After reading this note you will be able to define CKD, list the major local aetiologies, describe the typical presentation and examination findings, interpret the key investigations, stage disease severity and outline the immediate and definitive management plan (always verify doses and local protocols against the Kenya MoH guideline and your hospital formulary).
Definition
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, present for ≥3 months, with either:
- Glomerular filtration rate (GFR) < 60 mL/min/1.73 m², or
- Evidence of kidney damage (e.g., albuminuria ≥the protocol dose/g, haematuria, structural abnormalities on imaging) irrespective of GFR.
Anatomy and physiology you need
| Structure | Key Function | Relevance to CKD |
|---|---|---|
| Glomerulus | Filtration of plasma | Damage → proteinuria, ↓GFR |
| Proximal tubule | Reabsorption of Na⁺, glucose, amino acids | Tubular injury → loss of solutes, metabolic acidosis |
| Loop of Henle | Concentrating urine | Impaired concentrating ability → polyuria |
| Distal tubule & collecting duct | Acid‑base regulation, K⁺ handling | Dysfunction → metabolic acidosis, hyperkalaemia |
| Renal interstitium & vasculature | Support, oxygen delivery | Fibrosis → progressive loss of nephrons |
| Renal papillae | Urine drainage | Obstruction (e.g., stones) can accelerate CKD |
Causes and risk factors
| Category | Common local aetiologies | Key risk factors |
|---|---|---|
| Diabetes mellitus | Type 1 & 2 (urban rise) | Poor glycaemic control, obesity |
| Hypertension | Essential, renovascular | Uncontrolled BP, salt excess |
| Infectious | HIV‑associated nephropathy, TB (renal TB), malaria (acute kidney injury → CKD), schistosomiasis | Late presentation, co‑infection |
| Glomerulonephritis | Post‑streptococcal GN, lupus nephritis, IgA nephropathy | Recurrent infections, autoimmune disease |
| Hemoglobinopathies | Sickle cell disease (renal papillary necrosis) | Sickle cell trait, vaso‑occlusive crises |
| Tubulointerstitial | Chronic analgesic use, herbal nephrotoxins, lead exposure | Over‑the‑counter NSAIDs, traditional medicines |
| Obstructive | Prostatic hypertrophy, ureteric stones, congenital anomalies | Age, recurrent UTIs |
| Others | Rheumatic fever (cardiorenal), chronic heart failure, obesity‑related nephropathy | Low socioeconomic status, limited access to care |
Pathophysiology
- Initial insult (e.g., hyperglycaemia, hypertension, infection) →
- Glomerular / tubular injury →
- Proteinuria & loss of nephron mass →
- Activation of RAAS & sympathetic nervous system →
- Intraglomerular hypertension & fibrosis →
- Progressive decline in GFR →
- Accumulation of uremic toxins & complications
(Arrows indicate the causal flow from trigger to end‑stage renal disease.)
Clinical features
| History element | Why it matters |
|---|---|
| Gradual loss of appetite, nausea, early satiety | Uremic toxins accumulate as GFR falls, affecting gastrointestinal motility and taste. |
| Fatigue, reduced exercise tolerance | Anaemia of chronic kidney disease and reduced erythropoietin, plus uremic fatigue. |
| Swelling (edema) – ankles, periorbital, sacrum | Sodium‑water retention from impaired tubular handling and hypo‑albuminaemia when protein loss occurs. |
| Changes in urine output – oliguria, nocturia, frothy urine | Decreasing filtration, concentrating ability, and proteinuria from glomerular damage. |
| Hypertension or resistant hypertension | Sodium retention, activation of renin‑angiotensin‑aldosterone system (RAAS) and sympathetic over‑activity. |
| Bone pain, pruritus, restless legs | Secondary hyperparathyroidism, calcium‑phosphate imbalance and uremic neuropathy. |
| History of diabetes, hypertension, HIV, TB, malaria, sickle cell, rheumatic fever, herbal nephrotoxins | Identifies common local precipitants and guides aetiologic work‑up. |
| Medication review – NSAIDs, aminoglycosides, traditional medicines | Potential nephrotoxic exposures that may have accelerated decline. |
| Family history of renal disease | Inherited glomerulopathies (e.g., focal segmental glomerulosclerosis) are not uncommon. |
| Symptoms of volume overload – dyspnoea, orthopnoea, cough | Pulmonary oedema from fluid retention, a sign of advanced CKD. |
| Neurological symptoms – confusion, seizures | Uremic encephalopathy when GFR <15 ml/min/1.73 m². |
Examination findings and their pathophysiology
| Finding | Explanation |
|---|---|
| Elevated blood pressure, often with a narrow pulse pressure | Sodium retention and RAAS activation raise systemic vascular resistance; loss of arterial compliance in CKD narrows pulse pressure. |
| Peripheral edema, pitting | Reduced glomerular filtration → sodium and water retention; hypo‑albuminaemia from protein loss worsens oncotic deficit. |
| Jugular venous distension | Volume overload extending to central circulation; may indicate impending heart failure. |
| Auscultation: crackles at lung bases | Interstitial fluid from pulmonary congestion secondary to fluid overload. |
| Dry, pale skin; conjunctival pallor | Anaemia from decreased erythropoietin production. |
| Bone tenderness, calcific deposits in soft tissues | Secondary hyperparathyroidism leading to renal osteodystrophy and metastatic calcification. |
| Pruritus, especially on back of arms and thighs | Accumulation of phosphate and uremic toxins stimulates itch pathways. |
| Peripheral neuropathy – reduced vibration sense, tingling | Uremic neuropathy due to toxin buildup. |
| Abdominal bruit over renal arteries | Suggests renovascular disease, a reversible cause of CKD in some patients. |
| Signs of chronic liver disease (spider naevi, palmar erythema) | May coexist with hepatorenal syndrome in advanced disease. |
| Growth retardation or delayed puberty (in adolescents) | Chronic illness and hormonal disturbances from CKD. |
Differential diagnosis
| Condition | Points to it | How to separate from CKD |
|---|---|---|
| Acute kidney injury (AKI) | Sudden rise in creatinine, oliguria, recent nephrotoxin exposure | Rapid reversibility, urine sediment with granular casts, no chronic stigmata (e.g., bone disease) |
| Congestive heart failure | Dyspnoea, peripheral edema, elevated JVP | Normal renal size, cardiac imaging shows reduced ejection fraction, BNP elevated |
| Liver cirrhosis with ascites | Jaundice, spider naevi, portal hypertension | Low albumin, enlarged spleen, ultrasound shows nodular liver, renal function may be preserved |
| Nephrotic syndrome | Massive proteinuria (>3.5 g/day), oedema, hypo‑albuminaemia | Urine protein selective, serum cholesterol high, renal biopsy shows specific glomerular disease |
| Chronic obstructive pulmonary disease (COPD) with cor pulmonale | Chronic cough, wheeze, right‑sided heart signs | Spirometry confirms airflow obstruction, chest X‑ray shows hyperinflation |
| Sickle cell nephropathy | History of sickle cell disease, hematuria, papillary necrosis | Peripheral smear shows sickled cells, hemoglobin electrophoresis positive |
| Tubulointerstitial disease from TB or HIV | History of TB, low-grade fever, sterile pyuria | Imaging shows small kidneys, urine eosinophils absent, PCR for TB or HIV viral load positive |
Investigations
| Test | What it answers | Meaning of result |
|---|---|---|
| Serum creatinine & eGFR (CKD‑EPI) | Current filtration level | eGFR < 60 ml/min/1.73 m² for ≥3 months = CKD |
| Urine albumin‑to‑creatinine ratio (ACR) | Degree of proteinuria | ACR ≥ the protocol dose/g = albuminuria; >the protocol dose/g = overt proteinuria |
| Full blood count | Anaemia, infection | Hb < 12 g/dL suggests CKD‑related anaemia |
| Serum electrolytes, calcium, phosphate, bicarbonate | Metabolic derangements | Hyperkalaemia, hypocalcaemia, hyperphosphataemia, metabolic acidosis indicate advanced CKD |
| Lipid profile | Cardiovascular risk | Elevated LDL common in CKD |
| Renal ultrasound | Size, obstruction, cysts | Small, echogenic kidneys = chronic disease; hydronephrosis = obstructive cause |
| 24‑hour urine protein (or spot protein/creatinine) | Quantify protein loss | >1 g/day suggests glomerular disease |
| Serology: HIV, hepatitis B/C, ANA, anti‑dsDNA, complement levels | Identify systemic causes | Positive HIV = HIV‑associated nephropathy; low complement = lupus nephritis |
| Renal biopsy (when indicated) | Histologic diagnosis | Shows focal segmental glomerulosclerosis, membranous nephropathy, etc. |
| ECG & cardiac enzymes | Cardiovascular involvement | LVH, electrolyte‑related changes (e.g., peaked T waves) |
| Bone mineral studies (PTH, vitamin D) | Secondary hyperparathyroidism | Elevated PTH = renal osteodystrophy |
Diagnosis and severity
- Confirm chronicity – eGFR < 60 ml/min/1.73 m² persisting ≥3 months, or structural kidney damage (e.g., imaging, proteinuria).
- Stage CKD (KDIGO)
| Stage | eGFR (ml/min/1.73 m²) | Typical clinical picture |
|---|---|---|
| 1 | ≥90 + evidence of kidney damage | Normal filtration, proteinuria or imaging abnormality |
| 2 | 60–89 + evidence of kidney damage | Mild reduction, often asymptomatic |
| 3a | 45–59 | Early CKD‑related anaemia, mild electrolyte changes |
| 3b | 30–44 | More pronounced hypertension, metabolic acidosis may appear |
| 4 | 15–29 | Marked anaemia, hyperkalaemia, bone disease, preparation for renal replacement |
| 5 | <15 (or dialysis) | Uremic symptoms, severe electrolyte derangements, indication for dialysis or transplant |
- Assign a risk category – combine eGFR stage with albuminuria (A1 < the protocol dose/g, A2 30‑the protocol dose/g, A3 > the protocol dose/g). Higher albuminuria upgrades cardiovascular and renal risk.
- Document aetiology – based on history, serology, imaging, and biopsy when needed.
- Identify complications – anaemia, mineral‑bone disorder, electrolyte imbalance, cardiovascular disease, volume overload, infection risk.
The clinical approach proceeds from confirming chronicity, staging severity, pinpointing cause, and then instituting targeted management while monitoring for progression and complications.
Management
| Phase | Key actions | Rationale / safety notes |
|---|---|---|
| Immediate stabilisation | • Secure airway, breathing, circulation; give supplemental O₂ if SpO₂ < 94 % | CKD patients may have fluid overload and anaemia → risk of hypoxia |
| • Correct severe hyperkalaemia (calcium gluconate, insulin‑glucose, β‑agonist, dialysis if >6.5 mmol/L) | Avoid rapid shifts that precipitate arrhythmia; monitor ECG | |
| • Treat volume overload with loop diuretic (if urine output present) | Watch for hypotension, ototoxicity; stop if AKI suspected | |
| • Give IV bicarbonate only if severe metabolic acidosis (pH < 7.1) | Over‑correction can cause hypocalcaemia | |
| Definitive treatment | • Optimise blood pressure (ACE‑inhibitor or ARB, titrate to ≤130/80 mmHg) | Reduces proteinuria; monitor creatinine rise <30 % |
| • Control glycaemia (metformin avoided if eGFR < 30 mL/min/1.73 m²) | Prevents further nephron loss | |
| • Manage dyslipidaemia (statin) | Cardiovascular risk reduction | |
| • Treat anaemia (erythropoiesis‑stimulating agent, iron supplementation) | Target Hb 10–12 g/dL; avoid hypertension | |
| • Phosphate binders (calcium‑based or sevelamer) if serum phosphate >1.5 mmol/L | Prevent vascular calcification | |
| • Vitamin D analogues for secondary hyperparathyroidism | Monitor calcium and phosphate | |
| • Lifestyle: low‑salt diet, adequate hydration, smoking cessation, exercise | General renal protection | |
| Renal replacement | • Indications: refractory fluid overload, uncontrolled hyperkalaemia, severe acidosis, uremic symptoms, eGFR < 15 mL/min/1.73 m² | Choose peritoneal dialysis or haemodialysis based on resources and patient preference |
| Monitoring / follow‑up | • eGFR, serum creatinine, electrolytes, bicarbonate every 3 months (more often if unstable) | Detect rapid decline |
| • Urine albumin‑creatinine ratio every 6 months | Guide ACE‑I/ARB titration | |
| • Blood pressure at each visit | Goal ≤130/80 mmHg | |
| • Haemoglobin, iron studies every 3 months | Adjust ESA/iron | |
| • Calcium, phosphate, PTH every 6 months | Titrate binders and vitamin D | |
| Contra‑indications / safety | • ACE‑I/ARB in bilateral renal artery stenosis → stop if creatinine rises >30 % | • NSAIDs – avoid; they reduce renal perfusion |
| • Metformin in eGFR < 30 mL/min/1.73 m² – risk lactic acidosis | • Loop diuretics in hypovolaemia – precipitate AKI |
Complications and prognosis
- Cardiovascular disease – leading cause of death; accelerated atherosclerosis from hypertension, dyslipidaemia, uremia.
- Progression to end‑stage renal disease (ESRD) – median time varies; faster in HIV‑associated nephropathy, sickle‑cell nephropathy, uncontrolled diabetes.
- Anaemia – due to erythropoietin deficiency, iron loss; worsens cardiac workload.
- Mineral‑bone disorder – secondary hyperparathyroidism, renal osteodystrophy, vascular calcification.
- Electrolyte disturbances – hyperkalaemia, metabolic acidosis, hyponatraemia.
- Infections – impaired immunity, especially in HIV/TB co‑infection; peritoneal dialysis increases peritonitis risk.
- Malignancy – increased risk of renal cell carcinoma and urothelial cancer.
Prognosis hinges on eGFR trajectory, proteinuria level, control of BP and glycaemia, and presence of comorbid HIV, TB or sickle‑cell disease. Early nephrology referral improves survival.
High‑yield exam points
- Look‑alike conditions – Acute tubular necrosis vs. CKD with acute on chronic; differentiate by chronic stigmata (small kidneys on US, persistent proteinuria).
- Common wrong first step – Starting a diuretic without assessing volume status; may precipitate AKI.
- Bedside examiner questions
- “What does a shrunken kidney on ultrasound suggest?” → chronic irreversible loss of nephrons.
- “Why is an ACE‑inhibitor preferred in proteinuric CKD?” → reduces intraglomerular pressure and proteinuria.
- “How would you differentiate prerenal azotaemia from CKD on labs?” → BUN/creatinine ratio, urine sodium, FeNa.
Clinical case
Patient: 42‑year‑old male farmer, HIV‑positive (on ART), presents with progressive swelling of legs, fatigue, and reduced urine output over 6 months.
Key findings: BP 158/96 mmHg, bilateral pitting oedema to knees, serum creatinine 280 µmol/L, eGFR 22 mL/min/1.73 m², urine albumin‑creatinine ratio the protocol dose/g, ultrasound shows bilaterally small kidneys with increased echogenicity.
Questions
- What is the most appropriate next step in management?
Start an ACE‑inhibitor and arrange renal referral.
- Which complication is he at highest risk of developing in the next year?
Cardiovascular event (myocardial infarction or stroke) due to accelerated atherosclerosis.
- What bedside examination finding would support chronicity rather than acute kidney injury?
Presence of bilateral small kidneys on ultrasound and longstanding hypertension.
Practice questions
Question 1
A 55‑year‑old woman with diabetic CKD (eGFR 28 mL/min/1.73 m²) presents with sudden onset dyspnoea, SpO₂ 88 % on room air, and serum potassium 6.8 mmol/L. What is the most urgent intervention?
A. Start oral potassium binder
B. Give intravenous calcium gluconate
C. Initiate high‑flow nasal oxygen
D. Schedule urgent dialysis
Answer: B. Give intravenous calcium gluconate – stabilises cardiac membrane while definitive therapy is arranged.
Question 2
A 30‑year‑old man with sickle‑cell disease has eGFR 45 mL/min/1.73 m², proteinuria 1 g/day, and blood pressure 140/85 mmHg. Which medication class should be added first?
A. Loop diuretic
B. ACE‑inhibitor
C. β‑blocker
D. Calcium channel blocker
Answer: B. ACE‑inhibitor – reduces proteinuria and slows progression in sickle‑cell nephropathy.
Question 3
A patient on peritoneal dialysis develops cloudy dialysate, abdominal pain, and fever. Which is the best next step?
A. Increase dialysate dwell time
B. Start intraperitoneal antibiotics promptly
C. Switch to haemodialysis without antibiotics
D. Observe for 48 h
Answer: B. Start intraperitoneal antibiotics promptly – early treatment reduces morbidity of peritonitis.
Question 4
Which laboratory pattern most strongly suggests CKD rather than acute tubular necrosis?
A. BUN/creatinine ratio > 20:1, urine Na < 20 mmol/L
B. Fractional excretion of sodium > 2 %
C. Persistent low urine specific gravity, small kidneys on US
D. Rapid rise in creatinine over 24 h
Answer: C. Persistent low urine specific gravity, small kidneys on US – indicates chronic structural loss.
Question 5
A 68‑year‑old man with CKD stage 4 is started on a statin. Which statement is correct regarding monitoring?
A. Check liver enzymes weekly for the first month
B. No routine monitoring required unless symptomatic
C. Stop statin if CKD progresses to stage 5
D. Switch to fibrate if triglycerides rise above 200 mg/dL
Answer: B. No routine monitoring required unless symptomatic – statins are safe in CKD; liver tests only if clinical suspicion.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.