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1.Kidney morphology

The human kidneys:

Fig (1):- Discribe the kidney structure &morphology

Are two bean-shaped organs, one on each side of the backbone.Represent about 0.5%of the total weight of the body,but receive 2025% of the total arterial blood pumped

by the heart. Each contains from one to two million nephrons.


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Fig(2):-How the kidney work

2.Nephron morphology

Fig(3):-The image shows a cut section of the cortex of a mouse kidney as seen under the scanning

electron microscope. Near the top (center) can be seen a Bowman's capsule with its glomerulus. Directly

beneath is another Bowman's capsule with its glomerulus removed. The remainder of the field shows

the lumens of both proximal and distal tubules as they have been cut at various angles.


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The nephron (right) is a tube; closed at one end, open at the other.

It consists of:-

Bowman's capsule. Located at the closed end, the wall of the nephron is pushed

in forming a double-walled chamber.

Glomerulus. A capillary network within the Bowman's capsule. Blood leaving the

glomerulus passes into a second capillary network surrounding the loop of henle.

Proximal convoluted tubule. Coiled and lined with cells carpeted

with microvilli and stuffed with mitochondria.

Loop of Henle. It makes a hairpin turn and returns to the

Distal convoluted tubule, which is also highly coiled and surrounded by

capillaries.

Collecting duct. It leads to the pelvis of the kidney from where urine flows to the

bladder and, periodically, on to the outside world.

The Bowman's capsules are packed in the cortex of the kidney, the tubules andcollecting ducts descend into the medulla.

Formation of urine

The nephron makes urine by

-Filtering the blood of its small molecules and ions and then reclaiming the

needed amounts of useful materials.

-Surplus or waste molecules and ions are left to flow out as urine.In 24 hours the kidneys reclaim

~1,300 g of NaCl

~400 g NaHCO3

~180 g glucose ,almost all of the 180 liters of water that entered the tubules.


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The steps:

Blood enters the glomerulus under pressure.

This causes water, small molecules (but not macromolecules like proteins) and

ions to filter through the capillary walls into the Bowman's capsule. This fluid iscalled nephric Filtrate

(1)

3.Kidney function

Fig(4):-The function of the kidneys

a. Filtering the blood

The kidneys remove wastes and excess water (fluid) collected by, and carried in,

the blood as it flows through the body.

About 190 liters (335 pints) of blood enter the kidneys every day via the renal

arteries. Millions of tiny filters, called glomeruli, inside the kidneys separate wastes

and water from the blood.

Most of these unwanted substances come from what we eat and drink.


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The kidneys automatically remove the right amount of salt and other minerals from

the blood to leave just the quantities the body needs.

The cleansed blood returns to the heart and recirculates through the body.Excess

wastes and fluid leave the kidneys in the form of urine. Urine is stored in the bladder

until it is full and then leaves the body via the urethra. Most people pass about 2 liters

(4 pints) of urine every day.

b.Balancing fluid levels

By removing just the right amount of excess fluid, healthy kidneys maintain

what is called the body's fluid balance.

In women, fluid content stays at about 55% of total weight. In men, it stays at about

60% of total weight. The kidneys maintain these proportions by balancing the

amount of fluid that leaves the body against the amount entering the body.

Fluid comes into our bodies from what we drink, and from high-liquid foods such

as soup. If we drink a lot, healthy kidneys remove the excess fluid and we pass a lot

of urine. If we don't drink much, the kidneys retain fluid and we don't pass much

urine. Fluid also leaves the body through sweat, breath, and feces. If the weather is

hot and we lose a lot of fluid by sweating, then the kidneys will not pass so much

urine.

As your kidneys fail, maintaining this balance becomes more difficult. You may

suffer symptoms of too much fluid. You may need to watch your diet and what you

drink to maintain fluid balance.
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c. Kidney act as endocrine organ through release hormones

1-Substance effect directly or indirectly on the vascular system

One of the important functions of the kidneys is to regulate blood pressure.

Healthy kidneys make hormones such as renin and angiotensin.

These hormones regulate how much sodium (salt) and fluid the body keeps, and

how well the blood vessels can expand and contract. This, in turn, helps control

blood pressure.

Kidney secret renin in case of:

1. decrease in arterial volume.

2. decrease in presentation of sodium in renal tubule .

3. hypocalemia.

They helps control blood pressure by regulating:

The amount of water in the body. If there is too much water in the body (fluid

overload) blood pressure will go up. If there is too little water in the body(dehydration) the blood pressure will drop.

The width of the arteries. The arteries constantly change in width as blood flows

through them. The narrower the arteries, the higher the blood pressure. Renin helps

control narrowing of the arteries. Failing kidneys often make too much renin. This

raises blood pressure. If your blood pressure is high, your heart is working harder

than normal to pump blood through your body.High blood pressure (also called

hypertension) caused by a breakdown in these functions is common in people with

kidney failure. It is also a complication, a secondary condition caused by kidney

failure.(2)
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2.substance stimulate production of red blood cells

Healthy kidneys produce a hormone known as erythropoeitin (EPO), which

stimulate erythropiosis(production of RBCs) carried in bone marrow . These cells

carry oxygen throughout the body. Without enough healthy red blood cells you

develop anemia, a condition which makes you feel weak, cold, tired, and short of

breath.

Fig(5):-Stimulate production of red blood cells

3.substance regulate calcium metabolism

kidney regulate ca+2

,where when there is increase of ca+2

in blood and regulat

hydroxylation of vit.D3

by 7-dehydrocholesterol(under skin)---------------u.v (sun light)-----------

cholecalciferol (vit D3)--------liver------ Vit.D3-----kidney-------- 1,25(oH)2

vitD

Vit. D Help in: 1. absorbtion of ca+2

in the kidney

2.deposition of ca+2

in bone(3)
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Fig(6):-Regulate calcium metabolism

4.Kidney function tests

Blood or urine is commonly collected to test for how the kidneys arefunctioning. Some kidney function tests include: creatine, creatinine-urine,

creatine clearance, and BUN test

1. BUN test

BUN stands for blood urea nitrogen. Urea nitrogen is what forms when proteinbreaks down.

A test can be done to measure the amount of urea nitrogen in the blood.


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Normal Results

7 - 20 mg/dL. Note that normal values may vary among different laboratories.

What Abnormal Results Mean?

Higher-than-normal levels may be due to:

Congestive heart failure Excessive protein levels in the gastrointestinal tract Gastrointestinal bleeding Hypovolemia Heart attack Kidney disease, including glomerulonephritis, , and acute tubular necrosis Kidney failure Shock Urinary tract obstruction

Lower-than-normal levels may be due to:

Liver failure

Low protein diet Malnutrition Over-hydration

Considerations

For people withliver disease, the BUN level may be low even if the kidneys are

normal.
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2. Creatinineblood

Creatinine is a breakdown product of creatine, which is an important part of

muscle. This article discusses the laboratory test to measure the amount of

creatinine in the blood.

Creatinine can also be measured with a urine test

Why the Test is Performed?

The test is done to evaluate kidney function. Creatinine is removed from the

body entirely by the kidneys. If kidney function is abnormal, creatinine levels will

increase in the blood (because less creatinine is released through your urine).Creatinine levels also vary according to a person's size and muscle mass.

Normal Results

A normal value is 0.8 to 1.4 mg/dL.

Females usually have a lower creatinine than males, because they usually have less

muscle mass.

Note: Normal value ranges may vary slightly among different laboratories. Talk to

your doctor about the meaning of your specific test results.


Higher-than-normal levels may indicate:

Acute tubular necrosis Dehydration Diabetic nephropathy Glomerulonephritis Kidney failure Muscular dystrophy
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Pyelonephritis Reduced kidney blood flow (shock, congestive heart failure) Urinary tract obstruction

Lower-than-normal levels may indicate:

Muscular dystrophy (late stage) Myasthenia gravis

3. Creatinine clearance

Creatinine tests

A measurement of the serum creatinine level is often used to evaluate kidney

function. Urine creatinine levels can be used as a screening test to evaluate kidney

function, or can be part of the creatinine clearance test

The creatinine clearance test compares the level of creatinine in urine with the

creatinine level in the blood. (Creatinine is a breakdown product of creatine, which

is an important part of muscle.) The test helps provide information on kidney

function.

The creatinine clearance appears to decrease with age

Why the Test is Performed?

The creatinine clearance test is used to estimate the glomerular filtration rate

(GFR).

However, because a small amount of creatinine is released by the filtering tubes in

the kidneys, creatinine clearance is not exactly thto the same as the GFR. In fact,

creatinine clearance usually overestimates the GFR. This is particularly true in

patients with advanced kidney failure.
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Normal Results

Clearance is often measured as milliliters/minute (ml/min). Normal values are:

Male: 97 to 137 ml/min.

Female: 88 to 128 ml/min.

Note: Normal values ranges may vary slightly among different laboratories.


Abnormal results (lower-than-normal creatinine clearance) may indicate:

Acute tubular necrosis Congestive heart failure Dehydration Glomerulonephritis Renal ischemia (blood deficiency Renal outflow obstruction (usually must affect both kidneys to reduce the

creatinine clearance)

Shock

Acute renal failure Chronic renal failure End-stage renal disease

Considerations

Factors that may interfere with the accuracy of the test are as follows:

Incomplete urine collection Pregnancy Vigorous exercise

Drugs that damage the kidneys, such as cephalosporins.
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The creatinine clearance test should only be done for patients who are medically

stable. Such patients may have a rapidly changing creatinine clearance, and

therefore any result may be inaccurate.(4)

5. Kidney failure

Renal failure (kidney disease) is a disease condition referring to impaired kidney

function.

Types

There are 2 types of renal failure: acute and chronic.

1.acute kidney failure

Acute (sudden) kidney failure is the sudden loss of the ability of the kidneys to

remove waste and concentrate urine without losingelectrolytes.is an express

development of

decreasing kidney function, usually occurring over a period of days or several

weeks. Symptoms include edema of the extremities, weight gain progressing to

nausea, vomiting,

seizures and coma. Other possible symptoms include fluid accumulation in the

lungs (pulmonary edema) and brown cola-colored urine(5)

.

ARF is here defined as an abrupt decline in renal function resulting in retention ofnitrogenous end products of metabolism .Such adefinition includes conditions

which are
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primarily nonrenal, such as the rise in blood urea and serum creatinine which

accompanies hypovolaemic states and that due to obstruction of the urinary tract,

as these

conditions must always be considered in the differential diagnosis of the acutelyuraemic patient. This definition does not demand that the patient be oligouric or

anuric ;this

reflect the realization that non-oliguric ARF is relatively common ,and probably

becoming more so.

The causes of ARF as defined above ,together with the commoner underlying or

precipitating factor ,are listed in the table 17.1 in three main categories:pre- renal,renal and post -renal.

Table 1:- causes of acute renal failure


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Cause precipitating factor

Pre-renal

Reduced intravascular

volume

Decreased cardiac output

Bleeding,excess gastrointestinallosses

hepatic failure, cardiogenic shock

Post-renal

Obstructive uropathytumors , bleeding , fibrosis and Stone

Renal

Acute tubular necrosis

Nephrotoxins

Glomerular disease

Tubular disease

Vascular disease

renal ischemia , shock

antibiotic , contrast media

rapidly progressive

Glomerulonephritis ,acute- on

chronic renal failure

uric acid , myeloma, papillary

Necrosis , interstitial nephritis

arterial thrombosis


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Physical examination:

Physical examination must be equally comprehensive because of the wide range

of diseases which may present as ARF. A full review of possible

important physical findings relating to all of the possible causes of ARF is

unnecessary here, but there are a few important points which should be stressed. In

identifying the broad category of ARF (renal, pre-renal or post-renal) an

assessment of the state of hydration is critical. The presence of oedema or ascites

speaks against the presence of hypovolaemia but does not exclude it, particularly in

patients with cardiac, renal or hepatic disease on diuretic therapy. Tachycardia

increased by sitting or standing, peripheral vasoconstriction, loss of skin turgor andespecially an exaggerated drop in blood pressure on assuming the sitting or

standing position from lying all suggest that intravascular volume is decreased.

This may be supported by evidence of a recent sudden loss of weight. It should be

noted, however, that as most cases of ARF are of a highly complex nature, with

multiple organ damage and many contributory factors, and usually further

complicated by previous administration of blood, intravenous fluids and drugs, the

diagnosis of pre-renal ARF (hypovolaemia, hypoperfusion) is seldom a simple

matter of clinical observation.

Physical examination may also be helpful in identifying post-renal ARF

(obstructive uropathy). Rectal and vaginal examinations may reveal prostatic

hypertrophy or pelvic neoplasm, which are the two commonest cases of this

syndrome. Evidence of a previous nephrectomy makes urinary tract obstruction

more likely, and a distended bladder should be carefully sought. Actue urinary

tract obstruction is usually, but not always, associated with some pain, andsubacute or chronic obstruction may be quite painless. When ARF is secondary to

intrinsic renal disease, the finding of hypertension, particularly if of recent onset or

malignant, suggests glomerular disease, while a skin rash with arthralgias may

indicate an underlying vasculitis or allergic interstitial nephritis due to drugs.


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While any of the above findings may be helpful, it must be remembered that cases

of ARF are often complex, and one must guard against premature acceptance of

any diagnosis on the basis of history and physical examination alonethe

diagnosis usually rests on further biochemical testing and some form of renal

imaging.

The complications of Acute Renal Failure (ARF) can affect the entriebody, including the digestive system, heart, lungs, and nervous system.

Infection is one of the most common complications of ARF, because the

body's immune system may stop working properly.

Uremic syndrome (uremia) is a serious complication of severe or

prolonged Acuts Renal Failure. It can cause severe nausea, confusion,

psychosis, irregular heart beats, and pulmonary edema (fluid in lungs).

Increased potassium in the blooddue to inability to filter and excrete

the electrolytes properly.


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Diagnosis of ARF

Table 2:-Differential diagnosis of renal causes of acuts renal failure.

Renal cause Diagnostic test

Glomerular disease Red cells; red cell casts in

urine: renal biopsy

Vascular occlusion Radionuclide scanning;

arteriography

Acute interstitial nephritis Gallium67scanning,

eosinophilia; renal biopsy

Papillary necrosis Intravenous urography;

examination of tissue passed inurine.

2.chronic renal failure

Chronic renal failure, also known as chronic kidney disease (CKD) is

characterized by a gradual worsening, or loss of normal kidney function.

Developing over a period of many years, it occurs in stages ranging from very mildand moderate to severe and complete failure. It is during the later stages that CKD

may progress to end-stage renal disease (ESRD) as the kidneys can no longer

function as required for survival, which is below 10% of normal.


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Note In the mild to moderate stages, those with CKD report no symptoms otherthan needing to frequently urinate during the night. However, as the disease

progresses symptoms of uremia may develop: anorexia, mental confusion,

weakness, nausea, vomiting and seizures. Uremia is due to the build up of waste

products, namely urea within the blood.

Pathophysiology of chronic renal failure

The hallmark of chronic renal failure is a reduction of glomerular filtration rate.

This reflects decreased nephron mass and decreased overall excretory capacity. For

substances which are handled predominantly by filtration (e.g.creatinine and, to a

lesser extent, urea) metabolic balance is maintained by a compensatory increase in

plasma concentration. However, renal tubules have the capacity to adapt to the

increased solute load per nephron, and for substance such as sodium, phosphate,

potassium and hydrogen ions the rise in plasma concentration is blunted by

mobilizing spare capacity of these tubular functions. Thus metabolic balance is

maintained but patients are vulnerable to overload if these tubular functions are

stressed further, particularly in therapeutic situations. Examples include water

intoxication, volume overload (e.g. acute pulmonary oedema from excess sodium

retention) and hyperkalaemia.


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Sodium and water:

The kidney retains some regulatory ability with regard to soium and water

excretion. Decreased Nephron mass, overperfusion of the remaining nephrons and

excessive regulatory demands in patients with chronic renal failure lead to

decreased flexibility of response and a tendency to both overload and depletion in

certain clinical situations. The changes in sodium reabsorption required to maintain

sodium balance in a patient with stable chronic renal failure after a reduction in

GFR to 5 litres per day.

Altered renal function in chronic renal failure

Reduced excretory capacity

Retained metabolites

Overperfusion of remaining nephrons

Reduced flexibility

Tubular adaptation.

Intact nephron hypothesis

The similarity of adaptive processes in kidneys with predominantly glomerular

and predominantly tubular damage has given rise to the concept of glomerulo-

tubular balance. Despite considerable structural heteropgeneity there remains a

basic orderliness of function so the residual residual nephrons retain a predicatable,

definable and organized pattern of response. Thus it was demonstrated that in

humans and animals with unilateral kidney damage, kidney functions such as free

water and sodium re-absorption remained normal in each kidney if allowance was

made for the reduction in GFR.

Potassium


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Potassium balance is achieved by a marked increase in potassium secretion per

nephron, aided by an increase in urine flow rate and in the delivery of sodium and

non-reabsorbable anions to the distal nephron which favours potassium ion

exchange and excretion. Regulatory mechanisms affecting potassium excretion are

probably stimulated by changes in plasma and intracellular potassium and

hydrogen ion concentration. In advanced renal failure potassium excretion exceeds

filtered potassium but plasma potassium is often normal. However,

Hyperkalaemia may occur suddenly if distal mechanisms for potassium excretion

are compromised by a reduction in urine flow rate or sodium delivery. Some older

patients and diabetics have a defect in aldosterone production and are more prone

to hyperkalaemia. The same is true in patients who are given potassium sparing

diuretics which block distal potassium transfer and are potentially very dangerous

in renal failure.

Hydrogen ions

As GFR falls, metabolic acidosis develops and by providing a stimulus to

hydrogen ion secretion enables the diseased kidney to achieve a balance between

hydrogen ion production and excretion. Until the GFR falls below 20 ml perminute the defect in hydrogen ion secretion is usually well compensated; after this

a progressive fall in plasma bicarbonate becomes apparent. The changes in

hydrogen ion excretion occur in the context of an increased solute and phosplate

load. The same factors which impair proximal sodium reabsorption may cuse an

increased distal delivery of bicarbonate, with some urinary loss of bicarbonate, and

failure to fully utilize other urinary buffers and to achieve maximal urinary

acidification until a new steady state is reached. Hydrogen ion balance is achieved

largely by increased renal ammonia production. The rate at which acidosis

develops depends on protein intake (hydrogen ion load), urinary phosphate (buffer)

excretion and the rate of nephron loss, which also determines the rate of

adaptation. Persistent metabolic acidosis also causes gradual reduction of bone

carbonate buffers and loss of calcium from bone.


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Uraemic toxins

The role of uraemic toxins in the pathogenesis of uraemic has been debated for

many years. The extrarenal manifestations of uraemia dominate the clinical picture

and virtually all organs are affected. It is tempting to attribute such wide spread

changes to some or all of numerous metabolic products which accumulate in renal

failure.

Anaemia

Fig(7):-Healthy kidneys produce a hormone called erythropoietin, or EPO, which stimulates thebone marrow to make red blood cells needed to carry oxygen throughout the body. Diseased

kidneys dont make enough EPO, and bone marrow then makes fewer red blood cells.

In a group of chronic renal failure patients entering our dialysis programme plasma

haemoglobin varied from 5.7-12.5g/dl.


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Although anaemia rarely warrants treatment, patient notice

improvement in symptoms after renal transplantation. The anaemia is usually

normocytic and normochromic, with some variation in shape of the red blood cells

and few reticulocytes.

The bone marrow is inappropriately normocellular in contrast to the hypercellular

marrow of patients with a comparable degree of anaemia and normal renal

function. Marrow iron turnover is depressed and plasma erythropoietin levels are

appropriately low.the bone marrow response to erythropoietin is also impaired.Red

blood cell halflife is reduced; since normal cells have a reduced half-life in

uraemic plasma this defect is probably due to a circulating toxin. Anemia usually

worsens soon after commencement of dialysis, probably due to excessive bloodtaking for investigation. Predialysis haemoglobin levels are regained after 3-6

months and often rise, particularly in well-nourished patients who continue regular

physical activity. Anaemia is much more severe following bilateral nephrectomy.

Nowadays, long-term dialysis patients can expect to have a haemoglobin level

between 9-12g/dl, particularly those on peritoneal dialysis, who have less blood

loss.

External source of erythropoietin, such as liver, may play a part in this. Occasional

patients who develop hepatitis while on dialysis show a marked rise in

haemoglobin. It is rarely necessary to treat the anaemia of chronic renal failure.

Patients with incapacitating symptoms often have a correctable cause such as

chronic blood loss or another disease such as corony artery disease which focuses

attention on their anaemia. Therapy should be directed towards reducing blood

loss, uncovering and correcting non-renal causes of anaemia, and encouraging

good nutrition and regular activity.

Androgen therapy may cause a small rise in haemoglobin in dialysis patients but

the benefits rarely justify the use of repeated intramuscular injections. Nausea,

virilization and hyperlipidaemia are common and often unacceptable side effect.


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Blood transfusion in the predialysis phase should be reserved for patients who

cannot cope without it. Its effect is temporary and there is a danger of aggravating

fluid overload or heart failure and further impairing renal function. On the other

hand , patient awaiting transplantation are usually transfused ,as this improve the

results of transplantation .

In advanced renal failure bleeding time may be prolonged because of defective

release of platelet factor III. Platelet aggregation, platelet adhesiveness,

prothrombin consumption and prostaglandin release may all be reduced, and may

contribute to skin and mucosal bleeding and the predisposition to haemorrahagic

pericarditis. The prolonged bleeding time may be improved by blood transfusion or

dialysis.

Renal bone disease

The major factor contributing to hypocalacemia and renal bone disease is an

absolute or relative deficiency of 1,25-dihydroxycholecalciferol, the active

metabolite of vitamin D. Vitamin D3in the liver. Regulation of 25-hydroxyvitajin

D3 levels is normal in renal failure although patients who hate reduced levels

through malnutrition or other reasons are more likely to develop osteomalacia.

The kidney regulates the further metabolism of 25-hydroxyvitamin D3 by hydrox

ylation either to 1,25dihydroxyvitamin D3, which is a potent stimulus to calcium

absorption, or to other less active metabolites, normally renal hydroxylation of

vitamin D is modulated according to the calcium and phosphorus needs of the

body, but in renal failure deficiency of 1,25-dihydroxy-vitamin D3 causes impaired

intestinal calcium absorption, hypocalcaemia,

hypocalciuria, and skeletal resistance to PTH. The dual effects of

hyperphosphataemia and lack of 1.25-dihydroxy-vitamin D3 by lowering plasma

ionized calcium provides a stimulus or hyperparathyroidism.


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Fig(8):-Renal bone disease

Treatment to renal bone disease

Deficiency of vitamin D metabolites is also an important cause of impaired bone

mineralization in renal failure, and most patients with ostcomalacia due to renalfailure respond well to vitamin D therapv. However, the incidence of

osteompalacial in renal failure patients varies considerably in different parts of the

world and is relatively uncommon in Australia. In those patients who develop early

and scvee symptomatic osteomalacial it is likely that poor nutrition, lack of other

factors also contribute to the mineralization defect. Most patients with chronic

renal failure of more than a few year's duration have histological evidence of bone

diseae. Those with predominantly hyperparathyroidism show areas of bone

resorption, increased number of osteoblasts, marrow fibrosis and increased osteoid.

Diagnosis to bone disease


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The diagnosis of established bone disease is not difficult. Overt

hyperparathyroidism is indicated by hypoclacemia, hyperphosphataemia, and

elevated alkaline phosphatase level and subperiosteal bone resorption which can be

seen on magnified X-rays of the hands.

Soft tissue is usually seen in patient with uncontrolled hyperphosphataemia.

Calcification in the conjunctiva causes conjunctival irritation and around joints

and acute inflammatory response which simulates gout. Vascular calcification in

the small vessels of the hand usually indicates severe and prolonged

hyperparathyroidism. Extensive soft tissue calcification, pulmonary calcification or

ischaemic necrosis of vessels are fortunately very uncommon.

Metabolic and endocrine disturbances

The ready availability of immunossay and its application to renal failure has

shown increased plasma levels of a large number of peptide hormones, including

insulin, gastrin, glucagon, growth hormone ,prolactin, luteinizing hormone (LH),

follicle stimulating hormone (FSH) and neutrotensin. Increased levels of hormone

may be due to persistent direct stimulation of regulatory mechanism, indirect

stimulation through reduced end-organ responsiveness, or decreased hormonecatabolism. In many cases all three mechanisms are invoved. Persistently elevated

hormone levels may also imply interference with feed-back control loops involving

for instance the pituitary gland. Other hormone levels are reduced, for example

erythropoietin, 1,25-dihydroxycholecalciferol and testosterone, because of

destruction of hormone forming cells or their suppression by uraemic metabolites.

The clinical importance of these changes varies. Three hormonal abnormalities

which warrant some discussion are abnormalities of thyroid hormone, sexhormones and insulin.


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Thyroid function

Thyroid function is usually normal in patients with chronic renal failure

although there may be clinical features and abnormalities of thyroid hormone which

mimic hypothyroidism. There is an increased incidence of goiter, levels of protein

bound iodine are low, decreased total (and sometimes free) thyroxine (T4), tri-

iodothyronine(T3) and free thyroxin index have been reported. Although variable it

appears that the plasma concentration of thyroid hormones (particularly T3)

decreases progressively with increased duration of renal failure or dialysis.

Gonadal function

Infertility, menstrual abnormality, decreased libido and impotence are common

in chronic renal failure. Gynaecomastia may occur in male patients but is more

common in those undergoing dialysis.

Many women with chronic renal failure have amenorrhoea or oligomenorrhoea and

there is often reduced fertility. Furthermore, patients with advanced uremia who

become pregnant have a much higher risk or abortion or premature delivery and

contraceptive advice is necessary for women of childbearing age. Estrogen and

progesterone levels are often low but the level of gonadotropins varies.

Insulin and glucose intolerance

Mild glucose intolerance is common in renal failure and although it is of little

clinical importance this abnormality of carbohydrate metabolism has been

extensively studied. Investigation have shown an increased basal insulin level,

peripheral resistance to insulin, an impaired hypoglycaemic response to infused

insulin and an increased and prolonged insulin response to glucose. Insulin

degradation by the kidney and liver is decreased. All these abnormalities improve

with dialysis and this may be partly due to improved nutrition and correction of


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potassium depletion and acidosis. Insulin requirements may decrease in diabetic

patients as renal failure worsens.

Lipid metabolism

Arteriosclerosis is a common mode of death in chronic renal failure patients but

its incidence has not been definitely shown to be increased. Prolonged and

persistent hypertension is certainly a predisposing factor but it is questionable

whether changes in lipid metabolism play a major role. The main abnormality of

lipid metabolism is hypertriglyceridaemia associated with an increase in very low

density lipoproteins (VLDL).

This has been attributed to reduced clearance of VLDL triglyceride and to

suppression of lipase activity. High density lipoproteins. (HDL) are usually low

but return to normal after successful renal transplantation. The situation in chronic

renal failure resembles type 4 hyperlipoproteinaemia (as seen in diabetes, obesity

and patients with an increased alcohol intake ) and may be aggravated by certain

drugs, such as androgens, and by excessive dietary carbohydrate.

Hypercholesterolaemia is uncommon except in patient with nephritic syndrome.

The abnormalities of lipid metabolism may be related to disorders of insulin

production and degradation. Treatment is encouraging regular exercise and on

avoidance of excess carbohydrate and drugs which may aggravate

hypertriglyceridaemia.

Nitrogen metabolism

Changes in nitrogen balance include those due to uraemia, to associated

malnutrition, to changes in intestinal nitrogen breakdown and to dialysis.

It has been suggested that patients with chronic renal failure can reutilize urea to

synthesize protein but the quantities involved are too small to be of practical

significane. The normal molar ratio of plasma urea to creatinine is approximately

30: 1.


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Immunological disorders

An increased tendency to infection and reduced ability to heal wounds has been

recognized for many years but is of little clinical importance in well-managed

patients. There are defects in both antibody production and cellular response to

antigen and in various aspects of leucocyte activity. Patients with chronic renal

failure have an increased likelihood of becoming virus carriers, particularly of

hepaitiesB and cytomeglaovirus, and have an increased incidence of cancer,

both possibly related to immunological incompetence.

Cardiovascular system

Cardiovascular complications in uraemia are moat commonly due to

hypertension or extracellular volume expansion. Control of these plays a vital role

in conservative management and is associated with a significantly better prognosis.

Extracellular volume expansion is important in the pathophysiology of

hypertension but is also a compensatory mechanism which depresses proximal

tubular solute reabsorption. A prmary objective in treatment is to maintain sodium

balance by adjusting sodium intake to excretion and by avoiding sudden changes in

extracellular volume, which may compromise renal function. Most hyper ten sive

patients with chronic renal failure require antihypertensive drug therapy and blood

pressure can be controlled by standard drug regimens.


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Fig(9):-Cardiovascular system

However, once end-stage chronic renal failure supervenes, antihypertensive drugs

can usually be withdrawn and blood pressure controlled by a reduction inextracellular volume. In a small proportion of dialysis patients, usually those

presenting with malignant hypertension, blood pressure is more difficult to control

both before and after the institution of dialysis. In these cases peripheral resistance

and plasma rennin activity are often increased and sodium depletion causes severe

postural hypotension. Prior to dialysis it may be necessary to employ newer agents

such as angiotensin-converting enzyme inhibitors. After dialysis is started gradual

ECV reduction is combined with B-adrenoreceptor blockers or (very rarely)

bilateral nephrectomy.

Heart failure may be caused by uncontrolled sodium retention and aggravated by

anemia, preexisting coronary disease, hypertension and other metabolic

derangements associated with uraemia, such as chronic elevation of parathyroid


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hormone and catecholamines. Fluid overload may also cause functional aortic

insufficiency. Early diastolic murmurs require careful evaluation but do not often

indicate organic valve disease and may disappear after the correction of

hypertension and fluid overload. There are occasional patients with gross

cardiomegaly which is not explained by the above factors. Most of these are long-

established dialysis patients and the term uraemic cardiomyopathy has been.

However, this should not be taken to imply a common cause or recognized

aetiology. The term uraemic retinopathy has similarly been used but the changes

seen are mostly due to hypertension and arteriosclerosis, with occasional patients

showing retinopathy due to cerebral oedema, anaemia, retinal vien thrombosis and

other complications.

In advanced uraemia, uraemic pericarditis may cause retorsternal pain, fever and a

friction rub. Small pericardial effusions are often seen on equated control of

extracellular volume. Pericarditis or radiologically detectable effusion is usually an

indication for aggressive dialysis with reduction in extracellular volume. Bleeding

due to heparin or volume de pletion. If a reduction in ECV is accompanied by

hypotension without a corresponding fall in juaular venous pressure, cardiac

tamponade should be suspected. The classical signs of pericardial effusion and

compression are usually not present but volume repletion and drainage of the

pericardium should not be delayed on this account. Although echocardiography

and other techniques can be used to define left ventricular function and assess the

presence of pericardial fluid, appropriate management still rests on a rapid clinical

assessment of their significance. Pericarditis with fever and chest pain. This may

be relieved by indomethacin but persistent pericarditis is debilitating and the risk

of haemorrhage is always present. Unless there is a rapid and complete response to

drugs, partial pericardectomy is advisable and effectively cures the condition.


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Central nervous system

Early treatment has made overt neurological manifestation of uraemia relatively

uncommon. However, many patients experience slowing of mental function, poormemory, apathy and a reduced attention span, particularly if renal failure

progresses fairly rapidly. A number of studies point to defect in the reticular

activating system, which is responsible for maintaining an optimal level of arousal

and affects the assimilation and processing of new information. Asterixis and

myoclonic jerks are common in advanced uraemia and the latter may be a prelude

to generalized convulsions

Conservative management of chronic renal failure


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Despite the success of dialysis and renal transplantation there is no doubt that

most patients are better off without these forms of treatment even if renal function

is quite markedly impaired. There is every reason to assess such patients

thoroughly and to supervise their management with a view to delaying progression

of rena failure and treating any reversible complications. Treatment of the

underlying condition is of paramount importance and is dealt with under the

appropriate headings elsewhere. Practical examples where dramatic changes in

prognosis can be made are the treatment of malignant hypertension, cessation of

analgesics in patients with analgesic nephropathy, relief of obstruction and the

treatment of such conditions as systemic lupus erythematosus, goodpastures

syndrome and wegeners granulomatosis. Even after chronic renal failure is

established there is still much to be done to preserve renal function and improve

the lifestyle of patients nearing end-stage renal failure. The most important aspects

of conservative treatment are:

1- supervision and self-care:2- control of hypertension;3- maintenance of good nutrition;4- maintenance of fluid and electrolyte balance;5- prevention and treatment of bone disease.

Supervision and self

Patients with chronic renal failure should be involved in their own care as soon

as possible. They should understand the cause of their disease, the anticipated rate

of progression of renal failure and the things they can do to influence this. For

patients with a good prognosis it may be sufficient to emphasize the importance ofblood pressure control, good nutrition and sodium balance. As renal failure

progresses, the need for phosphate control should be explained, as should the

importance of reporting any symptoms such as headache, which may indicate or

lead to a complication.


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Control of hypertension

Progression of established renal may be delayed by Control of hypertension and

hyperphosphataemia. It is also possible that improved nutrition and reduction of

protein load may slow the rate of deterioration. With few exceptions, the treatment

of hypertension in chronic renal failure is the same as that in non-uraemic

hypertensive individuals. Although a number of antihypertensive druge are

excreted by the kidney, their use is simplified by the fact that there is a defined

therapeutic end- point, i.e. control of blood pressure, which together with the

presence of sid-effects determines the does used. Indications and contraindications

for individual drugs apply but the aims of blood pressure control should be more

stringent in patients with renal impairment.

Nutrition

Good nutrition remains a corner stone in the conservative management of

chronic renal failure and the emphasis should be on the positive aspects of nutrition

rather than an unnecessarily restricted diet. A reduced protein intake can relive

symptoms such as anorexia, nausea and vomiting, and reduce the load of hydrogenion, sulphate, phospate and potassium which the kidney has to excrete.

Fluid and electrolyte balance

Regular review of blood pressure, weigh and the state of hydration is

necessary and should be more frequent as renal failure progresses. It is good

practice to establish a routine of daily weighing and to teach patients the

importance of maintaining sodium balance and reporting any inter-current illness,

fluctuation in weight or unusual symptoms. Temporary electrolyte imbalance may

worsen quite if unattended and it often saves time to admit patients to hospital to

have this corrected.


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Prevention and treatment of bone disease

Although bone biopsy is necessary to accurately define the type and extent of

bone disease it is an unpleasant procedure and the histological techniques are

demanding. In practice many patients can be treated without recourse to biopsy.

Without treatment, hyperparathyroidism progresses at a variable rate. However, if

the plasma phosphate and calcium are maintained in the normal range, this may be

prevented. It should be possible to control the plasma phosphate with a

combination of protein restriction and phosphate binding agents but frequently

these measures are not introduced early enough. If the patient is hypoclacemic,

claium carbonate can be given in a dose of 1-2 g three times a day and, if this is not

effective , aluminium or magnesium hydroxide may be added.


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6.Management of complications

Patients with chronic renal failure may develop complications with alter the

course of the disease but many of these are reversible. Examples include acuteurinary infection, septicaemia, urinary tract obstruction, gastrointestinal

haemorrhage, dehydration or fluid overload with associated acute electrolyte

disturbances and drug toxicity. Some of these are dealt with under the appropriate

headings. These complications may be the cause of the patients initial presentation

and their correction often leads to improvement which can be maintained over

many years. Patients with established chronic renal failure should be encouraged to

report any change in health since relatively minor intercurrent illnesses may upsetthe delicate balance of compensated renal failure. For instance, vomiting may be

expected to cause volume depletion but at the same time the patients medications

are often not taken and a vicious cycle of events is established which leads to

progressive deterioration. If such patients are admitted to hospital this deterioration

can be prevented by intravenous fluid replacement, the use of parentral

medications and, sometimes, short periods of dialysis.

Drug intoxication is a common problem. Almost all drugs or their metabolitesare excreted by the kidney and chronic renal failure is a common cause of drug

toxicity. No drugs should be given without a definite therapeutic indication and a

knowledge of how the drug is handled in renal failure (see Ch. 26). The

prescription of anti-nausea drugs is usually unjustified and the patient would be

better served by a reduction in protein intake and investigation of other possible

causes of nausea, such as water intoxication, drug overdose or ulcer. Similarly,

patients should be encouraged to avoid regular use of sedatives. Adding drug-

related symptoms to the symptoms of uraemia does not improve the patients well

being.(6)


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7. Renal failure treatment

Dialysis and TransplantationWhen the function of the kidneys are no longer adequate for daily survival

needs, physicians will deem haemodialysis as a necessary treatment.

Haemodialysis is the process by which the blood is cleansed by way of an artificial

kidney. Those receiving haemodialysis will undergo minor surgery to construct a

fistula in order to obtain access. Fistulas are placed either in the arm or leg of those

preparing to begin receiving haemodialysis treatment. It is through these fistulas

that the blood can be gradually removed, cleansed and then returned to the body.

Haemodialysis may be done in the home, in the hospital or at a haemodialysis

center.

1-Heamodialysis

Fig(10):-Haemodialysis requires an artificial

kidney, the dialyser, which contains the

filtration membrane. Purification is achieved

by exchange between the bloodstream and a

dialysis bath created and controlled by a

generator. This technique requires an

accessible, high-flow, vascular outlet. A

surgically created arterial-venous fistula on the

forearm is the system of choice. The fistula is

pierced by two needles for the blood outflowand inflow. 3 sessions per week are necessary.

The sessions last 4 hours on average and take

place in a specialised Centre, an auto-dialysis

Centre, or at home after training.


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2-Peritoneal dialysis

Fig(11):-Peritoneal dialysis is carried out by

filling the abdominal cavity with a sterile

liquid. After a period of exchange across the

peritoneal membrane, the liquid is drained

off. Four, 2-litre sachets are required every

day. A catheter is inserted through the

abdominal wall and the abdomen is filled

either manually by gravity or using an

automatic machine. Sessions take place at

home after training. Around 10% of dialysisis undertaken using this method which is less

effective than haemodialysis.

Severe complications associated with dialysis

- Acute oedema of the lungs: excessive weight increase or overestimation

of the dry weight may provoke acute oedema of the lungs due to passage of

plasma into the alveoli causing progressive asphyxia. Lying down becomes

impossible. There is a sensation of gasping for breath. Weight reduction by

dialysis is necessary as quickly as possible.

- Hyperkalaemias: a potassium restricted diet must be strictly followed

when prescribed. An excess of potassium causes hyperkalaemia. This begins

with a general feeling of weakness with numbness of the feet, hands and

mouth. The pulse rate falls below 50/min. The heart may stop beating. Take

two units of Kayexalate and contact the Centre using the numbers shown

above who will act quickly

Other major complications


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- Anaemia: this is frequent and generally well controlled by EPOinjection.

- Accelerated cardiovascular ageing: cardiac follow up is necessary. It is

strongly recommended to avoid the use of tobacco.

- Hyperparathyroid: responsible for calcium and phosphorus problems.

Itching may occur when phosphorus levels are too high. Bones become

brittle and the blood vessels calcify.(7)

Reference

1.http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/G/GITract.html#intestine

2.http://www.renalinfo.com

3. the kidney book fifth edition edited by barry M.brenner

4.http://www.nlm.nih.gov/medlineplus/ency/article/000500.htm

National Kidney Foundation National Library of Medicine National Library of Medicine

5.http://healthtools.aarp.org/adamcontent/electrolytes

6.Text book of renal disease edited by tudith A.whit worth IR lawrnce.

Adam W R, Dawborn JK, Rosenbaum M 190 Transient early diastolic murmurs in patients

with renal failure.

Medical Journal of Austaralia 2: 10851086

Alvestrand A, Furst P, Bergstrom J 1982 Plasma and muscle free amino acid in uremia.

Influence of nutrition with amino acids. Clinical Nephrology 18: 297305.

Nephrology, vol. 7 Chronic renal failure. Churchill

Livingstone, New York, Edinburgh, London
http://www.renalinfo.com/http://www.renalinfo.com/http://www.renalinfo.com/http://www.nlm.nih.gov/medlineplus/ency/article/000500.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000500.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000500.htmhttp://www.kidney.org/kidneydisease/ckd/index.cfmhttp://www.kidney.org/kidneydisease/ckd/index.cfmhttp://www.nlm.nih.gov/medlineplus/ency/article/000471.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000471.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000493.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000493.htmhttp://healthtools.aarp.org/adamcontent/electrolyteshttp://healthtools.aarp.org/adamcontent/electrolyteshttp://healthtools.aarp.org/adamcontent/electrolyteshttp://healthtools.aarp.org/adamcontent/electrolyteshttp://www.nlm.nih.gov/medlineplus/ency/article/000493.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000471.htmhttp://www.kidney.org/kidneydisease/ckd/index.cfmhttp://www.nlm.nih.gov/medlineplus/ency/article/000500.htmhttp://www.renalinfo.com/


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Bricker N S 1972 On the pathogenesis of the uremic state, an exposition of the trade-off

hypothesis. New England

Journal of Medicine 286 (20): 1093 1099

Briker N S, Klahr S, Lubowitz H, Rieselbach R E 1965

Renal Function in chronic renal disease. Medicine 44(4): 263- 288

7.www.medindia.net

References And recommended reading

Trauma 15: 10561063

DElia J A, Gleason R W, Alday M 1982 Nonoliguric acute renal failure associated with a low fractional excretion

of sodium. Annals of internal Medicine 96: 597600

Kennedy A C, Burton J A, Luke R G 1972 Factors affecting the prognosis in acute renal failur. Quarterly Journal ofMedicine 42: 73-86

Kleinknecht D, Jungers P, Chanard J, Barvanel C, Geneval

D 1972 Uremic and non-uraemic complications in acute renal failur: evaluations of early and frequent dialysis on

prognosis. Kidney International: 1: 190-196

Levinsky N G 1977 Pathophysiology of acute renal failure.

Myers B D, Carrie B J, Yee R R, Hilberman M. Michaels A S 1980 Pathophysiology of hemodynamically mediated

acute renal failure in man. Kideny International 18: 495-504

Oken D E 1981 On thedifferential diagnosis of acute renal failure. Amercian Journal of Medicine 71: 916-920

Schrier R W 1979 Acute renal failure. Kidney International 15: 20516

Swann R C, Merrill J P 1953 The clinical course of acute renal failure. Medicine, Baltimore 32: 21592

Werb R, Linton A L 1979 Aetiology, diagnosis, treatment and prognosis of acute renal failure in an intensive care

unit. Resucition 7: 95 - 100
http://www.medindia.net/patients/patientinfo/acuterenalfailure_complications.htm#ixzz1HLMNUGV7http://www.medindia.net/patients/patientinfo/acuterenalfailure_complications.htm#ixzz1HLMNUGV7http://www.medindia.net/patients/patientinfo/acuterenalfailure_complications.htm#ixzz1HLMNUGV7http://www.medindia.net/patients/patientinfo/acuterenalfailure_complications.htm#ixzz1HLMNUGV7


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