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Chronic Renal Failure
The best indicator of renal failure is CREATININE b/c it is not significantly altered by
other factors. Measuring 24 hour creatinine clearane is the best measure of creatinine and
renal fx., but most use serum creatinine for convenience.
URINALYISIS FINDINGS
Test
Color
Normal
Amber Yellow
Abnormal Findings
-Dark, smoky color suggests hematuria
-Yellow brown to olive green indicates excessive
bilirubin; orange-red or orange brown caused by
phenazopyridine (pyridium); cloudiness of freshly
voided urine indicated infection; colorless urine
indicates excessive intake, renal disease or diabetes
insipidus
Smell
Aromatic
-On standing urine becomes more ammonia-like in
Smell; in UTI, urine smells unpleasant
Protein
0-150mg/24 hrs
0-18mg/dl
-persistent proteinuria is characteristic of acute and
chronic renal disease, especially involving
glomeruli. In absence of disease, positive reading
May be caused by high-protein diet, strenuous
exercise, dehydration, fever, or emotional stress.
Vaginal secretions may contaminate urine specimen
and give positive reading
Glucose
None
-Glycouria indicates diabetes mellitus or low renal
threshold reabsorption (if blood glucose is normal)
Ketones
None
-altered carbohydrate and fat metabolism indicates
diabetes mellitus and starvation. Findings can also
be seen in dehydration, vomiting and severe
diarrhea
Bilirubin
None
-presence of bilirubin is as significant as jaundice in
detection of liver disorders. Bilirubin may appear
in urine before jaundice becomes visible or may be
present with hepatic disorders who do not have
recognizable jaundice
Specific
Gravity
1.003-1.030
SP of morning urine specimen reflects maximum
concentrating ability of kidney and is 1.025-1.030.
Low SP indicates dilute urine and possible
excessive diuresis. High SP indicates dehydration.
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If it becomes fixed at about 1.010, this indicates
renal inability to concentrate urine, suggesting
kidney is progressing to end stage renal disease
Osmolality
300-1300mOsm/kg
-measurement is a more accurate method than SG
for determining diluting and concentrating ability of
kidneys. Deviations from normal indicate tubular
dysfunction. Findings indicate if kidney has lost
ability to concentrate urine.
pH
4.0-8.0
-if > 8.0 finding may be the result of standing of
urine or urinary tract infections b/c bacteria
decompose urea to form ammonia. If > 4.0 may
indicate respiratory or metabolic acidosis
RBC
0-4/hpf
-bleeding in urinary tract is caused by calculi,
cystitis, neoplasm, glomerulonephritis,
tuberculosis, kidney biopsy or trauma
WBC
0-5/hpf
-increased WBC in urine (pyuria) indicates urinary
Tract infection or inflammation
Casts
none or
occasional
hyaline
-casts are molds of the renal tubules and may
protein, WBC, RBCs or bacteria. Noncellular
casts are hyaline in appearance, and a few may
be found in normal urine. Casts indicate renal
dysfunction or upper urinary tract infections.
Culture
for
organisms
No
organisms
<10-4,
organisms/cc
result of normal
flora
-bacteria count > 100,000/cc indicate UTI;
organisms most commonly found in UTI are
E. coli, enterococci, Klebsiela, Proteus,
Streptococci
* most common cause of intra-renal failure is ischemic or nephrotoxic injury. Ischemic
injury occurs when systolic BP < 60mmHg for > 40 minutes.
Normal Adult GFR=125cc/minute
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Chronic Kidney Disease (CKD) involves progressive, irreversible destruction of the
nephrons in both kidneys
The kidneys have a remarkable functional reserve. Up to 80% of the GFR (reflected in
creatinine clearance measurements) may be lost with few overt changes in the
functioning of the body. A person is born with 2 million nephrons and can survive
without dialysis until almost 90% of the nephrons are lost. In the majority of cases the
individual passes through the early states of CKD without recognizing the disease state
b/c the remaining nephrons hypertrophy to compensate.
STAGES OF CHRONIC KIDNEY DISEASE: normal adult GFR 125cc/min.
Stage 1: Kidney damage with normal or increased GFR GFR at or > 90
Stage 2: Kidney damage with mild decrease GFR
GFR 60-90
Stage 3: Moderate decrease GFR
GFR 30-59
Stage 4: Severe GFR
GFR 15-29
Stage 5: Kidney Failure
GFR < 15
Stages are defined based on the fx. of the kidney (GFR). The last stage of kidney disease
occurs when the GFR is < 15cc/min.
Causes of chronic kidney failure
- Diabetes Nephropathy
- Hypertension
- Glomerulonephritis
- Cystic Kidney Disease
When creatinine clearance falls below 15ml/min. (usual 85-135/min/adult) some
form of dialysis or transplantation is required.
As renal fx. progressively deteriorates every body system becomes affected. The clinical
manifestations are a result of retained substances, including urea, creatinine, phenols,
hormones, electrolytes and water and many other substances. **toxins build up.
Uremia: a syndrome that incorporates all the signs and symptoms seen in various systems
throughout the body in chronic kidney disease
Urinary Manifestations of CKD
-polyuria (early manifestation)
-SG fixed around 1.010: this is due to the inability of kidneys to concentrate urine
-oliguria and then progresses to anuria (urine output < 40cc/24 hrs.)
-urine (if produced) contains proteinuria, casts, pyuria and hematuria could be present
depending on the cause of kidney disease
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Metabolic Manifestations of CKD
-Waste product accumulation
-as GFR DECREASED, the BUN and serum creatinine levels INCREASED. BUN is
increased not only by kidney failure, but also by protein intake, fever, corticosteroids and
catabolism. As BUN increase, N/V, lethargy, fatigue, impaired thought processes and
headache
-Altered Carbohydrate metabolism: defective carbohydrate metabolism is caused by
impaired glucose use resulting from cellular insensitivity to the normal action of insulin.
The exact nature of this insulin resistance is unclear, but it may be related to circulating
insulin antagonists, alteration in hormone receptors or abnormalities of transport
mechanism.
-Moderate hyperglycemia, hyperinsulinemia, and abnormal glucose tolerance may be
seen. Insulin and glucose metabolism may improve, but not to normal levels, after the
initiation of dialysis
-diabetics who become uremic may require less insulin than before the onset of CKD.
This is b/c insulin, which is dependent on the kidneys for excretion, remains in
circulation longer. The insulin dosing must be individualized and glucose levels
monitored carefully.
-Elevated triglycerides: hyperinsulinemia stimulates hepatic production of triglycerides.
Almost all pts. with uremia develop hyperlipidemia, with elevated very low density
lipoprotein (VLDL) normal or decreased low-density lipoproteins and lowered high
density lipoproteins (HDL). The reason for the alteration in lipid metabolism is related to
decreased levels of the enzyme lipoprotein lipase that is important in the breakdown of
lipoproteins. Hyperlipidemia is a definite risk factor for accelerated atherosclerosis. This
can worsen atherosclerotic changes in diabetes with ESRD.
-the serum level of triglycerides does not usually decrease after dialysis is started. For
pts. receiving chronic PD, the level frequently becomes higher as a result of the increased
amount of glucose absorbed from the peritoneal dialysate fluid. Elevated glucose levels
lead to increased insulin. Insulin stimulates the liver to produce triglycerides.
Electrolyte & Acid-Base Imbalances
-Potassium: hyperkalemia is a the most serious electrolyte disorder associated with
kidney disease. Fatal arrythmias can occur when serum potassium levels reaches 7-8
mEq/L. Hyperkalemia results from the decreased excretion by the kidneys, the
breakdown of cellular proteins, bleeding and metabolic acidosis. Potassium may also
come from the food consumed, dietary supplements, drugs and IV infusion.
-Sodium: Na may be normal or low in renal failure. B/c of impaired sodium excretion,
sodium along with water is retained. If large quantities of body water are retained,
dilutional hyponatremia occurs. Sodium retention can contribute to edema, hypertension
and congestive heart failure. Sodium intake must individually determined but is
generally restricted to 2g per day.
-Calcium & Phosphate: same as above
-Magnesium: primarily excreted by the kidneys. Hypomagnesaemia is generally not a
problem unless the pt. is ingesting magnesium (milk of magnesia, magnesium citrate,
antacids containing magnesium). Clinical manifestations of hypermagnesemia can
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include absence of reflexes, decreased mental status, cardiac arrhythmias, hypotension
and respiratory failure.
-Metabolic Acidosis: Results from the impaired ability of the kidneys to excrete the acid
load (primarily ammonia) and from defective reabsorption and regeneration of
bicarbonate. The average adult produces 80-90 mEq of acid per day.
-in renal failure, plasma bicarbonate, which is an indirect measure of acidosis, usually
falls to a new steady state at around 16-20 mEq/L. It generally does not progress below
this level b/c hydrogen ion production is usually balanced by buffering from
demineralization of the bone (the phosphate buffering system). Although Kussmal
respiration is uncommon in CRF, this breathing pattern reduces the severity of acidosis
by increasing CO2 excretion.
*hyperkalemia decreases acid secretion b/c inhibits renal ammonium production and
excretion. In hyperkalemic, hyperchloremic metabolic acidosis associated with selective
aldosterone deficiency, correction of potassium alone (diuretics of kayexalate) may
worsen the acidosis. Sodium bicarbonate tablets are the preferred source of alkali
replacement.
Hematologic System
-Anemia: iron deficiency, folic acid, which is essential for RBC maturation is dialyzable.
If not replaced in the diet or by drugs, megalobastic anemia may develop in pts. receiving
hemodialysis
Tx. of Anemia
Most common cause of anemia is erythropoietin.
-Epogen, Procrit (Erythropoietin) is used to tx. anemia
Adverse effects: Hypertension – related to hemodynamic changes; increased blood
viscosity; functional iron deficiency resulting from the increase demand for iron to
support erythropoietin; iron supplements given; GI side effects of iron (GI irritation,
constipation)
Adverse Effects of Erythropoietin**
-EXACERBATION of HYPERTENSION. The most common complication of
erythropoietin administration. This can be managed if the hematocrit rises slowly
-accelerated thombosis of hemodialysis
-decreased dialysis efficiency r/t hyperviscosity
Benefits of Erythropoietin
-erythropoietin administered to pts. with CRF improves sense of well being;
beneficial cardiac effects such as decreased LVF-left ventricular function.
Erythropoietin should be administered to anemic pts. with CRF to maintain the
hematocrit > 33%
**oral iron supplements should be given at the same time as phosphate binder b/c
calcium binds to iron.
-advise pts. of a change in stool color (dark)
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-AVOID TRANSFUSION if possible; undesirable side effects of transfusions include:
suppression of erythropoietin as a result of a decrease in the hypoxic stimulus, the
possible transmission of Hepatitis B or Co or HIV and possible iron overload b/c each
bag of blood contains 250mg of iron
-Decreased Erythropoietin: erythropoietin stimulates cells in the bone marrow to
produce RBC.
-nutritional deficiencies
-decreased RBC life span
-increased hemolysis of RBC
-frequent blood sampling
-GI bleeding
-blood loss in the dialyze
-elevated levels of PTH: (produced to compensate for low serum calcium levels) can
inhibit erythropoietin, shorten survival of RBC and cause bone marrow fibrosis, which
can result in decreased number of hematopoietic cells.
-Decreased platelets:
-impaired release of platelet Factor 3
-increased concentration of Factor VIII and fibrinogen
-hemorrhage
-GI bleeding
Tx. of platelet dysfunction
-bleeding tendency (ecchymoses, purpura, epitaxis, prolonged bleeding from
venipuncture sites), prolonged bleeding
**Cryoprecipitate 10 Units IV every 12-24 hrs. for emergent situations
-Infection: caused by changes in leukocyte function and altered immune response;
altered by both neutrophils and monocytes
-lymphopenia
-lymphoid tissue atrophy
-decreased antibody production
-suppression of delayed hypersensitivity response
Other contribution factors to infection:
-malnutrition
-hyperglycemia
-external trauma (catheters, needles, etc.)
There is an increased risk of cancer in pts. with renal failure to lungs, breast, uterus,
colon, prostate, and skin malignancies.
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Cardiovascular System
-hypertension
-increased sodium retention
-increased extracellular fluid volume
-MI
-stroke
-atherosclerotic vascular disease
-intrarenal arterial spasm
-left ventricular hypertrophy
-congestive heart failure
-cardiac arrhythmias
-pulmonary edema
-nephropathy
-pericarditis (friction rub, chest pain, low grade fever)
-pericardial effusion
-cardiac tamponade
-retinopathy
-encephalopathy
Respiratory System
-Cough reflex depressed
-“uremic lung”
-uremic pneumonitis: condition responds to dialysis treatment
GI System: every part of the GI tract is affected as a result of inflammation of mucosa
caused by excessive urea.
-mucosal ulceration: found throughout the GI tract and caused by increased ammonia
levels produced by bacterial breakdown of urea
-stomatitis: exudates and ulcerations
-metallic taste mough
-uremic fetor: urine odor to the breath
-anorexia, N/V
-malnutrition
-weight loss
-GI bleeding: contributed by irritation of the mucosa by waste products coupled with
platelet defect
-diarrhea: b/c of hyperkalemia and altered calcium level
-constipation: due to ingestion of iron salts and calcium containing phosphate binders;
also fluid limit and inactivity
Neurological System
-fatigue
-altered mental ability
-coma
-restless legs syndrome
-bilateral foot drop
-loss of deep tendon reflexes
-jerking
-nocturnal leg cramps
-irritability
-seizures
-peripheral neuropathy: due to slow nerve conduction
-paresthesias
-muscular weakness and atrophy
-muscle twitching
-asterixis (hand-flapping tremors)
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Musculoskeletal System
-Renal Osteodystrophy is a syndrome of skeletal changes found in chronic kidney
disease. This syndrome is a result of alterations in calcium and phosphate metabolism.
Normally, the calcium/phosphate ratio maintains the electrolytes in a soluble state. As
the GFR decreases, urinary phosphate excretion is impaired and the serum phosphate
increases.
-the kidneys metabolize Vitamin D to its active form. In renal failure the kidneys fail to
activate Vitamin D, calcium absorption is impaired and serum calcium decreased. Low
serum calcium stimulate the release of PTH, which causes reabsorption of calcium and
phosphate from the bone. This release causes increases serum Calcium and Phosphate
from the bone. The excess Phosphate will bind with calcium leading to the formation of
insoluble metastatic calcifications that are deposited throughout the body.
-common sites are the blood vessels, joints, lungs, muscles, myocardium and eyes
**“uremic red eye” is caused by the irritation from deposits in the eye. Metastatic
calcifications in the arteries of the fingers and toes may cause gangrene. Intracardiac
calcifications can disrupt the conduction system and cause cardiac arrest.
Treatment of Renal Osteodystrophy
-restrict phosphate < 1000mg/day
-calcium-based phosphate binders i.e.calcium barbonate (tums); calcium acetate (PhosLo)
are used to bind the phosphate which then is excreted in the stool
-Sevelamer (Renagel) is a phosphate binder that does not contain either calcium or
aluminum; also added benefit of lowering cholesterol and LDL
-Aluminum hydroxide gels or antacids (Alu-Caps, Amphojel, Basljel,Alternagel) should
not be used to bind phosphate b/c dementia and bone disease (osteomalacia) are
associated with excessive absorption of aluminum hydroxide gels or antacids.
-Magnesium containing antacids (Maalox, Mylanta) should not be given b/c magnesium
is dependent on the kidneys for excretion
Phosphate binders: Tums, PhosLo, should be administered with each meal to be effective
b/c most phosphate is absorbed within one hour after eating.
-Hypercalcemia may occur with calcium supplementation and is associated with
increased cardiac calcification and mortality in ESRD.
-Constipation is frequent side effect of phosphate binders and may necessitate stool
softeners
-Hypocalcemia results from the inability of GI tract to absorb calcium in the absence of
Vitamin D. If hypocalcemia persists in the setting of controlled serum phosphate levels
and supplemental calcium, the active form of Vitamin D is given.
-Active form of Vitamin D: Calcitrol, Rocaltrol
-Paricalcitrol (Zemplar) and doxercalciferol (Hectorol) are new synthetic Vitamin D
analogs that are designed to reduce PTH. They cause less hypercalcemia and
hyperphosphatemia level before administering calcium or Vitamin D. It is important to
lower serum phosphate level before administering phosphate or Vitamin D b/c these
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drugs may contribute to soft tissue calcification if both calcium and phosphate levels
are elevated.
-If renal osteodystrophy remains despite conservative treatment, subtotal
parathyroidectomy may be peformed to decrease the synthesis and secretion of PTH
-most common methods to evaluate the status of bone disease are x-rays, bone scan,
biopsy and bone densitometry.
-PTH and alkaline phosphatase levels should be monitored; Alkaline Phosphatase is
elevated when there is a demineralization of bone and increased in liver disease.
2 Types of Osteodystrophy
1-Osteomalacia: causes lack of mineralization of newly formed bone, hypocalcemia,
increased aluminium
2-Osteitis Fibrosa: causes marked elevated levels of PTH (causes bone reabsorption)
Integumetary System
-Yellow-Gray discoloration of skin: results from absorption and retention of urinary
pigments that normally give the characteristics color to urine. The skin also appears
pale as a result of anemia and is dry and scaly b/c of a decrease in oil and sweat
gland activity. Decreased perspiration results from a decreased in size of sweat
glands.
-Pruritis: mostly results from a combination of dry skin, calcium-phosphate deposition in
the skin, and sensory neuropathy. The itching may be so intense that it can lead to
bleeding or infection secondary to scratching. Uremic frost is a rare condition in which
urea crystallizes on the skin and is usually seen only when BUN levels are extremely
high. It occurs when a pt. refuses dialysis or is withdrawn from dialysis.
-Hair is dry and brittle and may fall out. The nails are thin, brittle and ridged.
-Petechiae and ecchymosis may be present and are due to platelet abnormalities.
Reproductive System
-infertility and decreased libido
-women decreased levels of estrogen, progesterone, luteinizing hormone; amenorrhea
-men decreased testosterone; low sperm count
Endocrine System
-Hypothyroidism: low levels of T-3, T-4
Psychological System
-personality and behavioral changes, emotional lability, withdrawal, depression, fatigue,
changes in body image, decrease ability to concentrate and slowed mental activity. Long
Labs/Diagnostics
-serum electrolyes
-protein-creatinine ratio in FIRST VOIDED SPECIMEN in the morning
-UA & culture
-hgb/hct levels
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Conservative mgmt. is attempted before maintenance dialysis. Every attempt is made to
detect and treat potentially reversible causes of renal failure (cardiac failure, dehydration,
infections, nephrotoxins, UTI, obstructions, renal artery stenosis). Goals of conservative
mgmt. are to preserve existing renal fx., treat clinical manifestations, prevent
complications, provide comfort, educate.
Treatment of Hypertension
-Na restriction
-fluid restriction
-antihypertensive agents
-diuretics
-Beta Blockers
-ACE inhibitors: decrease proteinuria and delay progression of renal failure. Must be
used cautiously with ESRD b/c they can further decrease GFR and increase serum
potassium.
-ACE inhibitors should be considered the primary choice as an antihypertensive agent in
pts. with CRF if no absolute contraindications are evident. Absolute contraindications for
ACE inhibitors include: bilateral renal artery steonis; and advanced renal failure GFR <
20ml/min.
-pts. receiving ACE inhibitors should be closely monitored for changes in renal fx. and
hyperkalemia b/c a decline in renal fx. and hyperkalemia represent the most significant
side effect of these agents with CRF.*************
-malignant hypertension, causing histologic changes and angiotensin-mediated
vasoconstriction decreases renal blood flow and GFR. If hypertension is corrected too
quickly, the injured renal vasculature may be unable to vasodilate appropriately in
response to the lowered renal perfusion pressure, and worsen renal fx.
** blood pressure should be lowered gradually and allow vascular relaxation to occur
along with improved control of hypertension.
-teach pt. how to take and monitor b/p
Volume Dysfunction
As a result of increases Na, many pts. become volume overloaded as renal fx.
deteriorates. These pts. may be started on diuretics combine with dietary salt restriction
which can result in volume depletion ECFV-depletion. Because serum sodium is
abnormal, any concomitant disturbance i.e. diarrhea emesis, which may be mild when
renal fx. is normal can result in severe volume depletion in pts. with CRF.
-In advanced CRF, there is relatively fixed amount of sodium excretion impairing ability
to regulate salt balance precisely. As a result, CRF pts. are more prone to volume
depletion and volume overload.
-close attention to the volume status in pts. with CRF is mandatory, particularly when
there is unexplained rise in serum creatinine level. This is especially a concern with
concurrent illness or change in therapeutic interventions.
**Monitor clinical parameters for ECVFD/ECVFE:
-weight
-jugular vein distention
-congestive heart failure
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-urine sodium concentration*
-urine osmolarity*
*these clinical indicators may not reflect true picture b/c of the relative fixed Na
excretion in CRF.
-tx. ECFVE w/ diuretics: thiazides, loop, avoid potassium sparing
**Thiazide diuretics are ineffective once the GFR < 30ml/min. In this case use loop
diuretics.
Potassium Disorders
-regulation of K+ by the kidney is accomplished by the regulation of K+ excretion in the
collecting tubules. As CRF progresses, K+ excretion decrease b/c of a decline in GFR
and defect in tubular secretion. Serum K+ level does not usually rise until GFR <
15cc/min. As renal excretion of potassium declines, the GI tract, particularly the colon,
increases fecal excretion of potassium.
-serum K+ level increases b/c the normal ability of the kidneys to excrete 80-90% of the
body’s potassium is impaired. Bleeding and blood transfusion cause cellular destruction,
releasing more K+ into the extracellular fluid.
-acidosis worsens hyperkalemia as hydrogen ions enter the cells and K+ is driven out of
the cells into the extracellular fluid. K+ > 6mEq/L or arrhythmia are identified, treat
IMMEDIATELY.: tall, peaked T waves, widening of QRS complex, depressed ST wave.
-handling of potassium loads after a meal is dependent on the mvmt. of potassium into
the cell. This process is facilitated by insulin, beta-adrenergic stimulation and a
functioning sodium-potassium triphosphate. Therefore, CRF or presence of aldosterone
deficiency, beta-blocker therapy, diabetes and digitalis can cause severe hyperkalemia.
Prompt tx. of hyperkalemia is urgent.
Potassium Excess
Serum potassium level increase b/c the normal ability of the kidneys to excrete 80-90%
of the body’s K+ is impaired. Bleeding and blood transfusion cause cellular destruction,
releasing more K+ into the extracellular fluid. Adrenal insufficiency (hypoaldosterone)
can cause HYPERKALEMIA. Decreased aldosterone alters sodium reabsorption and
potassium excretion. In adrenal insufficiency, sodium is not reabsorbed back into the
body (HYPONATREMIA) and potassium cannot be excreted (HYPERKALEMIA).
Signs/Symptoms of hyperkalemia
-ascending musckle weakness (usually beginning in the legs and traveling upward to arm
and trunk)
-lethargy, nausea, abdominal cramping
-diarrhea
-hyperactive bowel sounds
-numbness, tingling
-dysrhythmia: (peaked T waves, widened QRS complex, depressed ST wave;
bradycardia: no P waves; ventricular dysrhythmia: Asystole)
-b/c diaphragm and intercostals muscles are not usually involved in hyperkalemia,
respirations fx. is not affected.
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-Hyperkalemia usually associated with METABOLIC ACIDOSIS. Why? b/c potassium
rather than hydrogen ion is exchanged for sodium in the kidney. Metabolic acidosis
causes a shift of potassium out of the cell (intracellular) and into the extracellular fluid
plasma as hydrogen (an acid) enters the cell.
Treatment of hyperkalemia
-Regular Insulin Administration IV- potassium moves into the cell when insulin is
given. Glucose is given concurrently to prevent hypoglycemia. When effects of insulin
diminish, potassium shifts back out of the cell
-Sodium Bicarbonate- therapy can correct acidosis and cause shift of potassium back
into the cell. Both insulin and NaHCO3 temporarily shift potassium back into the cell,
but will eventually shift back out.
-Calcium Gluconate- therapy is given IV and generally used in advanced cardiac
toxicity. Calcium raises the threshold for excitation resulting in decreasing likelihood of
dysrhythmia.
-Dialysis- hemodialysis brings K+ levels to normal within 30 minutes to 2 hours
-Kayexalate (sodium polystyrene sulfonate)- cation-exchange resin is administered by
mouth or retention enema. When resin is in the bowel, potassium is exchanged for
sodium. Therapy removes 1mEq of potassium per gram of drug. It is mixed in water
with sorbitol to produce osmotic diuresis allowing evacuation of potassium rich stool
from body.
** Only dialysis and kayexalate actually removes K+
Water Disorder
CRF progresses loss of ability to dilute or concentrate urine.
-risk for water intoxication (hyponatremia)
-risk for dehydration (hypernatremia)
-treatment for hyponatremia (simple) is fluid restriction.
-treatment of hyponatremia (complex) stupor, coma, altered mental status; hypertonic
saline, often combined with loop diuretic to avoid sudden volume overload and osmotic
shifts.
-hypernatreimia usually less of a problem r/t thirst stimulus
-risk for hypernatremia:
-hyper-osmolar gastrostomy tube feeding
Goal is euvolemia is established by infusion of NS and any free water deficit with ½ NS
or 5% Dextrose and water.
Calcium Deficite: Phosphate Excess
A low serum calcium level results from decreased GI absorption of calcium. Vitamin D
is necessary to absorb calcium from the small intestine. Only functioning kidneys can
activate Vitamin D. When hypocalcemia occurs, PTH secrets parathyroid hormone
which stimulates bone demineralization thereby releasing calcium from the bones.
Hypocalcemia is rarely asymptomatic in the renal failure. This is b/c in the acidosis state
associated with kidney failure more calcium is in the ionized state (free physiologically
active) rather than bound to protein.
-in an acidotic state, hypocalcemia can lead to tetany.
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-in an acidotic state, INCREASEED phosphate is released worsening hyperphophatemia.
Elevated phosphate results from decrease excretion by kidneys.
Signs/Symptoms of hyperphosphatemia (increased phosphate, decreased calcium)
-neuromuscular irritability, muscle cramps, tetany (similar to hypocalcemia).
Tx. of hyperphosphatemia includes:
-normal saline and loop diuretic. Loop diuretics are used to prevent absorption of
calcium.
-pilcamycin stimulates bone uptake of calcium
-oral phosphate to bind calcium
Signs/Symptoms of hypophosphatemia (decreased phosphate, increased calcium)
-muscle weakness, thirst, polyuria, N/V, anorexia, malaise, renal calculi, kidney stones,
platelet dysfunction, hypoxia, metabolic acidosis (similar to hypercalcemia)
Complications of Drug Therapy
Many commonly used medications can compromise renal function either by direct
nephrotoxicity (aminoglycoside antibiotics) or by inciting interstitial inflammatory
response (analgesics, penicillin, sulfa-containing drugs). Meticulous monitoring of serum
levels of any potential nephrotoxic agent, adjusting the dose of medications based on the
estimated GFR and asking pts. to avoid certain medications altogether are all
-Demerol (Meperidine) should never be administered to pt. with CRD b/c the liver
metabolizes it to normeperidine, which is dependent on the kidneys for excretion. If normeperidine accumulates, seizures could result.
-NSAID should be avoided. These drugs block the synthesis of the renal postaglandins
that produce vasodilation. This can worsen renal hypo-perfusion. Acetaminophen can be
substituted.
-ACE inhibitors- pts.on ACE inhibitors should be monitored closely for changes in renal
fx. and hyperkalemia b/c decline in renal fx. and hyperkalemia represent the most
significant side effects of these agents in pts. with CRF.
-ACE inhibitors contradincated w/ GRF < 20m./min.
Limitations of Creatinine in CRF
-creatinine value must always be interpreted with a consideration of pt.s’ age, gender and
muscle mass b/c serum creatinine is directly proportion to muscle mass. Any change in
muscle mass affects the serum creatinine level independent of GFR. Women and elderly
have lower muscle mass and hence lower serum creatinine values. A normal creatinine
level does not ensure that the GFR is normal i.e. in a pt. with significant muscle wasting a
serum creatinine level in the normal range may represent a significant reduction in GFR.
Creatinine & protein restriction
The most important dietary source of creatinine is meat. Consuming a low-protein diet
can result in a decrease of serum creatinine level by 10-30%.
-pts. with CRF is placed on a low-protein diet to slow progression of the disease.
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Creatinine and mode of excretion
Creatinine is normally eliminated by glomelurar filtration (90%) with a small amount by
the tubular section (10%). As renal fx. deteriorates tubular secretion becomes responsible
for a larger portion of creatinine excretion. B/c creatinine clearance is a measure of both
filtration and secretion, it follows that as creatinine excretion increases in progressive
CRF, GFR can fall significantly with little change in serum creatinine level or creatinine
clearance. Therefore, creatinine clearance overstimulates GFR as renal disease
progresses to near end stage.
-just as filtration can decrease without significant change in serum creatinine levels, these
levels can increase when the GFR is stable. Drugs compete with creatinine for tubular
secretion raise serum creatinine level without affecting filtration.
**changes in levels of serum creatinine and creatinine clearance must be considered with
the knowledge of changes in musckle mass, diet, accompanying illness and medications
Nutritional Therapy
-Protein restriction: decrease protein intake 0.6-0.75g/kg of IBW b/c BUN is an end
product of protein metabolism.
-Decrease phosphorus
-add ketoacids of essential amino acids b/c in the body nonessential amino acids transfer
amine groups to the essential keto acids synthesizing essential amino acids
-start dialysis; protein intake 1.2-1.3g/kd of IBW
Water Restriction
-water depends on the previous 24 hour urine output
-600cc + previous days ouput = fluid limit
-foods that are liquid at room temp. should be counted as liquid (ice cream, gelatin)
-pt. should not gain > 1-3kg between dialysis
Sodium Restriction
-sodium and salt should not be equated
i.e. 1000mg of sodium chloride (salt) = 400 mg sodium
-advise to avoid high sodium foods: cured meats, pickled foods, canned soups and stews,
franks, cold cuts, soy sauce, salad dressing.
-most salt substitutes should not be used b/c they contain potassium chloride
Potassium & Phosphate Restriction
-limit potassium
-phosphate restriction
-foods high in phosphate include: milk, ice cream, cheese, yogurt, foods containing dairy
products, pudding
-most foods high in phosphate are also high in calcium
-restricting phosphate will automatically restrict calcium
Chronic Renal Failure 14 of 15
Chronic Renal Failure, Page 15 of 15
REMEMBER:
-phosphate binders should be taken with meals
-iron supplements should be taken between meals
-weight gain more than 4 lbs or 2kg should be reported
Clinical signs of Acidosis
-associated with neurological & cardiac symptoms
-headache, confusion, lethargy, coma
-CNS depression
-cardiac dysrhythmia
-hypotension
-decreased myocardial contraction
-hyperkalemia – pH decrease (acidosis) raises serum potassium
-acidosis moves K+ out of the cell (intracellular) so that hydrogen can move into the cell.
This is a compensatory mechanism to reduce the serum hydrogen content and reduce
acidosis. Therefore, in an acidotic state, the serum potassium level increases
HYPERKALEMIA
-pts. in renal failure develop progressive inability to excrete hydrogen b/c of their
decreased ability to excrete acid and ammonium ions. This results in acidosis.
-intestinal fluid below the stomach including pancreatic and biliary secretions are
alkaline. Severe diarrhea or removal of thse fluids (drainage/fistula) causes a loss of
HCO2 (bicarbonate) and METABOLIC ACIDOSIS.
-increased BUN
-increased creatinine
-decreased sodum
-increased potassium
-decreased pH
-decreased bicarbonate
-decreased calcium
-increased phosphate
Clinical signs of Alkalosis
-associated with central & peripheral nervous system
-lightheadeness
-alteration of consciousness
-cramps
-nervous, irritable, muscle tremors
-seizures
-signs of hypocalcemia & hypokalemia – pH increases (alkalosis) calcium combines with
proteins and reduces serum calcium level
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