CHRONIC RENAL

FAILURE
A PRESENTATION BY MR. GAVOR SAMUEL
FOR GROUP 3

OBJECTIVES
Overview

Clinical Manifestations

Epidemiology

Complications

Etiology

Investigation

Risk factors
Pathophysiology

Management and
Treatment

Clinical Manifestations

Prognosis

OVERVIEW
Chronic renal failure is the progressive irreversible destruction of
kidney tissue by disease which, if not treated by dialysis or
transplantation, will result in the death of the patient.
The aetiology of CRF (Chronic Renal Failure) encompasses the
spectrum of known kidney diseases. The end results of renal failure
all occur because of the loss of functioning nephrons.
It is a feature of CRF that patients may have a few if any symptoms
until the glomerular filtration rate falls bellows 15mL/minute (i.e.
10% of normal function), and the disease is far advanced.
According to Kidney Disease Outcomes Quality Initiative (KDOQI),
and the International Guideline group, Kidney Disease Improving
Global Outcomes (KDIGO), guidelines have been laid down which
define chronic renal failure as either kidney damage or decreased

EPIDEMIOLOGY
The ratio of the occurrence in black Americans to whites
is 4:1 due to the prevalence of hypertension in African
Americans.
It affects 5-10% of the worlds population
It is the 9th leading cause of death in the US
More prevalent in the elderly population over 60 years
Chronic renal failure in children is more common in boys
because of abnormalities in the posterior urethral valve.

AETIOLOGY
Type 1 diabetes
Type 2 diabetes
Glomerulonephritis
Interstitial nephritis
Polycystic kidney disease
Prolonged obstruction of the urinary tract
Vesicoureteral reflux
Recurrent kidney infection

RISK FACTORS
Diabetes
Hypertension
Heart and blood vessel
Smoking
Obesity
Being African American, Native American or Asian-American
Family history of kidney disease
Abnormal kidney structure
Old age

PATHOPHYSIOLOGY
There are many risk factors that lead to CRF but two major causes:
Hypertension and Diabetes
HOW HYPERTENSION LEADS TO CRF
Hypertension is one of the leading causes of CRF due to the
deleterious effects that increased BP has on kidney vasculature.
Long-term, uncontrolled high blood pressure leads to high
intraglomerular pressure, impairing glomerular filtration. Damage
to the glomeruli leads to leakage of large amounts of protein into
urine: proteinuria (microalbuminuria)
Microalbuminuria is the presence of small amounts of albumin in
the urine and is often the first sign of chronic renal failure
Proteinuria (in the light of a protein-to-creatinine ratio less
220mg/g) develops as CRF progresses.

PATHOPHYSIOLOGY (contd.)
HOW DIABETES LEADS TO CHRONIC RENAL FAILURE
With diabetes, the small blood vessels in the body are injured. When the blood
vessels in the kidneys are injured, the kidneys cannot clean the blood
properly.
The body then retains more water and salt than it should (which can result in
weight gain and ankle swelling)
Waste materials also start to build up in the blood
Diabetes can damage the nerves in the body. It becomes difficulty to empty
the bladder. As such, the pressure resulting from the full bladder backtracks
up into the ureters.
Again, if urine remains in the bladder for a long time, one can develop an
infection due to the rapid growth of bacteria in urine that has a high sugar
level.

PATHOPHYSIOLOGY (contd.)
UREMIA
Sclerosis of the glomerular apparatus leads to tubular
atrophy and shrinkage of the glomerular apparatus
thereby increasing the plasma concentration of
metabolic wastes such as urea and creatinine.
The build up of urea in the blood (uremia) is what is
responsible for most of the symptoms of chronic renal
failure

STAGING OF CHRONIC RENAL

FAILURE
Stage 1: kidney damage with normal or increased glomerular
filtration rate (GFR) >90mL/min/1.73m2
Stage 2: mild reduction in GFR (60-89 mL/min/1.73m 2)
Stage 3a: moderate reduction in GFR (45-59 mL/min/1.73m 2)
Stage 3b: moderate reduction in GFR (30-44 mL/min/1.73m 2)
Stage 5: kidney failure (GFR <15 mL/min/1.73m 2)
Individuals with stages 1-3 are often asymptomatic.

CLINICAL SYMPTOMS
Anemia due to decreased erythropoietin synthesis
Hypocalcemia due to vitamin D stimulation deficiency
Uremic frost
Nausea
Vomiting
Loss of appetite
Reduction in the amount of urine excreted

CLINICAL MANISFESTATIONS
Uremic symptoms can affect every organ system, most noticeably the following:
Neurological system: Cognitive impairment, personality change, asterixis
(involuntary jerking movements, especially in the hands), seizures (but these are
rare)
Gastrointestinal system: nausea, vomiting,
Blood-forming system anemia due to erythropoietin deficiency, bruising and
bleeding due to abnormal platelets
Pulmonary system: fluid build up in the lungs, respiratory difficulties
Cardiovascular system Chest pain due to pericarditis and pericardial effusion
(fluid accumulation around the heart)
Skin Generalized itching, uremic frost

COMPLICATIONS
Fluid retention, which could lead to swelling of the arms
and legs, hypertension, pulmonary oedema
Hyperkalemia
Cardiovascular diseases
Weak bones and an increased risk of bone fractures
Cardiac failure
Hyperlipidemia
Anemia

COMPLICATIONS (contd.)
Decreased sex drive, erectile dysfunction or reduced fertility
Damage to the central nervous system thereby leading to personality
changes, seizures or difficulty in concentrating,
Decreased immune response, making one more vulnerable to
infections
Pericarditis
Pregnancy complications that carry risks for the mother and
developing foetus
Irreversible damage to ones kidneys (End Stage Kidney Disease),
eventually requiring either dialysis or a kidney transplant for survival.

INVESTIGATIONS
Laboratory studies
FBC
Urinalysis
Serum albumin levels
Lipid profile
Imaging studies
Renal ultrasonography
Retrograde pyelography (usually when an obstructive renal disease is
suspected)
CT scan
MRI
Biopsy
This is useful when a diagnosis is unclear after several workups.

MANAGEMENT AND TREATMENT

Delaying/halting the progression of CKD by treating the
underlying condition
Diagnosing and treating the pathologic manifestations of CRF
Anaemia treated by using erythropoiesis-stimulating agents
Hyperphosphataemia treated by using dietary phosphate binders and phosphate
restrictors
Hypocalcemia treated with calcium supplements
Hyperparathyroidism treated with calcitriol, vitamin D or calcimimetics
Volume overload treated with loop diuretics
Metabolic acidosis treated with oral alkali supplements
Uremic manifestations treated with kidney transplant, hemodialysis or peritoneal
dialysis

Long-term renal replacement therapy

PROGNOSIS
Chronic renal failure is often insidious in its onset and
progression. The rate of progression is; however,
variable but usually, kidney function declines leading to
an End Stage Renal Disease

Thank you

INDEX NUMBERS OF GROUP

MEMBERS
SM/MED/14/0002
SM/MED/14/0006
SM/MED/14/0010
SM/MED/14/0014

SM/MED/14/0034
SM/MED/14/0039

SM/MED/14/0018
SM/MED/14/0022
SM/MED/14/0026
SM/MED/14/0030

SM/MED/14/0043