Chronic renal failure Short note from Harrison 22 edition only

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Harrison's Principles of Internal Medicine 22nd edition chronic kidney disease

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Chronic Renal Failure / Chronic Kidney Disease

Chronic renal failure is now termed chronic kidney disease (CKD). It comprises persistent abnormalities of kidney structure or function, usually with a progressive decline in glomerular filtration rate (GFR), and is assessed by eGFR, its rate of decline, and albuminuria. Stage 5 CKD replaces the older term “end-stage renal disease.”
Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322, p. 2429.

Etiology

Major causes are:

Diabetic nephropathy - a leading cause of progression to kidney failure
Glomerulonephritis
Hypertension-associated CKD, including ischemic and vascular nephropathy
Autosomal dominant polycystic kidney disease
Other cystic, congenital, hereditary, and tubulointerstitial nephropathies

Pathogenesis

CKD results from:

Initial disease-specific injury to glomeruli, vessels, tubules, or interstitium, for example immune injury, metabolic disease, toxins, or genetic defects.
Adaptive hyperfiltration and hypertrophy of surviving nephrons after nephron loss.

Initially, hyperfiltration sustains GFR. Over time, raised intraglomerular pressure and flow damage podocytes and the filtration barrier, causing glomerulosclerosis and further nephron loss. Increased intrarenal renin-angiotensin system activity contributes to this self-perpetuating progression.

Staging and risk

CKD risk is stratified by:

GFR category: G1 to G5
Albuminuria category: A1 to A3

Lower eGFR and greater albuminuria predict higher risks of CKD progression, all-cause mortality, and cardiovascular mortality. Adults at risk should have annual assessment of blood pressure, eGFR, and urinary albumin excretion.

Clinical features and complications

Patients may remain asymptomatic until advanced disease. Important manifestations include:

Hypertension and extracellular fluid expansion
Proteinuria or albuminuria
Hyperkalemia and metabolic acidosis
Normocytic anemia due to inadequate erythropoietin production
Mineral and bone disorder: reduced calcitriol, hyperphosphatemia, secondary hyperparathyroidism, and renal osteodystrophy
Malnutrition and altered carbohydrate, lipid, and protein metabolism
Increased cardiovascular risk and systemic inflammation
Uremic syndrome in advanced CKD: toxin accumulation together with loss of renal endocrine and metabolic functions, causing anorexia, nausea, pruritus, fatigue, cognitive symptoms, neuropathy, pericarditis, and bleeding tendency.

Small bilateral kidneys and cortical thinning on ultrasonography support chronic irreversible disease, although kidneys can remain large in diabetic kidney disease.

Management

Treat the underlying cause where possible.
Slow progression
- Monitor serial eGFR and albuminuria.
- Control hypertension and reduce albuminuria.
- Address hyperfiltration-mediated injury with appropriate renoprotective therapy.
- Avoid nephrotoxins, especially NSAIDs and unnecessary radiographic contrast.
- Investigate a sudden accelerated fall in GFR for reversible causes: volume depletion, uncontrolled hypertension, urinary infection, obstruction, nephrotoxic exposure, or relapse of the primary renal disease.
Treat complications: fluid overload, hyperkalemia, acidosis, anemia, and CKD-mineral and bone disorder.
Kidney replacement therapy: dialysis or kidney transplantation is required in stage 5 CKD when toxin, fluid, and electrolyte accumulation becomes incompatible with life.

Source: Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322 “Chronic Kidney Disease,” pp. 2429 onward.

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KDIGO CKD GFR categories G1 G5 albuminuria categories A1 A3

CKD Staging Table

GFR category	eGFR (mL/min/1.73 m²)	Description	Usual clinical status
G1	≥90	Normal or high GFR	CKD is diagnosed only if there is another marker of kidney damage, such as albuminuria, abnormal urine sediment, structural abnormality, or biopsy abnormality.
G2	60-89	Mildly decreased	Often asymptomatic; assess albuminuria and cause of kidney disease.
G3a	45-59	Mildly to moderately decreased	Early complications may begin; increased cardiovascular and progression risk.
G3b	30-44	Moderately to severely decreased	Complications become more frequent; monitor anemia, mineral-bone disorder, potassium, and acidosis.
G4	15-29	Severely decreased	Advanced CKD with major metabolic complications; prepare for renal replacement therapy.
G5	<15	Kidney failure	Uremic manifestations may occur; dialysis or transplantation is needed when indicated clinically.

Albuminuria Categories

Albuminuria category	Urine albumin-creatinine ratio (ACR)	Interpretation
A1	<30 mg/g (<3 mg/mmol)	Normal to mildly increased
A2	30-300 mg/g (3-30 mg/mmol)	Moderately increased
A3	>300 mg/g (>30 mg/mmol)	Severely increased

Risk assessment: CKD prognosis is based on the combination of cause, GFR category, and albuminuria category (CGA classification). Lower GFR and greater albuminuria indicate a higher risk of CKD progression, cardiovascular death, and all-cause mortality.

Complications of CKD

System	Complication	Main basis / clinical features
Fluid and cardiovascular	Hypertension, salt and water retention, edema, pulmonary edema, heart failure	Impaired sodium-water excretion and activation of neurohormonal mechanisms. Cardiovascular disease is a major cause of mortality.
Electrolytes	Hyperkalemia	Reduced renal potassium excretion, often aggravated by drugs or acidosis. May produce dangerous cardiac arrhythmias.
Acid-base	Metabolic acidosis	Decreased acid excretion and impaired bicarbonate regeneration. Associated with muscle catabolism, bone disease, and faster CKD progression.
Hematologic	Normocytic normochromic anemia	Reduced erythropoietin production, iron deficiency, inflammation, and reduced red-cell survival.
Bone-mineral disorder	Hyperphosphatemia, low calcitriol, hypocalcemia, secondary hyperparathyroidism, renal osteodystrophy	Diseased kidneys cannot adequately excrete phosphate or synthesize calcitriol. Bone pain, fractures, and vascular/soft tissue calcification may develop.
Neurologic	Uremic encephalopathy, peripheral neuropathy, sleep disturbance	Retention of uremic toxins, usually in advanced CKD.
Gastrointestinal and nutrition	Anorexia, nausea, vomiting, dysgeusia, malnutrition	Uremia and altered protein, lipid, and carbohydrate metabolism.
Skin	Pruritus, hyperpigmentation, xerosis	Common in advanced uremia; may be associated with mineral imbalance.
Endocrine and reproductive	Sexual dysfunction, infertility, menstrual abnormalities	Altered clearance, degradation, and regulation of hormones.
Immune/infectious	Increased susceptibility to infections	Uremia and malnutrition impair immune function.
Hemostatic	Bleeding tendency	Uremic platelet dysfunction, despite a normal platelet count.
Uremic syndrome	Pericarditis, encephalopathy, severe anorexia/vomiting, pruritus, neuropathy, serositis	Represents advanced kidney failure due to toxin accumulation plus loss of renal fluid, electrolyte, endocrine, and metabolic functions. It may require dialysis or transplantation.

Adapted from Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322 “Chronic Kidney Disease,” p. 2429 onward. Harrison emphasizes that CKD risk is stratified by both eGFR and albuminuria, and that stage 5 CKD may lead to the uremic syndrome requiring kidney replacement therapy.

6 page short note from Harrison 22 edition only

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Chronic Kidney Disease (CKD) / Chronic Renal Failure

Six-page short note based only on Harrison’s Principles of Internal Medicine, 22nd ed.

Page 1: Definition, significance, and causes

Definition

Chronic kidney disease (CKD) encompasses a spectrum of pathophysiologic processes associated with abnormal kidney function, usually with a progressive decline in glomerular filtration rate (GFR). The risk of progression is closely related to:

Current GFR
Rate of decline of GFR over time
Degree of urinary albumin excretion, that is, albuminuria

The term end-stage renal disease (ESRD) is replaced by stage 5 CKD. At this stage, retention of toxins, fluid, and electrolytes becomes fatal unless renal replacement therapy is provided by dialysis or kidney transplantation.
Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322, p. 2429.

Major causes

The leading clinical categories causing CKD are:

Major cause	Comments
Diabetic nephropathy	The most common cause in North America and Europe, usually associated with type 2 diabetes mellitus. Diabetes accounts for about half of patients with CKD who progress to stage 5 CKD.
Glomerulonephritis	Includes immune-mediated glomerular diseases causing proteinuria, hematuria, and progressive nephron loss.
Hypertension-associated CKD	Includes vascular and ischemic kidney disease, nephrosclerosis, and sometimes unrecognized primary glomerular disease with secondary hypertension.
Autosomal dominant polycystic kidney disease	A common inherited cause. Cyst enlargement progressively reduces functioning renal mass.
Other cystic and tubulointerstitial nephropathies	Includes hereditary, congenital, obstructive, toxic, and chronic tubulointerstitial disorders.

Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322, Table 322-4.

Risk factors for CKD and its progression

Important risk factors include:

Diabetes mellitus
Hypertension
Albuminuria
Tobacco use
Increased body mass index and sedentary lifestyle
A previous episode of acute kidney injury, even when apparently recovered
Previous childhood or adolescent kidney disease
Family history and genetic predisposition
Exposure to nephrotoxic agents
Vascular disease and older age

Genetic factors may contribute to a substantial proportion of adult-onset CKD. Some inherited disorders are Mendelian, including autosomal dominant polycystic kidney disease, type IV collagen-associated nephropathy, and autosomal dominant tubulointerstitial kidney disease. Variants in APOL1 contribute to susceptibility to some forms of CKD in people of sub-Saharan African ancestry.

Page 2: Pathophysiology

CKD develops through two broad mechanisms.

1. Disease-specific initiating injury

The first mechanism is the initial renal injury, which differs according to the cause. It may involve:

Genetic abnormalities of renal development
Immune-complex deposition
Inflammation
Metabolic disorders
Microvascular injury
Exposure to toxins
Primary vascular, glomerular, tubulointerstitial, or cystic disease

2. Common pathway: adaptive hyperfiltration followed by progressive damage

When nephron number falls, the surviving nephrons undergo:

Hypertrophy
Increased single-nephron GFR
Hyperfiltration

These adaptations initially preserve total GFR. However, sustained high intraglomerular pressure and flow eventually become harmful. They cause:

Distortion of glomerular architecture
Podocyte dysfunction
Disruption of the glomerular filtration barrier
Proteinuria
Glomerulosclerosis
Further nephron dropout

Thus, a reduction in nephron mass, whatever the original cause, can lead to a self-perpetuating decline in kidney function over many years.

The intrarenal renin-angiotensin system (RAS) and reduced tubuloglomerular feedback contribute to both compensatory hyperfiltration and later maladaptive hypertrophy and sclerosis.

Sequence of progression:
Primary renal injury → nephron loss → hyperfiltration of remaining nephrons → intraglomerular hypertension → podocyte and filtration-barrier injury → glomerulosclerosis → more nephron loss → progressive CKD.

Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322, p. 2429.

Page 3: Staging, evaluation, and diagnosis

CKD staging

CKD staging is based on the GFR category and the degree of albuminuria. Both worsening GFR and increasing albuminuria predict progression, all-cause mortality, and cardiovascular mortality.

GFR category	eGFR, mL/min per 1.73 m²	Description
G1	≥90	Normal or high
G2	60-89	Mildly decreased
G3a	45-59	Mildly to moderately decreased
G3b	30-44	Moderately to severely decreased
G4	15-29	Severely decreased
G5	<15	Kidney failure

Albuminuria categories

Albuminuria category	Urine albumin-creatinine ratio	Description
A1	<30 mg/g	Normal to mildly increased
A2	30-300 mg/g	Moderately increased
A3	>300 mg/g	Severely increased

The clinician should interpret CKD according to its cause, GFR category, and albuminuria category.

Clinical assessment

Adults at risk should be monitored yearly for:

Urinary albumin excretion
Estimated GFR
Blood pressure

The trajectory of GFR is important. A more rapid than expected fall in GFR should raise concern for a reversible superimposed disorder, such as:

Extracellular fluid-volume depletion
Uncontrolled hypertension
Urinary tract infection
Obstructive uropathy
New nephrotoxic exposure, for example NSAIDs or radiographic contrast
Recurrence or flare of the underlying disease, such as lupus or vasculitis

Features suggesting chronicity

When the duration of renal impairment is uncertain, chronicity is suggested by ultrasonography showing:

Bilaterally small kidneys
Renal length less than about 8 cm
Cortical thinning

However, kidney size may be preserved or enlarged despite kidney failure in certain conditions, particularly diabetic kidney disease.

The kidneys normally contribute to blood pressure regulation through renin production and to erythropoiesis through erythropoietin production. Reduced calcitriol production in CKD contributes to secondary hyperparathyroidism. Very high PTH levels also favor a diagnosis of chronic kidney disease rather than recent kidney injury.

Page 4: Uremia and clinical manifestations

Uremic syndrome

Uremia is the clinical syndrome resulting from reduced kidney function. It includes symptoms, signs, and laboratory abnormalities caused by the accumulation of substances normally excreted by the kidneys, loss of renal homeostatic and endocrine functions, and systemic inflammation.

Although serum urea and creatinine increase as GFR decreases, they are only convenient and incomplete surrogate markers of retained toxins. The manifestations of uremia cannot be explained by accumulation of urea and creatinine alone.

The retained solutes include multiple water-soluble, hydrophobic, protein-bound, charged, and uncharged nitrogen-containing metabolic products.

Three components of uremic syndrome

Harrison describes three major spheres of dysfunction:

Accumulation of normally excreted toxins
Loss of renal functions, including fluid-electrolyte homeostasis and hormone regulation
Systemic inflammation, with vascular and nutritional consequences

Clinical manifestations and complications

System	Manifestations in CKD
Fluid and cardiovascular	Sodium retention, extracellular fluid expansion, edema, hypertension, worsening cardiac disease
Electrolyte	Hyperkalemia, particularly in advanced CKD or with relevant medications and metabolic acidosis
Acid-base	Metabolic acidosis due to impaired acid excretion
Hematologic	Anemia, related partly to impaired erythropoietin production and the uremic milieu
Mineral and bone	Hyperphosphatemia, reduced calcitriol, hypocalcemia, secondary hyperparathyroidism, renal bone disease
Nutritional and metabolic	Anorexia, nausea, reduced dietary intake, protein-energy malnutrition, altered carbohydrate, lipid, and protein metabolism
Endocrine	Altered levels and regulation of PTH, FGF-23, insulin, glucagon, vitamin D, sex hormones, prolactin, and other hormones
Inflammatory and vascular	Elevated inflammatory markers, reduced albumin, accelerated atherosclerosis and vascular calcification
Neurologic and other uremic features	Fatigue, cognitive symptoms, neuropathy, pruritus, and other manifestations in advanced disease

Inflammation, malnutrition, and vascular disease

CKD is associated with systemic inflammation. Acute-phase reactants such as C-reactive protein rise, while negative acute-phase reactants, including albumin and fetuin, decline. This promotes the malnutrition-inflammation-atherosclerosis/calcification syndrome, contributing to accelerated vascular disease and morbidity in advanced CKD.

Page 5: Major metabolic complications

1. Sodium and water retention

Normally, renal sodium and water excretion matches intake. In CKD, reduced sodium excretion results in:

Sodium retention
Extracellular fluid expansion
Edema
Hypertension

Hypertension can further worsen glomerular hyperfiltration and kidney damage.

Management includes salt restriction and diuretics when appropriate. Loop diuretics are often required in more advanced CKD. Diuretic-resistant edema with uncontrolled hypertension can be an indication for dialysis.

Some patients with CKD may instead become volume depleted during vomiting, diarrhea, renal sodium loss, or excessive diuretic use, causing acute-on-chronic kidney dysfunction. Such patients may need temporary withholding or adjustment of diuretics and antihypertensive treatment during an intercurrent volume-depleting illness.

2. Hyperkalemia

Potassium excretion can remain relatively preserved despite reduced GFR because of:

Aldosterone-dependent potassium secretion in the distal nephron
Increased gastrointestinal potassium excretion

Nevertheless, hyperkalemia may be precipitated by:

High potassium intake
Hemolysis
Transfusion of stored red cells
Metabolic acidosis
RAS inhibitors
Mineralocorticoid receptor antagonists
Potassium-sparing diuretics

RAS blockade can reduce CKD progression and cardiovascular complications, so it is often continued with careful potassium monitoring rather than stopped automatically.

3. Metabolic acidosis

Metabolic acidosis in CKD results from impaired net acid excretion. Chronic acidosis is associated with:

Muscle catabolism
Bone disease
More rapid progression of CKD

In advanced disease, oral alkali may be used to raise and maintain serum bicarbonate above approximately 22-24 mmol/L.

4. CKD-mineral and bone disorder

The kidneys normally synthesize calcitriol and excrete phosphate. As CKD progresses:

Phosphate retention develops
Calcitriol production falls
Calcium balance becomes abnormal
PTH levels rise
Secondary hyperparathyroidism develops
Renal osteodystrophy may occur

The pathogenesis of secondary hyperparathyroidism is multifactorial. Increased FGF-23 inhibits renal 1-alpha hydroxylase, reducing 1,25-dihydroxyvitamin D and contributing further to increased PTH secretion.

Bone lesions may include:

High-turnover bone disease with increased PTH, including osteitis fibrosa cystica
Osteomalacia due to reduced vitamin D effect
Low-turnover or adynamic bone disease

Severe and prolonged secondary hyperparathyroidism may become autonomous, producing tertiary hyperparathyroidism.

5. Anemia and malnutrition

Anemia is a common manifestation of reduced renal endocrine function. CKD also causes abnormalities of protein, carbohydrate, and lipid metabolism. Reduced intake, metabolic acidosis, and inflammatory cytokines promote protein catabolism and protein-energy malnutrition, especially in advanced CKD.

Page 6: Principles of management and renal replacement therapy

General objectives

Management of CKD has two broad aims:

Treat the specific underlying cause
Slow progression caused by the common pathway of hyperfiltration and nephron loss

Measures to slow progression

Important principles include:

Identify and treat the cause of kidney disease where possible.
Monitor serial eGFR, albuminuria, and blood pressure.
Plot the rate of GFR decline over time.
Control hypertension and extracellular fluid excess.
Avoid or minimize nephrotoxic exposure, especially NSAIDs and unnecessary radiographic contrast.
Search actively for reversible causes if GFR decline accelerates.
Use renoprotective therapy directed at reducing maladaptive hyperfiltration when indicated.
Address lifestyle risk factors, including tobacco use, increased BMI, and physical inactivity.
Manage diabetes and vascular disease.
Monitor and manage hyperkalemia, metabolic acidosis, anemia, fluid retention, mineral-bone disorder, and malnutrition.

Etiology-specific therapy

Some disorders require cause-specific treatment. Examples discussed in Harrison include:

ADPKD: therapies directed at slowing cyst growth may be useful in appropriate patients.
Primary hyperoxaluria type 1: siRNA-directed therapy is available.
APOL1-mediated kidney disease: APOL1 channel inhibition has been shown to reduce urinary protein excretion in affected patients with focal segmental glomerulosclerosis.

Cause-specific therapy is generally most valuable before there is a substantial measurable fall in GFR.

Preparation for renal replacement therapy

Maintenance dialysis and kidney transplantation prolong life in patients with advanced CKD. Preparation should begin gradually and include education and multidisciplinary support.

Clear indications to initiate renal replacement therapy include:

Persistent anorexia and nausea not due to a reversible cause
Evidence of malnutrition
Refractory hyperkalemia
Refractory fluid overload or extracellular fluid expansion
Other medically refractory fluid, electrolyte, or uremic complications

The choice between conservative care, dialysis, and transplantation should be discussed early, allowing time for psychological, social, physical, and practical preparation.

Conclusion

CKD is a progressive disorder characterized by nephron loss, adaptive hyperfiltration, and eventual glomerulosclerosis. Its severity and prognosis depend on GFR, albuminuria, and cause. The principal clinical problems are progressive loss of renal function, cardiovascular disease, fluid and electrolyte disturbances, metabolic acidosis, anemia, mineral-bone disorder, malnutrition, and uremia. Early detection, treatment of the cause, renoprotection, prevention of complications, and timely preparation for renal replacement therapy are the central principles of care.

Source used exclusively: Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322 “Chronic Kidney Disease,” pp. 2429 onward; Chapter 319, “Chronic Kidney Disease and the Uremic Syndrome.”

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KDIGO 2024 CKD GFR G1 G5 albuminuria A1 A3 classification

Chronic Kidney Disease (CKD): One-Page Revision Summary

Definition

CKD is a spectrum of disorders with abnormal kidney function, often with a progressive fall in GFR. Progression risk depends on:

eGFR
Rate of eGFR decline
Albuminuria

Stage 5 CKD replaces the term ESRD. Without dialysis or transplantation, retained toxins, fluid, and electrolytes may be fatal.

Major Causes

Diabetic nephropathy
Glomerulonephritis
Hypertension-associated CKD: vascular, ischemic nephropathy, nephrosclerosis
Autosomal dominant polycystic kidney disease
Other cystic and tubulointerstitial nephropathies

Risk factors: diabetes, hypertension, obesity, smoking, sedentary lifestyle, prior AKI, childhood renal disease, nephrotoxins, family/genetic predisposition.

Pathogenesis

Primary renal injury
↓
Loss of nephrons
↓
Compensatory hypertrophy and hyperfiltration in surviving nephrons
↓
Increased intraglomerular pressure, podocyte dysfunction, filtration-barrier injury
↓
Proteinuria, glomerulosclerosis, further nephron loss
↓
Progressive CKD

Intrarenal renin-angiotensin system activation promotes maladaptive hyperfiltration and sclerosis.

CKD Staging

GFR category	eGFR (mL/min/1.73 m²)	Description
G1	≥90	Normal or high
G2	60-89	Mildly decreased
G3a	45-59	Mildly to moderately decreased
G3b	30-44	Moderately to severely decreased
G4	15-29	Severely decreased
G5	<15	Kidney failure

Albuminuria

Category	Urine ACR	Meaning
A1	<30 mg/g	Normal to mildly increased
A2	30-300 mg/g	Moderately increased
A3	>300 mg/g	Severely increased

Higher albuminuria + lower eGFR = higher risk of CKD progression, cardiovascular mortality, and all-cause mortality.

Clinical Features and Complications

System	Major manifestations
Fluid/CVS	Sodium and water retention, edema, hypertension, heart failure
Electrolytes	Hyperkalemia
Acid-base	Metabolic acidosis
Hematologic	Anemia due to reduced erythropoietin and the uremic milieu
Bone-mineral	Hyperphosphatemia, low calcitriol, hypocalcemia, secondary hyperparathyroidism, renal osteodystrophy
Nutrition	Anorexia, nausea, weight loss, protein-energy malnutrition
Endocrine	Abnormal regulation of PTH, FGF-23, insulin, vitamin D, sex hormones, prolactin
Neurologic/skin	Fatigue, neuropathy, cognitive symptoms, pruritus
Vascular	Systemic inflammation, atherosclerosis, vascular calcification

Uremic syndrome

Results from:

Retention of normally excreted toxins
Loss of fluid-electrolyte and hormonal functions
Systemic inflammation with nutritional and vascular consequences

Evaluation

Serial eGFR, urine albumin excretion, and blood pressure
Identify cause and assess rate of decline
Ultrasound clues to chronicity: small bilateral kidneys and cortical thinning
- Exception: kidneys may be large in diabetic kidney disease.
Rapid decline suggests a reversible added problem: volume depletion, infection, obstruction, uncontrolled hypertension, nephrotoxins, or flare of primary renal disease.

Management Principles

Treat the underlying cause.
Reduce progression related to hyperfiltration.
Control hypertension and extracellular-fluid excess.
Avoid nephrotoxins, especially NSAIDs and unnecessary contrast exposure.
Treat anemia, hyperkalemia, acidosis, mineral-bone disorder, and malnutrition.
Prepare early for dialysis or transplantation in advanced CKD.

Indications for renal replacement therapy

Refractory hyperkalemia or fluid overload
Persistent anorexia/nausea with no reversible explanation
Malnutrition
Severe or refractory uremic, electrolyte, or fluid complications

Source: Harrison’s Principles of Internal Medicine, 22nd ed., Chapter 322, “Chronic Kidney Disease,” pp. 2429 onward.

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