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ACUTE RENAL FAILURE

INTRODUCTION:-Before the advancement of modern medicine, acute kidney injury might be

referred to as uremic poisoning. Uremia was the term used to describe the contamination of the blood with urine. Starting around 1847 this term was used to describe reduced urine output, now known as oliguria, which was thought to be caused by the urine's mixing with the blood instead of being voided through the urethra.Acute kidney injury due to acute tubular necrosis (ATN) was recognised in the 1940s in the United Kingdom, where crush injury victims during the London Blitz developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function. During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids.Research studies show,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.Congenital defects :-10% of persons born have potentially significant malformations of the urinary system. Incidence: Community: Less than 1% Hospital: 2% to 7% Intensive care unit (ICU)/postoperative: 4% to 25%, Risk factors for postoperative renal failure:Age -70 years, Insulin-dependent diabetes mellitus,Chronic renal failure, Left ventricular dysfunction.Significant associated mortality in ICU:43% to 88. Independent predictor of mortality. DEFINITION:-Acute renal failure (ARF), or acute kidney injury (AKI) is defined as an abrupt or rapid decline in renal perfusion or renal filtration function(normal GFR in normal size man 125ml/mint), usually marked by decresed in urine output(<400ml/day),increasd blood urea nitrogen value, a rise in serum creatinine concentration or by azotemia,a rise of in BUN and serum creatinine proportionate to each other (ratio of >10:1)[specific criteria exist for the diagnosis-Rapid time course (less than 48 hours), absolute increase in serum creatinine of 0.3 mg/dl (26.4 mol/l),percentage increase in serum creatinine of 50% and reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours]
RELATED ANATOMY AND PHYSIOLOGY OF KIDNEY:-

The kidneys are bean shaped and sit near the posterior wall of the abdomen (one on each side of the vertebral column) and are located at the level of the 12th rib. A normal kidney measures about 10cm (length) 5cm (width) 2.5 cm (thick). The kidneys are protected from trauma and infection by connective tissue, and fascia (which connect the kidneys to the abdominal wall). The inner most layer of the kidney is comprised of adipose tissue which forms a protective cushion for the kidneys. The kidneys receive oxygen rich blood from the renal arteries (which come off the abdominal portion of the aorta); while the renal veins drain through the abdominal portion of the inferior vena cava. The hilum is the entry and exit port for the renal vessels and nerves.

The ureters measure approximately 25-30 cm long and are lined with smooth muscle. The ureters carry urine to the bladder and are situated in a downward position to assure that urine can only move in a downward direction. The outside region of the kidney (reddish brown in color) is referred to as the renal cortex; while the inner region (pinkish in color) is referred to as the renal medulla. The renal cortex houses the nephrons which are considered to be the functional parts of the kidneys.

One kidney contains ten lakh nephrons.The nephrons filter the blood of small molecules and ions (forming urine) while retaining useful minerals and sugars. In a 24 hour period it is estimated that the nephrons reclaim 1,300 grams of sodium (NaCl), 400 grams of sodium bicarbonate (NaHCO3), 180 grams of glucose and 180 liters of water. The Glomerulus (the main filter of the nephron system) is a semi-permeable membrane that is located within Bowmans capsule and allows water and solutes (in the form of urine) to be excreted via afferent and efferent arterioles. The urinary bladder is located midline in the abdominal pelvis. The urinary bladder is pyramid shaped and very muscular. The main function of the urinary bladder is to collect and store urine until it is excreted through the urethra. The kidneys (as well as the lungs) play a vital role in the ph balance by holding on to or excreting hydrogen ions and Co2 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. 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.Formula for creatinine clearance: C=UV P C = clearance rateU = urine concentrationV = 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: proximal tubule, loop of Henle, distal tubule, collecting duct. Then it reaches the pelvis and kidney for reabsorption: water, sodium, and other substances leave the lumen of the tubule and enter the blood. Glucose and amino acids - completely reabsorbed Filtered water - 99% reabsorbedUrea - about 50% reabsorbedCreatinine none Electrolytes determined by need. 4.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. 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 Renin - released by special cells located near the glomerulus (juxtaglomerular cells) in response to 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). Erythropoietin - released in response to hypoxia. Acts on bone marrow to stimulate production and release of RBCs. Vitamin D activated and converted in kidney affects calcium metabolism.
ETIOLOGICAL FACTORS(ACCORDING TO CAUSES):-

PRERENAL 1.Volume depletion(hypovolemia) resulting from -Haemorrhage

INTRARENAL 1.Acute glomerulonephritis -Interstitial nephritis

POSTRENAL 1.Benign prostate hyperplesia. -Bladder cancer

-Renal losses(excessive diuresis),hypoalbuminemia, -G.I losses(diarrhea,vomiting,nasogastric suction) 2.Impaired cardiac efficiency(cardiac dysrhythmias) -Decreased cardiac output -Myocardial infarction -Heart failure 3.Decreased peripheral vascular resistance -Anaphylaxis -Neurologic injury -Septic shock -Antihypertensive medication which causes vasodialation -Renal artery thrombosis 4.Decreased renovascular blood flow -Bilateral renal vein thrombosis -Hepatorenal syndrome -Nephrotoxic injury aminoglycosides gentamicin,amikacin radiocontrast agents) hemolytic blood transufusion reaction) chemical exposure(ethylene glycol,lead,arsenic,carbon tetrachloride) crush injury,burn

-Prostate cancer

2.Thrmbotic disorder Malignant hypertension

2.Blood clots Calculi formation

3.Toxemia of pregnancy Interstitial nephritis -Allergies(antibiotics : sulfonamide,rifampin),NS AIDS,ACE inhibitors) -Infections(bacterial-acute polynephritis,viralCMV,fungal-candidiasis) 4.Prolonged renal ischemia -Pigment nephropathy -Myoglobinuria -Hemoglobinuria

3.Spinal cord disease Strictures Neuromuscular disease

4.Trauma(back,pelvis,perini um)

PHASES OR TYPES OF ACUTE RENAL FAILURE:The Four Phases of Acute Renal Failure Onset Phase this period represents the time from the onset of injury through the cell death period. This phase can last from hours to days and is characterized by:--Renal flow at 25% of normal; Oxygenation to the tissue at 25% of normal ;Urine output at 30 ml (or less) per hour ;Urine sodium excretion greater than 40 mEq/L. In this phase only 50% of the patients are noted to be oliguric. With prompt treatment, irreversible damage can be achieved during this pre renal failure onset phase.

Oliguric/Anuric Phase this phase usually lasts between 8-14 days and is characterized by further damage to the renal tubular wall and membranes. Other characteristics in the oliguric-anuric phase include:---Great reduction in the glomerular filtration rate (GFR) ;Increased BUN/Creatinine ;Electrolyte abnormalities (hyperkalemia, hyperphosphatemia and hypocalcemia) ;Metabolic acidosis {BACKLEAK PHENOMENON:cracks or breaks in the tubuler wall->secondary to the ischemic event>glomeruler filtrate to leak back in renal tissue->oliguria} Diuretic Phase this phase occurs when the source of obstruction has been removed but the residual scarring and edema of the renal tubules remains. This phase usually lasts and additional 7-14 days and is characterized by:---Increase in glomerular filtration rate (GFR) ;Urine output as high as 2-4 L/day ;Urine that flows through renal tubules;Renal cells that cannot concentrate urine Increased GFR in this phase contributes to the passive loss of electrolytes which requires the administration of IV crystalloids to maintain hydration. Recovery Period Phase The recovery phase can last from several months to over a year. During this phase, edema decreases, the renal tubules begin to function adequately and fluid and electrolyte balance are restored (if damage was significant, BUN and Creatinine may never return to normal levels). At this point the GFR has usually returned to 70% to 80% of normal. PATHOPHYSIOLOGY:-

Vascular Factors Alterations in regional blood flow>Increased sensitivity to vasoconstrictor

Stimuli>Increased sensitivity to renal nerve stimuli>Impaired autoregulation>Endothelial injury>Decreased nitric oxide derived from endothelial nitric oxide synthase> Increased endothelin>Decreased prostaglandins>Leukocyte adhesion to endothelium Tubular FactorsSublethal Reversible Proximal Tubular Injury>Cytoskeletal disruption> Loss of polarity>Tubular obstruction>Abnormal gene expressionProximal tubular necrosis>Calcium influx>Metalloproteases>Oxygen radicals-Lipid peroxidation>Nitric oxide derived from inducible nitric oxide synthase>Defective heat shock protein response>Proximal tubular apoptosis Inflammatory Response Endothelial injury and leukocyte infiltration> Neutrophils T lymphocytes Monocyte/macrophages>Activation of leukocytes by inflammatory mediators Sepsis and Acute Renal Failure Renal vasoconstriction with intact tubular Function>Tumor necrosis factor
CLINICAL FEATURES:-

The clinical features that may be experienced with acute renal failure depend on the phase, the degree of azotemia (abnormal levels of urea and creatinine) and the degree of metabolic acidosis. The following signs and symptoms are consistent with acute renal failure: URINARY SYSTEM:--Decreased urine output (urine may be pink or reddish in color) ,Proteinuria, Casts, Specific gravity decreased, Osmolality decreased, Urinary sodium increased. CARDIOVASCULAR SYSTEM:--Volume overload ,Heart failure, Arrhythmias , Early hypotension, Hypertension(after development of fluid overload), Pericarditis, Pericardial effusion, Dysrhythmias. RESPIRATORY SYSTEM:-- Shortness of breath , Pulmonary edema, Kussmaul respirations, Pleural effusion. GASTROINTESTINAL SYSTEM:--Poor appetite, Nausea, Vomiting, Stomatitis, Bleeding, Diarrhoea, Constipations, Bitter or metallic taste in mouth INTEGUMENTARY SYSTEM:--Dry itchy skin , Easy bruising. HEMATOLOGIC SYSTEM:--Anemia(developed within 48 hours), Susceptibility to infection decreased, Leukocytosis, Defect in platelet functioning, Fatigue. NEUROLOGIC SYSTEM:-Seizures, Loss of consciousness, Seizures, Asterixis, Memory impairement. METABOLIC SYSTEM:--Level of BUN, CREATININE, POTASSIUM, PHOSPHATE increased, PH, SODIUM, BICARBONATE, CALCIUM decreased. Sudden weight gain.
COLLABORATIVE CARE OF ACUTE RENAL FAILURE:-

Acute renal failure is potentially reversible, the primary goals of treatement are to eliminate the cause,manage the sign and symtoms and prevent complications while the kidneys recover.If ARF is already established,then conservative therapy is needed.

DIAGNOSTIC EVALUATION:-A thorough history is essential for diagnosing the etiology of acute

renal failure. Comparing any previous measurements of serum creatinine with the patients current biochemistry. Pre-existing chronic renal impairment can be excluded if a relatively recent previous measurement of renal function was normal. A history of several months vague ill-health, nocturia or pruritus, and findings of skin pigmentation, anaemia, long-standing hypertension or neuropathy suggest a more chronic disease. A deciliter of normal blood contains 7 to 20 milligrams of urea. If a person's BUN is more than 20 mg/dL, the kidneys may not be working at full strength. A more sensitive test for protein or albumin in the urine involves laboratory measurement and calculation of the protein-to-creatinine or albumin-to-creatinine ratio. Basic bloods:Urea and electrolytes, Full blood count, Blood glucose, Coagulation screen, Liver function tests Calcium and phosphate, Blood cultures (if infection suspected) Arterial blood gases or venous bicarbonate, Inflammatory markers:C Reactive protein Electrocardiogram Chest radiograph Urine analysis: Confirmatory Lab Values for Acute Renal Failure Lab Test Prerenal Value Intrarenal Value Urine Specific Gravity Greater than 1.020 1.010 to 1.020 BUN/Creatinine ratio Greater than 20:1 10-20:1 Urine Osmolality Greater than 500 mOsm/kg 300-500 mOsm/kg Urine Sodium 10 mEq/L or less 20 mEq/L or more Urine Sediment (urinalysis) Hyaline casts Granular casts Fractional excretion of sodium percent (FENa) Less than 1% Greater than 1% (the fractional excretion of filtered sodium (FENa = [(urine sodium plasma creatinine) / (plasma sodium urine creatinine)]is less than 1%). Creatinine Clearance Test is believed to be the most accurate test to determine glomerular filtration rates. This test requires urine collection for a 24 hour period with normal clearance levels being 95 ml/min to 125 ml/min. Levels less than 50 ml/min are consistent with intrarenal disease. Prerenal disease levels vary depending on how long low renal flow has existed, with postrenal failure levels usually falling within normal limits. Renal Ultrasound can be effective in determining existing renal failure and or obstruction of the urinary collecting system. Kidney detection and possible obstruction can be difficult to evaluate in obese patients. An ultrasound that shows small kidneys can be a sign of chronic renal failure. Doppler Studies doppler scans can be effective in determining the presence and nature of renal blood flow. Doppler scans are also useful in detecting thromboembolic disease, renal vascular disease or hepatorenal syndrome. Nuclear Studies radionuclear imaging can be effective in determining renal blood flow and tubular function. The use of aortorenal angiography can be helpful in determining renal vascular disease, renal artery stenosis, atheroembolic disease, atherosclerosis with aortorenal occlusion and/or necrotizing vasculitis.

Renal Biopsy can be effective in diagnosing intrarenal failure, but should only be done if the result will alter the treatment plan. Renal biopsy is usually only indicated if there is a prolonged period of renal failure (without response to treatment) and it will assist with the development of a long term treatment plan. Renal scan,CT scan,MRI. Retrograde pyelogram.
MANAGEMENT:-COLLABORATIVE THERAPY

Treatment of precipitating cause. Fluid restriction (600ml plus previous 24hr fluid loss). Nutritional therapy-adequqte protein intake(0.6-2gm/kg/day)depending on degree of catabolism,potassium , sodium and phosphate restriction. Measures to lower potassium(if elevated) Calcium supplements or phosphate binding agents. Parental or enteral nutrition(if indicated). Initiation of dialysis or renal replacement therapy(if needed in progress in disease process). MEDICAL MANAGEMENT: In ATN, volume repletion does not restore renal function, and urine output usually remains low(<30 mL/h). Diuretics such as Furosemide (Lasix) a loop diuretic that can be used to increase urinary flow with the intent of flushing out cellular debris that may be causing an obstruction. There is a theoretical rationale for the use of loop diuretics in ARFinhibition of the Na+/K+/2Cl pump in the thick ascending limb of the loop of Henle.It seems reasonable to use diuretics only in adequately resuscitatedbut oliguric patients, at a dose suitable to the degree of renal impairment (250 mg furosemide intravenously over one hour is a standard regimen), and to stop diuretic treatment if oliguria persists. Many units give a trial of furosemide (e.g. 500 mg IV over 8 hours, or 1 g over 24 hours, if a small dose has produced no effect). Dopamine at low doses (1-5 mcg/kg/min), dopamine dilates renal arterioles and increases renal blood flow and glomerular filtration. Because dopamine (even at low doses) can cause tachycardia, myocardial ischemia and arrhythmias it use should be considered carefully . The use of low dose (13 g/kg/min) dopamine has been advocated to increase renal perfusion in critically ill patients. Recent studies, including a large randomised controlled trial, have shown it to lack efficacy on renal outcome or overall mortality.Use of dopamine may also reduce splanchnic perfusion, depress respiration, suppress anterior pituitary hormone release and function, and worsen renal function in hypovolaemic or normovolaemic patients. Mannitol an osmotic diuretic that can be used to dilate renal arteries by increasing the synthesis of prostaglandins (resulting in restored renal flow). Calcium antagonizes reduce the effects of hyperkalaemia, stabilising the myocardium within a few minutes of infusion and producing a more normal ECG trace without affecting serum potassium. It should be given immediately if P wave or QRS changes are present. A bolus of 1020 ml of 10% calcium gluconate or chloride is given intravenously over two to five minutesthe former is preferable because of a lower risk of tissue damage if extravasation occurs. High serum calcium concentrations potentiate the cardiac toxicity of digoxincalcium should be given as a slow infusion in hyperkalaemic patients taking this drug (that is, 10 ml 10% calcium gluconate in 100 ml 5% dextrose over 30 minutes). N-acetylcysteine (Mucomyst) this medication can help reverse acute renal failure when the cause is thought to be from a nephrotoxic source.

Regardless of the cause, the same general treatment principles apply to all patients who develop ARF. These include removing nephrotoxics (e,g. drugs): in some instances the nephrotoxins may need to be removed by dialysis or adsorption (e.g. after aspirin overdose) or specific antidotes may be needed in addition to dialysis (e.g. N-acetylcysteine in paracetamol overdose). Colloids Colloids (e.g. human albumin, dextrans,hydroxyethyl starch (HES), modified gelatins)are used in the hope that they will remain inthe vascular space for longer and hence restore microcirculatory flow more efficiently Ion exchange resins bind potassium in the gastrointestinal tract, in exchange for calcium or sodium, and result in increased potassium excretion in the stool. Calcium resonium (calcium polystyrene sulphonate) and Resonium A (sodium polystyrene sulphate) are the most commonly used, given at an oral dose of 15 g up to thrice daily, together with an osmotic laxative (for example, lactulose 10 ml) to prevent constipation. They can also be given rectally. An effect takes two to three hours. Side effects include hypercalcaemia and salt/water overload (with calcium and sodium containing resins respectively), and hypomagnesaemia. They are most suited for use in situations where potassium levels are moderately high (around 6.5 mmol/l), comparatively stable, and improvement in the patient's renal function is expected or dialysis is planned but can be delayed. 2 adrenergic agonists:- Salbutamol binds to 2 receptors and through cytosolic second messengers activates the Na+/K+ATPase, thus promoting cellular potassium uptake. Nebulised and intravenous salbutamol produce a similar effect to insulin, but at higher doses than used for bronchospasm (1020 mg via nebuliser, or 0.5 mg intravenously). The method should not be used in patients taking blockers or in those with a high risk of cardiac side effects. FLUID THERAPY:-These are often given in the hope that they will stimulate diuresis. It is both illogical and dangerous to give further fluid to a patient who has already been fully resuscitated. If the patient remains oliguric, the extra fluid load may cause life-threatening pulmonary oedema. The only rational use of a 500 mL fluid bolus is when given in combination with CVP measurements; administration of a fluid bolus to a hypovolaemic patient causes only a transient increase in CVP, whereas a more sustained rise is seen in patients. Once the patient is considered euvolaemic (normotensive, no postural drop, JVP and/or central venous pressure (CVP) normal), care should be taken to avoid fluid overload and a maintenance regimen started, which takes account of renal and insensible losses, aiming for a positive balance of 500 ml/day (hourly input = previous hour's output plus 25 ml). Crystalloids (e.g. 0.9% sodium chloride, 5% glucose, Hartmanns solution) are cheap and safe, but rapidly distribute between the vascular space and the extracellular space, resulting in oedema, pleural effusions and ascites if used in large volumes, particularly in the presence of increased endothelial permeability (as in systemic inflammatory response syndrome). In cases where the patient has symptomatic metabolic acidosis, 1.26% sodium bicarbonate solution may be infused instead of 0.9% sodium chloride. The two solutions are both isotonic with blood, but the bicarbonate will help correct the acidosis. NUTRITIONAL THERAPY:- Maintain adequate nutritional therapy: a good rough guide is a protein intake of 0.6 g/kg per day, increasing to 1 g/kg if the patient being dialysed. Calorie intake should be 50100% above the patients resting energy expenditure (25 kcal/kg per day). Consult a specialist renal dietician where possible.If the patient does not receive adequqte nutrition.catabolism of body proteins will occur. This process causes increased urea,phosphate and potassium levels. The daily calorie intake should be about 30-35kcal/kg of body weight.Protein intake is generally 0.6gm/kg body wt. to control

nitrogenous waste product production.Potassium and sodium are regulated in accordance with plasma levels.Sodium is restricted to prevent edema.Dietary fat intake(30%calorie from fat)is increased,fat emulsion iv infusion can also be given as a nonprotein calorie supplements.
THERAPIES TREAT ELEVATED POTASSIUM LEVEL:-

1.Regular insulin administration iv:-potassium moves into cells when insulin is given,glucose is given concurrently to prevent hypoglycemia. When effects of insulin diminish,potassium shifts back out of the cells. 2.Sodium carbonate:-therapy can correct acidosis and causes shift of potassium into cells. 3.Calcium gluconate iv:-therapy is given iv and generally used in advanced cardiac toxicity.Calcium raises the threashold for excitation,resulting in dysrhythmias. 4.Dialysis:-hemodialysis can bring potassium levels to normal within 30 mints to 2 hrs. 5.Sodium polystyrene sulfonate(karyexalate):-Cation exchange resin is administered by mouth or retention enema. When resin is in the bowel, potassium is exchanged for sodium. Therapy removes 1 mEq of potassium/gm of drug. It is mixed in water with sorbitol to produce osmotic diarrhea ,allowing for evacuation of potassium-rich stool from body. 5.Dietary resrtriction:-Daily potassium intake is limited to 40 mEq. PARENTAL NUTRITION:-Malnutrition is frequently present in patients with acute renal failure and may affect morbidity and mortality in this condition. When adequate nourishment cannot be given through the gastrointestinal tract, total parental nutrition with amino acids and hypertonic glucose may have beneficial results. Total parenteral nutrition has been reported to stabilize or reduce serum urea nitrogen, potassium and phosphorus levels, improve wound healing, enhance survival from acute renal failure, and possibly increase the rate of recovery of renal function. ENTERAL NUTRITION:- All patients were fed in a semirecumbent position, with the head elevated to 45. Feeding was always infused at a constant rate over 24 hours by a pump, and the containers and delivery systems were changed every 24 hours of use. Standard polymeric diets (Osmolite; (Abbott), 840 nonprotein kcal/L, 40 g proteins/L, with or without glucose polymers addition (Polycose; Abbott) 2 kcal/mL, or disease-specific diets: Dialycare (Abbott), 1720 nonprotein kcal/L, 70 g proteins/L or Renalcare (Abbott), 1880 nonprotein kcal/L, 30 g proteins/L. Diets were always administered at full strength. In the case of standard polymeric diet, the initial rate was set at 30 mL/hour and increased by 20 mL/hour/day every 24 hours. CALCIUM SUPPLEMENTS OR PHOSPHATE BINDING AGENTS:- Oral calcium supplementation is used in some patients with mild to moderate CKD to maintain adequate calcium nutrition. If calciumfree, phosphate-binding agents are used exclusively to manage hyperphosphatemia among patients with CKD, the diet becomes the sole source of calcium to satisfy nutritional requirements, except for amounts that may be transferred from dialysate to plasma during either hemodialysis or peritoneal dialysis procedures. CONTINUOUS RENAL REPLACEMENT THERAPY:- Renal replacement therapy for ARF generally involves intermittent hemodialysis (IHD) or continuous renal replacement therapy (CRRT), e.g., continuous veno-veno-hemofiltration (CVVH). Since the hemodynamic stress is less with CVVH than with IHD, it is possible that any additional hemodynamic or nephrotoxic insult, which might prolong the course of ARF and thereby increase mortality, might be less with CRRT. The most recent metaanalysis, however, of randomized results comparing IHD with CRRT in ARF has not shown any difference in survival.Many patients with mild-to-moderate ARF can be managed on general medical or surgical wards, but those with multiple organ failure should be managed on an ICU. Patients with

ARF requiring renal replacement therapy (RRT) (i.e. those with rapidly increasing serum creatinine, oliguria, especially those with impending or established pulmonary oedema, hyperkalaemia and severe metabolic acidosis) should be managed on either a renal ward or an ICU. Benefits to using CRRT as a method of dialysis include: Hemodynamic stability,Correction of metabolic acidosis,Quicker kidney recovery time,Correction of malnutrition and Solute removal. Transplantation:-A donated kidney may come from an anonymous donor who has recently died or from a living person, usually a relative. The kidney must be a good match for the patient's body. The more the new kidney is like the person receiving the kidney, the less likely the immune system is to reject it. The immune system protects a person from disease by attacking anything that is not recognized as a normal part of the body. So the immune system will attack a kidney that appears too "foreign." The patient will take special drugs to help trick the immune system so it does not reject the transplanted kidney. Unless they are causing infection or high blood pressure, the diseased kidneys are left in place. Kidneys from living, related donors appear to be the best match for success, but kidneys from unrelated people also have a long survival rate. Patients approaching kidney failure should ask their doctor early about starting the process to receive a kidney transplant.
DIALYSIS:-

The two major forms of dialysis are hemodialysis and peritoneal dialysis. Hemodialysis uses a special filter called a dialyzer that functions as an artificial kidney to clean a person's blood. The dialyzer is a canister connected to the hemodialysis machine. During treatment, the blood travels through tubes into the dialyzer, which filters out wastes, extra salt, and extra water. Then the cleaned blood flows through another set of tubes back into the body. The hemodialysis machine monitors blood flow and removes wastes from the dialyzer. Hemodialysis is usually performed at a dialysis center three times per week for 3 to 4 hours. A small but growing number of clinics offer home hemodialysis in addition to standard in-clinic treatments. The patient first learns to do treatments at the clinic, working with a dialysis nurse. Daily home hemodialysis is done 5 to 7 days per week for 2 to 3 hours at a time. Nocturnal dialysis can be performed for 8 hours at night while a person sleeps. Research as to which is the best method for dialysis is under way, but preliminary data indicate that daily dialysis schedules such as short daily dialysis or nocturnal dialysis may be the best form of dialysis therapy. In peritoneal dialysis, a fluid called dialysis solution is put into the abdomen. This fluid captures the waste products from a person's blood. After a few hours when the fluid is nearly saturated with wastes, the fluid is drained through a catheter. Then, a fresh bag of fluid is dripped into the abdomen to continue the cleansing process. Patients can perform peritoneal dialysis themselves. Patients using continuous ambulatory peritoneal dialysis (CAPD) change fluid four times a day. Another form of peritoneal dialysis, called continuous cycling peritoneal dialysis (CCPD), can be performed at night with a machine that drains and refills the abdomen automatically. Hemodialysis hemodialysis remains the primary method of renal replacement therapy in patients with acute renal failure. It provides ultrafiltration for rapid water removal and diffusion for solute removal. It is indicated for uremia, electrolyte imbalances, fluid overload and severe metabolic acidosis. Hemodialysis is recommended when there is a need for quick removal of water and toxins.It

has an immediate effect once started. Maximum removal occurs in the first hour of dialysis. Serum potassium may decrease by 1.21.5 mEq/l/h if potassium free dialysate is used, which can precipitate hypokalaemia and arrhythmias. One concern with using hemodialysis for critically ill patients with acute renal failure is that the process requires moving large amounts of fluid out of the intravascular system which can lead to acute and severe hypotension (secondary to hypovolemia). 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. Factors which influence clearance capacity :-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) .Factors which influence: transmembrane hydrostatic pressure ,surface area ,selective permeability of the membrane Indications i. volume overload ii. electrolyte imbalance iii. contraindications to peritoneal dialysis iv. uremic symptons Contraindications/disadvantages i. Hemodynamic instability ii. vascular access problems iii. adherence to rigid diet iv. disequilibrium syndrome v. hepatitis vi. muscle cramping vii. bleeding tendancies due to anticoagulant used Types of vascular access: i. Quinton or temporary double or single lumen catheters ii. AV fistulas iii. grafts (Gortex) iv. shunts (Scribner) Peritoneal Dialysis peritoneal dialysis is not commonly used as a treatment with acute renal failure. Although efficient, it is slow process that involves the transfer of fluid and solutes between the peritoneal cavity and the peritoneal capillaries. The clearance that occurs with peritoneal dialysis is thought to be less effective than other types of dialysis. Continuous Arteriovenous Hemodialysis (CAVHD) and Slow Continuous Ultra-filtration (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. Contraindications to SCUF or CAVHD a. inability to tolerate anticoagulation b. hematocrit greater than 45 Difference between SCUF and CAVHD: a. smaller volumes with SCUF, so control of uremia and electrolytes is impossible. Advantages 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 Disadvantage: a. limited ability to remove wastes and excess solutes b. need arterial and venous access. Some rebound of potassium levels occurs after dialysis, especially if initial levels were high or if treatments to increase cellular uptake were used predialysis Prevention of further potassium accumulation. This can be achieved through a low potassium diet. Special situations (1) Rapidly progressive glomerulonephritis:-Rapidly progressive glomerulonephritis (RPGN) can destroy kidney function within days to weeks if not correctly identified and treated. (2) Haemolyticuraemic syndrome:-This occurs in an epidemic form, usually associated with outbreaks of diarrhoea often caused by Shiga toxin producing E coli (3) Tubulointerstitial nephritis:-Drug induced tubulointerstitial nephritis should respond to cessation of offending agent but renal biopsy may be required to confirm the diagnosis (4) Contrast nephropathy:-The use of radiological contrast media is associated with the development of ARF in a number of at risk groups including patients with preexisting renal impairment (especially diabetic nephropathy), those with volume depletion, those taking drugs that interfere with the normal regulation of renal perfusion (ACEI, NSAIDs), and those requiring increased doses of contrast agent. (6) Liver diseasehepatorenal syndrome:-Hepatorenal syndrome (HRS) defines the ARF that occurs in conjunction with advanced cirrhotic liver disease when other causes of renal impairment such as prerenal failure, ATN (5) Rhabdomyolysis:-Severe skeletal muscle injury and cell lysis produces rhabdomyolysis with the release of muscle breakdown products into the circulation. ARF may result, partly from direct toxic effects of myoglobin, and partly from intravascular volume depletion (muscle oedema, plus blood loss from trauma) and renal hypoperfusion.
NURSING ASSESSMENT:-

Nursing assessment focus around the following physical findings (based on the phase of renal failure): Onset Phase: Mild reduction in normal daily urine output Mild lethargy Mild malaise Oliguric/Anuric Phase:

24 hour urine total 400 ml or less Listlessness/fatigue Confusion or altered LOC (from electrolyte imbalances) ECG changes (elevated T waves, depressed ST segment, prolonged PR interval, loss of P wave, wide QRS complex, arrhythmias) S3 or S4 gallop Pericardial friction rub Pulsus paradoxus Fever Chest pain Crackles upon lung auscultation (due to fluid overload) Shortness of breath (due to fluid overload) Jugular vein distention (due to fluid overload) Periorbital, peripheral or sacral edema (due to fluid overload) Ascites (due to fluid overload) Capillary fragility as evidenced by easy bruising Metabolic acidosis Anorexia, nausea, vomiting, diarrhea, constipation Uremic frost (pale, yellow, dry or itchy skin) Diuretic Phase: Urine output of 3 to 5 liters in a 24 hour period Lethargy or muscle weakness (due to hypokalemia) Decreased blood pressure (due to fluid depletion) Dry mucous membranes (due to fluid depletion) Poor skin turgor and delayed capillary refill (due to fluid depletion) Recovery Phase: Urine output of 1500 to 1800 ml in a 24 hour period Stabilization of serum potassium, bicarbonate, BUN and creatinine Stabilization of cardiac rhythm and rate Reduction in lethargy and shortness of breath
NURSING DIAGNOSIS:-

Alteration in urinary elimination evidenced by decresed urine output. the goal is that the patient is euvolemic and has no symptoms suggestive of fluid deficit or overload. Fluid volume deficit evidenced by-dry mouth, hypotension, poor skin turgor, delayed capillary refill the goal is that the patient is euvolemic; with urine output that is approximately 30 ml/hr and has no symptoms suggestive of fluid deficit. Fluid volume overload evidenced by edema, wt. gain, JVD. the goal is that the patient is euvolemic and has no symptoms suggestive of fluid overload. Altered nutrition (less than bodily requirement) evidenced by anorexia. the goal is that the patient will have balanced nutrition and fluid balance with weight within normal limits. Potential for impaired skin integrity evidenced by pressure ulcers and dry itchy skin. the goal is that the patient remains free from pressure ulcers and dry itchy skin. Knowledge deficit evidenced by verbalization.

the goal is that the patient/family has a better understanding of the disease process and understand the need for follow up care. Decreased cardiac output evidenced by cardiac arrythmia the goal for the patient is to have improved clinical findings based on adequate cardiac output i.e. normal vital signs, adequate capillary refill, absence of hypotension. Fear (anxiety) evidenced by verbalization. the goal for the patient will have a low level of anxiety and be able to effectively express concerns and questions regarding care. The patient will also be able to verbalize symptoms of anxiety and mechanisms for dealing with these symptoms. Activity intolerance the goal for the patient is to participate in activities of daily living without become exhausted. Ineffective individual/family coping the goal of the patient/family is to be able to participate in care without becoming overwhelmed. The goal is also to be able to verbalize where counseling/support can be found Body image disturbance the goal of the patient who may require a shunt for hemodialysis is to state or demonstrate acceptance of this change. Altered thought processes the goal of the patient is to demonstrate improved cognitive function and be able to participate in activities of daily living. Potential for injury the goal for the patient is to remain injury free and be able to verbalize and explain methods to prevent injuries and/or falls. Risk of infection the goal for the patient is to remain free from symptoms of infection (WBCs within normal limits) and to be able to state what symptoms of infection are. EXPECTED OUTCOMES: Insert an indwelling urinary catheter and measure output and specific gravity hourly. Monitor for signs of electrolyte imbalance. 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. 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. Observe the client for metabolic acidosis to identify complication of renal failure.Observe the fluid and electrolyte balance hourly. avoid an edema caused by excessive fluid intake. Monitor the client's diet to provid Maintaining volume homeostasis and correcting biochemical abnormalities-- Gathering a detailed patient history (pre-hospital and current) Maintaining adequate intravascular volume Maintaining mean arterial pressure Discontinuing all nephrotoxic medications (NSAIDS, Gentamycin) Eliminating exposure to any other nephrotoxins Correcting acidosis (sodium bicarbonate for severe acidosis) Correcting hemolytic abnormalities (blood transfusion may be required)

Correcting all electrolyte abnormalities (Hyperkalemia is very common) Strict monitoring on intake and output/daily weight (Hydration for prerenal failure) Serial monitoring of labs (BUN/Creatinine/Osmolality [urine/blood], etc) Diet and fluid restrictions/replacement (in a state of oliguria or polyuria) High carbohydrates, adequate fats, and low protein. Administer with meals to reduce gastric upset. Avoid using with neurotoxic drugs such as amikacin, gentamicin, vancomycin. Reduce the client's potassium intake to help prevent elevated potassium levels. Protein catabolism causes potassium release from cells into the serum. Provide frequent oral hygiene to avoid tissue irritation and sometime ulcer formation caused by urea and other acid waste products excreted through the skin and mucous membranes. Furosemide (Lasix) - promotes excretion of water, sodium, chloride and other electrolytes. Watch potassium levels to prevent hearing loss. Give with caution in patients receiving neurotoxic drugs When giving IV push - give 10 mg/min. Hydrochlorothiazide promotes excretion of water, sodium and chloride by inhibiting the reabsorption of sodium ions. Thiazide diuretic. Watch for potassium depletion, Electrolyte imbalance may increase when used with steroids. Maintain skin care with cool water to relive pruritus and remove uremic frost (white crystal formed on skin from excretion of urea. Observe for the arrhytmias and cardiac arrest to identify complications of high serum potassium. Administer stool softeners to prevent colon irritation from high levels urea and organic acids. Provide hemodialysis or peritoneal dialysis as ordered. Provide emotional reassurance to the client and family members to help decrease anxiety levels caused by the fact that the client has an acute illness with unknown prognosis.Explain treatments and progress to the client to help reduce anxiety. Algorithm for preventing acute renal failure in an oliguric patient Oliguria (<0.5ml/kg/h) | Correct volume depletion and usual blood pressure - if not possible refer to ICU | Catheterise or check catheter patency, measure urine output | Fluid challenge to raise CVP to 15mmHg | 2-5g/kg/h dopamine | 5-10mg/h frusemide | Fluid challenge to raise PAOP to 18mmHg | Abdominal ultrasound | Dialyse/haemofilter

Nursing Responsibilities for CRRT

Patient family teaching regarding the procedure and equipment Monitoring of hemodynamic stability Frequent observation of the patients response to fluid removal Continuous assessment of vital signs/CVP/PAWP/PAP/Cardiac Output Monitoring changes in mental status Assessing breath sounds Assessing skin turgor/edema Monitoring for signs of bleeding/infection Monitor specifically for hypotension in response to hypovolemia (aggressive fluid replacement with a crystalloid and/or alteration of the ultrafiltration rate may be necessary). Monitoring for fluid volume overload (requiring a decrease or temporary discontinuation of replacement fluid). Monitor that all equipment connections are secure (due to the risk for vast hemorrhage if a break in the system occurs). Close monitoring of electrolyte and acid-base imbalances (prompt replacement is required). Adjusting care based on the mobility restrictions that occur with CRRT equipment. Close monitoring of extremity distal to catheter placement (pulses/perfusion). Assessment of catheter insertion site/dressing changes as per policy.
REHABILITATION THERAPY IN ACUTE RENAL FAILURE PATIENTS:-

Rehabilitation is a process which results in the restoration of an individual to his or her maximum possible level of function and allround achievement. For people with kidney disease, it includes restoration of well-being, physical performance, emotional stability, social adjustment and work capacity.However, thousands of people with kidney disease are living proof that these fears can be overcome. Many dialysis and transplant patients are fully rehabilitated with physically active and interesting lives which often include jobs, sport and varied social activities. Vocational Rehabilitation A number of people with kidney failure maintain their present jobs and activities. Other may change their work for a variety of reasons. Rehabilitation services such as Commonwealth Rehabilitation The Benefits of Exercise Increasingly, there is evidence that a physical exercise program, integrated into your total treatment plan, has positive benefits for your general health, including weight loss, improved muscle strength, lower level of cholesterol and blood fats, increased cardiac output and greater physical exercise capacity. The psychological benefits of exercise are also important. Routine exercise can enhance feelings of self-esteem and create a sense of independence and may help control feelings of depression and anxiety which are sometimes present. Planning an Exercise Program; For people with end-stage renal disease, regular exercise is extremely beneficial. It is desirable that an exercise program be designed to fit your own physical capabilities. This will eliminate the likelihood that you will over-exert yourself or exercise to the point of exhaustion. Before beginning an exercise program, you must consult your doctor who may recommend you undergo a medical examination, and if need be, a cardiac examination. Consider the following when designing exercise program:

Type of exercise - best are continuous activities such as walking, swimming (particularly good for people with joint pain), bicycling (stationary or mobile), skiing or aerobic dancing. Frequency - a minimum of three and no more than five days per week, e.g. Monday, Wednesday, Friday, Sunday. Duration - begin at a level that is suitable e.g. five minutes per session. From there, gradually build up the duration of each session by adding one or two minutes each week. About thirty minutes per session is a good level to aim for, although you may feel like exercising longer. Intensity - it is difficult to give general advice on exercise intensity as this depends so much on individual capacity. In general, one should feel completely recovered within one hour of exercising and should not feel so much muscle soreness that heare unable to exercise the following day. Each session should being with a slow warm up, rise to a comfortable level of effort and then slow down again before the finish. Medical Treatment Can Aid Rehabilitation It was once thought that people with kidney disease could not participate in vigorous exercise because of fatigue caused by anaemia or complications of treatment. It is now known that the physiological changes brought on by regular exercise are beneficial and exercise may be just as important for kidney patients as it is for the general population. People with end-stage renal failure may feel tired and weak due to anaemia (a low red blood cell count). Researches have found that patients who exercise increase their red cell count significantly, providing more energy for an exercise program and for activities of daily life.
Complications:

Water overload Hyperphosphataemia Hyperkalaemia Chloride levels raised (plasma or serum) Hypernatraemia Amylase levels raised (plasma or serum) Hypocalcaemia Metabolic acidosis Reduced level of consciousness Nausea and vomiting Diabetes insipidus, nephrogenic Weight loss Pyruvic acid levels raised (blood) Urea levels raised (plasma or serum) Pericarditis Immune deficiency Hypermagnesaemia Bicarbonate levels low (plasma) Oedema Weight gain Creatinine levels raised (plasma or serum) Acute confusional state Bleeding tendency

Pulmonary oedema
Hope through Research-As understanding of the causes of kidney failure increases, so does the ability to predict and prevent these diseases. Recent studies have shown that intensive control of diabetes and high blood pressure can prevent or delay the onset of kidney disease.In the area of genetics, researchers supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) have located two genes that cause the most common form of PKD and learned that a person must have two defective copies of the PKD1 gene to develop PKD. Researchers have also found a gene in the roundworm that is identical to the PKD1 gene. This new knowledge will be used in the search for effective therapies to prevent or treat PKD. The National Kidney Disease Education Program (NKDEP) is an initiative of the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, U.S. Department of Health and Human Services. The NKDEP aims to raise awareness of the seriousness of kidney disease, the importance of testing those at high risk, and the availability of treatment to prevent or slow kidney disease.

A research on Correction of salt and volume depletion is paramount in the prevention of renal damage says-commonly, patients at risk are hypotensive, with severe vascular disease, cardiac failure, sepsis and/or are receiving nephrotoxic drugs. There are two main categories in which pre-disposition to renal damage is increased; firstly, patients with impaired renal perfusion pressure due to sodium depletion, diuretic therapy, low cardiac output or any other condition that tends to promote increased sodium reabsorption and secondly, patients with already impaired renal function, vascular disease, severe infection, diabetes or liver disease.
CASE STUDY Mr VC is a 65-year-old man (68 kg, 175 cm) who presents to casualty with nausea, vomiting and profound diarrhoea. Two weeks ago he presented to his GP with a painful right metatarsal pharyngeal joint (due to gout), for which his GP prescribed colchicine 500 g 4-hourly for 2 days. Unfortunately, the patient became violently sick after four doses and discontinued this medication and went back to the GP who then prescribed: Indometacin 50 mg three times a day Ranitidine 150 mg twice daily. The gout pain is now resolving. On admission, Mr VC was pale, lethargic and breathless. Past medical history: Hypertension 1 year Type 2 diabetes 5 years. Medication: Bendroflumethiazide 5 mg every morning (for the last six months increased from 2.5 mg)/ Ramipril 2.5 mg every morning (started six months ago)/Gliclazide 40 mg twice daily. Biochemistry: Sodium 137 mmol/L (135150 mmol/L)/ Potassium 6.9 mmol/L (3.55.2 mmol/L)/ Urea 28.5 mmol/L (3.26.6 mmol/L)/ Creatinine 386 mol/L (60110 mol/L)/ Bicarbonate 18 mmol/L (2231 mmol/L)/ Phosphate 1.7 mmol/L (0.91.5 mmol/L)/ Corrected calcium 2.6 mmol/L (2.22.5 mmol/L)/ pH 7.26 (7.367.44)/ Glucose 10.8 mmol/L/ 24-hour urine output 600 mL. Mr VC is admitted to hospital under the diabetic team. Q1. What patient and pharmaceutical factors may have precipitated acute renal failure in this patient? Q2. What are the main pharmaceutical problems and how might they be managed? Mr VC is treated for his hyperkalaemia, put on a sliding scale insulin infusion, and rehydrated

with 4 L of sodium chloride 0.9%, until he has a central venous pressure (CVP) of 12. After 2 days, his serum creatinine has fallen to 168 mol/L. However, a further 2 days later, it is noted that he is again failing to pass urine, although he appears to have a palpable bladder, and his serum creatinine has again risen to 272 mol/L. This suggests urinary retention, so the decision is made to insert a urinary catheter. Following insertion of the catheter, Mr. VC passed 2 L of urine in the next 24 hours, but then spiked a temperature of 38.5C and became hypotensive. A diagnosis of urinary sepsis was made, and because it was the weekend, and with no other laboratory data available, the new senior house officer (SHO) prescribed gentamicin 475 mg IV daily. Q3. Comment on the appropriateness of the prescribed antibiotic therapy. What advice would you provide regarding this? Mr VC is given the gentamicin dose of 475 mg IV on the Sunday. On Monday morning, the pharmacist notes that both the drug and the dose are inappropriate for Mr VC, given his degree of renal impairment. The drug is discontinued on the drug chart, but a gentamicin level is taken anyway, and is reported back as 8.6 mg/L, so it is calculated it will take Mr VC several more days to clear that one dose. The prescription is changed to co-amoxiclav IV 600 mg three times a day. His serum creatinine is monitored, and over the course of the next few days, the serial levels are 272, 284, 290, 237, 188, 135 mol/L. He is switched to oral co-amoxiclav, and his renal function continues to fall. Mr VC is discharged from hospital on day 10, with a serum creatinine of 112 mol/L. (1) PROGNOSIS

1.Prognostic factor: Serum Creatinine Increase:-Serum Creatinine >= 3 mg/dl,Mortality: 64% Serum Creatinine < 2mg/dl and non-oliguric,Mortality: 5-20% 2.Prognostic Factor: Oliguric ATN requiring dialysis,Mortality: 50% 3.Prognostic Factor: Multiple Organ Failure,Mortality: 30% per organ system that fails Specific organ related risks(Respiratory failure: 8 fold increased mortality,Liver disease: 2-3 fold increased mortality,Catabolic state: 2 fold increased mortality,Heart disease: 3-4 fold increased mortality) Non-Prognostic Factors (Factors not related to mortality)Advanced age,Admission Serum Creatinine,Number of prior episodes of renal insufficiency.
SUMMARISATION

Today I have discussed about the definition,causes,clinical features,investigations and different management regarding acute renal failure.The prognosis of the disease also help us to get a clear picture about the disease condition.
CONCLUSION: Acute renal failure is a life-threatening condition. In a series of more than 1000 patients requiring dialysis, mortality was 40%.12 Outcome depends directly on pathogenesis. If due to obstruction which is successfully relieved, or ATN where haemodynamic parameters return to normal quickly, then recovery approaches 100%. However if due to glomerulonephritis, prognosis depends on severity of damage and may be irrecoverable if too many glomeruli are involved. In such cases, the patient will need to remain on dialysis permanently. REFFERENCES:-

o Bare B, Smeltzers.C.S . Brunner & Suddarths textbook of Medical Surgical Nursing. 17th ed. USA: Lippincott William &Wilkins publications, 2007, p:1321-1326. o Black J, Hawks M, Hekansen J. Medical Surgical Nursing.7th ed. St.louis Missouri: Elsevier publications, 2009, p:1000-1003. o Chatterjee.C.C. Human Physiology. 10th ed. Kolkata: Medical allied agency, 2005, pg:324. o Chntamoni. Lewiss Medical Surgical Nursing.7th ed. Haryana: Elsevier publications, 2010, p:1202-1210. o Jana B. Human Pathology. 3rd ed. New Delhi: B.Jain publishers, 2005, p:200. o Colmer M. Moroneys surgery for nurses. 16th ed. Newdelhi: ChurchillLivingstone, 2002, p:490-496 o Acute Renal Failure, content available from 1.Needham, E., M.D. (2005). Management of acute renal failure. American Family Physician. Vol. 72/No. 9. Retrieved on August 4, 2007,available at:aafp.org/afp/20051101/1739.html o o o o http//www.wikipedia.com http//www.medicinenet.in http//www.niams.nih.gov.in http://www.nlm.nih.gov/medlineplus

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