Most Common Causes of Kidney Failure

2011-10-28 19:01 Kidney failure can be the result of many reasons like Hypertension, Diabetes, genetic diseases like Polycystic Kidney Disease (PKD), immunological related disease like IgA Nephropathy, or direct kidney injury by renal toxic drugs and so on. Kidney is an organ where blood filtration takes places. And the pathological changes of kidney are almost all related to blood circulation within and outside of the kidneys. In order to make explain how these above mentioned factors affect kidneys and lead to final kidney function decline, we need first to make clear the most important tissue of kidneys---glomerulus. Glomerulus consists of massive blood capillaries, and is the main place where blood filtration takes place. Once there is blood capillary break, squeeze, or block, pathological changes of blood vessel cells can easily take place and lead to overall kidney function decline. And, the above mentioned several factors damages kidneys mainly through affecting blood circulation within the kidneys. Hypertension can easily lead to blood hyper transfusion into kidneys. Hypertension within kidneys not only lead to blood capillary break down, but also damages of filtrating barriers (endothelial cells, basement membrane and the epithelial cells). The damage of glomerular filtrating barriers gives rise to further damages of other renal tissues like renal tubules and intestinal cells, which accelerates the aggravation of kidney failure. Diabetes damage kidneys through direct injuring kidney blood capillaries. It is known well that the most common complication of Diabetes is arteriosclerosis caused by dysfunction of glucose metabolism. Arteriosclerosis with in kidney capillaries can easily give rise to blood circulation blocks and following insufficient blood supply to kidney cells. Cellular necrosis and kidney function decline will be the final result. Immunological related kidney diseases like Lupus Nephropathy or IgA Nephropathy are closely related to the immune complexes deposition in kidneys, which leads to pathological changes of the kidneys. Pathological change of kidneys gradually gives rise to final kidney function decline. This is kind of similar to renal toxic drug influence to kidneys. Another common causation of kidney failure is Polycystic Kidney Disease (PKD). With the swelling up of these cysts, more and more pressure will be added to kidney functional tissues like glomerular blood capillaries and renal tubules. Finally, kidney function decline will finally be the result. In summary, hypertension, diabetes, PKD and renal toxic drugs can all be the causation of kidney function decline. Based on different causation there are corresponding treatment methods.

How to Prevent Chronic Renal Failure (CRF)

2012-01-11 10:22 As a progressive kidney disease, Chronic Renal Failure (CRF) can result in significant morbidity and mortality due to the progressive and slow impairment of kidney function. The impairment usually takes months or years to occur. With the deterioration of kidneys, patients have great risk of End Stage Renal Failure (ESRF). In this case, you have to receive frequent dialysis or kidney transplant to sustain life. Therefore, for those with kidney disease, it is of great importance to take the following effective precautions so as to avoid further deterioration of your condition. Regular examinations should be done in hospital so as to detect the potential risk factors of CRF as early as possible. In most of the cases, Diabetes and high blood pressure are the two most causes of this disease. For those who have a family history, you are also more at risk of CRF. Once you are diagnosed with these risks, you had better receive prompt treatment so as to prevent CRF in the very beginning. A low-protein diet can help you protect your kidneys, because too much protein intake may impose more burdens on kidneys. Except for the protein needed for the body, there is no need to take in too much protein. In addition, people had better eat less food rich in fat, since high fat food can easily cause high blood pressure and vascular sclerosis which can result in kidney damage. Maintain a healthy weight through doing regular exercises and reduce the number of calories you eat. In addition, physical activity such as walking, lawn mowing, bike riding, swimming or gentle aerobics are suitable for you to stay fit. Avoid using of nephrotoxic drugs. Due to the delayed discharge of drugs, easily depositing of medication in the blood and tissue may cause kidney damage, thus aggravating the disease. Besides, you should stop smoking and drink alcohol in moderation. If you are suffering from other medical condition, it is available to ask our online experts and take treatment for these

How Long Can You Live Once Your Kidneys Shut down
2012-01-18 09:44

Kidneys are important organs responsible for filtering blood in our body. However, in Chronic Renal Failure, if the patients do not receive effective treatment in time, the kidneys will lose their renal functions gradually thus shutting down. How long can you live once your kidneys shut down? In fact, there is no a clear answer to this question. However, if the patients with kidneys shut down can receive proper treatment, they will be able to live as long as the normal people. The conventional therapies for the patients with kidneys shut down are dialysis and kidney transplant. It can not be denied that these two treatments have played an irreplaceable role in the treatment of kidneys shut down and prolonging their life expectancy. However, both of them have huge side effects on the patients. Dialysis is just like a filter, which can only remove the excessive water and metabolic wastes out of body, but can not repair the impaired kidneys. As a result, the residual function will further decline until the kidneys cease to work. Whats worse, dialysis can lead to a series of complications like heart failure, hypotension/hypertension, infections and so on, some of which are the death cause for the patients with kidneys shut down. Therefore, the patients with Kidney Disease should measure the advantages and disadvantages before starting dialysis. As for kidney transplant, insufficient kidneys source is a main problem for the patients with kidneys shut down. Many patients even on list have to wait for a very long time until kidney transplant is available for them. Unfortunately, many of them may lose their lives during their endless waiting. Moreover, even if they have a successful kidney transplant, they have to depend on a large dosage of immunosuppressive agent to resist rejection reaction in the rest of their life. Moreover, according to some researches, the survival rate of transplanted kidneys is only 1% in ten years. Therefore, choosing a proper treatment is the key to prolonging life expectancy for the patients with kidneys shut down. All kinds of kidney diseases will develop into renal failure due to the necrosis of the renal functional cells. In order to prolong the life expectancy for the patients with

kidneys shut down, they should repair the impaired functional cells. In this way, they will be able to recover the normal function of their native kidneys. Consequently, their life expectancy will prolong.

Signs and symptoms f kidney failure may include some or many of the following: High blood pressure Decreased urine output or no urine output Darkly colored urine Anemia Nausea or vomiting Loss of appetite Sudden weight change A general sense of discomfort and unease (malaise) Fatigue and weakness Headaches that seem unrelated to any other cause Sleep problems Decreased mental sharpness Pain along your side or mid to lower back Muscle twitches and cramps Swelling of the feet and ankles Bloody or tarry stools, which could indicate bleeding in your intestinal tract Yellowish-brown cast to your skin Persistent itching Chronic kidney failure can be difficult for you or your doctor to detect initially. Signs and symptoms are often nonspecific, meaning they can also be attributed to other illnesses. In addition, because your kidneys are highly adaptable and able to compensate for lost function, signs and symptoms of chronic kidney failure may not appear until irreversible damage has occurred. What are the symptoms of kidney failure? In the beginning, kidney failure may be asymptomatic (not producing any symptoms). As kidney function decreases, the symptoms are related to the inability to regulate water and electrolyte balances, to clear waste products from the body, and to promote red blood cell production. Lethargy, weakness, shortness of breath, and generalized swelling may occur. Metabolic acidosis, or increased acidity of the body due to the inability to manufacture bicarbonate, will alter enzyme and oxygen metabolism, causing organ failure Inability to excrete potassium and rising potassium levels in the serum (hyperkalemia) is associated with fatal heart rhythm disturbances (arrhythmias) Rising urea levels in the blood (uremia) can affect the function of a variety of organs ranging from the brain (encephalopathy) with alteration of thinking, to inflammation of the heart lining (pericarditis), to decreased muscle function because of low calcium levels (hypocalcemia)

Generalized weakness can be due to anemia, a decreased red blood cell count, because lower levels of erythropoietin do not adequately stimulate the bone marrow. As waste products build in the blood, loss of appetite, lethargy, and fatigue become apparent. This will progress to the point where mental function will decrease and coma may occur Because the kidneys cannot address the rising acid load in the body, breathing becomes more rapid as the lungs try to buffer the acidity by blowing off carbon dioxide. Blood pressure may rise because of the excess fluid, and this fluid can be deposited in the lungs, causing congestive heart failure

renal failure, inability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes. The condition may be acute or chronic. Acute renal failure is characterized by oliguria and the rapid accumulation of nitrogenous wastes in the blood (azotemia). It results from hemorrhage, trauma, burn, toxic injury to the kidney, acute pyelonephritis or glomerulonephritis, or lower urinary tract obstruction. Many forms of acute renal failure are reversible after the underlying cause has been identified. Acute renal failure may have three typical phases: prodromal, oliguric, and postoliguric. Treatment includes restricted intake of fluids and of all substances that require excretion by the kidney. Antibiotics and diuretics are also used. Chronic renal failure may result from many other diseases. The early signs include sluggishness, fatigue, and mental dullness. Later, anuria, convulsions, GI bleeding, malnutrition, and various neuropathies may occur. The skin may turn yellow-brown. Congestive heart failure and hypertension are frequent complications, the results of hypervolemia. Urinalysis reveals greater than normal amounts of urea and creatinine, waxy casts, and a constant volume of urine regardless of variations in water intake. Anemia frequently occurs. The prognosis depends on the underlying cause. Treatment usually includes restricted water and protein intake and the use of diuretics. When medical measures have been exhausted, long-term hemodialysis or peritoneal dialysis is often begun, and kidney transplantation is considered.

Renal Failure and Critical Care Nursing

I. Introduction and Assessment A. The History, Presence, and Nature of Renal Failure B. Signs and Symptoms II. Anatomy - Structure and Function III. Physiology A. Filtration B. Creatinine C. Tubular reabsorption and secretion D. Urine concentrating ability of the kidney: 2 mechanisms (SLIDE) E. Sodium and potassium regulation F. Potassium regulation 6. Endocrine fuctions IV. Pathophysiologies A. Congenital defects B. Urinary Tract Infections (UTIs) C. Obstructive Disorders D. Glomerulonephritis E. Diabetic glomerulosclerosis F. Acute Renal Failure (ARF) 1. Pathogenesis 2. Categories of ARF a. Prerenal

b. Renal (or intrarenal) c. Postrenal G. Chronic Renal Failure (CRF) H. LUPUS NEPHRITIS J. GOODPASTURE'S V. Interventions A. Pharmacotherapy B. Hemodialysis Return to Nurse Bob's Page

Renal Failure and Critical Care Nursing I. Introduction and Assessment The kidneys, which are generally smaller than a person's hand, are required to filter approximately 1700 liters of blood every day and remove the waste products of this blood into about one liter of urine every day.this affects the composition of our blood tremendously. The kidneys filtered as top particles from the blood and selectively reabsorbed those that are needed to maintain life. By regulating the volume and composition of body fluids, the kidneys perform both a waste removal as well as a metabolic or endocrine. A. The History, Presence, and Nature of Renal Failure Some other things which my predispose patients to the development of renal failure are; chronic renal disease, previous radiation therapy, and urinary tract infections. Circulatory disease which is generally associated with the poor renal perfusion may also be a factor in the development of renal failure. Some of these problems may include; aorta aneurysm, peripheral vascular disease, cardiac disease, and of course hypertension. Diabetes is another major factor in the United States today. The use of nephrotoxic agents such as antibiotics, and chemotherapy may also predispose one to the development of renal failure. By obtaining a a good patient database the nurse can ascertain the risk of patients developing chronic or acute renal failure. B. Signs and Symptoms The general appearance of the patient in acute renal failure may be; anemia, pallor, itching, dryness of the skin, dry mucous membranes, costalvertebral angle angled tenderness, and

lumbosacral, periorbital or extremity edema. the kidneys may affect the heart are cardiovascular system by causing pericarditis, hypertension, or retinopathy. Pulmonary wise the patient in real failure may develop respiratory distress due to acidoses. The breath sounds may be diminished and there may be a uremic odor to the breath. Most of the time, there is a change in the urinary patterns of the patient. There may be a change in frequency, color, quality or odor of the urine. However, urinary output is not always an indicator of acute renal failure. A patient may be making more than adequate urine, but his system may not be removing the waste products from his body. The patient may complain of ammonia taste. He may have slight gastrointestinal disturbance such as; hiccups, anorexia, nausea, vomiting, coated tongue, or he may have none of the symptoms at all. As the patient becomes more and more uremic he may develop central nervous system disturbances. These may include headache, confusion, disorientation, drowsiness, insomnia, muscle twitch and, or weakness. The patient's vital signs may be affected as he becomes more uremic. He may develop orthostatic changes in his blood pressure and pulse. The skin may become cooler. His urinary elimination pattern, volume, frequency, specific gravity, and state of hydration may change. His weight may increase. All of these are things the nurse muthest assess. II. Anatomy - Structure and Function The kidneys are two main shape structures which lie in the retroperitoneal space between the 12 thoracic and third lumbar vertebra. The left kidney sets slightly behind the spleen, while the right kidney sets behind the liver and is slightly lower than the left. Each kidney is enclosed in a tough fibrous capsule and is supported and protected by fat tissue. There is a fissure in the central content portion of the kidney where the blood vessels enter and leave. This is called the hilus. Also coming from the hilus, are to the ureters which connect the kidney to the bladder. The cortex is a brownish-tissue which covers the outer third of the kidney. The medulla are lightcolored and cone-shaped, these are the renal pyramids. The papilla are formed by the free ends of the pyramids which opens into the renal pelvis. the renal pelvis is made up of calyces, which drained up or lower hands of the kidney. Days unite with a renal pelvis at the upper end of the ureter. The functional unit of the kidney are the nphrons, each kidney contains approximately 1.2 million of these. Within each nephron there is a glomerulus and a tubule. Within the glomerulus, there is a structure called Bowman's Capsule which contains a network of capillaries. fluid in particles from the blood and are filtered through this membrane. Water, nutrients and electrolytes, as well as other substances, are reabsorbed as they pass through these tubulars. There is collecting duct which collects fluid from several nephrons and passes this fluid into the renal pelvis.

Two capillary beds, a glomerulus, and a peritubular network supply the nephron. The glomerulus is a unique, high pressure capillary filtration system that is located between two arterioles, the afferent and efferent arterioles. The low-pressure reabsorptive system of the peritubular capillary network arises from the efferent arteriole. here down III. Physiology A. Excretory functions 1. Filtration - the process of removing fluids and small particles from the blood. a. the glomerulus, which lies between two arterioles, allows for high-pressure filtration system. Capillary filtration pressure in the glomerulus is 2-3 times as high as that of other capillary beds in the body. The filtration pressure and the glomerular filtration rate (GFR) are regulated by the constriction or relaxation of the afferent and efferent arterioles. During strong sympathetic stimulation, which causes marked constriction of the afferent arteriole, the filtration pressure is reduced to the point where GFR drops to almost 0. b. Capillary membrane of the glomerulus is composed of 3 layers:
1. endothelial layer of the capillary 2. basement membrane 3. a layer of epithelial cells that line Bowman's capsule

c. Glomerular capillary permeability is 100-1000 times as great as capillaries elsewhere in the body. All 3 layers allow water and dissolved particles, such as electrolytes, to leave the blood and pass rapidly into Bowman's capsule. Blood cells and plasma proteins are too large to pass through the glomerular membrane of a healthy kidney. d.Glomerular filtration rate (GFR) is normally about 125 ml per minute. GFR can provide a measure to assess renal function, and can be measured clinically by collecting timed samples of blood and urine. 2. Creatinine - product of creatine metabolism by the muscle. Is filtered by the kidney, but not absorbed in the renal tubule. Formula for creatinine clearance: C=UV P C = clearance rate U = urine concentration V = urine volume P = plasma concentration

Normal creatinine clearance is 115-125 ml/min (corrected for body surface area) Usually 24 hour collection with blood drawn when urine collection is completed. 3. Tubular reabsorption and secretion The filtrate from the glomerulus passes through:
1. 2. 3. 4. proximal tubule loop of Henle distal tubule collecting duct

Then it reaches the pelvis and kidney Reabsorption: water, sodium, and other substances leave the lumen of the tubule and enter the blood. Secretion: substances from the blood enter lumen of the tubule. Glucose and amino acids - completely reabsorbed Filtered water - 99% reabsorbed Urea - about 50% reabsorbed Creatinine - none Electrolytes - determined by need 3. Urine concentrating ability of the kidney: 2 mechanisms (SLIDE) 1. Increased solute concentration in the medullary area surrounding the collecting tubules. Loop on Henle and peritubular capillary (vasa recta) descending into the renal medulla. Here a countercurrent mechanism controls water ans solute flow. As a result, water is kept out of the peritubular area surrounding the tubules, and sodium and urea are retained. 2. Selective permeability of collecting tubules (controlled by ADH) During dehydration, the kidney plays a major role in maintaining water balance. Osmoreceptors in the hypothalamus sense the increase in extracellular osmolality and stimulate release of ADH from posterior pituitary. Collecting tubules (under influence of ADH) become permeable to water. In the absence of ADH, the renal tubules remain impermeable to water and a dilute urine is formed. Specific gravity (osmolality) of urine varies with its concentration of solutes. Specific gravity provides index of hydration status and functional ability of the kidneys. Concentrated urine: 1.030 - 1.040 (SLIDE) Marked hyration or dilute: 1.000 4. Sodium and potassium regulation Sodium and potassium regulation (SLIDE) glomerular filtrate reabsorbed in proximal tubule. Na and KC1 pumped (requires energy) into intercellular spaces, and absorbed into peritubular

capillaries. Water movement accompanies the movement of these particles. Na reabsorption in distal tubule is variable and dependent on aldosterone. In the presence of aldosterone, almost all of sodium is reabsorbed and urine becomes almost sodium free. 5. Potassium regulation Potassium regulation - aldosterone mediated secretion of K into tubular fluid. (Can be reabsorbed in distal and collecting tubules, but since dietary intake far exceeds need, secretion usually exceeds reabsorption.) 6. Endocrine fuctions 1. Renin - released by special cells located near the glomerulus (juxtaglomerular cells) in response to: Reduction in GFR Sympathetic stimulation - Combines with angiontensinogen, a plasma protein that circulates in the blood to form angiotensin I, then converted to angiotensin II (potent vasoconstrictor and stimulator of aldosterone release). 2. Erythropoietin - released in response to hypoxia. Acts on bone marrow to stimulate production and release of RBCs. Persons with chronic hypoxia often have increased RBCs (polycythemia) due to increased erythropoietin levels. Examples: congestive heart failure, chronic lung disease, living at high altitude. 3. Vitamin D - activated and converted in kidney. Affects calcium metabolism. V. Pathophysiologies 80,000 - 110,000 die per year due to renal problems. 1.2 million conditions requiring hospitalization are related to renal stones, UTIs and other conditions. Medicare covers 95% of dialysis and transplants. A. Congenital defects 10% of persons born have potentially significant malformations of the urinary system.
1. Unilateral agenesis - relatively common; people often unaware. 2. Agenesis - Incompatible with life; infants usually stillborn. 3. Hypoplasia - Kidneys are not normal size; often only affects 1 kidney. If both, it progresses to renal failure, dialysis, and/or death. 4. Horseshoe kidney - Fusion of the kidneys at the midline. Usually no problem. 5. Dysplasia - Most common; i.e.: multicystic kidney, atresia or obstruction of the ureter.

6. Polycystic disease - Inherited; requires interventions such as surgery, drug therapy, transplant, and dialysis.

B. Urinary Tract Infections (UTIs) Second most common type of infection (Respiratory is first). 20% of all women will have one in their lifetime.
1. Bacteriuria. Presence of 100,000 or more organisms per ml of urine. Common complication associated with the use of foley catheters. CDC recommends that patients with a foley catheter not share a room. 2. Cystitis. Infection of the bladder. Characterized by frequency, urgency, lower abdominal discomfort, and dysuria. 3. Pyelonephritis. Inflammed areas of the kidney and renal pelvis. Can develop scar tissue. Patient is usually very ill: symptoms inlcude pain and chills, decrease in renal function.

Chronic Pyelonephritis. Characterized by scarring an deformation. May lead to loss of tubular function. May have severe hypertension which contributes to a significant cause of renal failure. a. Treatments
a. Sulfonamides b. Fluids

C. Obstructive Disorders
1. Hydronephrosis. Dilatation of the renal pelvis with renal atrophy. Causes interference with blood flow and glomerular filtration. If obstruction continues, permanent damage occurs in 3 weeks. 2. Urolithiasis (stones). One-third of people with recurrent stones will lose a kidney. a. b. c. d. e. f. Types Staghorn - fills renal pelvis Calcium (oxalate or Phosphate) make up 80-90% of stones Magnesium ammonium phosphate bacteria causes splitting of urea then stone forms. Uric acid - found in people with gout Cystine - rare and genetic in cause.

D. Glomerulonephritis Most common following infections by strains of group A, beta-hemolytic streptococci. In this situation, there is an abnormal immune reaction, causing immune complexes to become entrapped in the glomerular membrane, inciting an inflammatory response. The capillary membrane swells and is then permeable to plasma proteins and blood cells. Usually follows a strep infection by 10 days to 2 weeks (the time needed for formation of antibodies). Oliguria is an early symptom, Na and H20 retention causes edema, particularly of the face and hands, along

with hypertension. Proteinuria and hematuria follow from the increased capillary permeability. This may give a smoky hue to the urine ("cola" colored). E. Diabetic glomerulosclerosis Most important manifestation of diabetic neuropathy. Diffuse type - thickening of basement membrane. Nodular type - (Kimmelstiel-Wilson syndrome) hyaline deposits on the glomerulus. Both types present with proteinuria, with a slow, steady progression to renal failure. F. Acute Renal Failure (ARF) Is a potentially reversible condition that results in acute suppression of renal function. Acute renal failure may rapidly present a life threatening situation which is amenable to appropriate medical management provided that the situation is recognized. Evidence of renal involvement may be masked by the primary medical, surgical, or obstetric condition. 1. Pathogenesis The pathogenesis remains controversial and inconclusive but the theories most often encountered include bakleak, tubular, obstruction, vascular obstruction, and reninangiotensin. Regardless of the pathoensis, pathologic studies have described two characteristic histologic insults: Iscemia-This tends to produce pathcy lesions affecting the proximal and distal tubular segments. The basement cell membrane is disrupted and tubular necrosisis present Nephrotic-This usually leaves the basement membrane intact while tubular destruction can range from simple cellular swelling to frank necrosis. Damage is seenprimarily in the proximal tubulaar segments. The influences that may bear on kidney function sare usually considered in terms of three separate but requently interrelated categories. 2. Categories of ARF a. Prerenal Prerenal causes of renal failure act by reducing glomerular perfusion either by vasoconstriction, or a reduction of mean arterial pressure. This may be due to locl or general causes:
i. ii. iii. iv. Local: -embolism or thrombosis, -surgical operation, -hepatorenal syndrome General: -hypovolemia due to hemorrhage, burns, cardiac insufficiency, -GI losses, -peripheral vasodilators associated with excessive anihypertensivetherapy, -bacteremic shock . Many of these conditions can occur in the presence of a normal blood pressure and go undetected until renal symptons present. Frequent consideration of the clinical situation will help assist in identifying prerenal causes for ARF.

b. Renal (or intrarenal)

Renal causes of ARF are due to parenchymal changes resulting from disease or nephrotoxic agents that induce renal disease. Diseases of the renal parenchyma other than ischemia account for 25% of all cases of ARF. These include glomerular lesions such as acute poststreptococcal glomerulonephritis, SLE, papillary necrosis, and vasculitides (polyarteritis nodosa), Goodpasture's, Wegener's, and malignant hypertension. Ischemia - occurs when perfusion to the kidney is obliterated or reduced below a mean systemic blood pressure of 60-70 mmHg in the afferent arteriole. Can be grouped into 5 categories:
i. ii. Injury to the glomerular membrane (acute glomerulonephritis) Acute tubular necrosis (ATN) characterized by destructive changes in the tubular epithelium due to ischemia or exposure to nephrotoxic agents. Shock and heart failure, for example, cause prerenal failure, tend to cause renal ischemia, and if allowed to progress, can produce tubular necrosis. As a rule, the blood supply to a normal kidney can be interrupted for about 30 minutes without inflicting damage to the kidney. Trauma, sepsis, and heart failure may interrupt blood flow for a longer duration. Nephrotoxic drugs may be ingested, inhaled therapeutically, accidentally, or with suicidal intent. Widespread use of nephrotoxic antibiotics has contributed to a high frequency of ATN. The sulfonamides, methicillin and cephalosporins, along with aminoglycosides such as gentamicin, tobramycin, vancomycin, and amikacin are some of the most common nephrotoxic antibiotics. The aminoglycosides bind avidly to proximal tubular epithelial cells with a half life of 109 hours (5 1/2 days). Radiologic contrast media can also produce tubular damage. Radiographic dye usually promotes an osmotic diuresis and urine losses of up to 7 ml for every 1 ml of dye used. Intratubular obstructions - due to accumulation of casts and cellular debris, secondary to severe hemolytic reactions or myoglobinuria. Skeletal and cardiac muscle contains myoglobin, which accounts for their rubiginous color. Myoglobin corresponds to hemoglobin in function, serving as an oxygen reservoir within the muscle fibers. Myoglobin is not normally found in the serum or urine. It has a low molecular weight, so should it escape into the circulation, it is rapidly filtered in the glomerulus. Myoglobinuria is most commonly due to muscle trauma, but may result from extreme exertion, hyperthermia, sepsis, prolonged seizures, potassium or phosphate depletion, alcoholism or drug abuse. Can be traumatic or non-traumatic. Hemoglobin may also escape into the glomerular filtrate due to severe hemolytic reaction. Both myoglobin and hemoglobin cause discoloration of the urine, ranging from the color of tea to red, brown, or black. Acute pyelonephritis or necrotizing papillitis - bacterial infection of the kidney and renal pelvis.

iii.

iv.

c. Postrenal Postrenal causes of ARF are due to urinary tract obstruction, secondary either to structural or fuctional lesions of the urinary passages. The obstruction may occur anywhere from the tubules to the kidneys to the external urethral orifice. The cause may vary from stricture through stone to tumors of the urinary passages or of adjacent pelvic or abdominal organs.

Functional obstruction may follow the use of drugs which interfere with the autonomic supply to bladder or urinary passages such as ganglion blockage or antihistamines. With diabetes mellitus the advent of an imbalance in the neurogenic supply may be sufficient to disturb the equilibrium and precipitate the obstruction. Anuria associated with ARF is usually indicative of a post renal cause. G. Chronic Renal Failure (CRF) A slow, progressive renal disorder culminating in end stage renal disease (ESRD). The decline in kidney function correlated with the degree of nephron loss.
1. Pathophysiology - Systemic changes occur when overall renal function is less than 20-25% of normal. 2. Pathogenesis- Bricker's "intact nephron" hypothesis provides an explanation for the kidney's ability to compensate and preserve homeostasis despite a significant loss of 80% of nephron function. 3. During CRF, regardless of etiology, injury occurs to the nephrons in a progressive manner. Significant damage to groups of nephrons will eliminate them from their contributing role in maintaining renal function. The remaining intact nephrons will compensate by experiencing cellular hypertrophy. This growth process will enable them to accept larger blood volumes for clearances resulting in the exertion of greater solute levels, thus compensation results. 4. Stages of CRF a. Diminished renal reserve b. 50% nephron loss c. Kidney function is mildly reduced while the excretory and regulatory function are sufficiently maintained to preserve a normal internal environment. d. The patient is usually problem free. e. The patient's normal serum creatinine will double. 5. Renal insufficiency a. 75% nephron loss b. --Evidence of impaired renal capacity that appears in the form of mild azotemia, slightly impaired urinary concentrating ability, and anemia. c. --Factors that can exacerbate the disease at this stage by increasing nephron damage are: infection, dehydration, drugs and cardiac failure.

6. End Stage Renal Disease (ESRD)

y y y y

90% of the nephrons are damaged Renal function has so deteriorated that chronic and persistent abnormalities exist in the internal environment. Patient requires artificial support to sustain life, i.e. dialysis, transplant Uremic Syndrome

--The body's systemic responses to the buildup of uremic waste products and the results of the failed organ system. --Usually described as the constellation of signs and symptoms demonstrated by the RF patient. --Symptoms may be avoided or diminished by initiation of early dialysis treatment. H. LUPUS NEPHRITIS Is the cause of approximately 3% of cases of ESRF (end-stage renal failure) requiring maintenance dialysis or transplantation. It is characterized by deposits of immune reactants in different sites along the nephron. There are many different forms of lupus nephritis each with its own characteristics. Treatment is based on the severity and progression of the disease. Many tests are used to follow the course of acute episodes and are used as a guideline to therapy. No one test is specific enough to be used individually. Treatment includes: corticosteroids, cytotoxic drugs, plasma exchange therapy, Cyclosporine A, and pulse methylprednisone. Presenting symptoms include: proteinuira and hematuria. J. GOODPASTURE'S Is a syndrome consisting of pulmonary hemorrhages and glomerulonephritis of primary crescentic type. Frequently the term Goodpasture's is used in a purely clinical sense without reference to pathology or immunopathology. The disease is most common in young adult males but occurs at any age. The onset is sometimes preceded by "flu-like" symptoms. VI. Interventions A. Pharmacotherapy 1. Bumetanide (Bumex) - acts on the ascending limb of the loop of Henle to inhibit reabsorption of water and electrolytes. Nursing Interventions - Monitor for signs of electrolyte imbalance. One or 2 daily doses appear to be more effective than small doses administered frequently. May need potassium supplements or potassium-sparing diuretics. Watch for hypokalemia. Concurrent use with aminoglycoside antibiotics may increase potential for ototoxicity. Avoid use of indomethacin or probenecid. 2. Ethacrynic acid (Edecrin) promotes the excretion of water, sodium, chloride and other electrolytes by inhibiting tubular reabsorption, especially in the medullary and cortical portions of the acending limb of the loop of Henle.

Nursing Interventions - Administer with meals to reduce gastric upset. Avoid using with neurotoxic drugs such as amikacin, gentamicin, vancomycin. Watch for hypokalemia. Concurrent use with corticosteroids can produce severe hypokalemia. 3. Furosemide (Lasix) - promotes excretion of water, sodium, chloride and other electrolytes by inhibiting tubular reabsorption, especially in the medullary and cortical portions of the ascending loop of the loop of Henle. Nursing Interventions - Watch potassium levels. Watch for hearing loss. Give with caution in patients receiving neurotoxic drugs (see Edecrin) When giving IV push - give 10 mg/min. 4. Hydrochlorothiazide (Esidrix, Hydro-diuril, Oretic) - promotes excretion of water, sodium and chloride by inhibiting the reabsorption of sodium ions in the ascending limb of the loop of Henle and in the early distal tubule of the nephron. Thiazide diuretic. Nursing Interventions - Watch for potassium depletion, Electrolyte imbalance may increase when used with steroids, corticotropin, or Ampho B. 5. Mannitol (Osmitrol) elevates blood plasma osmolality resulting in flow of water from tissues, including brain and CSF. Mannitol is not reabsorbed in the renal tubule, which increases osmolality of the glomerular filtrate, facilitates the excretion of water and inhibits reabsorption of Na, Cl, and solutes. Nursing Interventions - Use with in-line IV filter . B. Hemodialysis
1. most widely used treatment for renal failure. 2. Invented during WWII but not widely used until approximately 1960. 3. Hemodialysis replaces excretory functions of the kidney but not hormonal functions. Eliminates wastes, electrolytes and water by: a. Passive diffusion - solutes pass through a semipermeable membrane from an area of high concentration to low. i. Factors which influence clearance capacity
y y y

Pore size of the membrane Concentration gradient of the dialysate, Surface area of the dialyzer

b. Convection (ultrafiltration) - water movement encouraged by establishment of a hydrostatic pressure force across a membrane (some solute passes also)
y

Factors which influence: o transmembrane hydrostatic pressure o surface area o selective permeability of the membrane

b. Indications o i. volume overload o ii. electrolyte imbalance o iii. contraindications to peritoneal dialysis o iv. uremic symptons c. Contraindications/disadvantages o i. Hemodynamic instability o ii. vascular access problems o iii. adherence to rigid diet o iv. disequilibrium syndrome o v. hepatitis o vi. muscle cramping o vii. bleeding tendancies due to anticoagulant used d. Types of vascular access: o i. Quinton or temporary double or single lumen catheters o ii. AV fistulas o iii. grafts (Gortex) o iv. shunts (Scribner)

D. Continuous Arteriovenous Hemodialysis (CAVHD) and Slow Continuous Ultrafiltration (SCUF) Uses patient's arterial blood pressure to deliver blood to a low-resistance hemodialyzer primarily for water removal. Alternative for patients who are oliguric and require large quantities of parenteral fluids, such as hyperalimentation, antibiotics, or vasopressors. Also when other forms of dialysis are contraindicated.
y

1. Contraindications to SCUF or CAVHD o a. inability to tolerate anticoagulation o b. hematocrit greater than 45

2. Difference between SCUF and CAVHD:

o

a. smaller volumes with SCUF, so control of uremia and electrolytes is impossible.

3. Advantages
o o

a. Better for cardiovascualr stability since the process of volume removal is slower b. Can be managed by critical care nurse rather than hemodialysis staff

4. Disadvantage:
o o

a. limited ability to remove wastes and excess solutes b. need arterial and venous access

VI. Labs and Tests

A. Urea - an end-product of protein metabolism. Urea rises with high-protein diet, excessive tissure breakdown, or in presence of GI bleeding (blood protein broken down in the intestine and urea absorbed into the blood). Kidneys regulate BUN levels, filter urea in the glomeruli and reabsorb it in the tubules. *BUN increases during dehydration *Excretion is markedly decreased when GFR drops. (Longer the tubular fluid remains in the kdiney, the greater the reabsorption of urea into the blood.) B. Creatinine - product of creatine metablism inmuscle. is filtered in the glomeruli, but not reabsorbed in the tubules. Therefore, blood values depend closely on GFR. *Normal cretinine level is proportional to muscle mass. ex: smallwoman - 0.5 mg/100 ml blood, man - 1.0 mg/100ml, muscular man - 11.4 mg/100ml *If value doubles, GFR - and renal function - probably have fallen to half of normal state. *If value triples - suggests 75% loss of renal function. *Values of 10 mg/100 ml - 90% loss of function C. Urinalysis - Normal urine contains metabolic wastes and little, if any, plasma proteins, blood cells, or glucose. Casts - molds of distal nephron lumen. Tamm and Horsfall mucoprotein (gel-like substance) forms the matrix of casts. Hyaline casts - contain Tamm and Horsfall mucoprotein, without cells. Develop when protein content of urine is high (such as nephrotic syndrome) urine osmo high, urine pH low. D. Other Serum lab tests
1. potassium, phosphate - tend to increase in renal failure 2. Calcium, pH, bicarbonate - tend to decrease in renal failure.

E. Cystoscopy - visualize the urethra, bladder, and ureteral orifices. Biopsy specimens, small stones, lesions, small tumor, and foreign bodies can be removed from urethra, bladder, or ureters by this means. F. Radiologic exams
1. Computerized axial tomography (CAT) delineate tissue at any level. May be used to outline kidney and detect tumors therein. 2. Radiopaque iodine contrast medium - allows for visualization of urinary structures. Dye can be introduced into urinary system or into a vein.

3. Intravenous pyelogram (IVP) - allows for x-ray visualization of renal calyces, renal pelvis, and ureters as dye is excreted by the kidneys. 4. Retrograde pyelography - cystoscope is used to introduce dye into the ureters.