Chronic Kidney Disease

Chronic Kidney Disease
Learning Outcomes
 define chronic kidney disease (CKD) and end stage

renal disease (ESRD) and list the common causes.
 explain the pathophysiology of CKD and relate it to
the clinical features
 differentiate between AKI and CKD.
 outline the principles of management of CKD
Chronic Kidney Disease - Definitions
Based on
 proteinuria as an indicator of kidney damage
 glomerular filtration rate
1. kidney damage
OR
2. estimated glomerular filtration rate (eGFR) below 60
ml/min/1.73 m2
persisting for 3 months or more irrespective of the
cause
Kidney damage : proteinuria takes as indicator of “kidney

damage”
Proteinuria
Mild to moderate elevation may not necessarily indicate the
presence of CKD but a risk for progression to CKD
End Stage Renal Disease
End stage renal disease is when a patient with CKD begins to

require renal replacement therapy.
This occurs when the GFR falls below approximately 15 ml/ min.
This is often taken as the cut off point for defining ESRD.
Chronic Kidney Disease – Prognostic Classification
Pathogenesis of CKD
Two stages of pathogenesis

1. Specific mechanisms of kidney damage related to the specific
kidney disease
2. Mechanisms responsible for the progression of the damage

(after the initial specific mechanisms), irrespective of the
cause of CKD.
These involve hyperfiltration and hypertrophy of nephrons
Pathogenesis of CKD
Cause A Cause B Cause C Cause D Cause E
Specific
mechanisms
Kidney Damage
Common mechanisms
Chronic Kidney Disease

Pathogenesis of CKD
1. Specific mechanisms of kidney damage related to the specific

primary kidney disease
I. The disease process causes acute injury to nephrons –

glomeruli, tubules or both
II. Complete healing does not occur resulting in loss of
functional units (nephrons)
OR
III. The primary disease leads to chronic destruction of
nephrons, leading to nephron loss
Pathogenesis of CKD
2. Progression of the damage (after the initial specific mechanisms), irrespective

of the primary cause of CKD.
I. Hyperfiltration and hypertrophy of surviving nephrons / glomeruli as an

adaptation to loss of nephrons / parts of glomeruli
II. These adaptations give rise to intraglomerular hypertension and imbalances
among different cell types/components in the nephrons
III. Continuing increase in degree of adaptation results in a stage of
maladaptation due to these abnormalities
IV. Maladaptation causes loss of surviving nephrons
V. There is continuing
glomerular sclerosis
interstitial fibrosis
intra-renal vascular injury
Pathogenesis of CKD
progression of glomerular loss
Pathogenesis of CKD
progressive vascular and interstitial damage
Many mechanisms are involved. Different mechanisms assume

different degrees of significance in different individuals
Some important mechanisms include:
 Increased pressure/flow through surviving glomerular arterioles
causing endothelial/vascular dysfunction
 Vascular dysfunction leading to ischeamia of tubules
 Increased protein / lipids in tubular fluid causing tubular damage by
increasing reactive oxygen radicles and cytokines
 Excessive activation of renin-angiotensin system causing
exaggerated vascular responses and imbalanced cell growth
(affects glomeruli as well)
Causes of CKD
Common causes of CKD

 Diabetes mellitus
 Hypertension
 Glomerulonephritis
 Polycystic disease of the kidney
 Tubulo-interstitial disease
 Analgesic abuse
 Chronic infections
Risk factors of CKD
Irrespective of the causation of the initial kidney damage the presence of certain
factors appear to favour the progression of CKD
1. Non modifiable
Age (older), Race or ethnicity (non-Caucasian), Genetics, Birth weight (low)
2. Modifiable
Major
Systemic hypertension
Diabetes mellitus
Cardiovascular disease
Albuminuria
Minor
Obesity or metabolic syndrome, Dyslipidemia, Hyperuricemia, Smoking, Low
socioeconomic status, NSAIDs
Clinical Features of CKD
 May be asymptomatic until late stage

 Symptoms may not occur until 70-80% nephrons are lost
 Clinical features are non-specific
 Due to impaired kidney function causing ECF changes
 Due to loss of renal synthetic/secretory function –
(eryhtropoeitin, active vit D)
 Retention of biologically active molecules which are
inactivated by the kidney – (hormones)
 due to effects of accumulation of nitrogenous substances
(ureamia) on other systems
Consequences of CKD
Fluid and electrolyte

 Volume expansion and contraction
 Hypernatraemia and hyponatraemia
 Hyperkalaemia and hypokalaemia
 Metabolic acidosis
 Hypocalcaemia
Bone and mineral

 Renal osteodystrophy
 Osteomalacia
Consequences of CKD
Cardiovascular
 Arterial hypertension
 Congestive heart failure or pulmonary edema
 Pericarditis
 Cardiomyopathy
 Accelerated atherosclerosis
 Hypotension and arrhythmias
Consequences of CKD
Gastrointestinal
 Anorexia
 Nausea and vomiting
 Uremic fetor
 Gastroenteritis
 Peptic ulcer
 Gastrointestinal bleeding
 Hepatitis
 Peritonitis
Consequences of CKD
Neuromuscular
 Fatigue & Lethargy
 Sleep disorders
 Impaired mentation
 Tremors
 Muscular irritability, Restless legs syndrome, Muscle cramps ,
Myoclonus, Myopathy
 Peripheral neuropathy
 Seizures
 Coma
Consequences of CKD
Haematologic
 Normocytic, normochromic anemia
 Lymphocytopenia
 Bleeding diathesis
 Increased susceptibility to infection
 Splenomegaly and hypersplenism
Consequences of CKD
Metabolic
 Carbohydrate intolerance
 Hypothermia
 Hypertriglyceridemia
 Impaired growth and development
 Infertility and sexual dysfunction
 Amenorrhea
Consequences of CKD
Skin
 Skin pallor
 Hyperpigmentation
 Pruritus
 Ecchymoses
Na+ and Water Balance in CKD
1. Typically some degree of Na+ and water excess -reflecting loss of the
renal route of salt and water excretion.
Early stages asymptomatic
Large excess of Na+ - congestive heart failure, hypertension, ascites,
peripheral edema, and weight gain.
Excess of water in relation to Na+ - hyponatremia.
avoiding excess salt intake and restricting fluid intake so that it equals
urine output plus 500 mL (insensible losses) helps maintain balance
2. There is impaired renal salt and water conservation.
Easily develop ECF depletion
e.g. in sudden extrarenal Na+ and water losses (eg, vomiting, diarrhea)
or reduction of oral intake
K+ Balance in CKD
 Hyperkalemia is the commonest abnormality

 Worsened by
 Treatment with K+-sparing diuretics, ACE inhibitors, beta
blockers
 Increased gain from exogenous sources (eg, stored blood,
K+-rich foods, or K+-containing medications).
H+ Balance in CKD
 Metabolic acidosis is common

 The diminished capacity to excrete acid and generate base in
chronic renal failure results in metabolic acidosis.
 Mild to moderate until late stages – can be corrected with oral
sodium bicarbonate
 Highly susceptible to a sudden acid load or the onset of
disorders that increase the generated acid load or increase
loss of alkali
Ca2+ Metabolism in CKD
 Hypocalcaemia mediated through

 Impaired excretion of phosphate
 Decreased vitamin D activation
 Bone destruction
 Mineral dissolution due to metabolic acidosis
 Bone resorption due to increased PTH in response to
hypocalcaemia
Abnormalities in Ca2+ Metabolism in CKD
Haematological abnormalities in CKD
 Anaemia – normocytic normochromic

 lack of production of erythropoietin
Respond to treatment with erythropoietin
 bone marrow suppressive effects of uremic poisons, bone
marrow fibrosis due to elevated blood PTH
 Bleeding tendency
 Platelet dysfunction
 Coagulation defects
 Leukocyte dysfunction – susceptibility to infection
Principles of management of CKD
 Remove or minimise factors favouring progression

 Hypertension
 Diabetes mellitus
 Hyperuricaemia
 Maintain extracellular fluid volume and composition

 Control salt intake – no or little added salt in food,
variations in intake based on the hydration status
 Fluid volume regulated – based on urine output, take into
account insensible water loss, additional unusual losses
(e.g. diarrhoea)
 Restrict K+ intake – e.g. fruits
 Correct any severe abnormality

 Control of diet
 Limit proteins – allow only high quality proteins
 Provide adequate energy – minimise protein breakdown
 Regulate fat intake – close to minimum recommended
 Replace synthetic function of the kidney and/or correct

abnormalities due the loss of synthetic function
 Hypocalcaemia
• Active vit D, calcium, restrict phosphate
 Anaemia
• Erythropoeitin, blood transfusions (caution !)
 Reduce rate of progression

 Interrupt the excessive activation of RAS
ACE inhibitors, angiotensin II blockers
 Renal replacement therapy

 Dialysis
 Transplantation

Chronic Kidney Disease

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Chronic Kidney Disease

 define chronic kidney disease (CKD) and end stage

Kidney damage : proteinuria takes as indicator of “kidney

End stage renal disease is when a patient with CKD begins to

Two stages of pathogenesis

2. Mechanisms responsible for the progression of the damage

Cause A Cause B Cause C Cause D Cause E

Chronic Kidney Disease

1. Specific mechanisms of kidney damage related to the specific

I. The disease process causes acute injury to nephrons –

2. Progression of the damage (after the initial specific mechanisms), irrespective

I. Hyperfiltration and hypertrophy of surviving nephrons / glomeruli as an

Many mechanisms are involved. Different mechanisms assume

Common causes of CKD

 May be asymptomatic until late stage

Fluid and electrolyte

Bone and mineral

 Hyperkalemia is the commonest abnormality

 Metabolic acidosis is common

 Hypocalcaemia mediated through

 Anaemia – normocytic normochromic

 Remove or minimise factors favouring progression

 Maintain extracellular fluid volume and composition

 Correct any severe abnormality

 Replace synthetic function of the kidney and/or correct

 Reduce rate of progression

 Renal replacement therapy

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