Chronic Kidney Disease Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: CKD is an epidemic, primarily driven by Type 2 Diabetes. The Malaysian Renal Registry shows over 50,000 patients on dialysis, with diabetes being the cause in over 60% of new cases. As a House Officer, you will manage its acute complications (fluid overload, hyperkalemia, uremia) and play a key role in slowing its progression on the wards.
High-Yield Definition: (KDIGO) CKD is defined as abnormalities of kidney structure or function, present for >3 months, with implications for health. This requires one of the following:
eGFR <60 mL/min/1.73m²
Markers of kidney damage (e.g., albuminuria [ACR >30 mg/g], hematuria, structural abnormalities on imaging).
Clinical One-Liner: "CKD is irreversible, progressive kidney damage, usually from DM or HTN, that you must spot early to prevent dialysis and manage complications like fluid overload, high potassium, and anemia."
II. Etiology & Risk Factors
Etiology (Malaysian Context):
Diabetic Kidney Disease (DKD): The #1 cause.
Hypertension (Hypertensive Nephrosclerosis): The #2 cause.
Glomerulonephritis: (e.g., IgA nephropathy, lupus nephritis).
Obstructive Uropathy: (e.g., BPH, staghorn calculi).
Polycystic Kidney Disease (ADPKD).
Risk Factors:
Diabetes Mellitus
Hypertension
Cardiovascular disease
Obesity
Smoking
Family history of CKD
Prolonged use of nephrotoxins (NSAIDs, certain traditional/herbal remedies).
III. Quick Pathophysiology
The initial insult (e.g., hyperglycemia) damages the glomeruli. This leads to a compensatory hyperfiltration in the remaining healthy nephrons. This increased pressure is unsustainable and causes glomerulosclerosis and interstitial fibrosis. This common final pathway, regardless of cause, leads to a progressive, irreversible loss of nephron mass and GFR.
IV. Classification
We use the KDIGO Classification, which is based on CGA:
Cause
GFR Category (G1-G5)
G1: >90 mL/min/1.73m² (Normal or high GFR)
G2: 60–89 (Mildly decreased GFR)
G3a: 45–59 (Mildly to moderately decreased)
G3b: 30–44 (Moderately to severely decreased)
G4: 15–29 (Severely decreased)
G5: <15 (Kidney Failure or on dialysis)
Albuminuria Category (A1-A3)
A1: <30 mg/g (Normal to mildly increased)
A2: 30–300 (Moderately increased / Microalbuminuria)
A3: >300 (Severely increased / Macroalbuminuria)
These are combined into a 'heat map' to stratify the risk of progression, ESKD, and mortality.
V. Clinical Assessment
🚩 Red Flags & Immediate Actions:
Severe Hyperkalemia (K+ >6.5 or ECG changes): Risk of cardiac arrest.
Action: IV Calcium Gluconate 10mL 10% STAT (cardioprotection), then IV Insulin/Dextrose (10 units short-acting insulin in 50mL D50%), inform senior for urgent dialysis.
Acute Pulmonary Edema (APO): Pink frothy sputum, SpO2 <92%, bilateral crepitations.
Action: Sit patient up, high-flow O2, IV Frusemide 40-80mg STAT, nitrates (if BP allows), urgent nephrology consult.
Uremic Encephalopathy: Confusion, drowsiness, GCS drop, asterixis.
Action: Stat nephrology consult for urgent dialysis.
Uremic Pericarditis: Pleuritic chest pain, pericardial rub.
Action: Stat ECG (risk of tamponade), echo, urgent nephrology consult for dialysis.
History:
Key Diagnostic Clues: Often asymptomatic until GFR <30. This is the main pitfall.
Common (>50% in late stages): Fatigue, lethargy (anemia), pruritus, peripheral edema, nocturia (early sign of lost concentrating ability).
Less Common (10-50%): Reduced appetite, nausea, metallic taste, shortness of breath (fluid overload).
Rare (<10%): Uremic flap (asterixis), seizures (severe uremia), easy bruising.
Pertinent Negatives: Absence of acute fever, rigors, or loin pain (points away from AKI/pyelonephritis).
Physical Examination (OSCE Approach):
General Inspection: Sallow (yellowish) complexion, cachectic, pallor (anemia), excoriation marks (pruritus). Look for AV fistula, Tenckhoff catheter.
Vitals: Hypertension (volume overload & RAAS), tachypnea (if fluid overloaded or acidotic).
Disease-Specific Examination:
Fluid Status: Raised JVP, 3+ pedal/sacral edema, fine basal crepitations (APO).
Uremic Signs: Uremic fetor (ammonia smell), asterixis (flap), Kussmaul's breathing (metabolic acidosis), pericardial rub.
Etiology Clues: 'Glove & stocking' neuropathy (DM), ballotable kidneys (PCKD), femoral bruits (atherosclerosis).
Pertinent Negatives: No costovertebral angle tenderness (no acute pyelonephritis). No palpable, distended bladder (no acute outflow obstruction).
Differentiating Disease Stage:
Early (G1-G3a): Usually asymptomatic. May have HTN or A2 albuminuria.
Moderate (G3b-G4): Pallor, worsening HTN, mild edema, fatigue.
Late (G5): Overt uremic features (nausea, confusion, flap), significant fluid overload, cachexia.
Clinical Pearl: "Don't trust the urine output; non-oliguric renal failure is common. Your best bedside markers are the JVP, lung bases, and mental state. And always check for an AVF scar before taking a BP or setting a line on that arm."
VI. Diagnostic Workflow
Differential Diagnosis:
Acute Kidney Injury (AKI):
Points For: Acute rise in creatinine.
Points Against: History >3 months, known DM/HTN, small kidneys on USS.
Differentiate: Serial creatinine (AKI = rapid change; CKD = stable/slow rise), renal ultrasound (CKD = small, echogenic kidneys; AKI = usually normal size).
Nephrotic Syndrome:
Points For: Heavy proteinuria (A3), significant edema, hypoalbuminemia.
Points Against: Lack of other uremic features, normal GFR (initially).
Differentiate: 24-hr urine protein, serum albumin, lipid profile.
Cardiorenal Syndrome:
Points For: Overt signs of severe heart failure (orthopnea, PND, S3 gallop).
Points Against: Lack of primary renal disease features.
Differentiate: Echocardiogram, BNP. (Note: significant overlap exists).
Investigations Plan:
Bedside / Initial (First 15 Mins):
UFEME (Proteinuria, hematuria, casts).
ECG (Check for hyperkalemic changes, LVH).
USS KUB (Kidney size, echotexture, hydronephrosis).
First-Line Labs & Imaging:
Renal Profile (RP): Creatinine, Urea, eGFR. Must be serial to establish chronicity.
Urine Albumin:Creatinine Ratio (ACR): Essential for staging.
FBC: Normocytic, normochromic anemia (anemia of chronic disease).
Serum Electrolytes: K+, Ca2+, PO4- (CKD-MBD).
Serum Albumin.
Confirmatory / Gold Standard:
The diagnosis is clinical, based on eGFR <60 or markers of damage (e.g., albuminuria) persisting for >3 months.
Renal biopsy is not for routine CKD diagnosis. It's reserved for when a specific, reversible glomerulonephritis is suspected (e.g., rapid GFR decline, active urinary sediment).
VII. Staging & Severity Assessment
We use the KDIGO CGA classification. The GFR (G1-G5) and Albuminuria (A1-A3) stages are combined into the 'heat map' (see Section IV). This stratifies the patient's risk for CKD progression, ESKD, and all-cause mortality. A patient with G3a but A3 (macroalbuminuria) is at much higher risk than a G3a A1 patient. This guides follow-up frequency and management intensity.
VIII. Management Plan
A. Principle of Management:
Treat the underlying cause (if possible).
Slow the rate of GFR decline.
Manage complications.
Prepare for Renal Replacement Therapy (RRT).
B. Immediate Stabilisation (The ABCDE Plan):
Not relevant for stable chronic outpatient CKD. This is for acute complications. Refer to Section V Red Flags.
C. Definitive Treatment (The Ward Round Plan):
1. Slow Progression (The "Big 3"):
BP Control: Target <130/80 mmHg (Malaysian CPG).
RAAS Blockade: First-line if albuminuria (A2/A3) is present.
ACE-inhibitors (e.g., Perindopril 2-8mg OD) or ARBs (e.g., Losartan 50-100mg OD).
Action: Must check RP and K+ 1-2 weeks after initiation or dose titration.
SGLT2 Inhibitors: Now standard of care in DKD and many non-diabetic CKDs.
(e.g., Dapagliflozin 10mg OD, Empagliflozin 10mg OD).
Action: Proven to slow GFR decline and reduce cardiovascular events.
2. Manage Complications:
Anemia (Renal): Target Hb 10–11.5 g/dL.
Action: Correct iron deficiency first (PO or IV Iron). If Hb still low, start Erythropoietin Stimulating Agents (ESA) (e.g., Epoetin alfa, Darbepoetin).
CKD-Mineral Bone Disorder (MBD): Monitor Ca, PO4, PTH.
Action: Low phosphate diet. Phosphate binders (e.g., Calcium Carbonate) with meals. Active Vitamin D (Calcitriol) if PTH remains high.
Fluid Overload:
Action: Salt restriction (<2g/day), Loop diuretics (e.g., Frusemide 40-120mg PO BD).
Metabolic Acidosis:
Action: PO Sodium Bicarbonate if serum HCO3 <22 mmol/L.
D. Long-Term & Discharge Plan:
Referral to Nephrology: Refer all G4-G5, rapidly progressive CKD, or G3 with persistent albuminuria (as per CPG).
RRT Preparation: Patient education on hemodialysis (HD), peritoneal dialysis (PD), and transplant. This should start in G4.
AV Fistula: Creation of an arteriovenous fistula (AVF) should be planned ideally 6-12 months before anticipated dialysis.
"Sick Day Rules": Crucial. Advise patient to temporarily stop ACEi/ARBs, diuretics, metformin, and NSAIDs during acute illness (fever, diarrhea, vomiting) to prevent AKI-on-CKD.
Medication Review: Avoid nephrotoxins. Dose-adjust medications (e.g., Metformin, Gabapentin, certain antibiotics).
IX. Complications
Immediate (Acute-on-Chronic):
Hyperkalemia, Acute Pulmonary Edema (from non-compliance/illness).
Action: As per ABCDE plan.
Long-Term:
End-Stage Kidney Disease (ESKD): Requiring RRT.
Action: Timely referral for RRT planning and access creation.
Cardiovascular Disease (CVD): The #1 cause of death in CKD patients (MI, CVA, PVD).
Action: Aggressive BP, lipid (statins), and glycemic control.
Renal Anemia:
Action: Monitor FBC, iron studies; provide ESA/iron.
CKD-MBD (Mineral Bone Disorder):
Action: Monitor bone profile, PTH; provide binders/Vit D.
Malnutrition:
Action: Dietitian referral, monitor albumin.
X. Prognosis
Prognosis is guarded and directly tied to GFR, level of albuminuria, and underlying cause. Malaysian Renal Registry data shows diabetic patients starting dialysis have a 5-year survival rate of only ~40-50%. Cardiovascular events are the leading cause of death, not renal failure itself. Early detection and aggressive management of BP, glucose, and albuminuria are the only ways to improve this.
XI. How to Present to Your Senior
S: "Sir/Madam, I'm reviewing Mr. Tan, a 60-year-old man, known case of CKD Stage 4 secondary to Diabetic Kidney Disease."
B: "He is G4A3 with a baseline creatinine of ~280. He was admitted for cellulitis, which is resolving with IV Cloxacillin. His DM and HTN are sub-optimally controlled."
A: "His main issue now is fluid overload. He is 3L positive on the chart, JVP is up 4cm, and he has 2+ pedal edema with basal crepitations. BP is 160/90. Morning RP is stable, K+ is 4.8. His Hb is 9.5, consistent with renal anemia."
R: "My plan is to give IV Frusemide 40mg BD, tighten his fluid chart, and continue BP and glucose monitoring. I would also like to restart his oral Perindopril (which was held on admission) and refer to the dietitian for fluid/salt restriction. Is this agreeable?"
XII. Summary & Further Reading
Top 3 Takeaways:
CKD is defined by GFR <60 or kidney damage (e.g., albuminuria) for >3 months.
Staging is CGA (Cause, GFR, Albuminuria). This 'heat map' determines risk.
Management priorities: Slow progression (BP control, RAASi, SGLT2i) and manage complications (anemia, MBD, fluid). CVD is the #1 killer.
Bonus: Always teach "Sick Day Rules."
Key Resources:
Malaysian CPG: Management of Chronic Kidney Disease (2nd Edition, 2018).
UpToDate: "Overview of the management of chronic kidney disease in adults"
KDIGO Guidelines: (2024 Guideline for Evaluation & Management of CKD is now available, updating the 2012 version).
