RENAL

Chronic Kidney Disease (CKD)

from –https://assets.kidney.org.au/resources/KHA-CKD-Handbook-5th-Ed-July2024.pdf

Definition

CKD is characterized by abnormalities of kidney structure or function, present for >3 months, with implications for health. Diagnosis requires one or more of the following:

  • Decreased eGFR: <60 mL/min/1.73 m²
  • Markers of kidney damage, including:
    • Albuminuria:
      • ACR ≥2.5 mg/mmol (men) or
      • ≥3.5 mg/mmol (women)
    • Persistent hematuria (after exclusion of urological causes)
    • Electrolyte abnormalities due to tubular disorders
    • Structural abnormalities detected by imaging (scarring, polycycstic kidneys)
    • Histological abnormalities identified by biopsy

Epidemiology & Causes

CKD more common in:

  • Women with T2DM
  • Aboriginal and Torres Strait Islander peoples
  • Some non-European ethnic groups

Early treatment reduces morbidity and mortality.

Systolic BP is a key predictor of progression.

CKD in diabetes is often asymptomatic – rely on labs.

  • Diabetic nephropathy – 36%
  • Glomerulonephritis – 19%
  • Hypertension – 12%
  • Polycystic kidney disease – 5%
  • Reflux nephropathy
  • Tubulointerstitial disease – (e.g. NSAIDs, lithium, heavy metals)
  • Plasma cell dyscrasias – Myeloma, light chain deposition, amyloidosis
  • Unknown – 5%

Risk Factors

  • Non-modifiable:
    • Age ≥60 years
    • Family history of kidney disease
    • Aboriginal or Torres Strait Islander descent
  • Modifiable:
    • Diabetes mellitus
    • Hypertension
    • Smoking
    • Obesity (BMI ≥30 kg/m²)
    • Cardiovascular disease
    • History of acute kidney injury (AKI)
    • Exposure to nephrotoxic agents

📉 eGFR decreases ~8 mL/min/1.73 m² per decade after age 30
⚠️ eGFR <60 still carries increased risk of CVD and CKD progression


Clinical Features

CKD is often asymptomatic until advanced stages (≥ Stage 4–5).

Possible symptoms:

  • Fatigue, malaise, anorexia, nausea
  • Nocturia, pruritus, restless legs
  • Dyspnoea, volume overload
  • Hypertension
  • Haematuria

Screening Recommendations

  • BP
  • UEC: If eGFR < 60mL/ min/1.73m2 repeat within 7 days
  • ACR – first morning void, If ACR positive, require 2 further samples over 2 months

General Population

Risk CategoryScreening Frequency
Diabetes, HypertensionAnnually
Obesity, Smoking, FHx, ATSIEvery 2 years
Age ≥ 60 without other risk factorsNo routine screening recommended

Whilst being aged 60 years of age or over is considered to be a risk factor for CKD, in the absence of other risk factors it is not necessary to routinely assess these individuals for kidney disease.

Aboriginal and Torres Strait Islander Peoples

  • Ages 18–29 without risk factors: Annual screen (as part of MBS 715)
  • With ≥1 risk factor: Screen every 2 years (ACR, eGFR, BP)

🧪 ACR positive: Repeat twice over 3 months (preferably first-void)
🧪 eGFR < 60: Repeat within 7 day


Investigations

Urine

  • MSU MCS – Rule out infection
  • Microscopy – Dysmorphic RBCs, casts, crystals
  • Urine ACR – First morning void preferred
  • Urine immunoelectrophoresis – Bence-Jones proteins

Bloods

  • FBC, CRP, ESR
  • eLFTs, CMP, HCO₃⁻
  • Lipids, fasting glucose/HbA1c
  • B12, folate, iron studies, PTH
  • Autoimmune screen (ANA, ENA, C3/C4, ESR, ANCA, anti-GBM)
  • serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP)  – If aged >40 with suspicion of myeloma
  • Hepatitis B/C, HIV, syphilis serology (if not performed in past 12 months)

Imaging

  • Renal ultrasound – Assess size, structure, obstruction

eGFR (Estimated Glomerular Filtration Rate)

  • Best overall marker of kidney function (via CKD-EPI equation, validated across ethnicities).
  • Automatically reported with serum creatinine in adults ≥18 years.
  • More sensitive than serum creatinine alone — up to 50% kidney function may be lost before creatinine rises.
When eGFR May Be Unreliable / Misleading:
  • Acute changes (e.g. AKI)
  • On dialysis
  • Recent cooked meat consumption (<4 hours before test)
  • High or low protein intake, vegetarian diet, creatine supplements
  • Extremes of body size
  • Muscle conditions (paraplegia, amputees → overestimation; high muscle mass → underestimation)
  • <18 years of age
  • Severe liver disease
  • eGFR >90 mL/min/1.73m²
  • Drugs affecting creatinine (e.g., trimethoprim)
  • Pregnancy
  • Minor changes (≤15%) may reflect lab or physiological variability
eGFR and Drug Dosing
  • Valid for drug clearance estimation; check product info
  • Adjust for BSA in extremes of body size
  • Use therapeutic monitoring for narrow therapeutic index drugs
eGFR in Pregnancy
  • Not recommended
  • Use serum creatinine instead
Clinical Tip:
  • If eGFR <60 mL/min/1.73m²:
    • Repeat in 7 days to exclude AKI
    • Repeat at 3 months to diagnose CKD

Albuminuria / Urine Albumin:Creatinine Ratio (uACR)

CategoryACR (mg/mmol)Albumin excretion (mg/day)PCR (mg/mmol)Protein excretion (mg/day)Dipstick
MicroalbuminuriaM: 2.5–25
F: 3.5–35
30–300M: 4–40
F: 6–60
50–500Trace to +1
MacroalbuminuriaM: >25
F: >35
>300M: >40
F: >60
>500≥ +1

  • Detects albuminuria, an early and often missed CKD marker
  • Predicts risk of kidney failure and cardiovascular disease
  • uACR more sensitive than uPCR (especially for microalbuminuria)
  • Dipstick urine protein tests are not recommended
  • ≥2 abnormal uACRs (≥3.0 mg/mmol) over 3 months = albuminuria

Testing Recommendations

  • Use first-void urine sample for best accuracy
  • Random spot acceptable if first-void not practical
  • Positive uACR → repeat on first-void sample
  • 24-hour collection not routinely needed

Conditions that falsely elevate albuminuria:

  • UTI
  • High dietary protein
  • CHF
  • Fever
  • Recent heavy exercise (<24h)
  • Menstruation
  • Genital infection/discharge
  • NSAIDs

Albuminuria in Pregnancy

  • uACR thresholds not validated — interpret with caution

Staging of CKD

Based on eGFR

  • G1: ≥90 mL/min/1.73 m² (normal or high)
  • G2: 60–89 mL/min/1.73 m² (mildly decreased)
  • G3a: 45–59 mL/min/1.73 m² (mild to moderate decrease)
  • G3b: 30–44 mL/min/1.73 m² (moderate to severe decrease)
  • G4: 15–29 mL/min/1.73 m² (severely decreased)
  • G5: <15 mL/min/1.73 m² (kidney failure)

Based on Albuminuria (ACR)

  • A1: <3 mg/mmol (normal to mildly increased)
  • A2: 3–30 mg/mmol (moderately increased)
  • A3: >30 mg/mmol (severely increased)

Management Strategies

Lifestyle Modifications

ParameterTreatment Goal
Nutrition and Diet• Eat a healthy diet (vegetables, fruits, wholegrains, legumes, dairy, lean meats, fish, plant proteins)
• Limit salt to <5g/day
• Avoid ultra-processed foods and sugary drinks
• Drink water to satisfy thirst
Weight Management• BMI <25 kg/m² (Asians <23 kg/m²)
• Waist circumference: <94 cm (men), <90 cm (Asian men), <80 cm (women including Asian)
Physical Activity• Be active most days, ideally daily
• Aim 2.5–5 hrs/week of moderate activity
• Include strength training ≥2x/week
• Any activity better than none
Smoking/Vaping• Do not smoke or vape
• Offer counselling, NRT or meds
• Refer to Quitline 13 7848
Alcohol• Reduce alcohol
• General guideline: ≤10 standard drinks/week and ≤4/day
• No CKD-specific safe alcohol threshold
Immunisation
• Recommend: Influenza, Pneumococcal, COVID-Influenza: annually
Pneumococcal: every 5 years
COVID-19: per current guidelines
Herpes Zoster: as per NIP

Pharmacological Interventions

TARGET parameters

Hypertension• Maintain BP <130/80 mmHg in all CKD patients
Glycaemic Control• Fasting BGL: 6–8 mmol/L
• Postprandial BGL: 8–10 mmol/L
• HbA1c ≤53 mmol/mol (≤7%)
• Individualise per patient factors
Albuminuria• Aim ≥30% reduction in uACR
Lipids• No absolute cholesterol target
• Use statin ± ezetimibe if:
– eGFR ≥15 + CVD risk ≥10%
– First Nations Australians + CVD risk ≥5%
Potassium• Maintain serum potassium ≤6.0 mmol/L

Monitoring and Follow-up

  • Frequency:
    • Low risk: Annual review.
    • Moderate risk: Every 6 months.
    • High risk: Every 3 months.
  • Assessments:
    • eGFR and urine ACR.
    • Blood pressure.
    • Medication review.
    • Cardiovascular risk assessment.

Patient Education and Support

  • Inform about CKD progression: Emphasize the importance of lifestyle and medication adherence.
  • Discuss potential complications: Cardiovascular disease, anemia, bone mineral disorders.
  • Encourage self-management: Blood pressure monitoring, dietary choices, and recognizing signs of disease progression.

Contraception and Pregnancy in CKD

  • Pregnancy increases kidney workload and may:
    • Unmask undiagnosed CKD
    • Worsen existing CKD
  • CKD increases pregnancy risks, especially hypertensive disorders.
  • Fertility may be preserved despite advanced disease or dialysis.
  • Unexpected pregnancy is possible even with ESKD.

Recommendations

  • Preconception counselling essential.
  • Contraception should be offered to all sexually active individuals of reproductive age with CKD.
  • Prioritise effective contraception if:
    • On teratogenic drugs
    • Have uncontrolled HTN or CKD
    • Post kidney transplant
  • Avoid oestrogen if:
    • HTN, thrombotic history, proteinuria, lupus
  • Preferred methods:
    • IUDs
    • Permanent options (vasectomy, tubal ligation) if no future pregnancy desired
  • Refer to maternal medicine, obstetric nephrology, or high-risk pregnancy team:
    • Preconception ideally
    • At minimum, early in pregnancy

CKD in Older People

  • Individualised approach is key.
  • Consider:
    • Functional status
    • Life expectancy
    • Treatment goals (quality of life vs. survival)
  • eGFR more accurate than creatinine alone in elderly.
  • eGFR <60 is not normal for age—still indicates risk.

Dialysis vs. Conservative Management

  • In elderly with multiple comorbidities, dialysis may not improve survival.
  • Decision aid tools (e.g., My Kidneys My Choice) support shared decision-making.

Referral Guidance

  • Referral to nephrologist if:
    • eGFR <30 mL/min/1.73m²
    • Anaemia possibly due to CKD
    • Suspected glomerulonephritis or systemic disease
    • Electrolyte imbalances (e.g., hyperkalemia)
    • Resistant hypertension
    • Hematuria with proteinuria
    • Persistent significant albuminuria (ACR >30 mg/mmol)
    • Rapid decline in eGFR (>5 mL/min/1.73 m² per year)
  • Can manage in primary care if:
    • eGFR ≥30
    • Microalbuminuria present
    • BP controlled
  • Discuss with specialists via phone/email for shared care.

Medication Management in CKD and Older Adults

  • Dose adjustments needed with declining eGFR.
  • Monitor for side effects (increased risk in elderly).
  • Polypharmacy risk: falls, confusion, decline.
  • Support with:
    • Home Medicines Reviews (HMR)
    • Residential Medication Management Reviews (RMMR)

Avoid nephrotoxins

Commonly Prescribed Drugs That May Harm Kidney Function in CKD

  • Lithium
    • Risk: Nephrogenic diabetes insipidus, chronic tubulointerstitial nephritis
    • Requires monitoring of serum levels and renal function
  • Aminoglycosides (e.g., gentamicin, tobramycin)
    • Risk: Acute tubular necrosis (ATN)
    • Especially toxic with prolonged use or in dehydration
  • NSAIDs / COX-2 inhibitors
    • Risk: Afferent arteriole constriction → ↓ GFR
    • May lead to AKI, especially in hypovolaemic states
    • Avoid combination with ACEi/ARB + diuretic (“Triple Whammy”)
  • ACE Inhibitors / ARBs
    • Risk: Efferent arteriole dilation → ↓ intraglomerular pressure
    • Can cause a reversible decline in eGFR
    • Monitor urea, creatinine, potassium after initiation
  • Diuretics (loop or thiazide)
    • Risk: Hypovolaemia, electrolyte disturbances, pre-renal AKI
  • Metformin
    • Risk: Lactic acidosis in patients with significant renal impairment or during dehydration
    • Avoid if eGFR <30 mL/min/1.73 m²
  • Sulfonylureas (e.g., gliclazide)
    • Risk: Hypoglycaemia, especially in reduced renal clearance
  • SGLT2 inhibitors (e.g., dapagliflozin, empagliflozin)
    • Risk: Osmotic diuresis, volume depletion, transient eGFR dip
    • Can lead to AKI in setting of acute illness or dehydration

⚠️ Sick Day Rule: SADMANS Acronym

These medications should be withheld temporarily during acute illness (e.g. fever, vomiting, diarrhoea, reduced oral intake) to prevent AKI:

LetterDrug ClassExample Medications
SSulfonylureasGliclazide, glibenclamide
AACE InhibitorsRamipril, perindopril
DDiureticsFurosemide, indapamide
MMetforminMetformin
AARBsIrbesartan, candesartan
NNSAIDsIbuprofen, celecoxib
SSGLT2 inhibitorsEmpagliflozin, dapagliflozin

Clinical Tip: “Triple Whammy” AKI Risk

  • Concurrent use of:
    1. NSAID
    2. ACE inhibitor or ARB
    3. Diuretic
  • Increases risk of acute kidney injury, especially in dehydration or intercurrent illness.


MEDICATIONS


BP control

is crucial in slowing CKD progression and reducing cardiovascular risk.

  • Target BP:
    • <140/90 mmHg (general CKD population)
    • <130/80 mmHg (if diabetes or significant albuminuria)

Stepwise Pharmacological Approach

  • ACE inhibitor (ACEi) or Angiotensin II receptor blocker (ARB)
    • Initiate and up-titrate to maximum tolerated dose
    • Prescribe for all CKD patients with:
      • ACR > 3 mg/mmol and comorbid diabetes, IHD, or hypertension
      • ACR > 30 mg/mmol (proteinuria)
  • Therapeutic Goal: ≥ 50% reduction in albuminuria

Step 2: Add-On Antihypertensives (if BP target not achieved)

Step 3: Consider Other Agents


  • Dapagliflozin – 10 mg taken once daily, with or without food.
  • Next Step After Stabilised RAAS Blockade
  • Recommended for people with CKD and proteinuria, with or without diabetes.
  • Benefits:
    • slows CKD progression
    • reduces CV risk (DAPA-CKD trial)
  • Indications:
    • eGFR: 25–75 mL/min/1.73m²
    • ACR: 22.6–565 mg/mmol
  • Do not initiate if eGFR <25 mL/min/1.73m²
  • Reversible eGFR drop expected:
    • Greatest drop at ~4 weeks, then stabilises.
    • Routine eGFR testing post-initiation not necessary unless symptomatic.
  • Consider reducing diuretics or antihypertensives at initiation due to osmotic diuresis.

  • Use in people with CKD and albuminuria associated with type 2 diabetes.
  • Do not initiate if:
    • eGFR <25 mL/min/1.73m²
    • Serum potassium >5.0 mmol/L
  • Monitor for hyperkalaemia

  • Indicated for people with CKD and type 2 diabetes
  • Benefits:
    • Reduces albuminuria
    • Cardiovascular protection
  • Not recommended in patients with kidney failure

Clinical Tips

  • Temporarily withhold the following drugs during acute illness (e.g., sepsis, hypotension, dehydration):
    • ACE inhibitors
    • ARBs
    • SGLT2 inhibitors
    • Diuretics
  • Check eGFR within 2 weeks of initiating ACEi/ARB:
    • If <25% drop → continue
    • If >25% drop → cease and refer nephrology

💊 ACEi/ARB

🔬 Physiological Background: Renal Autoregulation

  • Glomerular filtration is maintained via a balance between:
    • Afferent arteriole – delivers blood into the glomerulus
    • Efferent arteriole – drains blood from the glomerulus
  • Angiotensin II preferentially constricts the efferent arteriole:
    • Maintains intraglomerular pressure
    • Helps preserve GFR during low perfusion states (e.g., dehydration, heart failure, CKD)

🧪 Mechanism of Action: ACEi/ARB

  • ACEi/ARB inhibit the renin–angiotensin–aldosterone system (RAAS), leading to:
    • Efferent arteriole vasodilation
    • ↓ Intraglomerular pressure
    • ↓ GFR (initial, hemodynamic effect)

📈 Renal and Cardiovascular Benefits

BenefitMechanismClinical Impact
↓ Glomerular hypertensionEfferent vasodilationProtects against hyperfiltration injury
↓ ProteinuriaReduced glomerular capillary pressureSlows progression of nephron loss
↓ Fibrosis/inflammationRAAS inhibitionPreserves structural kidney integrity
↓ BP and CV riskSystemic RAAS blockade↓ MI, stroke, CV mortality (independent of BP control)

🛡️ CKD-Specific Outcomes

Delays progression to end-stage kidney disease (ESKD)

  • Reduces albuminuria
    • Target: ≥50% reduction in urine ACR
    • Degree of ACR reduction correlates with slower eGFR decline
  • Prevention of albuminuria onset
    • Type 1 or 2 diabetes: prevents microalbuminuria onset
    • Slows progression from micro- to macroalbuminuria in normotensive and hypertensive diabetics
  • Lowers cardiovascular event rates in CKD populations

🔄 Expected eGFR Changes After Initiation

  • Up to 25% reduction in eGFR (or ~30% ↑ in creatinine) is:
    • Expected, transient, and due to hemodynamic changes
    • Usually stabilises within 1–2 weeks at a new baseline
  • Do not cease ACEi/ARB based on eGFR drop alone
  • Monitor:
    • Serum creatinine and potassium 1–2 weeks post-initiation or after dose increase

⚠️ When to Be Concerned

  • >25–30% fall in eGFR may indicate:
    • Bilateral renal artery stenosis
    • Volume depletion/dehydration
    • NSAID co-use (i.e., triple whammy with diuretic)
    • Severe heart failure
    • Advanced CKD (Stage 4–5)
  • Serum potassium: Acceptable up to 6.0 mmol/L if stable over 2 months
ParameterAcceptable Threshold
eGFR reduction≤25% from baseline
Serum potassium≤6.0 mmol/L (monitor closely)
If >25% eGFR declineCease ACEi/ARB and consider referral

Contraindications

  • Absolute:
    • History of angioedema
    • Pregnancy (Category D – teratogenic)
    • Bilateral renal artery stenosis
    • ACEi-induced hypersensitivity
  • Relative:
    • Significant aortic stenosis or hypertrophic cardiomyopathy
    • Dry cough (ACEi only – affects ~10%)
    • Hyperkalaemia
      • If intolerant to ACEi → Switch to ARB
  • Do not combine ACEi + ARB
    • ↑ Risk of AKI and hyperkalaemia
    • No added benefit (as shown in ONTARGET trial)

🩸 Glycaemic Control in CKD

Glycaemic Targets in CKD

Blood Glucose Levels (BGL)
  • Fasting BGL: 6–8 mmol/L
  • Postprandial BGL: 8–10 mmol/L
HbA1c
  • General target: ≤53 mmol/mol (≤7%)
  • Acceptable range: 48–58 mmol/mol (6.5–7.5%)
  • Individualise based on:
    • Comorbidities
    • Disease duration
    • Life expectancy
    • Vascular complications
  • Unreliable in:
    • Iron deficiency (falsely elevated)
    • Anaemia (falsely lowered)
  • Consider lower targets where appropriate
Management Considerations
  • Optimal glycaemic control reduces micro- and macroalbuminuria and nephropathy risk.
  • CKD increases hypoglycaemia risk:
    • ↓ renal clearance of insulin and hypoglycaemic drugs
  • Medication doses may need adjustment or cessation as CKD progresses.
  • Educate patients on lifestyle and “sick day” rules (withhold nephrotoxic/hypoglycaemia-inducing drugs during illness).
Medication Summary for Diabetes in CKD

ClassDrug ExamplesCKD Dosing GuidanceKey Points
MetforminMetformin– Full dose if eGFR >60
– Reduce dose if eGFR 30–60
– Avoid if eGFR <30
– Temporarily withhold during illness
– Risk of lactic acidosis
SGLT2 inhibitorsDapagliflozin, Empagliflozin, Ertugliflozin– Do not initiate if eGFR <25–30 (varies)
– Cease in ESKD or dialysis
– Renal + CV benefit
– Risk: eDKA, fungal infections
Non-Steroidal MRAFinerenone– Avoid if eGFR <25 or K⁺ >5.0 mmol/L
– Cease if K⁺ >5.5 mmol/L
Not for diabetes unless CKD present
– Monitor K⁺ closely
DPP-4 inhibitorsLinagliptin, Sitagliptin, Saxagliptin, Vildagliptin, Alogliptin– Linagliptin: No dose adjustment
– Others: Reduce dose if eGFR <45–60
– Caution if pancreatitis hx
– ↑ risk of hypoglycaemia with sulfonylureas
SulfonylureasGliclazide, Glibenclamide– Reduce dose if eGFR <30
– Avoid glibenclamide in CKD
– ↑ Hypoglycaemia risk as eGFR declines
GLP-1 RASemaglutide, Dulaglutide– No adjustment unless eGFR <15
– Not recommended in kidney failure
– Potential CV and renal benefits
– Limited data in eGFR <30
InsulinAll insulinsAdjust dose as needed
– Monitor BGL closely
– ↑ Hypoglycaemia risk with declining eGFR

Medications requiring dose reduction

  • Pharmacological management for CKD also includes adjusting doses of medicines cleared by the kidneys to reduce adverse effects
  • Dose reduction or cessation of medicines cleared by the kidneys is generally required once eGFR is < 60 mL
  • GFR can be assessed using serum creatinine-based formulae.
    • Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)
    • But for  extremes of body weight unless it is first corrected to the actual GFR for that patient
CKD-EPI eGFR. × Individual’s body surface area (BSA) = eGFR result in mL/min  
                                173
BSA = 0.007184 × Weight in kg^0.425 × Height in cm ^0.725 (Du Bois formula)

Drug ClassExamplesNotes
AntiviralsAcyclovir, TenofovirHigh renal clearance, risk of neurotoxicity or nephrotoxicity
BenzodiazepinesMidazolam, LorazepamAccumulation may lead to sedation, confusion
OpioidsMorphine, Codeine, TramadolUse with caution; prefer fentanyl or buprenorphine if severe CKD
Hypoglycemic agents
DPP-4 inhibitorsLinagliptin, Sitagliptin, Saxagliptin, Vildagliptin, AlogliptinLinagliptin: No dose adjustment
– Others: Reduce dose if eGFR <45–60
– Caution if pancreatitis history
– ↑ Hypoglycaemia with sulfonylureas
GLP-1 RASemaglutide, Dulaglutide– No adjustment unless eGFR <15
– Not recommended in ESKD
CV and renal benefit
Limited data in eGFR <30
SulfonylureasGliclazide, Glibenclamide– Reduce dose if eGFR <30
– Avoid glibenclamide in CKD
– ↑ Hypoglycaemia risk as renal function declines
MetformineGFR > 45: no dose change
eGFR 30–45: max 1g/day
eGFR < 30: avoid
InsulinReduced renal clearance → increased risk of hypoglycaemia


Adjust dose based on renal function
Monitor BGL closely
Cardiac medicationsDigoxin, Sotalol, AtenololRequire close monitoring; risk of bradycardia, arrhythmias
DiureticsThiazides, K⁺-sparing (e.g. amiloride)Risk of hyperkalemia and reduced efficacy in advanced CKD
AnticoagulantsEnoxaparin (LMWH), FondaparinuxRequire dose adjustment or monitoring of anti-Xa levels
Psychotropics / AnticonvulsantsLithium, Gabapentin, PregabalinAccumulate in CKD; risk of CNS toxicity
Gout medicationsAllopurinol, ColchicineReduce dose to prevent bone marrow suppression and neuromyopathy

🔴 Acute Kidney Injury (AKI)

Key Concepts

  • AKI is common and associated with high morbidity/mortality.
  • CKD is a major risk factor for AKI.
  • AKI can lead to progression of CKD, kidney failure, and death.

Risk Factors

Pre-existing:

  • CKD
  • Diabetes
  • Cardiopulmonary/liver disease
  • Cancer
  • Anaemia
  • Advanced age

Potentially modifiable exposures:

  • Pre-renal: Hypovolaemia, hypotension, blood loss, shock
  • Intrinsic: Drug toxicity, critical illness
  • Post-renal: Obstruction

AKI Prevention and Management

PhaseActions
Identifying Risk– All CKD stage 3–5 patients are high risk
– Avoid nephrotoxins (NSAIDs, aminoglycosides)
– Apply sick day rule for ACEi/ARB/diuretics in illness
Diagnosis↑ Creatinine ≥1.5x baseline in <7 days OR
Oliguria (reduced urine output)
During AKI– Identify and treat the cause
– Review meds & fluid status
– Consult nephrology early
Post-AKIRepeat Kidney Health Check at 3 months, then annually × 3 yrs
– Educate on AKI prevention
– Record episode in medical records

Medications to Withhold During Illness (↓ fluid intake, vomiting, dehydration):

  • ACEi
  • ARBs
  • NSAIDs
  • Diuretics
  • Metformin
  • Sulfonylureas
  • SGLT2 inhibitors

🟡 Kidney Cysts

Simple Cysts

  • Very common (~10% prevalence), benign, often incidental.
  • Features:
    • Not inherited
    • Asymptomatic
    • Increases with age
    • Not associated with kidney failure

Refer/Investigate if:

  • Multiple or bilateral cysts
  • Complex cysts (solid or septated)
  • Symptoms: pain, haematuria, infection
  • Rapid growth or malignancy suspicion

🟠 Polycystic Kidney Disease (PKD)

Autosomal Dominant PKD (ADPKD)

  • Most common inherited kidney disorder
  • ~10% cases occur without family history
  • May cause progressive CKD

Ultrasound Diagnostic Criteria

AgeDiagnostic Criteria
15–39 yrs≥3 cysts total (unilateral/bilateral)
40–59 yrs≥2 cysts in each kidney
≥60 yrs≥4 cysts in each kidney

Management of ADPKD

  1. Refer early to nephrologist
  2. Assess family history & progression risk
  3. Manage HTN, cyst growth, eGFR decline
  4. Evaluate for complications (e.g., haematuria, infection)
  5. Consider genetic testing
  6. Consider MRA for cerebral aneurysm screening (if family history)
  7. Tolvaptan (PBS listed): for Stage 2–3 rapidly progressing ADPKD

🧊 Kidney Stones

Epidemiology

  • Lifetime risk: ~10% men, ~3% women
  • Most common: calcium oxalate/phosphate
  • Recurrence risk:
    • 5–10% per year
    • 30–50% within 5 years

Stone Prevention

  • Cannot dissolve existing stones
  • Goals: Correct urine chemistries and reduce risk
  • Refer to dietitian for:
    • 3–6-month dietary trial before medications
    • Encourage ≥2 L/day urine output
    • ↑ Potassium, phytates (nuts, legumes)
    • Maintain normal calcium intake
    • ↓ Oxalate (spinach, tea), animal protein, sucrose, Na⁺, supplements

Drug Options

  • Allopurinol: for hyperuricaemia
  • Citrate: for hypocitraturia

Stone Workup

  • Serum labs: calcium, uric acid, PTH
  • Stone analysis (if passed)
  • 24-hour urine collection: volume, calcium, oxalate, citrate, uric acid

Acute Stone Management

  • Most <5 mm stones can be passed
  • Use alpha-blockers: e.g., prazosin or tamsulosin
  • Urgent referral if:
    • Infection
    • Large stone
    • Obstructive symptoms
    • Single kidney

CKD Complications and Management

ComplicationSummaryManagement Strategies
Metabolic AcidosisCommon with eGFR <30; ↓ acid excretion and HCO₃⁻ production– Sodium bicarbonate 840 mg OD-BD → titrate to normalise HCO₃⁻
– Limit dose to avoid fluid overload
– Base-producing diet (fruit/vegetables)
AlbuminuriaStrong prognostic marker for CKD/CVD progression– ACEi or ARB to max tolerated dose
– Add SGLT2i
– In T2DM: consider finerenone and/or GLP-1 RA
AnaemiaBegins at eGFR <60 due to ↓ EPO, iron, and inflammation– Target Hb 100–115 g/L
– Correct iron (Ferritin >100 / >200 if on ESA; TSAT >20%)
– ESA only via nephrologist
DepressionAffects ~20% CKD; worsens QOL and adherence– Screen with DASS-21/K10
– SSRIs preferred
– Address modifiable factors (sleep, nutrition, dialysis)
– GP Mental Health Plan referral
HaematuriaMay be glomerular or non-glomerular (UTI, cancer, menstruation, stones)– Confirm with urine microscopy
– Refer to urology or nephrology as appropriate
– Annual monitoring if isolated in <40s

ComplicationSummaryManagement Strategies
HyperuricaemiaCommon with CKD/metabolic syndrome; may cause gout– Allopurinol 50–100 mg/day (↓ dose with ↓ eGFR)
– Avoid colchicine if eGFR <10; reduce dose if eGFR <50
– Low-dose prednisolone in flares
– No benefit for CKD alone without gout
HyperkalaemiaCommon with CKD + RAS inhibitors/MRA; risk of arrhythmia if K⁺ >6.5 mmol/LTarget K⁺: ≤6.0 mmol/L
Risks ↑ with RAS inhibitors, MRAs
If K⁺ 6.0–6.5:
Diet: low K⁺, avoid salt substitutes
Correct acidosis
Use potassium-wasting diuretics
Consider resins (e.g., SPS, patiromer)
If K⁺ >6.5:
Emergency referral due to arrhythmia risk
LipidsCKD shows ↑ triglycerides, ↓ HDL; LDL often normalCharacteristic pattern: ↑triglycerides, ↓HDL, normal LDL
Management:
Statin (+/- ezetimibe) if eGFR ≥15 and CVD risk ≥10%
For First Nations patients: threshold ≥5%
No target lipid level recommended
MalnutritionAnorexia in CKD contributes; linked to poor prognosisRelated to anorexia and inflammation
Management:
– Refer to dietitian
– Use screening tools for appetite, unintentional weight loss
Mineral-Bone Disorder (CKD-MBD)Begins when eGFR <60; ↓ vitamin D, ↓ calcium, ↑ phosphate, ↑ PTH– Nephrology referral for CKD stage 3–5
– Monitor calcium, phosphate, PTH
– Consider DEXA if result affects management
– Avoid calcium overload
– Use calcitriol if advanced CKD and hypocalcaemia
ComplicationSummaryManagement Strategies
OedemaCommon in advanced CKD due to fluid overload, sodium retention, or nephrotic syndromeAssess for:
– Nephrotic syndrome
– CHF
– Sodium excess
– Medications (e.g., CCBs)

Management:
Mild: elevate legs, reduce sodium, compression stockings

Moderate–severe: loop ± thiazide diuretics (adjust for eGFR)

Refractory: consider dialysis initiation
Pain (CKD-related)Pain is often multifactorial (neuropathic, nociceptive) and affects QOL– Step 1: Paracetamol 1g QID (safe)
– Step 2: Codeine or tramadol (avoid if eGFR <20)
– Step 3: Strong opioids with renal dosing (avoid morphine if eGFR <20)
– Neuropathic pain: gabapentin/pregabalin (adjust dose), TCAs (e.g., amitriptyline), duloxetine
– Refer to pain/palliative care team if refractory
PruritusAffects up to 70% with CKD stage 4–5; multifactorial originExclude secondary causes (e.g., skin, calcium/phosphate imbalance)

Non-drug: moisturisers, cool showers, avoid irritants

Pharmacologic:
= Gabapentin (if co-existing restless legs)
= Topical capsaicin
= UVB therapy (dermatology)
= Difelikefalin (kappa opioid agonist for dialysis patients)
ComplicationSummaryManagement Strategies
Muscle CrampsCommon in advanced CKD; may be due to electrolyte imbalances or volume depletion– Correct electrolyte abnormalities (e.g., calcium, magnesium, sodium)
– Ensure adequate hydration
– Limited evidence for magnesium supplementation effectiveness
Restless Legs Syndrome (RLS)Frequently co-occurs with uraemic pruritus; often under-recognised– First-line: Gabapentin or pregabalin (dose adjust in CKD)
– Optimise iron stores (TSAT >20%, ferritin >200 mcg/L)
– Ensure adequate dialysis in ESKD
– Rule out contributing factors (e.g., anaemia)
ConstipationCommon due to reduced mobility, medications (e.g., phosphate binders, opioids), low fluid/fibre intake– Increase dietary fibre if safe (assess for potassium/phosphate content)
– Osmotic or stimulant laxatives (avoid phosphate-based laxatives)
– Manage contributing medications (e.g., opioids)
Cognitive Impairment / DeliriumCommon in advanced CKD and dialysis; multifactorial– Optimise medication regimen to reduce polypharmacy
– Assess for contributing factors (electrolytes, uremia, medications)
– Consider formal cognitive assessment and geriatric referral where appropriate
Falls & FrailtyCommon due to sarcopenia, poor nutrition, polypharmacy, orthostatic hypotension– Screen regularly (e.g., TUG test)
– Adjust antihypertensives if symptomatic
– Address sarcopenia: physical therapy, protein intake
– Home medication review to address polypharmacy

Metabolic Acidosis in CKD

Pathophysiology
  • Occurs when eGFR <30 mL/min/1.73m²
  • Due to:
    • ↓ Renal acid excretion
    • ↓ Bicarbonate regeneration
  • Leads to:
    • Bone demineralisation
    • Increased protein catabolism
    • Associated ↑ morbidity
Treatment Target
  • Maintain serum HCO₃⁻ >22 mmol/L
Management
  • Sodium bicarbonate (SodiBic 840 mg):
    • Start: 1 capsule once or twice daily
    • May titrate to 2 capsules twice daily
    • Monitor and adjust based on bicarbonate level
  • Precautions:
    • Monitor fluid status – high doses risk fluid overload
    • Sodium load may worsen hypertension

Albuminuria in CKD

Prognostic Significance
  • Albuminuria correlates with:
    • CKD severity
    • Risk of progression to ESKD
    • Cardiovascular risk
Treatment Target
  • Aim for ≥50% reduction in urine ACR
Management
  • ACE inhibitor or ARB:
    • First-line to reduce albuminuria and slow CKD progression
  • Salt restriction:
    • ↓ Sodium intake enhances antiproteinuric effect of ACEi/ARB
  • Spironolactone (on specialist advice):
    • Can reduce albuminuria further
    • Monitor potassium regularly

Anaemia of CKD

📉 Pathophysiology
  • Common when eGFR <60 mL/min/1.73m²
  • Causes:
    • Erythropoietin production
    • Iron deficiency
    • ESA resistance
Targets
ParameterTarget Before ESATarget After ESA
HbTrial iron first if <100 g/LMaintain 100–115 g/L
Ferritin>100 µg/L200–500 µg/L
TSAT>20%20–30%
Management
  • IV iron trial before ESA if:
    • Ferritin <100 µg/L or TSAT <20%
  • Erythropoiesis-Stimulating Agents (ESAs):
    • Consider if Hb <100 g/L despite adequate iron
    • Avoid overtreatment (risk of thrombosis/stroke)

Hyperparathyroidism and Increased Fracture Risk in CKD:

🔍 Biochemical Targets

  • Phosphate (PO₄): Keep within 0.8–1.5 mmol/L
  • Calcium (Ca): Maintain within 2.2–2.6 mmol/L
  • Vitamin D (25-hydroxyvitamin D): Adequate if >50 nmol/L
  • PTH: Refer to nephrologist if persistently elevated and rising above lab reference range

📉 Pathophysiology in CKD

As kidney function declines:

  • Renal phosphate clearance → ↑ serum phosphate
  • Calcitriol synthesis (kidney-dependent) → ↓ calcium absorption
  • Calcium from reduced GI absorption (due to ↓ calcitriol)
  • Vitamin D → ↓ calcium absorption and bone mineralisation

Combined effects:

  • PTH secretion (secondary hyperparathyroidism)
  • Bone resorption → ↑ fracture risk
  • Cardiovascular mortality (likely via vascular calcification)

💊 Management Strategies

1. Vitamin D Replacement

  • Cholecalciferol (Vitamin D₃):
    • Converted to 25(OH)D in liver
    • Renal function needed to convert to calcitriol
    • Use for vitamin D deficiency even in advanced CKD
  • Calcitriol:
    • Used when eGFR is low
    • Directly suppresses PTH
    • Preferred in advanced CKD for secondary hyperparathyroidism

2. Phosphate Management

  • Dietary phosphate restriction
  • Phosphate binders:
    • Calcium-based (e.g., calcium carbonate)
    • Non-calcium binders (e.g., Sevelamer, Lanthanum) – preferred in dialysis patients or where calcium overload is a concern

3. Calcium Management

  • If PO₄ is controlled, calcium usually stays in range
  • If Ca low with normal PO₄, consider Vitamin D supplementation
  • Avoid calcium excess – risk of vascular calcification

Shared Decision Making (SDM)

Definition:

  • A collaborative process where clinicians and patients make informed health decisions together.
  • Involves:
    • Discussing available options, their benefits and harms
    • Exploring the patient’s values, preferences, and circumstances
    • Is an ongoing process, not a one-off conversation
    • Applicable to decisions about screening, investigations, and treatments

Benefits:

  • Acknowledges patient values
  • Enhances engagement and empowerment
  • Improves knowledge and understanding
  • Supports evidence-based care

Key Questions to Facilitate SDM:

  1. What will happen if we watch and wait?
  2. What are your test or treatment options?
  3. What are the benefits and harms of these options?
  4. How do the benefits and harms weigh up for you?
  5. Do you have enough information to make a choice?

Decision Support Tools:

  • Not mandatory, but increasingly used to aid SDM

📝 Advance Care Planning (ACP)

Definition:

  • Planning for end-of-life care and preferences, separate from dialysis decisions
  • Can occur while patients are still on active treatment

When to Initiate ACP:

  • All competent patients ≥65 years
  • Competent patients of any age who have:
    • Reduced life expectancy due to medical conditions
    • Poor functional status
    • Chronic malnutrition
    • Poor quality of life

🏥 Multidisciplinary Team (MDT) Care in CKD

Objectives of MDT Care:

  • Provide diagnosis-based therapy
  • Slow CKD progression
  • Manage co-morbidities (e.g. diabetes, HTN, lipids)
  • Prevent/manage cardiovascular disease
  • Manage CKD-specific complications:
    • Anaemia
    • Renal bone disease
    • Fluid/electrolyte/acid-base disorders
    • Malnutrition
  • Plan for renal replacement therapy (RRT)
    • Dialysis modality, access, transplant preparation
  • Offer conservative and palliative care

Whole-of-Practice Approach to CKD

  • Collaborative care involving GP, practice nurses, admin staff.
  • Appoint a clinical lead for CKD.
  • Importance of correct CKD coding, clinical governance, and e-health systems.
  • MBS item numbers can support care:
    • Chronic disease management plans (721, 723)
    • GP Management Plans
    • Team Care Arrangements
    • Health assessments
    • Nurse and allied health visits
Team MemberRoles
GP– Ongoing therapeutic relationship
– Care coordination
– Advocacy for patient goals
Nephrologist– Specialist renal care
– RRT planning and complication management
Endocrinologist/Diabetologist– Optimise glycaemic control in diabetic CKD
Vascular/Transplant Surgeon– Create dialysis access
– Perform transplant assessment and surgery
Practice Nurse / Nurse Practitioner– Manage CKD to ESKD
– Case management and continuity of care
Renal Nurse– Educate on dialysis
– Monitor patient condition and provide support
Dietitian– Conduct nutritional assessments
– Provide dietary advice
– Assist with dialysis timing
Pharmacist– Review medications (especially elderly)
– Adjust doses for low eGFR
– Prevent polypharmacy
– Conduct HMRs and RMMRs
Physiotherapist– Maintain mobility
– Prescribe tailored exercise
Mental Health Professionals– Support psychological wellbeing and adjustment
Community Health Professionals– Provide home care and social support services
Patient Educator– Deliver group and 1:1 education (diet, anaemia, access)
– Promote self-management skills
Family / Lay Carers– Provide emotional and practical support
Social Worker– Address financial/insurance/travel issues
– Assist in system navigation
Aboriginal Health Worker– Provide cultural support for Indigenous patients/families
– Collaborate with social workers

Culturally Safe CKD Care for First Nations Australians

  • Care should be culturally safe and community-inclusive.
  • Involve family, community, Aboriginal Health Workers/Practitioners, and interpreters.
  • Refer to:
    • CARI Guidelines on cultural safety
    • Clinical Yarning program (WA Centre for Rural Health)
    • HealthInfoNet and NACCHO



Renal Replacement Therapy (RRT) Options

🟩 1. Transplant

Types:

  • Living donor
  • Deceased donor (may wait 3–7 years)

Involves:

  • Major surgery
  • Lifetime immunosuppression
  • Requires a compatible donor

Lifestyle Impact / Outcomes:

  • Best option for quality of life
  • Freedom to work and travel once stable
  • Requires maintenance of a healthy diet, but few restrictions
  • Good survival rates
  • Increased risk of infection and malignancy due to immunosuppression

—————————————————–

🟨 2. Home Peritoneal Dialysis (PD)

a. Continuous Ambulatory Peritoneal Dialysis (CAPD)

Involves:

  • Manual exchange of four daytime bags

Lifestyle Impact / Outcomes:

  • Requires PD catheter
  • Simple, gentle, portable dialysis option
  • ~1 week training required
  • Freedom to work and travel
  • Good quality of life
  • Treatment longevity: 2–5 years

b. Automated Peritoneal Dialysis (APD)

Involves:

  • Machine-managed overnight exchanges

Lifestyle Impact / Outcomes:

  • Same as CAPD but:
    • No need to manually change bags during the day

—————————————————–

🟦 3. Home Haemodialysis

Types:

  • Daytime: 3–5 sessions/week, each 4–6 hrs
  • Night-time: 3–5 nights/week, each 8 hrs

Involves:

  • Blood cleaned via artificial filter
  • Requires surgical fistula (3+ months prior to use)
  • ~3 months training required

Lifestyle Impact / Outcomes:

  • Allows flexible routines
  • Night dialysis offers better health outcomes
  • More frequent/longer dialysis associated with:
    • Improved blood pressure
    • Better phosphate control
    • Improved energy levels

—————————————————–

🟥 4. Centre-Based Haemodialysis

Types:

  • Delivered in hospital or satellite dialysis centres
  • Typically 3 sessions per week, each lasting 4–6 hours
  • Some clinics offer overnight dialysis

Involves:

  • Similar process to home haemodialysis (blood filtered through an artificial filter)
  • Managed entirely by staff – no patient training required

Lifestyle Impact / Outcomes:

  • Requires transport to and from the centre
  • Imposes a strict routine and strict dietary restrictions
  • Higher infection risk due to frequent vascular access
  • Suitable for patients unable or unwilling to manage home therapies

—————————————————–

🟫 5. Non-Dialysis Supportive Care (Conservative Management)

Types:

  • No dialysis or transplant
  • Managed in community settings
  • Supported by palliative care teams

Involves:

  • Medication and dietary control
  • Advance care planning
  • Focus on symptom relief, quality of life, and holistic care

Lifestyle Impact / Outcomes:

  • Reduced life expectancy compared to dialysis or transplant in most people
  • May be equally appropriate for elderly or multimorbid patients
    • Especially when dialysis provides limited benefit or adds burden
  • Focus on comfort, dignity, and patient goals

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