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 CrCl (UV/P) — gold standard but cumbersome

eGFR calculator available on the National Kidney Foundation website. ^[1]

GFR declines with age: ^[1]

Why this matters: A 75-year-old with eGFR 68 may have age-appropriate kidney function, not necessarily "CKD." Context is critical. However, if there is also albuminuria, that tips the diagnosis toward CKD regardless of age.

Proteinuria up to 150 mg/day can be normal. ^[1] In DM, a urine ACR > 3 mg/mmol is regarded as microalbuminuria, and requires ACE inhibitor or ARB. ^[1] ACR 3-30 mg/mmol for > 3 months indicates CKD. ^[1]

Other causes of albuminuria: Hypertension, High protein diet, Exercise, fever, UTI. ^[1]

The staging is a two-dimensional grid of GFR (G1-G5) and albuminuria (A1-A3). The combination determines prognosis ("heat map"):

^[3]

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]

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.

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.

Hypertension target < 120/80 (KDIGO 2021 Guideline) ^[1]

This is a tighter target than the general population (which is < 140/90 or < 130/80). The rationale: in CKD patients, lower BP reduces proteinuria, slows progression, and reduces CV events. However, the SPRINT trial-based target of < 120 systolic is recommended for measurement via automated office BP (AOBP), not conventional clinic BP — this distinction matters.

Antihypertensive choices in CKD: ^[1]

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 of hyperkalaemia (if K⁺ > 6.0-6.5 or ECG changes):

1. Cardiac membrane stabilization: IV calcium gluconate 10% (does NOT lower K⁺ — just protects the heart)
2. Shift K⁺ into cells: Insulin-dextrose infusion, nebulized salbutamol, IV NaHCO₃
3. Remove K⁺ from body: Potassium binders (calcium resonium, sodium zirconium cyclosilicate [Lokelma], patiromer), loop diuretics, haemodialysis

Chronic management:

• Low-K⁺ diet (< 1 mmol/kg/day)
• Potassium binders (newer agents like patiromer/SZC allow continued RAAS blockade)
• Avoid K⁺-sparing diuretics, potassium supplements
• Treat metabolic acidosis (NaHCO₃ → shifts K⁺ intracellularly)

CKD causes a normal anion gap metabolic acidosis (early, due to ↓ NH₄⁺ excretion — essentially a Type 4 RTA) and later a high anion gap metabolic acidosis (uraemic toxins — sulphates, phosphates, organic acids accumulate).

Treatment:

Sodium bicarbonate ^[1] — oral supplementation to maintain serum bicarbonate > 22 mmol/L. This slows CKD progression and reduces protein catabolism.

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.

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]

1. "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: RAAS blockade, SGLT2i, BP target < 120/80, statin, low-protein diet, monitor K⁺ and Cr 2 weeks after starting ACEI

2. "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

3. "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

4. "Why is SGLT2i considered renoprotective?"

   • Tubuloglomerular feedback activation → ↓ intraglomerular pressure → ↓ hyperfiltration → ↓ proteinuria

5. "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

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]