Risk factors/Predisposing factors

Acute Renal Failure

• Advanced age
• Chrinic infection
• Diabetes

Diabetes can also damage the kidneys because it may cause:

—fhigh blood pressure

—fhardening of the arteries

—fdamage to the nerves that control the bladder, making it difficult to know when you need to urinate

- repeated urinary tract infections (Bacteria grow rapidly in urine with a high sugar level.)

• High blood pressure

-If left uncontrolled, high blood pressure can damage the kidneys by causing the blood vessels of the kidneys to become thickened and rigid

-This reduces the blood supply, which destroys kidney tissue and significantly impairs the kidneys' ability to cleanse the blood and balance body chemicals

• Kidney diseases
• Liver diseases
• Prostate gland enlargement

f—can block the normal flow of urine, and cause the urine to back up into the kidney

• Bladder outlet obstruction

Obstructions, or blockages, can occur anywhere within the urinary system from the kidney itself to the ureter, bladder or urethra. Some of the causes of blockage

qkidney stones

qan enlarged prostate gland in men

q tumours or blood clots

Even when a blockage is only partial, damage can still occur.

Kidney Stones

- Kidney stones are not a major cause of kidney failure. However, recurrent kidney stones can cause damage to the kidney tissue and contribute to kidney failure

- Most stones begin when a tiny particle of solid material is deposited in calycesà more and more materials are added to the initial pebbleà it enlarges to become a stone.

f —Also, stones often make it easier to get infections in the urinary tract. If have repeated infections and/or scarring from kidney stones, the damage could contribute to decreased kidney function.

Chronic Renal Failure

• Diabetes
• High Blood Pressure
• Bladder outlet obstruction
• Lupus Erythematosus

—This condition is known as an autoimmune disease. Normally, the body's immune system makes proteins, called antibodies, which protect the body against infections and foreign materials, called antigens. In an autoimmune disorder, the immune system begins to destroy own tissues and organs because it cannot tell the difference between a foreign substance and the tissue of your body

—family history and environmental factors (e.g., infections, viruses, and toxic chemicals) may play key roles

• Chronic Glomerulonephritis

-—This disease causes inflammation of the part of the kidney that filters the blood, the glomeruli

—-Glomerulonephritis may be acute or chronic

—-Acute glomerulonephritis usually develops suddenly, often following an infection in the throat (such as strep throat) or on the skin. The problem usually is related to a malfunction in the immune system. The antibodies produced by the body to fight the infection persist after the bacteria have been destroyed, and these antibodies begin to damage the kidneys.

• Congenital Kidney disease

—These defects can range from absence of one or both kidneys to abnormalities in the position, form, size or structure of the kidneys and other parts of the urinary system.

—most common congenital problems

vdefects in the ureters (the tubes that carry urine from the kidneys to the bladder)

vurethra (the tube that drains urine from the bladder during urination)

These defects can block the normal flow of urine, causing urine to back up, or "reflux" to the kidneys. These problems are among the more common causes of kidney failure in children

• Family history of kidney disease

—Polycystic Kidney Disease (PKD)

÷The adult type, which is called autosomal dominant PKD, or ADPKD, occurs when an abnormal gene is inherited from one parent. The childhood variety, which is called autosomal recessive PKD, or ARPKD, occurs when both parents pass an abnormal gene to the child.

—-Polycystic kidney disease is characterized by the growth of cysts (soft, fluid filled sacs) that form in the kidney and other organs, such as the liver and pancreas. Outpouchings may also occur in the large intestine and blood vessels of the brain.

-—The cysts enlarge over time, and eventually, they can replace the kidney tissue, reducing kidney function and, in some cases, leading to kidney failure. The kidneys enlarge as the cysts enlarge, and they can weigh more than 20 pounds toward the end of the process.

Alport Syndrome

—-inherited form of kidney inflammation (nephritis)

—-mutation in a gene for a protein in connective tissue, called collagen

—-genetic condition characterized by kidney disease, hearing loss, and eye abnormalities

-—most often affects males

• Urinary Tract Infections

—occur when bacteria get into the urinary tract and cause symptoms such as pain, fever and an increased need to urinate. Usually, these infections remain in the bladder, but they sometimes spread to the kidney.

• Exposure to drugs and toxins

—Using large amounts of certain pain relievers may cause a risk of kidney damage called analgesic nephropathy. This is especially true for pain relievers that combine more than one active ingredient in one pill.

The kidneys get direct exposure to antibiotics because they are the pathway for eliminating these drugs from the body. The longer the kidneys are exposed to the drugs and the higher the dosages, the greater the chance of possible kidney damage

—Certain chemicals, drugs, or other substances can also harm the kidneys. These are called nephrotoxins.

—Industrial areas may be a source of environmental nephrotoxins, such as heavy metals (lead, cadmium, bismuth, arsenic, copper and mercury), carbon tetrachloride, ethylene glycol, trichloroethylene, carbon monoxide, and chlorinated hydrocarbons. Snake venom and certain mushrooms can also destroy kidney tissue.

References:

MedlinePlus

—http://www.nlm.nih.gov/medlineplus/ency/article/000521.htm

—http://www.nlm.nih.gov/medlineplus/ency/article/000504.htm

National Kidney Foundation Inc

—http://www.kidney.org/patients/plu/plu_intro/pluo_5.cfm

—http://ghr.nlm.nih.gov/condition=alportsyndrome

General Summary

Renal Function

Kidney is located around vertebra L2.

Nephron: Glomerulus, proximal convulated tubule, Loop of Henle, distal convulated tubule, collecting duct.

Renal function

1. Conversion of calcidiol to calcitriol (vitamin D3). Raises blood concentration of calcium by promoting intestinal absorption and slightly inhibiting loss in urine. More calcium available for bone deposition.
2. Secretes renin, converting angiotensinogen to angiotensin 1. Angiotensin-converting enzyme on the lining of blood capillaries converts it to angiotensin 2. This hormone causes vasoconstriction.
3. Secretes 85% of the body’s erythropoietin. Promotes RBC production and increases oxygen carrying capacity of blood.
4. Filter blood plasma, separates and eliminates waste from the blood.
5. Regulate blood volume and pressure
6. Regulate osmolarity of body fluids
7. In extreme starvation, they carry out gluconeogenesis by deaminating amino acids and excreting the amino group as ammonia.

Investigations:

Types of tests and investigations:

1. Urine Test

2. Blood Test

3. Ultrasound

4. Angiography

Renal Failure:

Pathophysiology/Aetiology

Acute renal failure :
-Severe and prolonged circulatory shock or heart failure
*Burns
*Crush injuries
*Sepsis
-Nephrotoxins
-Glumerulonephritis
-Mechanical obstruction
*Calculi
*Blood clots
*Tumour

Chronic renal failure :
-Chronic Kidney Disease :
*Bilateral pyelonephritis
-Systemic disorder
*Hypertension
*Diabetes

Signs/Symptoms

Acute renal failure

• Bloody stools
• Breath odour
• Bruising easily
• Prolonged bleeding
• Changes in mental status or mood
• Decreased apetite
• Decreased sensation, especially in the hands or feet
• Fatigue
• Flank pain (between the ribs and hips)
• Hand tremor
• High blood pressure
• Metallic taste in mouth
• Nausea or vomiting, may last for days
• Persisent hiccups
• Nosebleeds
• Seizures
• Slow, sluggish movements
• Swelling-generalised 
• Swelling of the ankle, feet, and leg swelling
• Urination changes
• Shortness of breath

Chronic renal failure

Initial symptoms

• Fatigue
• Frequent hiccups
• General ill feeling
• Generalised itching
• Headache
• Nausea, vomiting
• Unintentional weight loss

Later symptoms

• Blood in the vomits or in stools
• Decreased alertness, including drowsiness, confusion, delirium, or coma
• Decreased sensation in the hands, feet, or other areas
• Easy bruising and bleeding
• Increased or decreased urine output
• Muscle twitching or cramps
• Seizures
• White crystals in and on the skin (uremic frost)

Additional symptoms

• Abnormally dark or light skin
• Agitation
• Breath odour
• Excessive nighttime urination (nocturia)
• Excessive thirst
• High blood pressure

Differential Diagnosis

• UTI
• Urinary Obstruction
• Urinary Incontinence
• Chronic Renal Failure
• Acute Renal Failure

Predisposing Factors/Risk Factors

Risk factors for developing acute Renal Failure

• Advanced age
• Chronic infection
• Diabetes
• High blood pressure
• Kidney diseases
• Liver diseases 
• Prostate gland enlargement
• Bladder outlet obstruction

Risk factors for developing chronic Renal Failure

• Diabetes
• High blood pressure 
• Sickle cell disease 
• Systemic Lupus erythematosus 
• Chronic glomerulonephritis 
• Kidney disease present at birth (congenital) 
• Bladder outlet obstruction 
• Overexposure to toxins and to some medications 
• Family history of kidney disease 
• Age 60 or older 

treatment and management

wk

Prevention

Fluid balances will be carefully monitored.

o    Your intake and output will be measured, and you may be weighed every day.

o    Your blood pressure will be checked frequently. You may be given IV fluids to help maintain normal blood pressure.

·         You will have frequent blood tests to make sure your electrolytes are in the proper balance.

·         Your diet will be managed to make sure that you receive at least 100 grams of carbohydrates each day. The amount of protein in your diet may be restricted.3

·         Your medicines will be carefully checked. Medicines that contain magnesium may be stopped. The dosages of your other medicines may be adjusted.

Sociological Access to Health Care

Barriers to Access for immigrants and migrants.
1. Structural access
 Universal i.e. made open & available to all(no discrimination)
 Financial i.e. affordable
 Geographical i.e. physically reachable
2. Socio-cultural access ie.“culturally acceptable” to patients
3. Factors affecting the presence of barriers:Legal or illgegal migrants,
origin of migrant, healthcare policies laws, type of foreigner (refugee,
migrant workers), aid of NGOs ie principle of goodwill, presence of
social activists and advocates.

Ethical Legal Issues of Organ Transplant
Donors
-Live Donors
~ consent
~ risks
~ organ tourism
- Cadaveric Donors
~Consent
~ Definition of death
Allocation of Organs
- in particular, kidneys in malaysia
~criteria

Kidney Transplant Compatibility

1. Blood type matching
2. Tissue Matching
3. Crossmatching

TREATMENT

DIET
-Low protein diet
Help slow down build up of protein waste (blood urea nitrogen and creatinine) in blood and limit nausea and vomitting
-Avoid foods high in potassium
Banana, apricots,potato, nuts
Leads to abnormal heart rhythms
-Avoid food high in phosphorous
Milk, cheese, nuts
Cause Secondary hyperthyroidism
Excess phosphate in blood reduce levels of blood calcium
Low blood calcium triggers parathyroid gland to release more PTH (Parathyroid hormone)
PTH dissolve bone tissue to release stored calcium to raise level of calcium in blood
Causes osteoporosis and fractures
-Salt restriction
4-6 grams a day to avoid fluid retention (oedema)
Help control high blood pressure
-Decrease fluid intake
Decrease workload for kidney
Consumption based on amount of urine excreted the day before
Only in severe cases of swelling or end stage or renal failure

MEDICATION
Sevelamer (Renagel)
Binds dietary phosphate in intestine, inhibiting absorption
Calcium carbonate (Caltrate)
Normalize phosphate concentrations
Binds with dietary phosphate to form insoluble calcium phosphate to be excreted in faeces
Calcitriol (Rocaltrol)
Suppress parathyroid production and secretion in secondary hyperparathyroidism
Treats hypocalcemia by Increasing intestinal calcium absorption
Ferrous SulfateBuilding block for hemoglobin synthesis
Darbepoetin (Aranesp)
Interacts with stem cell to increase red blood cell production

DIALYSIS
HemodialysisUses a machine filter called dialyzer to remove excess water and salt
This balances the other electrolytes in the body and removes waste products of metabolism
Blood flows through tube into machine, where it passes next to a filter membrane
Dialysate is present on the other side of membrane
Absorbs impurities from blood through membrane
Access to blood vessels is surgically created
Arteriovenous fistula is made
Connection between a large artery and vein in the body, usually the arm
Causes large amount of blood flow into vein
Causes vein to enlarge and thicken to tolerate repeated needle sticks to attach tube
2 needles placed: 1 to withdraw blood, 1 to return
If kidney failure happens acutely and there is no time to build fistula, special catheters inserted into larger blood vessel
Left in place for up to 3 weeks
Act as bridge until fistula can be planned, placed and matured
Side effects
Prone to infections
May cause blood vessels to clot or
narrow
Arteriovenous graft
Patients who have small veins
Fistula fails to develop
Made of artificial material
Polytetrafluoroethylene(PTFE)
Occurs 3 times a week and last 3-5 hours at a time
Travels to outpatient center to have dialysis
If inconvenient, home hemodialysis possible
Patient starts learning at clinic with dialysis nurse
Clinic provides machine or help patient get from supplier
Blood tests taken once a month to ensure HD working and detect problems such as anemia or high potassium levels
Risks
Infection
Blood loss
If cathether may seperate
Air embolism
Air is introduced into blood stream, preventing heart from pumping blood adequately

Peritoneal Dialysis
Uses lining of abdominal cavity (peritoneum) as dialysis filter
Catheter placed in the cavity through the abdominal wall through surgery
2-3 litres of dialysate dripped into cathether and left for few hours and then drained out
Waste products excreted from blood
Two types
Continuous Ambulatory Peritoneal Dialysis
Empties a fresh bag of dialysate into abdomen
After 4-6 hours of dwell time, patient repeats cycle with fresh bag of solution
Does not require machine
Continuous Cycler-Assisted Peritoneal Dialysis
Uses machine to fill and empty abdomen 3-5 times during night while person sleeps.

KIDNEY TRANSPLANT
May come from living related donors, living unrelated donors or cadaveric donors
Extensive testing to ensure compatibility for transplant
Shortage of organs, have to wait for months or years
Requires four to seven days in hospital
Require lifelong immunosuppressant medication to prevent rejection by body

aetiology

Acute renal failute :
-circulatory shock:
Inadequate cardiac output
Decrease in arterial pressure
Renal blood flow is reduced
GFR and amount of NaCl filtered by the glomeruli are reduced
Decreases the amount of NaCl that must be reabsorbed by the tubules
which uses most of the energy and oxygen consumption by the kidney
Renal blood flow and GFR fall, the requirement for renal oxygen consumption is also reduced.
Renal cells start to become hypoxic
Decrease in renal blood flow
If prolonged – damage or even death of renal cells

-Nephrotoxins :
a toxin with specific destructive properties for the kidneys.
Tubule necrosis
directly affect the glomerulus or the renal tubules
Lead nephropathy, arising from lead poisoning
nephropathy, from ingestion of the solvent carbon tetrachloride
Another toxin may create other substances conditions
causing the cells of these structures to die.
Drugs : antibiotics, analgesics
drug provokes an allergic reaction that destroys the kidneys
converting the hemoglobin of red blood cells into methemoglobin
interfering with the blood's transport of oxygen
Analgesic nephropathy is most prevalent in women over 30.
Uric acid nephropathy
not caused by exposure to an external toxic
arises from the body's overproduction of uric acid
usually in persons with diseases of the lymph nodes or bone marrow

Glomerulonephritis :
Caused by an abnormal immune reaction that damages the glomeruli
Group A beta streptococci
Streptococcal sore throat
Streptococcal tonsillitis
Streptococcal infection of the skin
Antibodies develop against the streptococcal antigen
React with each other to form an insoluble immune complex
Entrapped in the glomeruli
Many cells of the glomeruli begin to proliferate
Large number of WBC become entrapped in the glomeruli
Glomeruli become blocked by this inflammatory reaction
Those that are not blocked become excessively permeable
Allowing both protein and RBC to leak fr the blood of the glomerular capillaries into glomerular filtrate
Complete renal shut down

Burns:
Damaged erythrocytes break down in circulation
Releasing free haemoglobin
Accumulate in the tubule
Causing obstruction
Haemoglobin is toxic to tubular epithelium
Causing inflammation and necrosis

Mechanical obstruction:
-Calculi – Kidney stone
calcium in combination with either oxalate or phosphate
uric acid
amino acid cystine.
may not produce symptoms until they begin to move down the tubes (ureters)
block the flow of urine out of the kidneys
cause infection

-Blood clot
an obstruction in a blood vessel due to a blood clot
travel through the bloodstream
lodge in the renal artery
reduction of blood flow through the renal artery
can impair kidney function.
If prolonged, a complete blockage of blood
Renal failure

Chronic renal failure :
-bilateral pyelonephritis
persistent kidney inflammation that can scar the kidneys
bacteria from outside the body traveling back up the urinary stream
urethra → bladder → kidneys
ascending infection
The flow of urine backward
reflux
instead of a tight valve between the bladder and the ureter, there is a wide opening.
When the bladder contracts during urination, the urine goes both ways,
the urethra→ ureters.
The defect is not easy to correct and those who have it are subject to repeat infections.
from infection or inflammation in the urethra
insertion of catheters or instruments such as cystoscopes for diagnosis or treatment

-Polycystic kidney disease
common inherited cause of kidney failure.
occurs when multiple cysts form on each kidney.
As these cysts enlarge, they block normal kidney function.
If the disease is severe, the kidney can stop working altogether.

-Hypertension:
Chronic increase in pressure stretch the small arterioles and glomeruli
Sclerosis occurs in the glomeruli
Glomerulosclerosis
Leakage of plasma through the intimal membrane of these vessels
Fibrinoid deposits develop in the medial layers of these vessels
Progressive thickening of the vessel wall
Constrict the vessels
In some cases, occludes them
No collateral circulation among the smaller renal arteries, occlusion of one or more of them
Causes destruction of a comparable number of nephrons
Loss of glomeruli and overall nephron function
Decrease in both renal blood flow and GFR


-Diabetes
The body cannot break down glucose (sugar).
filtering function of the kidneys is actually higher
This extra glucose in the blood damages the nephrons
no longer filter blood effectively.
Kidney damage
Leads to hypertension

Renal function

Kidney is located around vertebra L2.
Nephron: Glomerulus, proximal convulated tubule, Loop of Henle, distal convulated tubule, collecting duct.
Renal function
1)Conversion of calcidiol to calcitriol (vitamin D3). Raises blood concentration of calcium by promoting intestinal absorption and slightly inhibiting loss in urine. More calcium available for bone deposition.
2)Secretes renin, converting angiotensinogen to angiotensin 1. Angiotensin-converting enzyme on the lining of blood capillaries converts it to angiotensin 2. This hormone causes vasoconstriction.
3)Secretes 85% of the body’s erythropoietin. Promotes RBC production and increases oxygen carrying capacity of blood.
4)Filter blood plasma, separates and eliminates waste from the blood.
5)Regulate blood volume and pressure
6)Regulate osmolarity of body fluids
7)In extreme starvation, they carry out gluconeogenesis by deaminating amino acids and excreting the amino group as ammonia.

Excretion will be explained during PCL =) need to do it with pics.

Prevention

·         Fluid balances will be carefully monitored.

o    Your intake and output will be measured, and you may be weighed every day.

o    Your blood pressure will be checked frequently. You may be given IV fluids to help maintain normal blood pressure.

·         You will have frequent blood tests to make sure your electrolytes are in the proper balance.

·         Your diet will be managed to make sure that you receive at least 100 grams of carbohydrates each day. The amount of protein in your diet may be restricted.³

·         Your medicines will be carefully checked. Medicines that contain magnesium may be stopped. The dosages of your other medicines may be adjusted.

SIGNS & SYMPTOMS OF RENAL FAILURE

`Acute renal failure

• Bloody stools
  
• Breath odour
  
  • Ammonia breath
    
  • Due to buildup of waste in the body
    
• Bruising easily
  
  • Platelet dysfunction
    
• Prolonged bleeding
  
• Changes in mental status or mood
  
  • Anaemia
    
• Decreased apetite
  
  • Due to buildup of waste in blood
    
• Decreased sensation, especially in the hands or feet
  
• Fatigue
  
  • Decreased erythropoietin synthesis
    
  • Anaemia
    
• Flank pain (between the ribs and hips)
  
  • Polycystic kidney disease, which causes large, fluid-filled cysts on the kidneys and sometimes the liver, can cause pain.
    
• Hand tremor
  
• High blood pressure
  
  • Fluid overload
    
• Metallic taste in mouth
  
  • Accumulation of uremic toxins
    
• Nausea or vomiting, may last for days
  
  • Accumulation of uremic toxins
    
• Persisent hiccups
  
  • Due to GI disturbance
    
• Nosebleeds
  
  • Due to accumulation of toxic products
    
• Seizures
  
  • Hypocalcaemia
    
  • because the impaired kidney no longer produces calcitriol and because hyperphosphatemia causes Ca phosphate precipitation in the tissues
    
• Slow, sluggish movements
  
• Swelling-generalised
  
  • fluid retention
    
• Swelling of the ankle, feet, and leg swelling
  
  • Fluid retention
    
• Urination changes
  
  • Decrease in amount of urine
    
  • Excessive urine at night (nocturia)
    
    • Peripheral oedema (abnormal infiltration of tissues with blood fluids) may be reabsorbed when the patient lies down in bed at night.
      
  • Urination stops completely (end stage)
    
• Shortness of breath
  
  • Fluid retention in lungs
    
  • anemia
    

 

 

 

 

Chronic renal failure

Initial symptoms

• Fatigue
  
  • Decreased erythropoietin synthesis
    
• Frequent hiccups
  
  • GI disturbances
    
• General ill feeling
  
  • Potassium accumulates in the blood
    
• Generalised itching
  
  • Pruritis
    
  • Due to buildup of waste in blood
    
• Headache
  
• Nausea, vomiting
  
  • Due to accumulation of uremic toxins
    
• Unintentional weight loss
  
  • Due to loss of appetite
    

Later symptoms

• Blood in the vomits or in stools
  
• Decreased alertness, including drowsiness, confusion, delirium, or coma
  
  • anemia
    
• Decreased sensation in the hands, feet, or other areas
  
• Easy bruising and bleeding
  
  • Platelet dysfunction
    
• Increased or decreased urine output
  
• Muscle twitching or cramps
  
  • Hypocalcaemia
    
• Seizures
  
  • hypocalcaemia
    
• White crystals in and on the skin (uremic frost)
  
  • Due to accumulation of urea in the body
    

Additional symptoms

• Abnormally dark or light skin
  
  • Due to increased melanin production
    
• Agitation
  
• Breath odour
  
  • Ammonia breath
    
  • Due to buildup of waste in body
    
• Excessive nighttime urination (nocturia)
  
• Excessive thirst
  
  • High level of urea in the blood
    
• High blood pressure
  
  • Fluid overload
    
• Loss of apetite
  
  • accumulation of uremic toxins
    
• Nail abnormalities
  
  • Due to increased melanin production
    
• Paleness
  
  • anemia
    

Pathophysiology of Renal Failure

Pathophysiology of renal failure

Renal Failure:

Acute

Chronic

Acute renal failure

Occurs in 3 clinical patterns: 

(1) as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons; 

(2) in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage; and 

(3) with obstruction to the passage of urine.

Thus classified as prerenal, intrinsic, and postrenal  

Prerenal Failure

Problems lie in the inability of the circulatory system to deliver the proper perfusion to the kidney to produce a normal GFR (90 - 120 mL/min )

Causes:

a) hypovolemic states (haemorrage, dehydration)

b) impairment of renal autoregulation (seen with cyclooxygenase inhibitors like NSAIDs and aspirin, or angiotensin converting enzyme (ACE) inhibitors)

c) low effective plasma flow state (low cardiac output states –arrythmias, valvular disease, congestive heart failure, systemic vasodilation – sepsis, antihypertensives, congestion – cirrhosis with ascites -> hepatorenal syndrome)

Kidneys recover rapidly once underlying deficit is corrected

Intrinsic Renal Failure

Hallmark: structural injury (most common form – acute tubular injury (ATN), either ischemic or cytotoxic)

Initial phase of ischemic injury – loss of integrity of actin cytoskeleton leads to flattening of the epithelium, with loss of brush border, loss of focal cell contacts, and subsequent disengagement of the cell from the underlying substratum.

Inflammatory response is responsible for some features of ATN

Reduced GFR – caused by intrarenal vasoconstriction (mediators are unknown)

Urine backflow and intratubular obstruction (from sloughed cells and debris) are causes of reduced net ultrafiltration

hallmark of ATN is a failure to maximally dilute or concentrate urine (isosthenuria).

The injured kidney fails to generate and maintain a high medullary solute gradient because the accumulation of solute in the medulla depends on normal distal nephron function.

Glomerulonephritis can be a cause of AKI and usually falls into a class referred to as rapidly progressive glomerulonephritis (RPGN). The pathologic correlation of RPGN is the presence of glomerular crescents (glomerular injury) on biopsy; if more than 50% of glomeruli contain crescents, this usually results in a significant decline in renal function. Although comparatively rare, acute glomerulonephritides should be part of the diagnostic consideration in cases of AKI.

Postrenal Failure

Hallmark: severe urinary tract obstruction

Men: prostate enlargement from benign prostatic hyperplasia or prostate cancer

Women: cervical cancer

Other causes: 

obstruction by bladder, kidney stones (lodged in the urinary tract such that flow from both kidneys is obstructed), phimosis (non-retractable foreskin), neurogenic bladder

Chronic renal failure

Involves several stages 

Decreased renal reserve -> Renal insufficiency -> End-stage renal failure/uremia

Decreased renal reserve

Around 60% nephrons lost

Decrease in GFR

Serum creatinine levels consistently higher than average but within normal range (0.8 to 1.4 mg/dL )

Serum urea levels normal (blood urea nitrogen: 7 to 20 mg/dL) 

No apparent clinical signs

Renal insufficiency

Around 75% nephrons lost

Indicated by a change in blood chemistry and manifestation

GFR decreased to 20% normal

Significant retention of nitrogen wastes (urea and creatine) in the blood

Tubule function decreased

Results in failure to concentrate the urine and control the secretion and exchange of acids and electrolytes.

Osmotic diuresis occurs at the remaining functional nephrons filter an increased solute load

Marked by excretion of large volumes of dilute urine.

Erythropoiesis decreased, patient’s blood pressure elevated (why?)

End-stage renal failure/uremia

More than 90% nephrons lost

Occurs when GFR is negligible

Fluids, electrolytes, and wastes retained in body, all body systems affected

Marked oliguria (reduced urine output) or anuria (no urine output) develops

Investigations

Types of tests and investigations:
1. Urine Test
2. Blood Test
3. Ultrasound
4. Angiography

What can a Urine Test reveal?
 Urine is normally sterile
 Blood cells in urineàmay be a sign of different diseases in the kidneys, the

urinary system or the bladder.
 Glucose in urine à may be a sign of diabetes
 Protein in urineà may be a sign of a kidney disease and can be used to detect the early signs of kidney damage from long-standing diabetes.

Types of urine collection
 24-hour urine collection
 Clean catch urine specimen
 Important! Stop some of the medication before urine tests as drugs may affect the results of test.

24-hour urine collection
 Collect urine for 24 hours.
 Normal resultsà800 to 2000 milliliters per day (with a normal fluid intake of about 2 liters per day)
 Abnormal results:
 Reduced urination à dehydration, inadequate fluid intake, or renal insufficiency or failure.
 Increased urination à Diabetes, end-stage renal disease, high fluid intake, kidney failure

Clean Catch Urine Culture
 About 1 - 2 ounces of urine is needed for a test.
 Remove the container from the urine stream without stopping the flow. Individual may finish urinating into the toilet bowl.
 Sample is sent to the lab.
 Clean Catch Urine Specimen can be used for urine specific gravity.

Urine Specific Gravity
 Requires clean catch urine specimen
 Used to evaluate body's water balance and urine concentration
 Normal values are between 1.002 to 1.028.

Urine pH
 Clean Catch Urine Specimen
 Measure the acidity of urine
 Normal Range: 4.6-8.0
 High pH à Kidney Failure, UTI
 Low pH à emphysema

RBC in Urine
 Clean catch urine specimen
 Normal values are 4 RBC per high power field (RBC/HPF) or fewer. Normal value ranges may vary slightly among different laboratories.
 Greater than normal value: cystitis, pyelonephritis, kidney tumor, kidney stones, glomerulonephritis.

Blood Test
 Blood sample can be analyzed for creatinine, estimated glomerular filtration rate and blood urea nitrogen (BUN)
 The level of these waste products in the blood increases as kidney filtration declines.

Creatinine
 The breakdown product of creatine, which is an important part of muscle.
 The normal value is 0.8 to 1.4 mg/dL.
 Females usually have lower creatinine than males, because they usually have less muscle mass.

Higher than normal results:
 Glomerulonephritis
 Kidney failure
 Pyelonephritis
 Reduced kidney blood flow (shock, congestive heart failure)
 Urinary tract obstruction

Glomerular Filtration Rate
 Used to check how well the kidneys are working
 A formula is used to get the results, where age, gender, height, weight and race are taken into account
 According to the National Kidney Foundation(US), the normal results range from 90 - 120 mL/min.
 Older people will have lower normal GFR levels, because GFR decreases with age.
 Normal value ranges can vary slightly among different laboratories.

Blood Urea Nitrogen (BUN)
 Also to check kidney function
 Normal result: 7 - 20 mg/dl.
 Abnormal results (higher)à hypovolemia, kidney failure, glomerulonephritis, pyelonephritis, acute tubular necrosis, UT obstruction

Angiography
• X-ray examination that shows blood flow in the arteries and veins.
• Needle inserted into artery
• Femoral artery usually used
• Needle is in place, long thin guide wire guided into blood vessle that needs to be examined (using fluorescent screen)
• Catheter is slipped over it pushed along until tip is in the right position
• Guide wire removed and dye injected
• Image viewed on screen / rapid sequence of X-ray pictures for further investigation (flouroscopy)


References:
http://www.netdoctor.co.uk/health_advice/examinations/urinesample.htm
http://www.nlm.nih.gov/medlineplus/ency/article/003425.htm
http://www.nlm.nih.gov/medlineplus/ency/article/007305.htm
http://www.nlm.nih.gov/medlineplus/ency/article/003777.htm

Guys!

Can we compile this week's anatomy practical answers next week? Just bring your respective answers next Mon and we can compile them together! :)

Summary for Alan & Bill =)

AIDS VS HIV
AIDS
Official criteria- HIV-infected people who have fewer than 200 CD4 T cells.
HIV infection
Case definition- Adults, adolescents, or children aged ≥ 18 months, Children aged ≤ 18 months
Notifiable diseases
These are some of the notifiable diseases: AIDS, HIV infection, Cholera, Malaria, Measles, severe acute respiratory syndrome
Incidence and Prevalence
The number of cases reported in the world increases by year. In Malaysia, majority of the cases reported are male. (more will be shown during presentation)
Etiology
There are 3 major routes of transmission of the HIV(Sexual Transmission, Transmission via blood or blood products, Mother to Child Transmission)
The risk of transmission via tears, urine and saliva is considered to be negligible
Pathophysiology
• Entry to host cells (CD4+ lymphocytes, macrophages and monocytes) using gp120 with the help of chemokine co-receptors.
• Life cycle of HIV (8 stages):
1. Viral binding
2. Entry and Uncoating
3. Reverse transcription
4. Integration into host chromosomal DNA
5. Synthesis of viral DNA
6. Translation and production of Viral proteins
7. Assembly of virus and budding from the host cell
8. Maturation
• Then the virus is ready for infection
Investigation and Diagnosis
• HIV Antibody Testing :
-Detects HIV antibodies in blood or other body fluids
weeks after exposure or an HIV RNA test (viral load)
>detects the presence of the virus
• ELISA - (Enzyme-linked Immunosorbent Assay Test)
-A common serological test for the presence of particular antigens or antibodies (Serum)
-Direct and indirect
• Western Blot Test
• Home Collection Kit
• HIV Viral Load
• p24 Antigen Count Test
• CD4 Count
-measurement of how many functional CD4 T-cells are circulating in the blood.
Modes of transmission
• Having vaginal or anal sex without a condom with someone who is infected.
• Having contact with the blood of someone who has HIV. This could be having a blood transfusion from someone who is infected with HIV
• From a mother who has HIV to her baby: HIV can pass to the baby during pregnancy, during the birth of the baby, or through breast-feeding. Only about one in three babies born to HIV-positive mothers get HIV.
• Receiving an injection from an unsterilized needle that was previously used by someone with HIV.
• Heterosexual transmission is the route by which most people with AIDS have become infected with HIV worldwide
This category of AIDS cases is also among the most rapidly increasing.
Signs and Symptoms of HIV infection
Symptoms Early After Infection - Acute HIV : fever, headache, muscle and joint pain, sore throat, rash, diarrhea.
Later Symptoms Of HIV Infection
it takes about eight to nine years between the time of infection and the appearance of later symptoms, although this varies from person to person.
These symptoms signal that immune system function is deteriorating, due to declining numbers of CD4+ T cells
Symptoms of the Immune System: Swollen lymph nodes in the neck, axilla, or groin (lymphadenopathy), fever / night sweats
Symptoms of the GI Tract : Rapid weight loss, Diarrhea, Poor appetite, Profound fatigue
Respiratory Symptoms
usually occur later in course of the disease
Any cough or shortness of breath could be a sign of bacterial pneumonia or pneumocystis (carinii) jiroveci pneumonia (PCP).
Shortness of breath
Dry cough / productive cough
Symptoms of the Skin and Mucous Membranes
result of infection by other viruses, fungi or bacteria. Often, these infections involve the skin or mucous membranes (for example, inside the mouth).
HIV Effects on Dental Health
Skin rash
Genital sores (sores around the penis or vagina)
Red, brown, pink or purple lesion on the skin - suggestive of Kaposi's sarcoma
White patches on the tongue, inside of the mouth, or gums - could be signs of thrush, candida, or hairy oral leukoplakia
Canker sores / apthous ulcers
Neurological / Emotional Symptoms
Depression
Numbness, tingling, or burning in the feet, hands, or face. (peripheral neuropathy)
Confusion, weakness, or changes in level of consciousness
memory loss
Blurred vision
Complications
Bacterial
- Pneumonia
- Mycobacterium avium complex
- Tuberculosis
- Salmonellosis
Viral
- Cytomegalovirus
- Viral hepatitis
- Herpes simplex virus
- Human papillomavirus
Fungal infections
- Candidiasis
- Cryptococcal meningitis
Parasitic
- Pneumocystis carinii pneumonia
- Toxoplasmosis
- Cryptosporidiosis
Cancers
- Kaposi’s sarcoma
- Non-Hodgkin’s lymphoma
Neurological complications
Management and Treatment
Counsellingproper counselling before and after testing with informed consent especially patients tested positive to address issues such as stigma and the fear of disclosure of one's HIV status
Support Groups
Initiation of Antiretroviral Therapy (Antiretroviral drug treatment)
Combination Therapy (combination of 2 or more drugs)
Home based care (patient staying at homeable to work and do daily chores)
Traditional/Alternative Medicine
Prevention
Effective HIV prevention interventions include
• Condom use, Male circumcision, Provision of clean injecting equipment, Opioid substitution therapy, treatment of sexually transmitted infections, HIV testing and counselling, A set of interventions to prevent mother-to-child transmission of HIV, Sex education
In health care settings, transmission of HIV can be prevented through
• primary prevention measures
• secondary prevention measures
In addition, there is increasing evidence indicating that
• antiretroviral therapy programmes
• Current research on new prevention technologies such as microbicides, topical and oral antiretroviral pre-exposure prophylaxis
HIV prevention - combination behavioural change approach has been
• Abstinence, including delay of sexual initiation or debut
• Being safer by being faithful to one’s partner or reducing the number of sexual partners, and
• correct and consistent Condom use.
Legal and Ethical Issues
o Consent for medical examination and treatment
o Prenatal HIV Testing
 Recommended by Institute of Medicine Panel:
o Confidentiality
 Exception
o The Doctor & The Law Courts
o Release of Information to a third party