Pathophysiology

Predisposing Factor (Non

Modifiable)
Hypertension, Diabetes

Precipitating Factors (Modifiable)

UTI, Smoking, Alcohol,
Glomerulonephritis

Damage to the
nephrons

Progressive lost of
functional nephrons

Diminished renal reserve (30

~ 50% loss of kidney
function)

Hyposthenuria
Polyuria

Renal Insufficiency (51 ~ 75%

loss of kidney function)

Oliguria
Isosthenuria
ESRD (90% loss of kidney
function)
Anuria

Excessive amounts of metabolic waste are

accumulated

Kidneys are unable to

maintain homeostasis

Metabolic
Changes

Excessive
accumulation of
sodium

Hypertension
Hypernatremia

Excessive
accumulation of
Potassium

Edema (peripheral
or pulmonary)

Hyperkalemia

Dysrhythmia

Production of Vit D
Ca Absorption
On GI tract

Hypocalcemia
Release of PTH

Phosphate retention

Bone resorption
Hyperphosphatemia
Renal Osteodysthrophy

Acid Base
Imbalance

Metastatic Calcifications
Acid excretion
(Hydrogen ions)
Metabolic Acidosis
Rate and depth of
breathing
Too much Co2
is released

Respiratory
Alkalosis

Cardiac
Changes

Malfunction in RAAS
Sodium & H2o
retention

BP

Edema (pulmonary
of peripheral)

Hypertension

Workload
of the heart
Left Ventricular
hypertrophy
Heart Failure

Hematologic
Changes
Erythopoietin
RBC Production

Anemia

Fatigue

Uremia
Accumulation of toxins
in the blood

Impaired platelet
aggregation and impaired
release of platelet factor III

Uremic toxins
reach the heart

Inflammation of
pericardial sac

Impairs Immune
system
Risk for
Infection

Bleeding
tendencies
Chest pain

Fever
Cardiac
Tamponade
Dysrhythmias

Cardiac
Effusion

GI
disturbances

Normal Flora
of the mouth
changes due to
uremia

Production
of Urease

Uremic Halitosis

Nausea &
Vomiting

Breaks down
Urea to
Ammonia

Anorexia

Uremic toxins
reach the
brain

Ammonia

Stomatitis

Lethargy

Irritability

Peptic Ulcer
Uremic Colitis
Bleeding

Seizure
Hemorrhagic
shock

Coma

Uremic Encephalopathy
Uremic toxins
reach the skin

Urochrome
pigment is
deposited in the
skin

Jaundice

Pruritus

Uremic Frost
Ecchymoses

Purpura

 Level of estrogen,
Progesterone and
luteinizing hormone

Reproductive
Disturbances

Fatigue
from
anemia

Anovulation

Amennorrhea

Testosterone Level

Decrease
libido

Low Sperm
Count

If treated

Hemodialysis

Impotence

If not treated

Kidney Transplant

Continued
systemic
breakdown

Peritoneal Dialysis
Anasarca

Dietary Management

Congestive Heart
Failure

Protein
Carbohydrates,
Fat, Calories
Potassium

Death

Sodium and Fluid

intake

Palliative Care
Palliative State

Chronic renal failure results from the destructive effects of many forms of renal
disease. Regardless of the cause, the consequences of nephron destruction in ESRD are
alterations in the filtration, reabsorption, and endocrine functions of the kidneys. The
progression of chronic renal usually occurs in four stages: diminished renal reserve, renal
insufficiency, renal failure and ESRD. Renal insufficiency represents a reduction in the
GFR to approximately 20% to 50% of normal; renal failure, a reduction to less than 20%
to 25% of normal; and ESRD, a decrease in GFR to less than 5% of normal.
End-stage renal disease affects almost every body system. It causes an
accumulation of nitrogenous wastes (i.e. azotemia), alters sodium and water retention,
and alters regulation of body levels of potassium, phosphate, calcium, and magnesium. It
also causes skeletal disorders, anemia, and alterations in cardiovascular function,
neurologic disturbances, gastrointestinal dysfunction, and discomforting skin changes.
CKD can be roughly categorized as diminished renal reserve, renal insufficiency,
or renal failure (end-stage renal disease). Initially, as renal tissue loses function, there are
few abnormalities because the remaining tissue increases its performance (renal
functional adaptation); a loss of 75% of renal tissue causes a fall in GFR to only 50% of
normal.
Decreased renal function interferes with the kidneys ability to maintain fluid and
electrolyte homeostasis. Changes proceed predictably, but considerable overlap and
individual variation exist. The ability to concentrate urine declines early and is followed
by decreases in ability to excrete phosphate, acid, and potassium. 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 hyperbolic rise as GFR diminishes. These changes are
minimal early on. When the GFR falls below 10 mL/min/1.73 m2 (normal = 100
mL/min/1.73 m2), their levels increase rapidly and are usually associated with systemic
manifestations (uremia). Urea and creatinine are not major contributors to the uremic
symptoms; they are markers for many other substances (some not yet well defined) that
cause the symptoms.
Despite a diminishing GFR, sodium and water balance is well maintained by
increased fractional excretion of sodium and a normal response to thirst. Thus, the plasma
sodium concentration is typically normal, and hypervolemia is infrequent unless dietary
intake of sodium or water is very restricted or excessive. Heart failure can occur due to
sodium and water overload, particularly in patients with decreased cardiac reserve.
For substances whose secretion is controlled mainly through distal nephron
secretion (eg, potassium), adaptation usually maintains plasma levels at normal until
renal failure is advanced. Potassium-sparing diuretics, ACE inhibitors, beta-blockers,
NSAIDs, cyclosporine, tacrolimus,trimethoprim/sulfamethoxazole, pentamidine,

or

angiotensin II receptor blockers may raise plasma potassium levels in patients with less
advanced renal failure.
Abnormalities of calcium, phosphate, parathyroid hormone (PTH), and vitamin D
metabolism and renal osteodystrophy can occur. Decreased renal production
of calcitriol contributes to hypocalcemia. Decreased renal excretion of phosphate results

in hyperphosphatemia. Secondary hyperparathyroidism is common and can develop in

renal failure before abnormalities in calcium or phosphate concentrations occur. For this
reason, monitoring PTH in patients with moderate CKD, even before hyperphosphatemia
occurs, has been recommended.
Renal

osteodystrophy

(abnormal

bone

mineralization

resulting

from

hyperparathyroidism, calcitriol deficiency, elevated serum phosphate, or low or normal

serum calcium) usually takes the form of increased bone turnover due to
hyperparathyroid bone disease (osteitis fibrosa) but can also involve decreased bone
turnover due to adynamic bone disease (with increased parathyroid suppression) or
osteomalacia. Calcitrioldeficiency may cause osteopenia or osteomalacia.
Moderate acidosis (plasma bicarbonate content 15 to 20 mmol/L) is characteristic.
Acidosis causes muscle wasting due to protein catabolism, bone loss due to bone
buffering of acid, and progression of kidney disease.
Anemia is characteristic of moderate to advanced CKD ( stage 3). The anemia of
CKD is normochromic-normocytic, with an Hct of 20 to 30% (35 to 40% in patients with
polycystic kidney disease). It is usually caused by deficient erythropoietin production due
to a reduction of functional renal mass. Other causes include deficiencies of iron, folate,
and vitamin B12.
The treatment of ESRD can be divided into two types: conservative management
of renal insufficiency and renal replacement therapy with dialysis or transplantation.
Conservative treatment consists of measures to prevent or retard deterioration in
remaining renal function and to assist the body in compensating for the existing
impairment. Interventions that have been shown to retard significantly the progression of

chronic renal insufficiency include dietary protein restriction and blood pressure
normalization. Activated vitamin D can be used to increase calcium absorption and
control secondary hypothyroidism, Recombinant human erythropoietin is used to treat the
profound anemia that occurs in persons with ESRD.