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Renal Diseases Kidney Functions Nephron The Functional unit of the kidney is called Ureters • Where the final urine product travels through to reach the bladder Bladder • Place where urine is temporarily stored Kidney Functions Kidneys have a remarkable role in : Regulate extracellular fluid volume and osmolarity Regulate electrolyte concentrations Regulate acid-base balance Excrete metabolic waste products like urea and creatinine and a number of drugs and toxins Help to regulate blood pressure by secreting the enzyme renin Produce the hormone erythropoietin, which stimulates the production of red blood cells in the bone marrow Convert vitamin D to its active form thereby plays a primary role in calcium regulation and bone formation Acute Renal Failure Acute Renal Failure in acute renal failure the kidney function deteriorates rapidly over hours or days. The loss of kidney function reduces urine output and allows nitrogenous wastes to build up in blood The degree of kidney dysfunction may be mild to severe With treatment acute renal failure is often reversible although the mortality rate are high ranging from 36-86 % Causes of Acute Renal Failure Acute Renal Failure is a consequence of : • Severe illness • Injury • Surgery To aid in diagnosis and treatment, its cauces are commenly classified as: prerenal- intrinsic- postrenal Causes • Prerenal factors : cause a sudden reduction in blood flow to the kidneys; often involve a severe stress – heart failure, shock, or blood loss • Intrinsic causes : infections, toxins, drugs, or direct trauma • Postrenal factors : those that prevent excretion of urine due to urinary tract obstructions Consequences of acute renal failure A decline in renal function alters the composition of blood and urine. The kidney may become unable to regulate the levels of electrolytes , acid, and nitrogenous wastes in the blood. Urine may be diminished in quantity or absent, leading to fluid retention Fluid and electrolyte imbalances • Edema ( is an early symptom )appear as puffiness in face and hands and swelling of the feet and ankles • Edema may be related to absence of urine or oliguria Oliguria: an abnormally low amount of urine often less than 400 mL/day The reduced excretion of electrolytes Consequences results in : 1- Sodium retention which contributes to edema 2- Hyperkalemia ( elevated serum potassium levels) can alter heart rate and lead to heart failure 3- Hyperphosphatemia ( elevated serum phosphate levels ) can increase secretion of parathyroid hormones and reduce blood calcium levels Consequences Uremia • • Abnormal accumulation of the body’s nitrogencontaining waste products especially blood urea nitrogen (BUN), creatinine, and uric acid in the blood. Moreover, the tissue catabolism that accompanies illness produces additional nitrogenous wastes than usual. • Symptoms of uremia: fatigue, lethargy, confusion, headache, anorexia, a metallic taste in the mouth, nausea and vomiting, and diarrhea In more serious cases: rapid pulse, elevated blood pressure, seizures, and delirium or coma MNT for acute renal failure Primary goal : Treat the underlying illness in order to prevent further damage to the kidneys. Protein and energy Due to catabolic condition associated with hypermetabolism and muscle wasting , sufficient protein and energy needed to preserve body’s protein content and muscle mass. Initially , the patient may be provided with 35 kcalories/kilogram body weight/day and body weight is monitored to ensure that energy intake is adequate. • protein increases the kidney workload, but intake should be sufficient to prevent negative nitrogen balance and additional weasting. • Protein usually restricted to about 0.6 – 0.8 g/kg body weight/day • With dialysis or kidney function improvements – protein allowed up to 2 g/kg body weight/day. Fluids Fluid status can be assessed by: 1. 2. 3. 4. Monitoring weight fluctuations, Blood pressure, Pulse rates, Appearance of skin and mucous membranes Measure serum sodium concentrations: Low sodium level indicates excessive fluid intake High sodium level suggests inadequate intake • Daily fluid needs determined by measuring urine output and adding 500 mL to replace the water lost through skin, lungs and perspiration • Individuals with fever, vomiting, or diarrhea require additional fluid • Patients undergoing dialysis can ingest fluids more freely. Electrolytes • Hyperphosphatemia : limit phosphorus • Potassium limited to 2000–3000 mg/day Serum electrolyte levels monitored closely • With oliguria : sodium intakes limited to 1100 - 3300 • • mg daily. Sodium intake can be adjusted to match urinary sodium losses unless edema is present. If on dialysis: generally can consume electrolytes more freely • In oliguric patients (those with reduced urine production), recovery from renal failure sometimes begins with a period of diuresis, in which large amounts of fluid are excreted may need electrolyte replacement to compensate for urinary losses Enteral and parenteral nutrition • • • • Some patients need enteral or parenteral nutrition support to obtain adequate energy Renal formulas: more kcalorically dense and have lower concentrations of protein and electrolytes than slandered formulas Enteral support (tube feeding) is generally preferred over parenteral nutrition because it is less likely to cause infection Total parenteral nutrition used only if patients are severely malnourished or cannot consume food for more than 14 days Dialysis: Treatment that removes wastes and excess fluid from the blood after the kidneys have stopped functioning Dialysis 1- Hemodialysis : • Blood is circulated through a dialyzer (artificial kidney), where it is bathed by dialysate, a solution that selectively removes fluid and wastes • It takes 3-4 hours and required for 2-3 times /week 2- Peritoneal dialysis : Dialysate is infused into a person’s peritoneal cavity, and blood is filtered by the peritoneum (the membrane that surrounds the abdominal cavity) after several hours ( 4-6 hours), the dialysate is drained, removing unneeded fluid and wastes Dialysis The basics of dialysis • Removal of solutes • Removal of fluid • Evaluation of dialysis treatment Chronic Kidney Disease CKD Chronic Kidney Disease Generally progresses over many years without causing symptoms Typically diagnosed late in the course of illness, after most kidney function has been lost Most common causes : Diabetes mellitus (45%) Hypertension (27%) 1- Altered electrolytes and hormones • • • • Usually develop during the final stage of renal failure Hormonal adaptations occur to help regulate electrolyte levels but may cause complications too Increased aldosterone secretion helps to maintain serum potassium levels but contributes to the development of hypertension Increased secretion of parathyroid hormone keeps serum phosphate levels normal, but contributes to bone loss (renal osteodystrophy) Electrolyte imbalances may develop when GFR becomes extremely low: < 5 mL/minute 2- Uremic syndrome Develops during the final stages of CKD • GFR < 15 mL/per minute • BUN > 60 mg/dL • Complications of uremic syndrome 1. Subtle خفيفmental dysfunctions 2. Neuromuscular changes : muscle cramping, twitching, 3. Impaired hormone synthesis : erythropoietin – anemia 4. Bleeding abnormalities – defects in platelet function and clotting factors Uremic syndrome cont’d • Chronic kidney disease worsens cardiovascular disease risk : hypertension, increased insulin resistance, and abnormal blood lipids in addition , elevated parathyroid hormone levels lead to calcification of blood vessels and heart tissue • Reduced immunity : poor immune responses – develop infections, a frequent cause of death 3- Protein-energy malnutrition • Anorexia : believed to be a primary cause of poor food intake secondary to nausea and vomiting, restrictive diets, uremia and medications • Nutrient losses : consequence of vomiting, diarrhea, gastrointestinal bleeding, concurrent catabolic disease and dialysis MNT of CKD The goal of CKD is to: Slow disease progression and prevent symptoms. Prevent PEM and weight loss The following table summarizes the dietary guidelines apply to patients in stage 1 to 4. By stage 5 either hemodialysis or peritoneal dialysis is necessary. Actual nutrition recommendation should be based on the results of nutrition assessment. 1- Energy Energy intake should be high enough to allow patients to maintain a healthy weight and to prevent wasting. 35 cal/ kg body weight˂ 60 years 30-35 ˃60 years • Foods and beverages of high energy and nutrient density is recommended • Malnourished patients may require oral formulas or tube feedings to maintain weight • Patients • undergoing peritoneal dialysis can absorb a substantial amount of glucose from the dialysate ( in order to draw fluid from blood to peritoneal cavity by osmosis) that may contribute as many as 800 kcalories daily . These calories must be included in the estimation of energy intake -weight gain is sometimes a problem 2- Protein • Predialysis : 0.6 to 0.75 grams/kg body weight/day • Low-protein diets produce fewer nitrogenous wastes so reduce risk of uremia • Low-protein diets supply less phosphorus so reducing risks associated with hyperphosphatemia • 50% of the protein should be from highquality sources Protein • Care taken to provide enough protein to meet needs and prevent wasting • Once dialysis begun: protein restrictions relaxed ≥ 1.2 to 1.3 grams/kg body weight/day • Dialysis removes nitrogenous wastes • results in some amino acids losses during the procedure • 50% of the protein should be from high-quality sources 3- Lipids • Some renal patients at risk for coronary heart • disease and are therefore advised to restrict saturated fat , trans fat and cholesterol Amount taken as necessary to maintain a As necessary to maintain healthy lipid profile • Renal diets include high-fat foods to increase calories but patients should be encouraged to select foods providing mostly unsaturated fats such as nuts, seeds, salad dressings, mayonnaise, avocados and soybean products 4- Fluids and sodium • As CKD progresses, the patient excrete less urine and the kidneys can’t handle normal sodium and fluid intake • Recommendations depend on total urine output, changes in body weight ,blood pressure and serum sodium levels. 1. Decrease in body weight – low blood pressure means fluid and sodium loss 2. Increase in body weight - high blood pressure means fluid and sodium retention • Fluids are not restricted until urine output decreases • Fluid intake should match the daily urine output in patient who is neither dehydrated or over-dehydrated Once on dialysis – sodium and fluid intakes controlled so that water weight gain is 2 pounds(= 908 gm) between dialysis treatments 5- Potassium • Predialysis – can handle typical intakes of • potassium Potassium restriction are usually necessary only in patients with elevated potassium levels • Supplementation may be needed for patients using potassium-wasting diuretics Potassium • Dialysis patients should control potassium intakes to prevent hyperkalemia and in some cases hypokalemia Hyperkalemia : abnormal elevation of serum potassium levels Hypokalemia: low serum potassium levels • Patients are taught foods that contain levels of potassium acceptable for renal diets. • They should avoid foods rich in potassium such as banana, beet, dried fruits, orange, milk and milk products, spinach and tomato. 6- Calcium, phosphorus and vitamin D To prevent bone disease calcium and phosphorus may need adjustment • Foods high in phosphorus should be avoided – protein-restricted diets are low in phosphorus • Before dialysis calcium intake = 800-1000 mg/ day ) • After dialysis begun calcium and vitamin D supplementation is required Calcium: ≤ 2000 from diet and medications 7- Vitamins and minerals The restrictive renal diet interferes with vitamin and mineral intakes . Patients treated with dialysis lose water soluble vitamin and some trace minerals into the dialysate. • Folate – 1 mg/day • Vitamin B6 – 10 mg/day • Vitamin C – < 100 mg/day because excessive intake can contribute to kidney stone formation in individuals at risk • supplementation with vitamins A and E not recommended because they may accumulate in renal failure patients • Intravenous administration of iron with erythropoietin therapy is more effective than oral intake of iron alone. Kidney Stones Kidney Stones Kidney stone : crystalline mass that forms within the urinary tract. Also called renal calculi Formation of Kidney Stones About 70% of kidney stones is made up primarily of calcium oxalate Less commonly , stones are composed of uric acid, amino acid cystine, calcium phosphate Factors that predispose to stone formation: Dehydration or low urine volume which promotes the crystallization of minerals or other compounds in the urine. Obstruction that prevent the flow of urine and encourage salt precipitation Urine acidity which affect the dissolution of urinary constituents Renal disease which is associated with calcium or phosphate accumulation 1- Calcium oxalate stones Commonly associated with: 1- Hypercalciuria ( elevated urinary calcium levels) • Excessive calcium in urine may result from: • Excessive calcium absorption • Impaired reabsorption of calcium in kidney tubules • Elevated serum levels of parathyroid hormone or vitamin D • Hyperoxaluria (Excessive urinary oxalate ) also promotes • • the formation of calcium oxalate crystals Hyperoxaluria may reflect an increase in the body synthesis of oxalate or increase the absorption from dietary sources People who form calcium oxalate stones are advised to reduce their dietary intake of oxalate • Avoid supplementation with vitamin C which degrades to oxalate in the body. 2- Uric acid stones • Uric acid stones develop when urine is abnormally acidic, contains excessive uric acid or both • Frequently associated with gout Gout: a metabolic disorder characterized by elevation uric acid levels in the blood and urine • Other diseases that increase the uric acid stones include leukemia and lymphoma which are associated with overproduction of purines • Purines : products of nucleotide metabolism that degrade to uric acid. • Purine-rich diet contributes to high uric acid levels( organ meats and sea foods) 3- Cystine stones • It occurs as a consequence of cystinuria • Cystinuria :inherited disorder of amino acid metabolism cystine • Renal tubules are unable to reabsorb cystine normally • Stones occur when cystine concentration is excessive in the urine leading to subsequent crystallization and stone formation. Consequences of kidney stones In most cases, small stones can readily pass through the ureters and out of the body with minimal treatment. 1- Renal colic: • A stone passes through the ureter can produce severe pain called renal colic • The pain begins suddenly in the back and intensifies as the stone follows the ureter’s course down to the abdomen toward the bladder • Pain may be severe enough to cause nausea and vomiting 2- Urinary tract complications • Hematuria as a result of damaging the kidney or ureter lining Hematuria: blood in the urine • May cause urinary tract obstruction or infection Treatment of kidney stones Drinking 12-16 cups of fluids/day Additional fluids if in hot weather or if individual is extremely active Medication which reduce urinary calcium , reduces oxalate absorption , reduces uric acid production in the body and reduce cystine levels MNT for Calcium oxalate stones • • Diet containing 800 – 1200 mg of calcium per day is recommended because calcium combines with oxalate in the intestines , reducing its absorption and in turn helping to control hyperoxaluria Moderate protein and sodium restriction is advised because high protein and sodium intakes increase urinary calcium excretion • Foods high in oxalate should be restricted because it increase urinary calcium excretion • Protein 0.8 – 1 gm / kg/ day • Sodium no more than 3450mg/ day • Vitamin C limited to DRI(75-90 mg/day) MNT for Uric acid stones • High fluid intakes • restriction of Purine rich l foods MNT for Cystine stones • High fluid intakes