2. Structure of the kidney
• Specific components are nephrons,
collecting ducts and a unique
microvasculature
• Multipapillary kidney of humans – 1 million
nephrons
• This number already established
prenatally
– Lost nephrons cannot be replaced
3. Nephrons
• A renal corpuscle (glomerulus)
– A knot of capillaries
– Connected to a complicated and twisted tubule
– Finally drains into a collecting duct
5. Renal physiology
• Prime function – to maintain a stable
milieu interieur
– By selective retention and elimination of
• Water
• Electrolytes
• And other solutes
6. Contribution of different nephron
segments to solute and water
hemostasis (1)
• Glomerulus – forms an ultrafiltrate of plasma
• Proximal tubule
– Reabsorbs 65-70% of filtered NaCl and water
– Reabsorbs 90% of bicarbonate
– Major site of ammonia production
– Reabsorbs almost all of glucose and amino
acids
– Reabsorbs K, phosphate, calcium, magnesium,
urea, and uric acid
– Secretes organic anions (urate) and cations
7. Contribution of different nephron
segments to solute and water
hemostasis (2)
• Loop of Henle
– Reabsorbs 15-25% of filtered NaCl
– Major site of active regulation of Mg excretion
• Distal tubule
– Reabsorbs a small fraction of filtered NaCl
– Major site of active regulation of calcium
excretion
8. Contribution of different nephron
segments to solute and water
hemostasis (3)
• Connecting segment and cortical
collecting tubule
– Principal cells reabsorb Na and Cl and secret K
– Intercalated cells secrete H, reabsorb K and in
metabolic alkalosis – secrete HCO3
– Reabsorb water in presence of ADH
9. Contribution of different nephron
segments to solute and water
hemostasis (4)
• Medullary collecting tubule
– Site of final modification of urine
– Reabsorb NaCl
– Reabsorb water and urea relative to amount of
ADH present
– Secrete H, and NH3
– Contribute to K balance by reabsorption or
secretion of K
10. ANTIDIURETIC HORMONE REGULATION
MECHANISMS
Osmoreceptors in
↑Osmolarity hypothalamus
Hypothalamus
↓Blood Volume receptor
↓ ↑ADH Kidney
volume
Atria and great veins tubules
or ↓BP Posterior
pituitary gland
↑H2O
reabsorption
Narcotics, Stress,
Anesthetic agents, Heat, ↑vascular
Nicotine, Antineoplastic volume and
agents, Surgery ↓osmolarity
11. ALDOSTERONE-RENIN-ANGIOTENSIN
SYSTEM
Juxtaglomerular RENIN Angiotensinogen in
↓Serum Sodium
↓Blood volume cells-kidney plasma
Angiotensin I
Angiotensin-
converting enzyme
Via vasoconstriction of arterial smooth muscle
↑Sodium Angiotensin II
resorption
Kidney tubules ALDOSTERONE
(H2O resorbed
with sodium); Adrenal
↑ Blood Cortex
volume Intestine, sweat
glands, Salivary
glands
12. REGULATION OF BODY COMPONENTS
• Osmosis
– Fluid shift from the region of low solute
concentration to the region of high solute
concentration until the solutions are of equal
concentration.
– Tonicity is the ability of the solutes to cause as
osmotic driving force that promotes water
movement from one compartment to another.
• Diffusion
– The natural tendency of a substance to move
from an area of a higher concentration to one
lower concentration. It occurs through a random
movement of ions and molecules.
Ex. exchange of the oxygen and the carbon
dioxide
Rate of Diffusion Varies Accdg. To:
Size of the molecules
Concentration of the solution
Temperature of the solution
13. • Filtration
– Hydrostatic pressure in the capillaries tends to filter fluid out of
the vascular compartment to the interstitial fluid. Movement of
water and solutes occurs from an area of high hydrostatic
pressure from an area of a lower hydrostatic pressure.
– Hydrostatic pressure- pressure exerted by a fluid within a closed
system on the walls of a container in which it is contained.
16. RENAL FAILURE
• Results when the kidneys cannot remove
the body’s metabolic wastes or perform
their regulatory functions. The substances
normally eliminated in the urine
accumulate in the body fluids as a result of
impaired renal excretion, leading to a
disruption in endocrine and metabolic
functions as well as fluid, electrolyte, and
acid-base disturbances.
• It is a systemic disease and is a final
common pathway of many different kidney
and urinary tract diseases
17. ACUTE RENAL FAILURE
Is a reversible clinical syndrome where
there is a sudden and almost complete
loss of kidney function (decreased GFR)
over a period of hours to days with failure
to excrete nitrogenous waste products and
to maintain fluid and electrolyte
homeostasis.
ARF manifests as an increase in serum
creatinine (M=53-132umol/L; F=44-
97umol/L) and BUN (7-20mg/dl). Urine
volume may be normal, or changes may
occur. Possible changes include oliguria
(<400ml/day), nonoliguria (>400ml/day), or
anuria (<50 ml/day)
18. Categories of Acute Renal Failure
1. Prerenal- occurs in 60%-70% of cases,
is the result of impaired blood flow to
that leads to hypoperfusion of the
kidney and a decrease in the GFR.
Common clinical conditions are
volume-depletion states (hemorrhage
or GI losses), impaired cardiac
performance (MI, HF, or cardiogenic
shock), and vasodilation (sepsis or
anaphylaxis)
19. 2. Intrarenal- is the result of actual parenchymal damage
to glomeruli or kidney tubules. Nephrotoxic agents
such as aminoglycosides and radiocontrast agents
account for 30% of cases of acute tubular necrosis
(ATN), and ischemia due to decreased renal
perfusion accounts for more than 50% of cases
Characteristics of ATN are intratubular back leak (abnormal
absorption of filtrate and decreased urine flow through the
tubule), vasoconstriction, and changes in glomerular
permeability. These processes result in a decrease of GFR,
progressive azotemia, and impaired fluid and electrolyte
balance.
Conditions such as burns, infections, crush injuries, and
severe blood transfusion reactions can lead to intrarenal ARF
and ultimately ATN
With burns and crush injuries, myoglobin (a CHON released
from muscle when injury occurs) and hemoglobin are liberated,
causing obstruction, renal toxicity, and ischemia
Medications such as NSAIDs and ACE inhibitors interfere with
the normal auto regulatory mechanisms of the kidneys and
may cause hypoperfusion and eventual ischemia.
20. 3. Postrenal – is usually the result
of an obstruction somewhere
distal to the kidneys. Pressure
rises in the kidney tubules and
eventually, the GFR decreases
21.
22. Comparing Categories of Acute Renal Failure
Characteristics Categories
Prerenal Intrarenal Postrenal
Etiology Hypoperfusion Parenchymal Obstruction
damage
BUN value Increased Increased increased
Creatinine Increased Increased Increased
Urine output Decreased Varies, often Varies, may be
decreased decreased, or
sudden anuria
Urine sodium Decreased to < 20 Increased to Varies, often
mEq/L >40mEq/L decreased to
20mEq/L or less
Urinary sediment Normal, few hyaline Abnormal casts Usually normal
casts and debris
Urine osmolality Increased to About 350 mOsm Varies, increased
500mOsm similar to serum or equal to serum
Urine specific Increased Low normal Varies
gravity
23. Causes of Acute Renal Failure
A. Prerenal
1. Volume depletion resulting from:
a. hemorrhage
b. renal losses (diuretics)
c. GI losses (vomiting, diarrhea, NG suctioning)
2. Impaired cardiac efficiency resulting from:
a. MI
b. Heart failure
c. Dysrhythmias
d. Cardiogenic shock
3. Vasodilation resulting from:
a. sepsis
b. anaphylaxis
c. antihypertensive medications or other
medications that cause vasodilation
24. Causes of Acute Renal Failure
B. Intrarenal
1. Prolonged renal ischemia resulting from:
a. pigment nephropathy (associated with the breakdown of
blood cells containing pigments that in turn occlude
kidney structures)
b. Myoglobinuria (trauma, crush injury, burns)
c. Hemoglobinuria (transfusion reaction, hemolytic anemia)
2. Nephrotoxic agents such as:
a. Aminoglycosides antibiotics (gentamicin, tobramycin)
b. Radiopaque contrast media
c. Heavy metals (lead, mercury)
d. Solvents and chemicals (carbon tetrachloride, arsenic)
e. NSAIDs, ACE inhibitors
3. Infectious processes such as:
a. acute pyelonephritis
b. acute GN
25. Causes of Acute Renal Failure
C. Postrenal
1. Urinary tract obstruction, including:
a. calculi (stones)
b. tumors
c. BPH
d. Strictures
e. Blood clots
26. Phases of ARF
1. Initiation – begins with the initial insult and
ends when oliguria develops
2. The oliguria period is accompanied by an
increase in the serum concentration of
substances usually excreted by the kidneys
(uric acid, urea, creatinine, organic acids). In
this phase uremic symptoms first appear
and life-threatening conditions such as
hyperkalemia develop.
3. The diuresis period is marked by a gradual
increase in urine output, which signals that
glomerular filtration has started to recover.
4. The recovery period signals the improvement
of renal function and may take 3-12 months.
Lab values return to normal level. Although
a permanent 1%-3% reduction in the GFR is
common.
27. Preventing ARF
1. Provide adequate hydration to patients at risk of
dehydration:
a. surgical patients before, during and after surgery.
b. Patients undergoing intensive diagnostic studies
requiring fluid restrictions and contrast agents
c. Patients with neoplastic disorders of metabolism and
those receiving chemotherapy
2. Prevent and treat shock promptly with blood and
fluid replacement.
3. Monitor CV and arterial pressures and hourly urine
output of critically ill patients to detect the onset
of renal failure as early as possible.
4. Treat hypotension promptly.
5. Continually assess renal function when appropriate.
28. Preventing ARF
6. Take precautions to ensure that the
appropriate blood is administered to the
correct patient in order to avoid severe
transfusion reactions, which can precipitate
renal failure.
7. Prevent and treat infections promptly.
Infections can produce progressive renal
damage.
8. Pay special attention to wounds, burns and
other precursors of sepsis
9. To prevent infections from ascending in the
urinary tract, give meticulous care to
patients with indwelling catheters. Remove
catheter ASAP.
10. To prevent toxic drug effects, closely monitor
dosage, duration of use, and blood levels of
all medications metabolized or excreted by
the kidneys.
29. Medical Management:
1. Pharmacologic therapy
a. hyperkalemia is the most life-threatening of the F/E
changes that occur in RF, the elevated K levels
may be reduced by administering cation-exchange
resins (sodium polystyrene sulfonate [Kayexalate]
orally or by retention enema. It works by
exchanging sodium ions for potassium ions in the
intestinal tract.
b. Sorbitol may be administered in combination with
Kayexalate to induce diarrhea type effect (induce
water loss in the GIT)
c. If hemodynamically unstable, IV dextrose 50%,insulin
and calcium replacement may be administered to
shift potassium back into the cells.
d. Diuretics are often administered to control fluid
volume, but they have not been shown to hasten
the recovery form ARF.
30. Medical Management
2. Nutritional Therapy
a. Dietary proteins are individualized to provide
the maximum benefit. Caloric requirements
are met with high-carbohydrate meals,
because carbohydrates have a protein-
sparing effect.
b. Foods and fluids containing potassium or
phosphorous such as banana, citrus fruits
and juices, coffee are restricted
31. Nursing Management
• Monitoring fluid and electrolyte balance
• Reducing metabolic rate
• Promoting pulmonary function
• Preventing infection
• Providing skin care
• Providing support
32. CHRONIC RENAL FAILURE/END STAGE
RENAL DISEASE (ESRD)
Is a progressive, irreversible
deterioration in renal function
in which the body’s ability to
maintain metabolic and fluid
and electrolyte balance fails,
resulting in uremia and
azotemia.
33. ESRD
Causes:
1. DM, HPN, chronic glomerulonephritis,
pyelonephritis, obstruction of the urinary
tract, hereditary lesions as in polycystic
kidney disease, vascular disorders,
infections, medications, or toxic agents.
2. Environmental and occupational agents
that have been implicated in CRF
include lead, mercury and chromium.
Dialysis or kidney transplantation
eventually becomes necessary for
patient’s survival.
34. Pathophysiology
As renal function declines, the end products of CHON
metabolism (which are normally excreted in urine)
accumulate in the blood. Uremia develops and
adversely affects every system in the body.
Stages of CRF: are based on the GFR. The normal
GFR is 125cc/min/1.73m2
1. Stage 1 = GFR > 90 ml/min/1.73m2. Kidney
damage with normal or increased GFR.
2. Stage 2 = GFR = 60-89 mL/min/1.73m2. Mild
decrease in GFR.
3. Stage 3 = GFR = 30-59 mL/min/1.73m2. Moderate
decrease in GFR.
4. Stage 4 = GFR = 15-29 mL/min/1.73m2. Severe
decrease in GFR.
5. Stage 5 = GFR <15 mL/min/1.73 m2. Kidney failure
35. Clinical Manifestations
1. CV manifestations:
a. HPN – due to Na and H20 retention or from R-A-A
activation,
b. heart failure and edema - due to fluid overload
c. pericarditis - due to irritation of pericardial lining by
uremic toxins
2. Dermatologic manifestations
a. severe pruritus is common
b. uremic frost, the deposit of urea crystals on the
skin.
3. GI manifestations:
a. anorexia, nausea and vomiting, and hiccups
b. The patient’s breath may have the odor of urine
(uremic fetor); this may be associated with
inadequate dialysis
4. Neurologic manifestations
a. altered LOC, inability to concentrate, muscle
twitching, agitation, confusion and seizures.
b. Peripheral neuropathy, a disorder of the peripheral
NS, is present in some patients
36. Assessment and Diagnostic Findings
1. GFR
2. Sodium and water retention
3. acidosis – due to inability of the kidneys to
excrete increased load of acid
4. Anemia
5. calcium and phosphorous imbalance –
hypocalcemia and increase in
phosphorous
37. Complications
1. Hyperkalemia due to decreased excretion,
metabolic acidosis, catabolism and
excessive intake (diet, meds and fluids)
2. Pericarditis, pericardial effusion and pericardial
tamponade due to retention of uremic waste
products and inadequate dialysis.
3. Hypertension due to sodium and water
retention and malfunction of the R-A-A
system
4. Anemia due to decreased erythropoietin
production, decreased RBC life span,
bleeding in the GIT from irritating toxins and
ulcer formation, and blood loss during
hemodialysis
5. Bone disease and metastatic and vascular
calcifications due to retention of
phosphorous, low serum calcium levels,
abnormal vitamin D metabolism and
elevated aluminum levels.
38. Medical Management
1. Pharmacologic Therapy
a. calcium carbonate (Os-cal) or calcium acetate
(Phoslo) are prescribed to treat
hyperphosphatemia and hypocalcemia
b. Antiseizure agents – diazepam (Valium) or
phenytoin (Dilantin)
c. Antihypertensive and CV drugs - digoxin
(Lanoxin) and dobutamine (Dobutrex)
d. Erythropoietin (Epogen) to treat anemia. It is
initiated to reach a hematocrit of 33% - 385
and a target hemoglobin of 12g/dl.
2. Nutritional Therapy
a. low sodium, low CHON and low K diet
3. Dialysis
39. Nursing Management
Nursing Management:
1. Assessing fluid status and identifying
potential sources of imbalance.
2. implementing a dietary program to ensure
proper nutritional intake
3. promoting positive feelings by
encouraging increased self-care and
greater independence.
4. Provide explanations and information to
the patient and family concerning ESRD,
treatment options and potential
complications.
5. Provide emotional support to the patient
and family.
40. DIALYSIS Is used to substitute some kidney functions
during renal failure.
It is used to remove fluid and uremic waste
products from the body when the kidneys
are unable to do so.
It may be indicated to treat patients with
edema that do not respond to treatment.
Acute dialysis is indicated when there is a
high and increasing level of serum
potassium, fluid overload, or impending
pulmonary edema, increasing acidosis,
pericarditis and severe confusion. It may
also be used to certain medications or other
toxins in the blood.
41. DIALYSIS
Chronic or maintenance dialysis is
indicated in ESRD in the following
instances:
1.Presence of uremic signs and symptoms
affecting all body systems (nausea and
vomiting, severe anorexia, increasing
lethargy, mental confusion)
2.Hyperkalemia and fluid overload not
responsive to diuretics and fluid
restriction.
3.General lack of well-being.
An urgent indication for dialysis in patients
with CRF is pericardial friction rub.
43. PERITONEAL DIALYSIS
• Indwelling catheter is implanted into the
peritoneum.
• A connecting tube is attached to the external
end of peritoneal catheter T –tube.
• Plastic bag of dialysate solution is inserted to
the end of T-tube; the other end is recap.
• Dialysate bag is raised to shoulder level and
infused by gravity in the peritoneal cavity
• Infusion time = 10 minutes/2 liters; dwelling
time is 4-6 hours depending on doctor’s order.
• At the end of dwelling time, dialysis fluid is
drained from the peritoneal cavity by gravity
• Draining time is 10-20 minutes/2 liters
• Then repeat the procedure when necessary
44. Peritoneal Dialysis
• Usually for patients with absolutely no
other options of dialysis
• Or as a temporary measure until options
of dialysis sorted out
45. Pre and post operative care for
Tenckhoff catheter insertion
• Pre operative care
– Fast for 8 hours
– Allow essential medications
– Bowel preparation not necessary
– Removal of body hair limited to that
necessary to facilitate performance of
procedure
– Empty bladder
– Single dose of prophylactic antibiotic
– Operating room or well equipped
procedure room
46. Pre and post operative care for Tenckhoff
catheter insertion
• Post operative care
– Catheter irrigation with 1 L of heparinized saline
performed as an in-and-out flush within 72
hours following surgery and weekly thereafter
until PD initiated
– Delay PD for a min of 2 weeks to allow wound
healing
– Change dressings weekly for 2 weeks
– Then patient should begin a routine of daily
exit-site cleansing with antibacterial soap
– Showering only permitted after 1 month if
wound healing uncomplicated
– Avoid catheter movement at the exit site
– Use sterile gauze dressing over exit site
– No tub bathing and swimming
49. PERITONEAL DIALYSIS
NURSING CONSIDERATIONS:
1. Dialysate must be room-warmed before use ( for better
absorption)
2. Drugs (heparin, potassium and antibiotics) must be
added in advance.
3. Allow the solution to remain in the peritoneal cavity for
the prescribed time.
4. Check outflow for cloudiness, blood and fibrin (early
peritonitis).
5. NEVER PUSH THE CATHETER IN.
6. Monitor the VS regularly.
7. Keep a record of patient’s fluid balance (daily weighing)
8. Monitor blood chemistry
9. Turn the patient side to side if drainage stop
10.Observe for abdominal pain (cold solution), dialysate
leakage (prevent infection)
11.Intake must be equal to output.
50. HEMODIALYSIS
Is the process of cleansing the blood of
accumulated waste products
Patient’s access is prepared and cannulated
surgically
One needle is inserted to the artery (brachial)
then blood flow is directed to dialyzer (dialysis
machine)
The machine is equipped with semi-permeable
membrane surrounded with dialysis solution
Waste products in the blood move to the
dialysis solution passing through the membrane
by means of diffusion
Excess water is also removed from the blood by
way of ultrafiltration
The blood is then returned to the vein after it
has been cleansed.
54. HEMODIALYSIS
NURSING CONSIDERATIONS:
1. Blood can be heparinized unless it is contraindicated
to prevent blood clot.
2. Dialysis solution has some electrolytes and acetate
and HCO3 added to achieve proper pH balance.
3. Methods of circulatory access: AV fistula; AV graft or
U-tube
4. Assess the access site for bruit, signs of infections
and ischemia of the hand.
5. Absence of thrill may indicate occlusion
6. No BP taking on the access site.
7. Cover the access site with adhesive bandage
8. Dietary adjustments of CHON, Na and fluid intake.
9. Monitor VS regularly
10.Check blood chemistry
11.Constant monitoring of hemodynamic status,
electrolytes and acid-base balance.
55. KIDNEY TRANSPLANT
Indicated for ESRD
TYPES OF DONOR
1.Living
2.Cadaveric
Rejection and infection remain the
major complication after surgery.
T and B lymphocytes are involved in
the rejection response
To reduce the rejection process,
immunosuppressive drugs are given
Watchout for infection after
immunosuppressive medications
56. KIDNEY
TRANSPLANT
REJECTION RESPONSE
1. Hyper acute – occurs in the OR, kidney turns blue
and flabby.
Treatment: remove the kidney
2. Accelerated Acute – occurs 48-72 hours post-op;
abrupt oliguria is seen.
Treatment: dialysis, steroid and immunsuppressive
drugs are initiated; with poor prognosis.
3. Acute – occurs 1 week to several weeks post-op,
weight gain, oliguria, HPN, increased BUN, enlarged
kidney are seen.
Treatment: same with accelerated acute; with good
prognosis.
4. Chronic – occurs months to years post-op,
progressive decreased renal function is seen.
Treatment: same as above; poor prognosis.
