Acute renal failure & Calcimate

Under supervision of:

Dr: Fatma Saied

 ‫بسم هّٰللا الرحمن الرحيم‬
‫والصالة والسالم على رسولنا الكريم‬
‫نبدأ بسم هّٰللا وندعوا ونتضامن مع أهلنا في فلسطين فـ‬
‫اللهم اجعل ألهلنا في فلسطين النصر والعزة والغلبة والقوة‬
‫اللهم ان نستودعك فلسطين وأهلها ونسائها واطفالها وشيوخها ورجالها‬
‫‪Prepared by:‬‬

‫‪ ‬مصطفى محمود على حسن‬

‫‪ ‬احمد حمدى عبد العال خليفه‬

‫‪ ‬معتز رفاعي عبدالباسط على‬

‫‪ ‬مايكل عصام ادیب شحاته‬

‫‪ ‬طارق على محمد البدرى‬

‫‪ ‬عبد الرحمن احمد محمد سلیمان‬

‫انوار عبد الحليم فتوح محمدين‬ ‫‪‬‬

‫‪ ‬عزالدين شحاته عبدالرحمن احمد‬

‫‪ ‬ايمان فتحى فوزى عطية‬

‫‪ ‬نهله مراد عرفه همام‬

 Acute renal failure
Outlines:
 Introduction
 Definition
 Pathophysiology
 Causes & Risk factors
 Signs and Symptoms
 Nursing management
 Acute renal failure

Introduction

Kidneys are a pair of organs that are responsible for filtering

out the waste products from the body. Not only that, but they
also have a role in electrolyte balance maintenance, hormonal
regulation, regulation of blood pressure and RBC synthesis.
When any of these functions ceases to occur properly, it leads
to renal failure.
 Acute renal failure

Introduction

The term renal failure denotes inability of the kidneys to

perform excretory function leading to retention of nitrogenous
waste products from the blood. Acute and chronic renal failure
are the two kinds of kidney failure. When a patient needs renal
replacement therapy, the condition is called end-stage renal
disease (ESRD).
 Definition

Kidney failure, also called renal failure, partial or complete

loss of kidney function. Kidney failure is classified as acute
(when the onset is sudden) or chronic.
 Pathophysiology

Initiation phase

This phase lasts for hours to days. It involves reduction in

glomerular filtration rate from decreased renal blood flow.
Ischemic injury to the tubular epithelial cells and renal
parenchyma causes the tubular cells to slough off and form
casts that block the flow of glomerular filtrate down the
nephron.
 Pathophysiology

Oliguric (anuric) phase

This phase lasts for 8 to 14 days or longer, depending on

nature of acute kidney failure and dialysis initiation. It
involves decreased urine output (below 400 mL/day) ,
increases in blood urea nitrogen (BUN) and creatinine levels,
electrolyte disturbances, acidosis, and fluid overload (from
kidney's inability to excrete water).
 Pathophysiology

Diuretic phase

This phase lasts for 7 to 14 days. It involves It involves

increased urine output (above 400 mL/day), renal tubule
scarring and edema, increased glomerular filtration rate and
possible electrolyte depletion from excretion of more water
and osmotic effects of high blood urea nitrogen (BUN).
 Pathophysiology

Recovery phase

This phase lasts for several months to 1 year. This stage

essentially involves regeneration of renal tubular epithelial
cells and restoration of urine output. It involves decreased
edema, normalization of fluid and electrolyte balance and
increased glomerular filtration rate.
 Causes

Pre-renal causes
 Significant bleeding
 Severe diarrhea
 Severe vomiting
 Septic shock
 Anaphylaxis
 Heart failure
 Reactions to medications such as:
 Angiotensin converting enzyme inhibitors

 Causes

Intrinsic causes
 Reactions to medications such as nonsteroidal anti-
inflammatory drugs or amphotericin B
 Reactions to contrast dye
 Lupus
Post-renal causes
 Large kidney stones
 Blood clots
 Tumor in or around the bladder
 Pre-
renal
causes

Causes

Post-
Intrinsic
renal
causes
causes
 Signs and symptoms

Signs of acute kidney failure include:

 Suddenly not urinating as much or at all

 Nausea  Irregular heartbeat
 Fatigue  Chest pain or pressure
 Weakness  Confusion
 Shortness of breath  Seizures
 Swelling of the legs, feet, or ankles
 Signs and symptoms

Symptoms of acute kidney failure include:

 Loss of appetite
 Shortness ofbreath
 Irregular heart beat
 Chest pain
 Decreased urine output
 Edema
Signs and symptoms
 Nursing management

A.Impaired Urinary Elimination related to renal malfunction

Nursing Interventions

 Evaluate and maintain urinary catheters and drains.

 Observe for changes in urine characteristics.
 Observe for changes in mental status, behavior, or level of
consciousness.
 Monitor electrolytes, BUN, creatinine, albumin, and arterial
blood gases (ABGs).
 Nursing management

 Provide routine voiding measures, such as privacy, normal

position, running water in the sink, and pouring warm water
over the perineum.
 Encourage fluid intake as prescribed.
 Provide and teach adequate perineal care.
 Insert a urinary catheter as indicated.
 Encourage the client to improve mobility and engage in
physical activities.
 Maintain patency of the urinary catheter; keep the drainage
 Nursing management

B. Hypovolemia related to impairment of excretion of water

and electrolyte
Nursing Interventions
 Assess the level of consciousness.
 Investigate changes in mentation and the presence of
restlessness.
 Assess skin, face, and dependent areas for edema.
 Evaluate the degree of edema .
 Monitor vital signs.
 Nursing management

 Auscultate lung and heart sounds.

 Record intake and output.
 Monitor urine-specific gravity.
 Weigh daily at the same time of day, on the same scale, with
the same equipment and clothing.
 Monitor echocardiography results as indicated.
 Administer and/or restrict fluids as indicated.
 Promote sodium and fluid restriction as indicated.
 Insert indwelling catheter, as indicated.
 Nursing management

C. Deficient knowledge related to deficient learning

resources

Nursing Interventions

 Review disease process and prognosis and future expectations.

 Review dietary restrictions, including phosphorus (carbonated
drinks, processed foods, poultry, corn, peanuts) and
magnesium (whole grain products, legumes).
 Enforce fluid and sodium restrictions when indicated.
 Nursing management

 Discuss other nutritional concerns such as regulating protein

intake according to the level of renal function.
 Encourage adequate calorie intake, especially from
carbohydrates in the non-diabetic patient.
 Discuss drug therapy, including the use of calcium
supplements and phosphate binders such as aluminum
hydroxide antacids and avoidance of magnesium antacids, and
vitamin D.
 Nursing management

 Stress the importance of reading all product labels (drugs and

food) and not taking medications without prior approval of the
healthcare provider.
 Review measures to prevent bleeding and hemorrhage, (use of
a soft toothbrush, electric razor); avoidance of constipation,
forceful blowing of the nose, strenuous exercise, and contact
sports.
 Instruct in self-observation and self-monitoring of BP,
including scheduling a rest period before taking BP, using the
 Nursing management

 Establish a routine exercise program within the limits of

individual ability; intersperse adequate rest periods with
activities.
 Identify available resources as indicated. Stress the necessity
of medical and laboratory follow-up.
 Identify signs and symptoms requiring immediate medical
evaluation.
 Review strategies to prevent constipation, including stool
softeners and bulk laxatives but avoiding magnesium
 Calcimate

Definition: Calcimate is a combination medication used to

prevent or treat low blood calcium levels in people who do not
get enough calcium from their diets.

Trade name: Calcimate

Scientific name: Calcium Carbonate 500mg

 Mechanism of action

The extracellular calcium-sensing receptor on the parathyroid

cell surface negatively regulates secretion of parathyroid
hormone. Its activation by small changes in the extracellular
concentration of ionized calcium decreases PTH secretion and
secondarily bone turnover. Calcium-sensing receptor is an ideal
target for compounds that may be developed to modulate its
activity - activating calcimimetics and inhibiting calcilytics.
Calcimimetics can amplify the sensitivity of the calcium-sensing
receptor to ionized calcium, thereby suppressing PTH levels and
 Mechanism of action

They dose-dependently reduce the secretion of PTH in cultured

parathyroid cells, in animal models and in humans. In uremic
animals, these compounds prevent parathyroid cell hyperplasia
when given at the onset of the disease and stop cell proliferation
if they are administered afterwards, when the hyperplasia
already exists. They normalize plasma PTH levels and bone
remodeling. In uremic patients undergoing hemodialysis,
calcimimetics reduce plasma PTH concentrations in the short
(12 weeks) and long (2 years) terms. They also reduce serum
 Mechanism of action

Calcimimetics are therefore an alternative for the treatment of

secondary hyperparathyroidism, particularly in dialysis patients,
when increased serum levels of calcium-phosphorus product, the
attendant risk of cardiovascular calcification, and its lack of
efficacy limit use of the standard treatment.
 Indications

 Indigestion.
 Antiacid:
 Gastric ulcer.
 Gastroesophageal reflux disease (esophageal reflux).
 Osteoporosis.
 Chronic renal failure.
 Hypothyroidism.
 Calcium deficiency during pregnancy and lactation
 Calcium and vitamin D deficiency
 Contraindications

 Hypercalcemia (with hyperfunction of the parathyroid

glands)
 Hypercalciuria
 Urolithiasis disease
 Decalcifying tumors (myeloma, bone metastases,
sarcoidosis)
 Osteoporosis due to immobilization
 Pulmonary tuberculosis (active form)
 Increased sensitivity to drug components
 Side effects

 Abdominal distension.
 Nausea and vomiting.
 Anorexia
 Loss of appetite
 Constipation
 Vomiting
 High calcium levels
 Low phosphate levels
 Milk-alkali syndrome
 ‫بسم هّٰللا الرحمن الرحيم‬
‫والصالة والسالم على رسولنا الكريم‬
‫نبدأ بسم هّٰللا وندعوا ونتضامن مع أهلنا في فلسطين فـ‬
‫اللهم اجعل ألهلنا في فلسطين النصر والعزة والغلبة والقوة‬
‫اللهم ان نستودعك فلسطين وأهلها ونسائها واطفالها وشيوخها ورجالها‬
Thank you