Medicine – Chronic Kidney Disease

Chronic kidney disease (CKD) is the modern term that has largely replaced chronic renal failure (CRF). CKD describes persistent abnormalities of kidney structure or function that are present for at least 3 months and have implications for health.

CKD can gradually lead to loss of functioning nephrons, reduced glomerular filtration rate (GFR), accumulation of metabolic waste products, disturbances of fluid and electrolyte balance, endocrine abnormalities, cardiovascular complications and eventually end-stage kidney disease (ESKD).

1. Definition of Chronic Kidney Disease

CKD is present when, for at least 3 months, there is either:

Reduced GFR

or

Evidence of kidney damage.

A commonly used GFR criterion is:

eGFR <60 mL/min/1.73 m² for at least 3 months.

However, a patient can have CKD despite an eGFR above 60 if there is persistent evidence of kidney damage, such as:

Albuminuria.

Abnormal urinary sediment.

Structural kidney abnormalities.

Histological abnormalities.

2. CKD versus Chronic Renal Failure

The older term:

Chronic renal failure – CRF

usually referred to relatively advanced loss of kidney function.

The preferred modern term is:

Chronic kidney disease – CKD.

CKD includes the entire spectrum from relatively mild chronic kidney damage to:

Kidney failure / ESKD.

3. Major Causes of CKD

The original notes give historical UK percentages for individual causes.

These percentages should not be memorised as fixed current values because the distribution changes over time and depends on whether statistics refer to:

All CKD

or

Patients reaching kidney replacement therapy.

The important causes include:

Diabetes mellitus.

Hypertension and vascular disease.

Glomerular disease.

Inherited kidney disease.

Reflux and congenital urinary tract disease.

Chronic obstruction.

Tubulointerstitial disease.

Plasma-cell disorders.

4. Diabetes Mellitus

Diabetes mellitus is one of the most important causes of CKD and kidney failure.

Persistent hyperglycaemia damages the glomerular filtration barrier and produces:

Diabetic kidney disease.

5. Diabetic Kidney Disease

The pathological changes include:

Glomerular basement membrane thickening.

Mesangial expansion.

Glomerular hyperfiltration and intraglomerular hypertension early in disease.

Progressive glomerulosclerosis.

A classic advanced lesion is:

Kimmelstiel–Wilson nodular glomerulosclerosis.

6. Clinical Progression of Diabetic Kidney Disease

Patients may develop:

Albuminuria.

Proteinuria.

Hypertension.

Progressive decline in GFR.

Eventually, some patients progress to:

ESKD.

However, CKD progression can also occur in diabetes without marked albuminuria.

7. Chronic Glomerulonephritis

Chronic glomerular diseases are another important cause of CKD.

Examples include:

IgA nephropathy.

FSGS.

Membranous nephropathy.

Lupus nephritis.

MPGN and C3 glomerulopathy.

Repeated or persistent glomerular injury eventually causes:

Glomerulosclerosis and nephron loss.

8. Hypertension and Vascular Kidney Disease

Long-standing hypertension can contribute to progressive kidney damage.

Chronic vascular injury causes:

Arteriolar narrowing.

Renal ischaemia.

Glomerulosclerosis.

Tubular atrophy.

Interstitial fibrosis.

This is traditionally described as:

Hypertensive nephrosclerosis.

9. The Kidney–Hypertension Cycle

CKD itself also causes hypertension through:

Sodium retention.

Water retention.

RAAS activation.

Therefore:

Hypertension damages the kidney → kidney disease worsens hypertension → hypertension accelerates CKD.

Breaking this cycle is an important goal of treatment.

10. Renovascular Disease

Atherosclerotic narrowing of the renal arteries may cause:

Renovascular hypertension

and

Ischaemic nephropathy.

Progressive bilateral disease, particularly in patients with widespread atherosclerosis, can contribute to CKD.

11. Reflux Nephropathy

Reflux nephropathy results from renal scarring associated with:

Vesicoureteric reflux, often combined with recurrent urinary infection.

It is particularly important when reflux begins during:

Childhood.

12. Consequences of Reflux Nephropathy

Progressive renal scarring may produce:

Proteinuria.

Hypertension.

Reduced renal function.

CKD.

Severe bilateral disease can eventually cause:

ESKD.

13. Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease – ADPKD is an important inherited cause of CKD.

Progressive development and enlargement of renal cysts causes:

Kidney enlargement.

Hypertension.

Haematuria.

Pain.

Recurrent infections.

Stones.

Progressive loss of renal function.

14. ADPKD and ESKD

Some patients with ADPKD eventually progress to:

ESKD

and require:

Dialysis

or

Kidney transplantation.

Important extrarenal associations include:

Hepatic cysts

and

Intracranial saccular aneurysms.

15. Chronic Urinary Tract Obstruction

Long-standing urinary obstruction can cause:

Hydronephrosis.

Tubular atrophy.

Interstitial fibrosis.

Progressive nephron loss.

This is sometimes called:

Post-obstructive nephropathy.

16. Causes of Chronic Obstruction

Possible causes include:

Benign prostatic enlargement.

Urinary tract malignancy.

Ureteric obstruction.

Stones.

Urethral stricture.

Neurogenic bladder.

Bilateral obstruction or obstruction affecting a solitary functioning kidney is particularly important.

17. Multiple Myeloma

Multiple myeloma can cause CKD through several mechanisms.

These include:

Light-chain cast nephropathy.

AL amyloidosis.

Monoclonal immunoglobulin deposition disease.

Hypercalcaemia.

Recurrent infection.

18. Myeloma Kidney

Excess monoclonal light chains can pass through the glomerulus and interact with proteins within the renal tubules.

This can produce:

Obstructing casts

and

Tubular injury.

This is called:

Light-chain cast nephropathy.

19. Amyloidosis

Amyloidosis can cause progressive renal disease through deposition of:

Amyloid fibrils within the kidney.

Renal amyloidosis often initially causes:

Heavy proteinuria

or

Nephrotic syndrome.

Progressive damage may eventually result in:

CKD and ESKD.

20. Chronic Tubulointerstitial Nephritis

Chronic tubulointerstitial nephritis primarily damages:

Renal tubules

and

Interstitial tissue.

Over time, this causes:

Tubular atrophy.

Interstitial fibrosis.

Progressive decline in renal function.

21. Causes of Chronic Tubulointerstitial Disease

Possible causes include:

Chronic drug exposure.

Lithium.

Chronic obstruction.

Reflux nephropathy.

Certain metabolic disorders.

Some autoimmune diseases.

22. Analgesic Nephropathy

Analgesic nephropathy is a form of chronic tubulointerstitial injury associated historically with prolonged consumption of certain analgesic combinations.

Classically it can produce:

Chronic interstitial nephritis

and

Renal papillary necrosis.

Its epidemiology has changed substantially following withdrawal or restriction of older analgesic preparations.

23. Renal Calculi

Recurrent or extensive:

Renal calculi

can contribute to CKD, particularly when associated with:

Recurrent obstruction.

Recurrent infection.

Staghorn calculi.

Bilateral disease.

An isolated uncomplicated kidney stone does not usually cause CKD.

24. CKD after Acute Kidney Injury

The original notes use:

“Post-ARF.”

The modern term is:

CKD following acute kidney injury – AKI.

Severe or repeated AKI can result in incomplete renal recovery and subsequent:

CKD.

25. AKI and CKD Are Closely Related

AKI increases the future risk of:

CKD.

At the same time, pre-existing CKD increases susceptibility to:

AKI.

Therefore:

AKI and CKD can form a mutually reinforcing cycle of kidney injury.

26. Clinical Features of CKD

Early CKD may be:

Completely asymptomatic.

As renal function declines, patients may develop:

Fatigue.

Anorexia.

Nausea.

Pruritus.

Oedema.

Breathlessness.

Nocturia.

Hypertension.

Muscle cramps.

Reduced exercise tolerance.

27. Advanced CKD and Uraemia

Advanced kidney failure can cause:

Uraemia.

Possible manifestations include:

Anorexia.

Nausea and vomiting.

Pruritus.

Cognitive disturbance.

Peripheral neuropathy.

Pericarditis.

Bleeding tendency due to platelet dysfunction.

Severe symptomatic uraemia may indicate a need for:

Kidney replacement therapy.

28. Major Complications of CKD

Important complications include:

Hypertension.

Fluid overload.

Hyperkalaemia.

Metabolic acidosis.

Anaemia.

CKD-mineral and bone disorder.

Cardiovascular disease.

Malnutrition in advanced disease.

29. Management of CKD

Management has several major goals:

Identify and treat the underlying cause.

Slow progression of kidney disease.

Reduce proteinuria or albuminuria.

Control cardiovascular risk.

Treat CKD complications.

Avoid further renal injury.

Prepare appropriately for kidney replacement therapy when necessary.

30. Blood Pressure Control

Blood-pressure control is one of the most important interventions for slowing CKD progression and reducing:

Cardiovascular risk.

The original notes give a universal target of:

<130/75 mmHg.

This is an older simplified target.

Modern blood-pressure targets are more:

Individualised

and depend on factors such as:

Albuminuria.

Diabetes.

Age.

Cardiovascular disease.

Treatment tolerance.

31. ACE Inhibitors

ACE inhibitors reduce systemic blood pressure and also dilate the:

Efferent arteriole.

This reduces:

Intraglomerular pressure.

As a result, ACE inhibitors can reduce:

Albuminuria and proteinuria.

32. ARBs

Angiotensin receptor blockers – ARBs provide similar kidney-protective effects.

Therefore:

ACE inhibitor OR ARB

is particularly important in many patients with:

Albuminuric CKD.

33. ACE Inhibitors and Creatinine

Starting an ACE inhibitor or ARB may produce a modest initial rise in:

Serum creatinine.

This occurs because efferent arteriolar dilation lowers intraglomerular pressure.

Renal function and:

Serum potassium

should therefore be monitored after initiation or dose adjustment.

34. ACE Inhibitors and Hyperkalaemia

ACE inhibitors and ARBs can increase:

Serum potassium.

This is particularly important in advanced CKD.

Therefore treatment requires monitoring of:

Potassium

and

Renal function.

35. Avoid Routine ACE Inhibitor plus ARB Combination

ACE inhibitors and ARBs should generally:

Not be routinely combined.

Dual blockade increases the risk of:

Hyperkalaemia.

Hypotension.

Acute kidney injury.

without sufficient additional benefit for most patients.

36. Other Antihypertensive Drugs

Additional drugs may be required to achieve adequate blood-pressure control.

These can include:

Calcium-channel blockers.

Diuretics.

Beta blockers in selected patients.

Other agents may be added according to the patient’s clinical circumstances.

37. Diuretics

Diuretics are particularly useful when CKD is accompanied by:

Fluid retention

and

Hypertension.

Loop diuretics such as:

Furosemide

are often useful in advanced CKD with volume overload.

38. Reduction of Proteinuria

Proteinuria is not merely a marker of renal disease.

Persistent albuminuria can also contribute to:

Progressive kidney injury.

Reducing albuminuria is therefore an important therapeutic goal.

39. RAAS Blockade and Proteinuria

ACE inhibitors and ARBs reduce:

Intraglomerular pressure

and therefore:

Urinary albumin excretion.

This provides renal protection in many forms of:

Albuminuric CKD.

40. SGLT2 Inhibitors

An important modern addition to the original notes is:

Sodium-glucose cotransporter-2 – SGLT2 – inhibitors.

These drugs have become major kidney-protective therapies for many suitable patients with CKD.

Examples include:

Dapagliflozin.

Empagliflozin.

41. SGLT2 Inhibitors and Kidney Protection

SGLT2 inhibitors can:

Slow CKD progression.

Reduce albuminuria.

Reduce heart-failure events.

Reduce cardiovascular risk in appropriate patients.

Importantly, their kidney-protective benefits extend beyond glucose lowering and can apply to selected patients:

With or without diabetes.

42. Finerenone

In selected patients with:

Type 2 diabetes + CKD + persistent albuminuria,

another modern kidney-protective treatment is:

Finerenone.

Finerenone is a:

Non-steroidal mineralocorticoid receptor antagonist.

Potassium must be monitored because:

Hyperkalaemia can occur.

43. Treatment of Anaemia

Anaemia becomes increasingly common as CKD progresses.

The major mechanism is:

Relative erythropoietin deficiency.

However, iron deficiency and inflammation frequently contribute.

44. Investigation of Anaemia

Assessment should include:

Haemoglobin.

MCV.

Ferritin.

Transferrin saturation – TSAT.

Other causes such as:

B12 deficiency, folate deficiency and blood loss

should be investigated when appropriate.

45. Iron Treatment

Iron deficiency may be treated with:

Oral iron

or

Intravenous iron.

IV iron is particularly commonly used in:

Haemodialysis patients.

The original instruction to use IV iron routinely is therefore too broad.

46. Erythropoiesis-Stimulating Agents

Persistent significant CKD-related anaemia may be treated with:

Erythropoiesis-stimulating agents – ESAs.

Examples include:

Epoetin

and

Darbepoetin.

These replace the inadequate erythropoietic stimulus caused by CKD.

47. Haemoglobin Target

The original note states:

“Maintain Hb >10 g/dL.”

Modern ESA treatment does not simply aim to normalise haemoglobin.

The treatment target is:

Individualised.

Excessively raising haemoglobin with ESA therapy can increase:

Hypertension.

Thrombosis.

Cardiovascular complications.

48. Dietary Management

Dietary treatment should be:

Individualised according to the patient’s CKD stage and biochemical abnormalities.

It is incorrect to assume that every patient with CKD requires universal restriction of:

Potassium

or other nutrients.

49. Salt Intake

Reducing excessive dietary:

Sodium

can help control:

Blood pressure.

Oedema.

Fluid overload.

It can also improve the effectiveness of antihypertensive treatment.

50. Potassium Intake

The original notes recommend:

Low potassium intake.

This should not be applied automatically to every patient with CKD.

Potassium restriction is mainly required when there is:

Hyperkalaemia

or a significant risk of developing it.

Unnecessary restriction may reduce dietary quality.

51. Protein Intake

Excessive protein intake may increase:

Nitrogenous waste production

and

Intraglomerular pressure.

However, severe protein restriction can cause:

Malnutrition.

Therefore dietary protein intake should be appropriate rather than excessively restricted.

52. Calorie Intake

Adequate energy intake is important, particularly in advanced CKD.

Insufficient calorie intake can contribute to:

Protein-energy wasting.

This is associated with poorer outcomes.

53. CKD-Mineral and Bone Disorder

Reduced kidney function disturbs:

Phosphate excretion.

Vitamin D activation.

Calcium balance.

PTH regulation.

This produces:

CKD-mineral and bone disorder – CKD-MBD.

54. Hyperphosphataemia

As GFR declines, phosphate excretion becomes impaired.

Advanced CKD may therefore produce:

Hyperphosphataemia.

Management may include:

Dietary phosphate management

and

Phosphate binders.

55. Phosphate Binders

Examples include calcium-containing agents such as:

Calcium acetate

and non-calcium agents such as:

Sevelamer.

The choice depends on:

Calcium concentration.

Phosphate concentration.

PTH.

Overall calcification risk.

56. Vitamin D and Alfacalcidol

The kidney normally activates vitamin D to:

Calcitriol – 1,25-dihydroxyvitamin D.

Advanced CKD impairs this process.

Selected patients with secondary hyperparathyroidism may therefore receive:

Active vitamin D or analogues such as alfacalcidol.

These treatments require monitoring because they can increase:

Calcium and phosphate.

57. Secondary Hyperparathyroidism

CKD causes:

Phosphate retention + reduced calcitriol + altered calcium regulation → increased PTH.

This produces:

Secondary hyperparathyroidism.

Persistent severe disease contributes to:

Renal osteodystrophy.

58. Calcimimetics

Selected dialysis patients with secondary hyperparathyroidism may receive:

Calcimimetics

such as:

Cinacalcet.

These increase sensitivity of the parathyroid calcium-sensing receptor and reduce:

PTH secretion.

59. Diabetes Control

In patients with diabetes, appropriate glycaemic management helps reduce:

Microvascular complications

and contributes to slowing diabetic kidney disease.

However, glycaemic targets should be:

Individualised.

60. Diabetes Medication in CKD

Renal function affects the choice and dosing of:

Glucose-lowering medications.

Some drugs require dose adjustment or avoidance as eGFR declines.

SGLT2 inhibitors have a particularly important role because they provide:

Renal and cardiovascular protection

in suitable patients.

61. Lipid Management

Patients with CKD have high:

Cardiovascular risk.

Therefore lipid management is important.

Many appropriate CKD patients are treated with:

Statin therapy

according to their age, CKD stage and cardiovascular risk.

62. Cardiovascular Risk

Cardiovascular disease is one of the major causes of morbidity and mortality in CKD.

Management therefore includes attention to:

Blood pressure.

Lipids.

Diabetes.

Smoking.

Exercise and physical activity where appropriate.

Weight and overall cardiovascular health.

63. Volume Status Monitoring

The kidneys regulate:

Sodium and water balance.

As kidney function deteriorates, patients may develop:

Fluid retention.

Clinical assessment includes:

Body weight.

Peripheral oedema.

Blood pressure.

Breathlessness.

Signs of pulmonary congestion.

64. Fluid Overload

Fluid overload may cause:

Peripheral oedema.

Pulmonary oedema.

Hypertension.

Heart failure.

Management may involve:

Salt restriction.

Diuretics.

Fluid management.

Dialysis in severe advanced kidney failure.

65. Hyperkalaemia

CKD reduces the ability to excrete:

Potassium.

Severe hyperkalaemia can cause:

Life-threatening cardiac arrhythmias.

Therefore potassium should be monitored, particularly in advanced CKD and patients receiving:

ACE inhibitors.

ARBs.

Mineralocorticoid receptor antagonists.

66. Metabolic Acidosis

Reduced renal acid excretion can produce:

Metabolic acidosis.

Chronic metabolic acidosis may contribute to:

Muscle wasting.

Bone disease.

CKD progression.

Selected patients may require:

Oral bicarbonate therapy.

67. Avoid Nephrotoxic Drugs

An important principle is:

Avoid unnecessary nephrotoxins.

Particularly important drugs include:

NSAIDs.

NSAIDs reduce renal prostaglandin synthesis and may precipitate:

AKI

especially in susceptible CKD patients.

68. Medication Dose Adjustment

Many medications are eliminated by the kidneys.

As GFR declines, some drugs require:

Dose reduction

or

Longer dosing intervals.

Failure to adjust doses can cause:

Drug accumulation and toxicity.

69. Contrast and Other Renal Insults

Potential renal insults should be considered carefully, particularly in patients with advanced CKD.

The key principle is to:

Minimise avoidable additional kidney injury

while still performing clinically necessary investigations and treatments.

70. Smoking

Smoking accelerates:

Cardiovascular disease

and may contribute to:

CKD progression.

Smoking cessation is therefore an important component of CKD management.

71. Vaccination and Infection Prevention

Advanced CKD and dialysis can increase susceptibility to infection.

Appropriate vaccination may include protection against:

Influenza.

Pneumococcal disease.

Hepatitis B, particularly when dialysis is anticipated or used.

Recommendations depend on local guidelines and individual circumstances.

72. Monitoring CKD Progression

Patients with CKD require periodic monitoring of:

Serum creatinine.

eGFR.

Urine ACR.

Blood pressure.

Potassium.

Bicarbonate.

Depending on disease severity, monitoring may also include:

Haemoglobin.

Calcium.

Phosphate.

PTH.

73. Albuminuria Categories

Modern CKD classification does not depend only on GFR.

Albuminuria is also important.

It is commonly divided into:

A1 – normal to mildly increased albuminuria.

A2 – moderately increased albuminuria.

A3 – severely increased albuminuria.

Higher albuminuria generally predicts:

Greater renal and cardiovascular risk.

74. GFR Categories

CKD can also be staged according to GFR:

G1 – normal or high GFR with evidence of kidney disease.

G2 – mildly reduced.

G3a – mild-to-moderately reduced.

G3b – moderately-to-severely reduced.

G4 – severely reduced.

G5 – kidney failure.

75. Why Both GFR and Albuminuria Matter

Two patients with the same eGFR may have very different risks depending on their:

Albuminuria.

Therefore modern CKD assessment combines:

Cause + GFR category + albuminuria category.

This is often called:

CGA classification.

76. Kidney Replacement Therapy

Advanced CKD may eventually require:

Kidney replacement therapy.

The principal options are:

Haemodialysis.

Peritoneal dialysis.

Kidney transplantation.

77. Preparing for Kidney Replacement Therapy

Preparation should begin before an emergency develops.

Depending on the patient, this may include:

Education about treatment options.

Transplant assessment.

Creation of dialysis access.

Planning for peritoneal dialysis.

Conservative kidney management when appropriate.

78. Conservative Kidney Management

Not every patient with advanced CKD chooses or benefits from dialysis.

For selected patients, particularly those with substantial comorbidity or personal preference against dialysis, treatment may focus on:

Symptom control.

Fluid management.

Anaemia management.

Quality of life.

Supportive and palliative care where appropriate.

79. Causes of CKD – Note Form

Diabetes mellitus:

Diabetic kidney disease.

Albuminuria and progressive GFR decline.

Kimmelstiel–Wilson nodules classically.

Chronic glomerular disease:

IgA nephropathy.

FSGS.

Lupus nephritis.

Other chronic glomerulopathies.

Hypertension and vascular disease:

Nephrosclerosis.

Renal ischaemia.

Progressive nephron loss.

Reflux nephropathy:

Childhood vesicoureteric reflux.

Renal scarring.

Hypertension and CKD.

ADPKD:

Inherited cystic kidney disease.

Hypertension.

Progressive CKD.

Chronic obstruction:

Prostatic disease.

Tumours.

Stones.

Neurogenic bladder.

Multiple myeloma:

Light-chain cast nephropathy.

AL amyloidosis.

Monoclonal deposition disease.

Amyloidosis:

Heavy proteinuria.

Nephrotic syndrome.

Progressive CKD.

Chronic tubulointerstitial nephritis:

Tubular atrophy.

Interstitial fibrosis.

Progressive CKD.

Previous severe or recurrent AKI:

Incomplete recovery.

Subsequent CKD.

80. Management of CKD – Note Form

Control blood pressure:

ACE inhibitor or ARB particularly in albuminuric CKD.

Additional antihypertensives as necessary.

Reduce albuminuria:

ACE inhibitor OR ARB.

SGLT2 inhibitor in suitable patients.

Finerenone in selected patients with type 2 diabetes and albuminuric CKD.

Treat anaemia:

Assess ferritin and TSAT.

Replace iron when indicated.

ESA therapy when appropriate.

Manage CKD-MBD:

Control phosphate.

Treat vitamin D abnormalities appropriately.

Control secondary hyperparathyroidism.

Diet:

Avoid excessive sodium.

Restrict potassium only when clinically indicated.

Maintain adequate nutrition and energy intake.

Diabetes:

Individualised glycaemic control.

Use kidney-protective therapy where appropriate.

Cardiovascular risk:

Blood-pressure control.

Lipid management.

Smoking cessation.

Fluid status:

Monitor weight and oedema.

Use diuretics when appropriate.

Prevent further renal injury:

Avoid unnecessary NSAIDs and other nephrotoxins.

Adjust renally cleared medications.

Prevent and promptly treat AKI.

Advanced disease:

Plan transplantation, haemodialysis, peritoneal dialysis or conservative kidney management as appropriate.

81. Important Corrections to the Original Notes

The term:

“Chronic renal failure – CRF”

should generally be replaced by:

CHRONIC KIDNEY DISEASE – CKD.

The percentages given for causes of CRF in the UK are:

Historical figures.

They should not be treated as fixed modern epidemiological percentages.

The universal blood-pressure target:

“<130/75 mmHg”

is outdated as a single target for every patient.

Modern treatment is:

Individualised according to albuminuria, cardiovascular risk, age and tolerance.

The original management focuses on:

ACE inhibitors.

An important modern addition is:

SGLT2 INHIBITORS

which now play a major kidney-protective role in many suitable CKD patients.

The statement:

“Low potassium diet”

should be changed to:

POTASSIUM RESTRICTION WHEN HYPERKALAEMIA OR A SIGNIFICANT RISK OF HYPERKALAEMIA IS PRESENT.

It is not necessary for every CKD patient.

The statement:

“Maintain Hb >10 g/dL”

is an older simplified ESA target.

Modern anaemia management is:

Individualised and does not aim to normalise haemoglobin completely.

The term:

“Post-ARF”

should be replaced by:

CKD FOLLOWING ACUTE KIDNEY INJURY – AKI.

82. CKD Progression – High-Yield Sequence

A useful overall sequence is:

UNDERLYING RENAL DISEASE

↓

NEPHRON LOSS

↓

COMPENSATORY HYPERFILTRATION OF REMAINING NEPHRONS

↓

INTRAGLOMERULAR HYPERTENSION

↓

PROTEINURIA + FURTHER GLOMERULAR DAMAGE

↓

GLOMERULOSCLEROSIS + INTERSTITIAL FIBROSIS

↓

PROGRESSIVE FALL IN GFR

↓

ADVANCED CKD / ESKD

This explains why reducing:

Blood pressure

and

Intraglomerular pressure

can slow progression.

Key Clinical Pattern

Think of CKD as:

KIDNEY ABNORMALITY FOR ≥3 MONTHS.

The major causes to remember are:

DIABETES + HYPERTENSION/VASCULAR DISEASE + GLOMERULAR DISEASE + INHERITED/STRUCTURAL DISEASE + OBSTRUCTION + TUBULOINTERSTITIAL DISEASE.

The major complications are:

FLUID OVERLOAD + HYPERKALAEMIA + METABOLIC ACIDOSIS + ANAEMIA + CKD-MBD + CARDIOVASCULAR DISEASE.

The major management principles are:

CONTROL BP → REDUCE ALBUMINURIA → ACEi/ARB WHEN INDICATED → SGLT2 INHIBITOR WHEN APPROPRIATE → CONTROL DIABETES → TREAT ANAEMIA → MANAGE CKD-MBD → CONTROL FLUID/ELECTROLYTES → AVOID NEPHROTOXINS → REDUCE CARDIOVASCULAR RISK.

And in advanced disease:

PLAN EARLY FOR TRANSPLANTATION, DIALYSIS OR CONSERVATIVE KIDNEY MANAGEMENT.