CHRONIC

RENAL
FAILURE
Chronic kidney disease (CKD)
or chronic renal failure (CRF)
progressive deterioration of kidney function over a period
of months or years

kidneys attempt to compensate for renal damage by

hyperfiltration within the remaining functional nephrons

Over time, hyperfiltration causes further loss of function


Chronic kidney disease (CKD)
or chronic renal failure (CRF)
Chronic loss of function
• generalized wasting (shrinking in size) and
progressive scarring within all parts of the kidneys

obscures the site of the initial damage

Patients experience symptoms when there is already 70%

damage to the normal function of both kidneys
 Chronic kidney disease (CKD)
or chronic renal failure (CRF)
Chronic kidney disease is identified by a blood
test for creatinine
• Higher levels : falling glomerular filtration rate
• normal in the early stages


Chronic kidney disease (CKD)
or chronic renal failure (CRF)
National Kidney Foundation (NKF) defines chronic kidney
disease as either kidney damage or a decreased kidney
glomerular filtration rate (GFR) of less than 60
mL/min/1.73 m2 for 3 or more months.
Stage 1 Kidney damage with (>90 mL/min/1.73 m2
normal or increased GFR

Stage 2 Mild reduction in GFR 60-89 mL/min/1.73 m2

Stage 3 Moderate reduction in 30-59 mL/min/1.73 m2

GFR

Stage 4 Severe reduction in GFR 15-29 mL/min/1.73 m2

Stage 5 Kidney failure GFR <15 mL/min/1.73

m2 or dialysis
Signs and Symptoms

initially without specific symptoms

can only be detected as an increase in serum creatinine or

protein in the urine


Azotemis -> uremia

‘Uremic frost’

Hyperkalemia

anemia
Signs and Symptoms

Fluid Overload (mild edema to life-threatening pulmonary

edema)

Hyperphosphatemia

Hypocalcemia (tetany)

Metabolic acidosis
Causes

diabetes and high blood pressure

multiple myeloma
Causes

Pre-Renal CRF 
• Some medical conditions cause continuous
hypoperfusion of the kidneys
• include poor cardiac function, chronic liver failure,
and atherosclerosis of the renal arteries
 Causes
 Post-Renal CRF 

 Interference with the normal flow of urine can produce

backpressure within the kidneys, can damage nephrons, and lead
to obstructive uropathy, a disease of the urinary tract
• Bladder outlet obstruction 

• Neurogenic bladder

• Kidney stones 

• Obstruction of the tubules

• Retroperitoneal fibrosis

• Diabetic nephropathy

• Vasculitis

• Hereditary diseases of the kidney (Alport’s syndrome)

 Diagnosis

Ultrasound
• are small in size and echogenic
• (< 9 cm) than normal kidneys

Sometimes, renal biopsy

Electrolytes, BUN, creatinine, phosphate, Ca, CBC,

urinalysis (including urinary sediment examination)


 Diagnosis

a combination of symptoms and elevated blood urea

nitrogen (BUN) and creatinine (Cr) levels

Anemia

High level of parathyroid hormone

Hypocalcemia

Hyperphosphatemia

 Diagnosis

Hyperkalemia

Hyponatremia

Low blood level of bicarbonate

Low plasma pH


Pathophysiology
CKD can be roughly categorized as diminished renal
reserve, renal insufficiency, or renal failure (end-stage
renal disease).

renal functional adaptation

a loss of 75% of renal tissue produces a fall in GFR to only

50% of normal
Decreased renal function interferes
with the kidneys' ability to maintain
fluid and electrolyte homeostasis
ability to concentrate urine declines
early and is followed by decreases in
ability to excrete phosphate, acid, and
K.
When renal failure is advanced (GFR ≤ 10 mL/min/1.73 m2),
the ability to dilute urine is lost; thus urine osmolality is
usually fixed close to that of plasma (300 to 320
mOsm/kg), and urinary volume does not respond readily
to variations in water intake.
Plasma concentrations of creatinine and
urea (which are highly dependent on
glomerular filtration) begin a nonlinear
rise as GFR diminishes.
Despite a diminishing GFR, Na and water
balance is well maintained by increased
fractional excretion of Na and a normal
response to thirst.
Factors other than the underlying disease process and glomerular
hypertension that may cause progressive renal injury include the
following:
• Systemic hypertension
• Acute insults from nephrotoxins or decreased perfusion
• Proteinuria
• Increased renal ammoniagenesis with interstitial injury
• Hyperlipidemia
• Hyperphosphatemia with calcium phosphate deposition
• Decreased levels of nitrous oxide
• Smoking


Renal Diet
 Protein
Protein restriction:
• 0.6 – 0.8 gProtein/kg Body Weight/day (Non-
Dialyzed)
• 1.2 – 1.3 gProtein/kg Body Weight/day (Dialyzed)

More of High Biologic Value proteins

Meat, fish, egg white


Carbohydrates
Main source of energy

Adjusted depending on the comorbities

Fruits, breads, grains, vegetables

Fats
Another source of calories

Adjusted depending on the comorbities

Prioritize monounsaturated or polyunsaturated fats (plant

sources)


Calcium and Phosphorus
Limit intake of phosphorus rich items such as milk, yogurt
and cheese

Fruits and vegetables contain low levels of phosphorus

Calcium and Vitamin D supplements can be taken


Sodium intake: < 2g/day

Iron: take supplements as needed

Fluids: not limited in early stages of kidney disease