitutes, juices and some animal products) rather than automatically banning all fresh fruit and vegetables
- Potassium binders (newer agents like patiromer/SZC allow continued RAAS blockade)
- Avoid K⁺-sparing diuretics, potassium supplements
- Treat metabolic acidosis (NaHCO₃ → shifts K⁺ intracellularly)
| Line | Action |
|---|---|
| 1st — Address correctable factors | Review non-RASi medications (NSAIDs, trimethoprim); assess dietary K⁺ intake with dietitian referral |
| 2nd — Medications | Appropriate use of diuretics; optimise serum bicarbonate; licensed potassium exchange agents (patiromer, SZC) |
| 3rd — Last resort | Reduce dose or discontinue RASi/MRA (associated with ↑ CV events); review and restart when possible |
| Drug (FDA approval) | Mechanism & location | Onset | Key adverse effects | Cost |
|---|---|---|---|---|
| SPS (1958) | Non-specific resin; exchanges Na⁺ for K⁺; colon | Hours to days | GI effects, colonic necrosis, electrolyte disorders | Low |
| Patiromer (2015) | Non-specific resin; exchanges Ca²⁺ for K⁺; colon | Within 7 h | GI effects, hypomagnesaemia, hypokalaemia (3-6%) | Very high |
| SZC (2018) | Selective inorganic; exchanges Na⁺/H⁺ for K⁺; entire GI tract | Median 2 h | GI effects, oedema, dose-dependent hypokalaemia | Very high |
Monitor serum K⁺ 1-2 weeks after initiating or up-titrating RAAS inhibitors. Exclude pseudohyperkalaemia if K⁺ > 5.0 mmol/L. [1]
| K⁺ level | Action |
|---|---|
| < 5.0 mmol/L | Routine monitoring |
| 5.0-5.4 mmol/L | If no acute illness/AKI: dietary modification, treat acidosis, avoid hyperkalaemia-associated drugs, consider K⁺-binding resin, consider diuretic |
| 5.5-5.9 mmol/L | Same as above; if acute illness/AKI present → treat urgently |
| ≥ 6.0 mmol/L | Urgent treatment (see acute management above) |
The slide algorithm uses K⁺ < 5.0 mmol/L as its follow-up target. Apply local thresholds and repeat-testing intervals because urgency also depends on trend, ECG and clinical context. [1]
CKD may first cause a normal-anion-gap (hyperchloraemic) acidosis through reduced ammoniagenesis/NH₄⁺ excretion, and later a high-anion-gap acidosis as sulphate, phosphate and organic anions accumulate. Type 4 RTA is an additional hypoaldosterone/resistance mechanism—especially in diabetic kidney disease or with RAS-blocking drugs—not a synonym for all early CKD acidosis.
Treatment:
The lecture recommends sodium bicarbonate to maintain serum bicarbonate > 22 mmol/L. [1]
Current KDIGO 2024 guidance is less target-driven: consider pharmacological treatment, with or without dietary measures, to prevent clinically important acidosis (an adult serum bicarbonate < 18 mmol/L is given as an example), then monitor so treatment does not push bicarbonate above normal or worsen BP, potassium or fluid status. Evidence that routine correction to > 22 mmol/L slows kidney failure is not definitive. [8]
10.5 CKD-Mineral Bone Disorder (CKD-MBD)
This is the most pathophysiology-heavy complication and a perennial exam favourite.
CKD-MBD: [1]
- Hyperphosphataemia
- Vitamin D deficiency (1α-hydroxylase)
- Secondary hyperparathyroidism (PTH)
- Osteitis fibrosa cystica
- Adynamic Bone Disease
- Osteoporosis
- Gout, pseudogout
- ↓ GFR → phosphate retention; FGF23 and PTH initially increase fractional phosphate excretion, so overt hyperphosphataemia often appears later
- ↓ functioning renal mass → ↓ 1α-hydroxylase activity → ↓ calcitriol (active vitamin D)
- ↓ calcitriol → ↓ intestinal Ca²⁺ absorption → hypocalcaemia
- Hyperphosphataemia directly binds Ca²⁺ → further hypocalcaemia
- Hypocalcaemia + ↓ calcitriol + hyperphosphataemia → stimulates PTH secretion → secondary hyperparathyroidism (SHPT)
- Chronically elevated PTH → parathyroid gland hyperplasia → eventually autonomous secretion (tertiary hyperparathyroidism)
- ↑ PTH → ↑ bone turnover → osteitis fibrosa cystica
- If PTH is over-suppressed (by excessive vitamin D or calcium) → adynamic bone disease (too low turnover)
- Persistent phosphate/calcium/PTH disturbance promotes bone disease and soft-tissue/vascular calcification → fractures and cardiovascular morbidity
As kidney function declines, secondary HPT develops — the lecture shows rising iPTH and phosphorus with falling calcium as creatinine clearance drops. [1]
Overview of SHPT pathogenesis: ↓ calcitriol → ↓ VDR stimulation + ↓ CaR stimulation → ↑ PTH secretion, ↑ PTH synthesis, ↑ cell proliferation [1]
Coronary artery calcifications increase with years of dialysis. [1] Cardiovascular calcification is associated with mortality in dialysis patients. [1] CV mortality in dialysis patients vs general population: 10-100× higher across all age groups. [1]
CKD can produce both intimal calcification (within atherosclerotic plaque) and medial calcification (arterial stiffening). The latter raises pulse pressure and afterload, contributing to LVH and heart failure; the coronary CT slide demonstrates the visible calcium burden but does not by itself distinguish the two compartments. The lecture's survival and dialysis-duration graphs show associations, not proof that calcification alone caused the excess mortality. [1]
CKD-MBD is a triad of overlapping domains: laboratory abnormalities, bone abnormalities, and vascular calcification — whose intersection drives CVD, fractures, and mortality (KDIGO / Sharon Moe 2006). [1]
Radiographic manifestations of high-turnover renal osteodystrophy include subperiosteal resorption (classically at the radial aspect of the middle phalanges) and pathological fractures (the slide shows a pelvic fracture). Metastatic calcification may appear as dense periarticular soft-tissue deposits. In contrast, the adynamic-bone histology slide represents low turnover: little osteoid formation and sparse tetracycline labels, often after excessive PTH suppression. Bone biopsy with histomorphometry is the definitive turnover assessment when the result would change treatment. [1]
Calciphylaxis [1] — a devastating condition, usually in advanced CKD, in which exquisitely painful retiform purpura can progress to black eschar and ulceration. The histology image shows medial calcification and intimal fibrosis/thrombosis of small dermal/subcutaneous vessels, producing tissue ischaemia. It is not diagnosed by a high Ca × PO₄ product alone. Management is urgent and multidisciplinary: wound and infection care, analgesia, optimization of CKD-MBD and review of contributors such as warfarin/calcium loading. Sodium thiosulfate is commonly used, but outcome evidence is limited; biopsy is individualized because a poor-healing lesion can worsen. [1]
MBD Treatment: [1]
- Dietary phosphate restriction
- Calcium-based and non-calcium-based phosphate binders
- 25-OH Vit D and active Vit D (1-α)
- Calcimimetics (cinacalcet)
- Parathyroidectomy
Different types of phosphate binders: [1]
| Binder | Notes |
|---|---|
| Calcium carbonate | Cheap, effective; risk of hypercalcaemia and vascular calcification with overuse |
| Calcium acetate | Similar to CaCO₃ but binds more PO₄ per unit calcium |
| Sevelamer | Non-calcium, non-aluminium; also ↓ LDL; expensive |
| Lanthanum carbonate | Non-calcium; effective; concerns about tissue accumulation |
| Sucroferric oxyhydroxide | Iron-based; newer |
| Ferric citrate | Iron-based; also provides iron supplementation |
| Tenapanor | Not a binder: NHE3 inhibitor that reduces paracellular intestinal phosphate absorption |
| (Aluminium hydroxide) | Most effective but causes neurotoxicity (dialysis dementia) and osteomalacia → only short-term use |
Choosing Phosphate Binders — Exam Logic
Base phosphate-lowering therapy on progressively or persistently elevated phosphate, not one result. Restrict calcium-based binder exposure in adults—especially with hypercalcaemia, vascular calcification, adynamic bone disease or low PTH—and individualize the non-calcium alternative. Aluminium-based binders are reserved, if used at all, for short courses because of toxicity. [11]
Calcimimetics (cinacalcet): act on calcium-sensing receptor (CaR) → increase receptor sensitivity to Ca²⁺ → ↓ PTH secretion, ↓ PTH synthesis, ↓ cell proliferation [1]
This is elegant pharmacology: cinacalcet doesn't add calcium — it makes the parathyroid gland "think" there is more calcium around, thereby suppressing PTH without the risks of hypercalcaemia.
| Agent | iPTH | PO₄ | Ca | Ca × P | FGF23 |
|---|---|---|---|---|---|
| Vitamin D (VDRA) | ↓ | ↑ | ↑ | ↑ | ↑ |
| Ca-based PO₄ binders | ↘ slight ↓ | ↓ | ↑ | ↘ slight ↓ | ↑ |
| Non-Ca-based PO₄ binders | ↘ slight ↓ | ↓ | → neutral | ↓ | ↓ |
| Cinacalcet (& PTX) | ↓ | ↓ | ↓ | ↓ | ↓ |
Exam Logic — Reading the MBD Table
This table is high-yield for MCQs: note that VDRA raises both Ca and PO₄ (and therefore Ca × P and FGF23) — this is why active vitamin D can worsen vascular calcification if phosphate is uncontrolled. Non-Ca-based binders are the only class that lowers Ca × P, PO₄, AND FGF23 without raising calcium. Cinacalcet lowers everything.
A 50-year-old F with CKD G3bA2: Ca 1.95 mmol/L, P 1.80 mmol/L, PTH 75 pg/mL (15-65), albumin 39 g/L, ALP 90 U/L, 25-OH Vit D 20 ng/mL. [1]
- Interpretation: ↓Ca, ↑PO₄, PTH marginally raised, ↓25-OH Vit D
- The slide's stated aim is near-normal Ca × PO₄ product and PTH
- For ↑PO₄: choose wisely between calcium and non-calcium-based phosphate binder, replete Vit D, and monitor
Modern interpretation is trend-based: make decisions from serial phosphate, calcium and PTH considered together, rather than chasing a calculated Ca × PO₄ product or one mildly high PTH. In non-dialysis CKD G3a-G5, the optimal PTH is unknown and a modest rise may be adaptive; first correct modifiable factors (hyperphosphataemia, hypocalcaemia, high phosphate intake and vitamin D deficiency). Replete native vitamin D when deficient. Calcitriol/active vitamin-D analogues are not routine in non-dialysis CKD and are generally reserved for severe, progressive SHPT in G4-G5 because they can worsen hypercalcaemia and hyperphosphataemia. [11]
CKD 3-5 patients aged > 50 years has a high risk of coronary deaths or incident MI in excess of 10 per 1000 patient-years regardless of the cholesterol level. In those patients with CKD 3-5, treatment with statin or statin plus ezetimibe is recommended (KDIGO 2013). [1]
The SHARP trial demonstrated that simvastatin + ezetimibe reduced major atherosclerotic events in CKD patients. The key exam point: in CKD, you treat with statin based on CKD stage and age, not on LDL level.
11. Management of CKD — Comprehensive
CKD Therapy Aim: [1]
- Delay kidney failure
- Control hypertension
- Reduce albuminuria
- Treat anaemia and MBD disorder
- Treat acidosis, high K
- Control lipid and CV risk
Dietary recommendations in CKD: [1]
- Reduce sodium to < 2 g (< 90 mmol), NaCl to < 5 g daily (for BP and volume control)
- In CKD 3-5, moderate restriction of dietary protein possibly reduces uremic toxin and hyperfiltration and reduces clinical symptoms and delays maintenance dialysis
- In DN, daily protein recommendation is 0.8 g/kg
Why low protein: Each gram of protein generates nitrogenous waste (urea). High protein intake also increases intraglomerular pressure via amino acid-mediated afferent arteriolar dilation → hyperfiltration → accelerated nephron loss. However, too much restriction → malnutrition (especially in dialysis patients). Balance is key.
Sodium excretion and cardiac risk in CKD patients (JAMA 2016) — the lecture references evidence that high sodium intake increases cardiovascular events in CKD. [1]
CKD Drug Therapy: [1]
| Category | Drugs |
|---|---|
| Diuretics, Antihypertensive, Antiproteinuric | ACEI/ARB |
| Newer renoprotective agents | SGLT2i, GLP1-RA, ns-MRA |
| Acidosis | Sodium bicarbonate |
| Hyperkalaemia | Potassium lowering drugs |
| Anaemia | EPO, HIF-PHi |
| CKD-MBD | Phosphate binders, Vitamin D therapy including 1-alfacalcidol, Calcimimetics |
11.4 Diabetic Kidney Disease (DKD) — Special Focus
The lecture dedicates several slides to DKD because it is the most common cause of CKD globally.
The renal histology image shows nodular mesangial sclerosis (Kimmelstiel-Wilson nodules) with expansion of the mesangial matrix, a classic advanced diabetic-glomerulosclerosis pattern. It supports the mechanism of chronic hyperglycaemic injury and intraglomerular hypertension, but nodular sclerosis is not completely specific to diabetes; integrate it with the clinical history and other biopsy features. [1]
Empagliflozin reduced doubling of serum creatinine, initiation of RRT, or death due to renal disease (EMPA-REG OUTCOME, Wanner et al. NEJM 2016) [1]
Mechanism: SGLT2i block sodium-glucose co-transporter 2 in proximal tubule → ↑ sodium delivery to macula densa → activates tubuloglomerular feedback → afferent arteriolar vasoconstriction → ↓ intraglomerular pressure → ↓ hyperfiltration → ↓ proteinuria → renoprotection. Additionally: weight loss, ↓ BP, ↓ inflammation, ↓ oxidative stress.
Key trials: CREDENCE (canagliflozin), DAPA-CKD (dapagliflozin, including non-diabetic CKD) and EMPA-KIDNEY (empagliflozin, including people without diabetes and a broader albuminuria range). [4][8]
EMPA-REG OUTCOME renal endpoint (Wanner et al. NEJM 2016): HR 0.54 (95% CI 0.40–0.75, P < 0.001) for the composite of doubling of serum creatinine (with eGFR ≤ 45), initiation of RRT, or renal death. [1]
Diabetic medication comparison table: [1]
| Drug | Kidney | CAD | HF | Glycaemia | Hypo risk | Weight | Cost |
|---|---|---|---|---|---|---|---|
| Metformin | n | +/- | + | ++ | low | n | low |
| SGLT2i | ++ | ++ | ++ | + | low | ↓ | high |
| GLP-1RA | + | ++ | + | ++ | low | ↓ | high |
| DPP-4i | n | n | - | + | low | n | high |
| Insulin | n | n | n | ++ | high | ↑ | - |
| PPARγ (TZD) | n | +/- | worse | ++ | low | ↑ | low |
| Sulphonylurea | n | n | n/a | ++ | high | ↑ | low |
n = neutral
| Agent | Initiation threshold | Dose adjustment | Discontinuation |
|---|---|---|---|
| Metformin | eGFR ≥ 30 | Reduce dose at eGFR < 45 | eGFR < 30 or dialysis |
| SGLT2i | eGFR ≥ 20 | — | Do not initiate if eGFR < 20; discontinue on dialysis |
Once initiated, SGLT2i can be continued until dialysis or transplant. [1]
Additional glucose-lowering agents (in order of preference if further glycaemic control needed): GLP-1 RA (preferred) > DPP-4i > insulin > sulfonylurea > TZD > alpha-glucosidase inhibitor. Selection is guided by patient preferences, comorbidities, eGFR, and cost. [1]
SGLT2i + GLP-1RA + Finerenone — The Triple Pillar
KDIGO 2022 DKD Guideline recommends a layered approach for T2DM with CKD:
- First-line: Metformin + SGLT2i
- If persistent albuminuria despite RAAS blockade + SGLT2i: Add ns-MRA (finerenone)
- If additional glycaemic or CV benefit needed: Add GLP-1RA A Circulation 2024 study estimated that combining all three on top of RAAS blockade provides the greatest lifetime cardiovascular, kidney, and mortality benefits. [1]
Proposed Mechanisms of the Triple Pillar Agents
| Drug class | Proposed mechanisms of action |
|---|---|
| SGLT2i | Reduce intraglomerular pressure; decrease volume overload (natriuresis/osmotic diuresis); improve cardiac energy metabolism; reduce inflammation and fibrosis |
| GLP-1 RA | Lower inflammation and oxidative stress; reduce atherosclerosis progression; improve endothelial function; promote weight loss and BP reduction |
| ns-MRA (finerenone) | Reduce fibrosis and inflammation in heart and kidneys; decrease sodium retention and volume overload; improve endothelial function |
Finerenone is a non-steroidal MRA with proven cardiorenal benefit in T2DM with CKD (FIDELIO-DKD and FIGARO-DKD). Consider it when eGFR is > 25, serum K⁺ is normal and albuminuria persists despite the maximum tolerated ACEI/ARB; it may be layered with an SGLT2i. It still increases hyperkalaemia risk, so select and monitor patients carefully rather than assuming it is potassium-neutral. [2][8]
From the nephrology interactive tutorial, if a diabetic patient has CKD, suspect a non-diabetic cause if: [2]
- Gross haematuria
- Rapid/sudden decline in GFR
- Short duration of diabetes (< 5 years for T1DM; though many T2DM are undiagnosed for years)
- Absence of diabetic retinopathy (expect microvascular complications to travel together)
Preparation for RRT is one of the nephrologist's key roles. [1]
Indications for starting RRT in CKD:
- Symptoms/signs attributable to kidney failure (for example uraemic neurological features, pericarditis, anorexia or intractable pruritus)
- Medically resistant acid-base/electrolyte disturbance or inability to control volume/BP
- Progressive nutritional deterioration despite intervention, or cognitive impairment attributable to kidney failure
Start dialysis from a composite assessment of symptoms, signs, quality of life, preferences, GFR and laboratory abnormalities—not from eGFR < 5 “regardless of symptoms.” These indications often, but not invariably, emerge at GFR 5-10 ml/min/1.73 m². Begin planning for pre-emptive transplant and/or dialysis access earlier, around GFR < 15-20 or a validated 2-year KRT risk > 40%. [8]
RRT modalities:
- Peritoneal dialysis (PD) — HA "PD-first" policy in Hong Kong
- Haemodialysis (HD)
- Kidney transplantation — treatment of choice when available [5]
The CKD patient journey also includes conservative/palliative care as a recognised pathway alongside transplantation, HD, and PD — particularly for patients who are not candidates for or decline RRT. [1]
The slide's journey is not a one-way “stage 1 to dialysis” conveyor belt. Monitoring, cause-specific treatment, cardiovascular prevention and complication management run throughout CKD; people may move between dialysis modalities and transplantation, choose comprehensive conservative care, or die—often from cardiovascular disease—at any stage. [1]
From the senior notes and lecture context: [6]
| Area | Findings to Look For |
|---|---|
| General | Consciousness (uraemic encephalopathy), fluid status, café au lait complexion, scratch marks, uraemic frost |
| Face | Pallor, band keratopathy (hypercalcaemia), gingival hyperplasia (CNI), uraemic fetor |
| Hands/Arms | Palmar crease pallor, asterixis, AV fistula/graft, nail changes, carpal tunnel |
| Neck | JVP (fluid status), parathyroidectomy scar, previous dialysis catheter sites |
| Chest | LVH, signs of heart failure, pericardial rub (uraemic pericarditis), pleural effusion |
| Abdomen | Tenckhoff catheter, nephrectomy/transplant scars, ballottable kidneys (PKD), renal bruit |
| Legs | Oedema, purpura, livedo reticularis, peripheral neuropathy, gout |
| Back | Sacral oedema, bony tenderness |
15. Exam Intelligence
-
"A 55-year-old diabetic man has serum creatinine 180 µmol/L and urine ACR 45 mg/mmol. Calculate his CKD stage and outline your management plan."
- Markscheme: Calculate eGFR (using CKD-EPI), stage by GFR + albuminuria (e.g. G3bA3), confirm chronicity, identify cause (DKD), manage: RAS blockade, SGLT2i, standardized-office SBP target < 120 if tolerated, statin, individualized nutrition, and monitor BP/K⁺/Cr within 2-4 weeks after starting or increasing ACEI/ARB
-
"List 4 complications of CKD and explain the pathophysiology of ONE."
- Markscheme: Anaemia (↓ EPO), CKD-MBD (↑ PO₄ → ↓ Ca → ↑ PTH), Hyperkalaemia (↓ excretion + RAAS blockers), CVD (vascular calcification + volume overload + LVH). Pathophysiology: full stepwise explanation
-
"A CKD stage 4 patient on ACEI develops K⁺ 6.8 with ECG changes. Outline your immediate management."
- IV calcium gluconate → insulin-dextrose → salbutamol nebulizer → potassium binder → consider dialysis
-
"Why is SGLT2i considered renoprotective?"
- Tubuloglomerular feedback activation → ↓ intraglomerular pressure → ↓ hyperfiltration → ↓ proteinuria
-
"A dialysis patient has Ca 2.8, PO₄ 2.5, PTH 800 pg/mL. What is the diagnosis and management?"
- Tertiary hyperparathyroidism; manage with non-calcium phosphate binder, cinacalcet, consider parathyroidectomy
| Trap | Correct Answer |
|---|---|
| "CKD patients should have Hb normalized to > 13" | NO — if using ESA, KDIGO 2026 recommends Hb ≤11.5 g/dL, typically 10-11.5; higher targets increase harm |
| "ACEI and ARB should be combined for better renoprotection" | NO — dual RAAS blockade causes ↑ hyperkalaemia and AKI without benefit |
| "Stop ACEI immediately if creatinine rises after starting" | NO — check within 2-4 weeks; if rise > 30% within 4 weeks, evaluate reversible causes and then decide whether dose reduction/cessation is needed |
| "Calcium-based phosphate binders are always first-line" | Not if patient has hypercalcaemia or vascular calcification |
| "Metformin is contraindicated in all CKD" | Only in eGFR < 30; dose reduce at eGFR 30-45; safe at eGFR > 45 |
| "CKD patients die of kidney failure" | Most die of CVD, not ESRD |
From past summative papers (2016-2025): CKD questions frequently appear as SAQs asking for staging, complications, management principles (especially RAAS blockade + SGLT2i), and data interpretation (elevated creatinine + MBD biochemistry). MCQs test drug choices in CKD (which drugs are contraindicated, which are renoprotective) and interpretation of Ca/PO₄/PTH patterns. [7]
High Yield Summary
- Definition: abnormal kidney structure/function for > 3 months—eGFR < 60, ACR ≥3 mg/mmol or another damage marker.
- Stage: cause + G category + A category; heat-map risk rises down and right.
- Major risks: cardiovascular disease, progression/kidney failure, anaemia, hyperkalaemia/acidosis and CKD-MBD.
- Kidney/CV protection: maximally tolerated ACEi/ARB when indicated, SGLT2 inhibitor, individualized BP control (standardized-office SBP < 120 if tolerated), lipid therapy, smoking/exercise/nutrition care and diabetes therapy where relevant.
- Monitoring: check BP/creatinine/K⁺ within 2-4 weeks after RASi initiation or titration; investigate > 20% serial eGFR change or doubled ACR.
- Complications: correct iron deficiency and other anaemia causes before ESA; if ESA is used, maintain Hb ≤11.5. Treat hyperkalaemia without reflexively abandoning RASi. Base CKD-MBD treatment on serial Ca/PO₄/PTH together.
- KRT: plan early when risk is high, but start dialysis for a composite clinical indication—not an isolated eGFR number.
Active Recall - Chronic Kidney Disease and its Complications
[1] Lecture slides: GC 034. Chronic Kidney Disease and its Complications [update 2025].pdf (pages 1-92) [2] Senior notes: Block A - Nephrology Interactive Tutorial.pdf (pages 3-4) [3] Senior notes: Block A – Nephrology Data Interpretation.pdf (pages 1-11) [4] Senior notes: Maksim Medicine Notes.pdf (pages 220-222) [5] Senior notes: Block A - Renal Replacement Therapies.pdf (page 36) [6] Senior notes: Ryan Ho Fundamentals.pdf (pages 111-112) [7] Past papers: 2018-2025 Fourth Summative MCQ and SAQ papers [8] KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease [9] KDIGO 2021 Clinical Practice Guideline for the Management of Blood Pressure in Chronic Kidney Disease [10] KDIGO 2026 Clinical Practice Guideline for the Management of Anemia in Chronic Kidney Disease [11] KDIGO 2017 Clinical Practice Guideline Update for CKD-Mineral and Bone Disorder
GC033 Chronic Diarrhea: Irritable Bowel Syndrome And Inflammatory Bowel Disease
Chronic diarrhea in the context of irritable bowel syndrome (a functional disorder with altered bowel habits and abdominal pain without structural pathology) versus inflammatory bowel disease (chronic immune-mediated intestinal inflammation, including Crohn's disease and ulcerative colitis, with mucosal damage and systemic manifestations).
GC035 Clinical Pharmacokinetics
Clinical pharmacokinetics is the application of pharmacokinetic principles to the safe and effective therapeutic management of drugs in individual patients, involving the study of absorption, distribution, metabolism, and excretion to optimize dosing regimens.