General Santos Doctors' Medical School Foundation,

Incorporated
Bulaong, General Santos City

Nursing Department

CASE CONFERENCE
In Partial Fulfilment of the Requirements in NCM 103 RLE
Medical-Surgical Ward Exposure

Submitted to:

Ms. Felicidad Sta.Ana, RN, MAN

Submitted by:
ALUMBRO, Anna Rose L. SN
COLANO, Afra B. SN
GIMPAYAN, Jerica May F. SN
TUDAYAN, Ivana Kim G. SN
VALERIO, Stephanie Z. SN

Chronic Renal Failure

I. Anatomy and Physiology
Kidney
The two kidneys are located in the upper abdominal cavity on either side of the
vertebral column, behind the peritoneum (retroperitoneal). The upper portions
of the kidneys rest on the lower surface of the diaphragm and are enclosed
and protected by the lower rib cage. The left kidney is slightly higher than the
right one. The right kidney is lower because of the presence of the liver in the
upper right abdominal quadrant. The kidneys are embedded in adipose tissue
that acts as a cushion and is in turn covered by a fibrous connective tissue
membrane called the renal fascia, which helps hold the kidneys in place.
Each kidney has an indentation called the hilus on its medial side. At the hilus,
the renal artery enters the kidney, and the renal vein and ureter emerge. The
renal artery is a branch of the abdominal aorta, and the renal vein returns
blood to the inferior vena cava.
A. Internal Structure of the Kidney
The lateral and middle areas are tissue layers, and the medial area at the
hilus is a cavity. The outer tissue layer is called the renal cortex; it is made
of renal corpuscles and convoluted tubules. These are parts of the
nephron. The inner tissue layer is the renal medulla, which is made of
loops of Henle and collecting tubules (also parts of the nephron). The renal
medulla consists of wedgeshaped pieces called renal pyramids. The tip of
each pyramid is its apex or papilla.
The third area is the renal pelvis; this is not a layer of tissues, but rather a
cavity formed by the expansion of the ureter within the kidney at the hilus.
Funnel-shaped extensions of the renal pelvis, called calyces (singular:
calyx), enclose the papillae of the renal pyramids. Urine flows from the
renal pyramids into the calyces, then to the renal pelvis and out into the
ureter.
B. The Nephron

The nephron is the structural and functional unit of the kidney. Each kidney
contains approximately 1 million nephrons. It is in the nephrons, with their
associated blood vessels, that urine is formed. Each nephron has two
major portions: a renal corpuscle and a renal tubule.
a. Types of Nephron
Cortical Nephron
80-85 % of the total number of nephrons located in the outermost
part of the cortex
Juxtamedullary nephrons
15-20% located deeper in the cortex

b. Parts of Nephrons
Renal Corpuscle
A renal corpuscle consists of a glomerulus surrounded by a Bowmans
capsule. The glomerulus is a capillary network that arises from an
afferent arteriole and empties into an efferent arteriole. The diameter
of the efferent arteriole is smaller than that of the afferent arteriole,
which helps maintain a fairly high blood pressure in the glomerulus.
Bowmans capsule (or glomerular capsule) is the expanded end of a
renal tubule; it encloses the glomerulus. The inner layer of Bowmans
capsule is made of podocytes; the name means foot cells, and the

feetof the podocytes are on the surface of the glomerular capillaries.

The arrangement of podocytes creates pores, slits between adjacent
feet, which make this layer very permeable. The outer layer of
Bowmans capsule has no pores and is not permeable. The space
between the inner and outer layers of Bowmans capsule contains renal
filtrate, the fluid that is formed from the blood in the glomerulus and will
eventually become urine.

Renal Tubule
The renal tubule continues from Bowmans capsule and consists of the
following parts: proximal convoluted tubule (in the renal cortex), loop
of Henle (or loop of the nephron, in the renal medulla), and distal
convoluted tubule (in the renal cortex). The distal convoluted tubules
from several nephrons empty into a collecting tubule. Several
collecting tubules then unite to form a papillary duct that empties urine
into a calyx of the renal pelvis. All parts of the renal tubule are
surrounded by peritubular capillaries, which arise from the efferent

arteriole. The peritubular capillaries will receive the materials

reabsorbed by the renal tubules.

C. Blood Vessels of the Kidney

The pathway of blood flow through the kidney is an essential part of the
process of urine formation. Blood from the abdominal aorta enters the
renal artery, which branches within the kidney into several interlobar
arteries (between the renal pyramids). Each interlobar artery becomes an
arcuate artery (arches over a pyramid), which branches into many
interlobular arteries that enter the renal cortex. The interlobular arteries
give rise to afferent arterioles in the renal cortex. The interlobar veins all
unite at the hilus to form the renal vein, which empties blood into the
inferior vena cava.

II.

Renal Failure
Renal failure refers to temporary or permanent damage to the kidneys that result
in loss of normal kidney function which cannot remove the bodys metabolic
wastes (Brunner & Suddarth, 2010). There are two different types of renal
failure--acute and chronic. Acute renal failure has an abrupt onset and is
potentially reversible. Chronic renal failure progresses slowly over at least three
months and can lead to permanent renal failure. (hopkinsmedicine.org)

III.

Chronic Renal Failure

Termed as an End-Stage Renal Disease (ESRD).
A progressive and irreversible deterioration in renal function in which the
bodys ability to maintain metabolic and fluid and electrolyte balance fails,
resulting in uremia or azotemia. Usually end result of gradual tissue destruction.
The incidence of ESRD has increased by almost 8% per year from the
past 5 years. In the US, more than 280,000 patients with CRF (65%) are
receiving hemodialysis, more than 120,000 (28%) have functioning renal
transplants, and more than 24,000 (7%) are receiving peritoneal dialysis (United
States Renal Data System [USRD], 2004)

IV.

Stages of Chronic Kidney Disease

Stages are based on the GFR.
Normal GFR: 90 - 125 mL/min/1.73 m2 (According to National Kidney Foundation)

V.

Risk Factors and Causes of CRF/ ESRD

Chronic kidney disease (CKD)
Injury or trauma to the kidneys
Major blood loss
Diabetes Mellitus
Hypertension
Chronic Glomerulonephritis
Pyelonephritis
Obstruction of the Urinary tract
Hereditary Lesion (Polycystic Kidney Disease)
Vascular Disorders
Infections
Medications
Exposure to toxic agents (lead, cadmium, mercury, and chromium)

VI.

Pathophysiology of CKD and CRF/ESRD

http://img.docstoccdn.com/

As renal function declines, the end products of protein metabolism (which are
normally excreted in urine) accumulate in the blood thus, increased solute load
per nephron. Uremia develops and adversely affects every system in the body.
The greater the buildup of waste products, the more severe the symptoms and
alteration of GFR might occur.

http://intranet.tdmu.edu.ua/

VII.

SIGNS/SYMPTOMS/ Clinical Manifestations

1. Neurologic
Weakness and fatigue
Confusion

Inability to concentrate
Disorientation
Tremors

Seizures
Asterixis
Restlessness of legs
Burning of soles of feet
Behavior changes

2. Integumentary

Gray-bronze skin color

Dry, flaky skin
Pruritus
Ecchymosis
Purpura
Thin brittle nails
Coarse thinning hair

3. Cardiovascular
Hypertension
Pitting edema (feet,
hand, sacrum)
Periorbital edema
Pericardial friction rub
Engorged neck vein
Hyperkalemia
Hyperlipidemia

4. Pulmonary
Crackles
Depress cough reflex
Pleuritic pain

Shortness of breath
tachypnea
5. Gastrointestinal
Ammonia odor of breath
( uremic fetor)
Metallic taste
Mouth ulceration and
bleeding
Nausea and vomiting
Constipation and
diarrhea
6. Hematologic
Anemia
Thrombocytopenia
7. Reproductive

Amenorrhea
Testicular atrophy
Infertility
Decrease libido

8. Musculoskeletal

Muscle cramps
Loss of muscles strength
Renal osteodystrophy
Bone pain
Bone fractures
Foot drop

VIII. Diagnostic Findings

A. Laboratory Assessment
Glomerular Filtration Rate
As glomerular filtration decreases (due to nonfunctioning glomeruli), the
creatinine clearance value decreases, whereas the serum creatinine and BUN
levels increase. Serum creatinine is the more sensitive indicator of renal
function because of its constant production in the body. The BUN is affected
not only by renal disease but also by protein intake in the diet, catabolism
(tissue and RBC breakdown), parenteral nutrition, and medications such as
corticosteroids
Sodium and Water retention
Some patients retain sodium and water, increasing the risk for edema, heart
failure, and hypertension. Hypertension may also result from activation of the
reninangiotensinaldosterone axis and the concomitant increased
aldosterone secretion.
Acidosis
With advanced renal disease, metabolic acidosis occurs because the kidney
cannot excrete increased loads of acid. Decreased acid secretion primarily
results from inability of the kidney tubules to excrete ammonia (NH3) and to
reabsorb sodium bicarbonate (HCO3). There is also decreased excretion of
phosphates and other organic acids.
Anemia
Anemia develops as a result of inadequate erythropoietin production, the
shortened life span of RBCs, nutritional deficiencies, and the patients
tendency to bleed, particularly from the GI tract. Erythropoietin, a substance
normally produced by the kidney, stimulates bone marrow to produce RBCs. In
renal failure, erythropoietin production decreases and profound anemia
results, producing fatigue, angina, and shortness of breath.
Calcium and Phosphorus Imbalance
With decreased filtration through the glomerulus of the kidney, there is an
increase in the serum phosphate level and a reciprocal or corresponding
decrease in the serum calcium level. The decreased serum calcium level
causes increased secretion of parathormone from the parathyroid glands.
In renal failure, however, the body does not respond normally to the increased
secretion of parathormone; as a result, calcium leaves the bone, often
producing bone changes and bone disease. In addition, the active metabolite

of vitamin D (1,25-dihydroxycholecalciferol) normally manufactured by the

kidney decreases as renal failure progresses. Uremic bone disease, often
called renal osteodystrophy, develops from the complex changes in calcium,
phosphate, and parathormone balance. There is also evidence of calcification
of blood vessels (Schrier, 2005)
B. Radiographic Assessment
Bone x-rays of the hand can show renal osteodystrophy. With long term
ESRd, the kidneys are atrophic and may be 8 to 9 cm or smaller. This small
size results from renal atrophy and fibrosis.

IX.

Medical Management
The goal of management is to maintain kidney function and homeostasis for as
long as possible. All factors that contribute to ESRD and all factors that are
reversible (eg, obstruction) are identified and treated. Management is
accomplished primarily with medications and diet therapy, although dialysis may
also be needed to decrease the level of uremic waste products in the blood and
to control electrolyte imbalance.
A. Pharmacological Therapy
Calcium and Phosphorus Binders
Hyperphosphatemia and hypocalcemia are treated with
medications that bind dietary phosphorus in the GI tract
Calcium Carbonate or Calcium Acetate
Antihypertensive and Cardiovascular Agents
Hypertension is managed by intravascular volume control and a
variety of antihypertensive agents.
Digoxin or Dobutamine
Antiseizure Agents
Neurologic abnormalities might occur
IV Diazepam (Valium) or Phenytoin (Dilantin)
Erythropoietin
Treatment for Anemia
Epogen

B. Nutritional Therapy
Dietary Intervention is necessary with deterioration of renal function and
includes:
Careful regulation of protein intake
Fluid intakes to balance fluid losses

Sodium intake to balance sodium losses

And some restriction of potassium
Adequate caloric intake
Vitamins supplementation

C. Dialysis
It is used to remove fluid and uremic waste products from the body when the
kidneys are unable to do so. It may also be used to treat patients with edema
that does not respond to other treatment, hepatic coma, hyperkalemia,
hypercalcemia, hypertension, and uremia.
Methods of therapy includes:
Hemodialysis
Most common method of dialysis. It used for patient who are
acutely ill and require short-term dialysis (days to weeks) and for
patients with ESRD who require long term or permanent therapy. A
dialyzer (also referred to as an artificial kidney)serves as a
synthetic semipermeable membrane , replacing the renal glomeruli
and tubules as the filter for the impaired kidneys
CRRT (Continuous Renal Replacement therapies)
Indicated for patients with acute or chronic renal failure who are
too clinically unstable for traditional hemodialysis, for patients with
fluid overload secondary to oliguria (low urine output) renal failure,
and for patients whose kidney cannot handle their acutely high
metabolic or nutritional needs.
Peritoneal Dialysis
Goal is to remove toxic substances and metabolic wastes and to
re-establish normal fluid and electrolyte balance. The treatment of
choice for patient with renal failure who are unable or unwilling to
undergo hemodialysis or renal transplant
D. Renal/ Kidney Transplant
Kidney transplantation has become the treatment of choice for most patients
with ESRD. Patients choose kidney transplantation for various reasons, such
as the desire to avoid dialysis or to improve their sense of well-being and the
wish to lead a more normal life. Additionally, the cost of maintaining a
successful transplantation is one-third the cost of treating a dialysis patient.
Criteria for Candidate in Kidney Transplantation
Free of medical problems that might increase the risk from the
procedure
2 to 7 years old
Advanced and uncorrectable cardiac disease are excluded
Metastatic Cancer

Chronic Infection
Severe Psychosocial problems (chemical dependency)
Long-standing pulmonary disease- respiratory infections
GIT problems (Peptic Ulcer, Diverticulosis)- made worse by the
large doses of steroid used after transplantation
Donors
Usually 18 years old above and are seldom older than 65 years of
age
Absence of systemic Disease and infection
No history of cancer
No hypertension or renal disease
Adequate renal function as determined by diagnostic studies

X.

Nursing Diagnosis for CRF/ End-Stage Renal Disease

Excess fluid volume related to decreased urine output, dietary excessive
and retention of sodium and water.
Imbalance nutrition; less than body requirements related to anorexia,
nausea, vomiting, dietary restrictions and altered oral mucous
membranes.
Risk for infection related to inadequate primary defenses (broken skin),
chronic disease and malnutrition.
Risk for injury related to internal biochemical risk factor associated with
renal failure (increased susceptible to bleeding, falls and fractures)
Deficient knowledge regarding condition and treatment
Activity intolerance related to fatigue, anemia, retention of waste
products, and dialysis procedure
Risk for situational low self-esteem related to dependency, role changes,
change in body image and change in sexual function

Reference:
Scanlon, V. and Sacnders, T. (2011). Essentials of Anatomy and
Physiology (7th Edition)

LaCharity, Linda A. Interventions for Clients with Acute and Chronic

Renal Failure
Smeltzer, Bare, Hinkle, Cheever, (2008). Brunner & Suddarths
Textbook of Medical-Surgical Nursing (11th Edition)
Ignatavicus & Workman (2006) Medical Surgical Nursing: Critical
Thinking for Collaborative Care (5th Edition)
Pathophysiology an Incredibly Easy (Pocket Guide)
Doenges, Moorhouse & Murr, (2010). Nursing Care Plans: Guidelines
for Individualizing Client Care Across the Life Span (9 th Edition)
http://www.hopkinsmedicine.org/
http://www.kidneyfund.org/
http://www.netwellness.org/