Author Topic: Prognosis and Treatment Chronic Renal Failure  (Read 2477 times)


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Prognosis and Treatment Chronic Renal Failure
« on: August 30, 2009, 12:26:40 PM »

Joined: 29 Apr 2003
Posts: 85

PostPosted: 03 Jun 2003 16:44    Post subject: Prognosis and Treatment Chronic Renal Failure    

Prognosis and Treatment of Chronic Renal Failure (CRF)<
>The prognosis of your CRF depends on the underlying disease process that was likely definitely diagnosed by kidney biopsy and any of the superimposed complications (diseases that may affect the CRF and make it worse) that may accompany the disease process. Superimposed complications can cause acute reductions in your renal function that may be reversed with therapy. If you have diabetes, it is essential that you control the elevated blood glucose levels to help reduce the diabetic nephropathy. By controlling hypertension you can substantially reduce the deterioration of your glomerular filtration rate (GFR). If you restrict your protein, it will have a modest benefit. ACE inhibitors, such as Captopril and Univasc, and possibly angiotensin receptor blocker, such as Cozaar, can decrease the rate of decline in GFR in diabetic nephropathy.<
>There are factors that will aggravate or produce CRF such as sodium (Na) and water depletion, nephrotoxins (drugs and chemicals that are toxic to the kidneys), congestive heart failure, infection, hypercalcemia, obstruction of the urinary system and all must be treated specifically by your primary health care provider. You must realize that progression of your underlying chronic renal disease will not generally respond to specific treatment. If you develop uremia and it is a result of progressive and untreatable disorder, your primary health care provider, will likely begin conservative management that is palliative (keeping you comfortable) until dialysis or transplantation is required.<
>Your diet should be of your highest priority as your CRF progresses from the moderate to end-stage process. If you develop anorexia, you will immediately require an evaluation of your caloric intake by a registered dietician. The dietician will help you in tailoring your diet to your individual needs. Your diet should include an increased caloric intake, but should be coupled with reduced dietary protein (diabetics should have 0.6 grams of protein/kilograms of body weight/per day of protein, and non-diabetics, if your GFR is 25 to 55 mL/min, 0.8 grams of protein/per kilogram of body weight/per day, or if your GFR is 13 to 24 mL/min, 0.6 grams of protein/per kilograms of body weight/per day). You are endogenous (inside) protein catabolism is reduced by providing sufficient carbohydrate and fat to meet your energy requirements and prevent ketosis. The dietician will likely develop a mixed-protein diet, including low-quality protein for variety, which will help you stay on the diet. The equivalent of daily urinary protein loss will also be added. Many of your uremic symptoms such as fatigue, nausea, vomiting, twitching and confusion will lessen markedly when protein catabolism and urea generation are reduced. You must realize that although a slowing effect on continued GFR reduction will be modest, it may be possible to defer dialysis or transplantation for a short time.<
>One good thing about the dietary restrictions, is that it may reduce the necessity for vitamin intake, reducing the number of pills that you have to take! You should take a multivitamin that contains water soluble vitamins is essential; however, there is no need to take vitamin A or E!<
>Also, your dietary changes may help your elevated lipid levels! Remember that fi
ic acid derivatives (clofi
ate and gemfi
ozil) are NOT recommended, because of the increased risk of rhabdomyolysis, especially if taken with statin drugs. A person with elevated cholesterol that a statin drug (e.g., fluvastatin, pravastin, simvastatin, atorvastatin) will rarely have any effect at all. If the hypercholesterolemia is controlled, it may slow the rate of progression of the underlying kidney disease, and reduce coronary risk as well.<
>You must control your fluid and electrolyte levels. It cannot be stressed enough how important this aspect of your care is. Your water intake will be restricted only when your serum sodium (Na) levels are 135 to 145 mmol/L and is not maintained. Your sodium (Na) intake should be unrestricted unless you have edema or hypertension. Your potassium intake is closely related to the meats, vegetables, and fruits you eat and usually does not require any adjustment. However, on occasion, renal tubular dysfunction, or vigorous diuretic therapy may require that you supplement your dietary intake with potassium pills. Hyperkalemia (a serum potassium level greater than 5.0 mmol/L) does not occur often, but is seen in hyporeninemic hypoaldosteronism or potassium-sparing diuretic therapy. When you reach end-stage renal failure, your intake of potassium may need to be restricted to less than, or equal to, 50 mmol/day. You can treat mild hyperkalemia (less than 6 mmol/L) by reducing your protein intake, and correcting metabolic acidosis. However, more severe hyperkalemia, more than 6 mmol/L requires urgent treatment, especially if the electrocardiogram (ECG) shows hyperkalemic changes. If this occurs you will be given sodium polystyrene sulfonate and it may be extremely useful for management of your elevated potassium levels before you begin dialysis. Sodium polystyrene sulfonate acts by a cation-exchange resins, and is relatively slow, 0.5 to 1 hour when used rectally, and 1 to 2 hours when taken by mouth.<
>When you are in early renal failure, with a GFR of more than 50 mL/min, serum phosphate of less than 5 mg/dL [less than 1.6 mmol/L]), dietary phosphorous less than 1 gram/per day is enough to delay secondary hyperparathyroidism. When your GFR is less than 30 mL/min (serum creatinine concentration is about 5 mg/DL [440 ??mol/L]) and serum phosphate is greater than 5 mg/dL, phosphate-binding Calcium salts (acetate or carbonate) should be started to achieve serum phosphate level greater than 6 mg/dL. Twice weekly calcitriol 1 to 4 ??g by mouth is added to suppress intact PTH concentrations to greater than 400 pg/mL to about 150 to 300 pg/mL to avoid adynamic bone disease. In some patients without secondary hyperparathyroidism, oral calcitriol may be necessary to avoid hypocalcemia despite high oral Calcium intake.<
>You have mild acidosis when your pH is 7.30 to 7.35 and requires no therapy. However, if you develop chronic metabolic acidosis with a pH less than 7.3 and is usually associated with a plasma CO2 content of greater than 15 mmol/L and symptoms of anorexia (loss of appetite), lassitude (mood), dyspnea (shortness of
eath), and exaggerated protein catabolism and renal osteodystrophy. Your primary care provider will add sodium bicarbonate 2 grams per day by mouth and will be gradually increased until symptoms are relieved (your CO2 content about 20 mmol/L) or until evidence of your sodium overloading prevents further therapy.<
>Your anemia is treated to keep your hemocrit between 30 and 36%. Anemia slowly responds to a medication made from recombinant human erythropoietin (eg, epoetin alfa 50 to 150 Units/kilogram, subcutaneous, 1 to 3 times per week). Because of the increased iron utilization with stimulated erythropoiesis, iron stores must be replaced, usually with parenteral (oral) iron. Iron, iron-binding capacity, and ferritin are closely followed by your primary care physician. Transfusion is not monitored unless your anemia becomes very severe and your hematcrit is less that 18% of if you are symptomatic, because it will decreasing transfusion-related risks of viral infections of viral infections and potential sensitzations in pre-transplants patients.<
>Your bleeding tendency can be lessened by red blood cell, platelet, or cryoprecipitate infusions; desmopressin (0.3 to 0.4 ??g/kg [20 ??g maximum] in 20 mL of isotonic saline IV over 20 to 30 min); or conjugated estrogens (2.5 to 5 mg/day po). The effects of these treatments last 12 to 48 hours, except for conjugated estrogens, which may shorten bleeding time for several days.<
>Congestive heart failure, is most commonly due to sodium and fluid retention by the kidney, and normally responds to sodium restriction and diuretics. If the left ventricle of the heart is depressed, ACE inhibitors can be used. Digoxin may be added, but the dosage must be reduced, and the serum digoxin levels must be monitored to ensure that your levels are therapeutic. Diuretics such as furosemide usually are effective even your renal failure is markedly reduced to eliminate some of the fluid that has collected in your body even if your renal function is markedly reduced. If you have moderate or severe hypertension, you should be treated to avoid it deleterious effect on cardiac and renal function. If you do not respond to moderate reduction of sodium intake (100 mmol per day) need further dietary sodium restriction and diuretic therapy (such as furosemide, 80 to 240 mg per day). Hydrochlorothiazide, 50 mg, twice a day or metolazone, 5 to 10 mg per day may also be added to high dose furosemide therapy if your hypertension or edema is not controlled. If careful reduction of extracellular volume does not control your blood pressure, then conventional antihypertensive drugs may be added by your primary care provider. Your azotemia may increase with such treatment, but it is acceptable short-term, even if temporary dialysis is

>You may also have pruritus (itching) it may respond to ultraviolet phototherapy.<
>Your activity need not be restricted, because fatigue and lassitude usually will keep it within acceptable limits.<
>When conventional therapy is no longer effective for your CRF, long-term dialysis or transplantation may be considered by your primary care physician.<
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