Diseases of the Renal System

dr.Agustin Faizah

Introduction

An estimated 13.1% of adults ages 20 or older (26 million adults) have physiological evidence of chronic kidney disease (CKD) the National Health and Nutrition Examinations Survey between 1999 and 2004. The medical interventions for these diseases are among the most expensive treatments.

The Kidneys
Anatomy
Renal pyramid

Renal Cortex
Renal medulla Renal Pelvis

Renal vein Inferior vena cava Urinary bladder Urethra

Ureter Renal artery Kidney Aorta Ureter (b) Longitudinal section of a kidney

(a) Components of the urinary system

 The functioning unit of the kidney is called the nephron. Each kidney consists of approximately 1.2 million nephrons. Each nephron is made up of a glomerulus , which is a capillary tuft located between two arterioles (the afferent and the efferent) The afferent arteriole carries blood to the glomerulus and the efferent arteriole carries blood away from it. The nephron extends through three sections of the kidney called the cortex, outer medulla, and inner medulla . The cortex contains the glomeruli and the proximal and distal convoluted tubules. The medulla consists of the collecting ducts, loops of Henle, and vasa recta.

Physiological Functions
The primary functions of the kidney : 1. Maintenance of homeostasis through control of fluid, pH, and electrolyte balance and blood pressure. 2. Excretion of metabolic end-products and foreign substances. 3. The production of enzymes and hormones. Urine formation is a crucial component in the maintenance of homeostasis. The glomerulus the first step in urine formation occurs filters large proteins and blood cells The ultrafiltrate , is similar in composition to the blood. The tubules the second phase of urine production most of its components are reabsorbed (amino acids, glucose, selective minerals, and water) Vasopressin controls the final phase of urine production, as it directs concentration of urine and assists in maintaining overall fluid balance . Urine osmolality can vary widely from 500 mOsm to 1200 mOsm. Volume varies as well; as little as 500 mL or as much as 12 liters of urine can be produced to maintain normal homeostasis.

 Sodium is reabsorbed in the proximal tubule under the influence of aldosterone. If serum sodium levels are elevated, sodium is exchanged with potassium so that homeostasis is restored. The kidney additionally plays a significant role in blood pressure control. Cardiac output and blood pressure are dependent on plasma volume Vasopressin, secreted by the pituitary gland. The formation of urine also serves as the route for excretion of waste products, including the by-products of metabolism such as uric acid, creatinine, and urea. Other wastes excreted are drugs and environmental toxins. The kidneys role in controlling both hydrogen and bicarbonate ions is a critical component of the maintenance of Ph homeostasis.

 The kidney also produces important enzymes and hormones. Renin, is produced by the kidney and is necessary for the initiation of the reninangiotensin control of fluid balance. The hormones 1,25-dihydroxycholecalciferol and erythropoietin are also synthesized by the kidney. The active form of vitamin D is synthesized in the kidney after the inactive direct precursor 25hydroxycholecalciferol, 25(OH)D3) is hydroxylated in the liver. Erythropoietin (EPO) is a glycoprotein synthesized in the kidneys that stimulates erythropoiesis in the bone marrow.

Laboratory Evaluation of Kidney Function

Most commonly, kidney function is measured by the glomerular filtration rate (GFR) measure the rate at which substances are cleared from the plasma by the glomeruli. The normal GFR is 135200 liters per day. Of this large volume, 98% to 99% of filtrate is reabsorbed with urine output, usually averaging 12 liters per day. The GFR is used to evaluate kidney health, estimate the severity of diagnosed disease, and monitor kidney disease progression.

 The two equations most frequently cited are the Modification of Diet in Renal Disease (MDRD) equation and the Cockcroft-Gault equation.
The Cockcroft-Gault equation:
GFR = [(140 - age) x body weight (kg) x 0.85 if female] 72 x serum creatinine (mg/dL)]

Modification of Diet in Renal Disease (MDRD) equation: GFR = 170 x serum creatinine x age x (0.762 if female) x (1.20 if black race) x BUN x serum albumin

Chronic Kidney Disease

The clinical definition of CKD includes a longterm reduction in GFR, decreased creatinine clearance, and a corresponding increase in serum creatinine concentration. Other biochemical assessments : tubular function tests, microscopic evaluation of the urine , radiological evaluation (intravenous pyelogram (IVP), renal ultrasonography, renal radionuclide imaging, computing tomography, MRI, renal arteriogram), and biopsy of the organ.

Pathophysiology Overview Signs and symptoms associated with inadequate kidney function to perform the normal homeostatic control. Advanced impairment of kidney function results in edema, metabolic acidosis, hyperkalemia, anemia, uremia, azotemia, hyperphosphatemia, oliguria, hypertension, and bone and mineral disorders.

CKD Response to Low Serum Calcium and/or High Phosphorus

Chronic Kidney Disease

Definition and Medical Diagnosis

Chronic kidney disease (CKD) is a syndrome of progressive and irreversible loss of the excretory, endocrine, and metabolic functions of the kidney secondary to kidney damage. CKD progresses slowly over time, and there may be intervals during kidney functions remain stable.

 The onset of renal failure is not usually apparent until 50% to 70% of renal function is lost. The National Kidney Disease Education Program (NKDEP) has defined CKD as having a GFR of less than 60 mL/min/1.73 m2 for 3 months or longer and/or albuminuria of more than 30 mg of urinary albumin per gram of urinary creatinine

 NKDEP describes 5 stages of CKD : - Stage 1 : kidney damage with normal or increased GFR . GFR 90 mL/min/1.73 m2 - Stage 2 : kidney damage with mild decrease in GFR . GFR: 6089 mL/min/1.73 m2 - Stage 3 : a moderate decrease in GFR. GFR: 3059 mL/min/1.73 m2 - Stage 4 : a severe decrease in GFR. GFR: 1529 mL/min/1.73 m2. - Stage 5 : kidney function is inadequate to sustain life and requires initiation of renal replacement therapy. GFR: 15mL/min/1.73 m2.

Epidemiology
CKD is a growing health concern. The incidence of CKD is very high among the U.S. adult population. An estimated 11.5% of adults ages 20 or older have evidence of CKD (The National Health and Nutrition Examination Survey) The incidence of CKD is even higher among patients with diabetes mellitus, cardiovascular disease, and hypertension. 1990 2000: the number of persons with kidney failure requiring dialysis or transplantation more than doubled 2006: > 500,000 individuals in the U S were receiving dialysis.

Etiology
Diabetes, hypertension, and glomerulonephritis are the leading causes of kidney failure. The following additional causes and risk factors :
EthnicityAfrican-Americans 4x white Americans

Native Americans 2x white Americans Hispanic Americans 2x non-Hispanic whites

Family history . Hereditary factors such as polycystic kidney disease (PKD) A direct and forceful blow to the kidneys. Prolonged consumption of over-the-counter painkillers that combine aspirin, acetaminophen, and other medicines such as ibuprofen.

How Does Diabetes Lead to CKD? Diabetic nephropathy is the most common cause of CKD in US. People with either type 1 or 2 diabetes are at increased risk. The risk is greater if blood sugars are not controlled. The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. Increasing numbers of glomeruli are destroyed and increasing amounts of albumin are excreted, can be detected by a urinalysis. As the number of functioning nephrons declines, each remaining nephron must clear an increasing solute load. Eventually, the limit to the amount of solute that can be cleared is achieved and the concentration in body fluids increases, leading to azotemia and uremia. Because the progression is slow (microalbuminuria can continue up to 510 years before other symptoms develop), the body can partially adapt to the changes.

Treatment
The goal of medical and nutritional management of kidney disease is to treat the underlying renal pathophysiology in order to delay the progression of the disease. Medical and nutritional care correlates with the level of kidney dysfunction. Progression of the disease is highly individualized, and many patients may remain at these initial stages for months to years. When CKD progresses to end-stage renal disease (ESRD or CKD stage 5) and harmful wastes build up in the blood, blood pressure rises, and excess fl uid is retained, more extensive treatment is needed to replace the work of the kidneys. Treatment options include hemodialysis, peritoneal dialysis, and kidney transplantation.

Dialysis
Dialysis is a renal replacement procedure that removes excessive and toxic by-products of metabolism from the blood, thus replacing the filtering function of healthy kidneys. It can maintain life once CKD progresses to the end stage, even though endocrine and metabolic functions of the kidney are not totally replaced. The decision to initiate dialysis depends on the severity of symptoms. Symptoms considered to be definite indications for dialysis therapy include pericarditis, uncontrollable fluid overload, pulmonary edema, uncontrollable and repeated hyperkalemia, coma, and lethargy. Less severe symptoms such as azotemia, nausea, and vomiting require a subjective determination that takes into consideration the patients quality of life.

 Currently two major types of renal replacement therapy are used for patients with CKD Stage 5: hemodialysis (HD) and peritoneal dialysis (PD). The most common method is hemodialysis. Selection the type of dialysis based on several factors, including underlying kidney disease and other comorbid factors such as cardiovascular disease, age, family support, and proximity to a dialysis center. Regardless of the modality, both methods require a selective semipermeable membrane that allows passage of water and small-to middle-molecular weight molecules and ions but excludes largemolecular weight molecules such as proteins.

Hemodialysis

The selective membrane is a man-made dialyzer sometimes referred to as an artificial kidney. The most common types are the hollow fiber and parallelplate dialyzers. Patients receiving hemodialysis first need to undergo a procedure that allows continual access to the bloodstream. The preferred permanent access site is an arteriovenous fistula (AVF), created surgically by fashioning in the forearm subcutaneous joining of the radial artery and the cephalic vein The AV fistula requires four to six weeks to become fully functional. The subclavian route may be used temporarily if HD is required before the AV fistula is ready for use.

 While blood passes through the dialyzer, dialysate simultaneously passes around the artificial membrane. Waste products and excess electrolytes from the blood to the dialysate via diffusion, ultrafiltration, and osmosis. The filtered blood then returns to the patient through the venous side . Hemodialysis treatments are typically prescribed three times a week for an average of 4 hours per treatment

 Although most hemodialysis treatments are done at a dialysis center, home treatments can be an option for some patients. Daily home hemodialysis (DHHD) is conducted five to seven days per week for two to three hours at a time, and nocturnal home hemodialysis (NHHD) is performed three to six nights per week during sleep. The major advantage of home dialysis is the ability to set ones own schedule; however, it is necessary to have a trained partner and it may also be stressful to the patients family.

Example of a Hemodialysis System

Peritoneal Dialysis
Access to the patients blood supply is gained via a catheter of silicone rubber or polyurethane, placed surgically into the peritoneal cavity. Dialysate is introduced into the peritoneum through the peritoneal catheter. Solutes from the plasma circulating in the vessels and capillaries perfusing the peritoneal wall pass across the peritoneal membrane into the dialysate, which is subsequently removed and discarded. The dialysate for PD is available with a range of dextrose concentrations that alter its osmolality and assist in fluid removal. The dwell time (i.e., how long the dialysate remains in the peritoneum) and the number of exchanges (i.e., how many bags of dialysate and the total volume of each used in twentyfour hours) also aff ect the amount of fl uid and solute removal.

Peritoneal Dialysis

Renal Transplantation For an organ transplant to occur, the immunological characteristics of the donated organ must be matched with the recipients medical and immunological characteristics. The role of the major histocompatibility complex (MHC) in determining acceptability for a transplanted organ was discussed. MHC antigens play an important role in transplant rejection. The immune system attacks the transplanted cells presenting MHC antigens that are different from those found on the recipients tissues.

 A national databaseUnited Network for Organ Sharingprovides the information and coordination that allow the recipient to be matched with a potential donor. After transplantation, patients are maintained on a variety of immunosuppressive regimens to prevent rejection of the donated kidney. Immunosuppressive medications include corticosteroids, cyclosporine, tacrolimus, mycophenolate mofetil, and sirolimus.

Nutrition Therapy for Chronic Kidney Disease

Medical nutrition therapy (MNT) is an essential component of medical care for early, progressive, and end-stage CKD. Malnu trition, cardiovascular disease, bone and mineral disorders, and anemia are the most common complications that accompany kidney disease. Each of these complications requires both medical and nutritional intervention. Many patients with CKD also have comorbid conditions such as hypertension and diabetes mellitus that also require medical nutrition therapy. Nutrition therapy for CKD can help prevent and manage complications as well as slow progression of the disease and compensate for impaired renal function and/or limitations of treatment modalities.

Nutrition Assessment
Malnutrition is very common in patients with CKD, especially those who are on dialysis. Evidence suggests that the prevalence of protein-energy malnutrition (PEM) ranges from approximately 20% to 70% among adult dialysis patients. Signs and symptoms of malnutrition present when the GFR declines to 30 mL/minute, and may progress to significant malnutrition at a GFR of 10 mL/minute. it is extremely important to evaluate the many complex factors that contribute to poor nutritional status in patients with CKD as part of a comprehensive nutrition assessment. The dietary restrictions associated with CKD add to the potential for inadequate nutrient intake. It is especially important to assess for usual dietary patterns and food intake, intolerance of specific foods, nutrient restrictions of the diet, and fear of eating wrong foods.

In summary, a nutrition assessment of the CKD patient should include: Review of the medical record for comorbid conditions, drug/nutrient interactions, or potential issues with digestion and absorption of nutrients. Nutrition interview for usual food/nutrient intake as well as changes in appetite, changes in food intake with the onset/ progression of CKD, and changes in elimination (urine output and stool). Interview to evaluate social barriers to adequate nutritional intake. Physical assessment, including height, weight, frame size, subjective global assessment and physical signs/symptoms of nutrient deficits Review of biochemical/laboratory indices that might be affected by CKD Assessment of current food intakekcalories, protein, fat, sodium, potassium, calcium, phosphorus, fluid, vitamins, and minerals.

Nutrition Diagnosis
Given the complexity of nutrition implications associated with CKD, many nutrition diagnoses may be present. The following is a list of possible nutrition diagnoses for patients with CKD: Inadequate energy intake Inadequate oral/food beverage intake Excessive fluid intake Malnutrition Excessive protein intake Excessive mineral intake (potassium, phosphorus,sodium) Altered GI function Altered nutrition-related laboratory values

 Food-medication interaction Involuntary weight loss Involuntary weight gain Food and nutrition-related knowledge deficit Disordered eating pattern Limited adherence to nutrition-related recommendations Undesirable food choices Impaired ability to prepare foods/meals Poor nutrition quality of life Limited access to food

Nutrition Intervention CKD is not a static medical condition. Disease progresses through a series of stages. The nutrition goals and intervention therefore need to be individualized based on the stages of CKD, and overall health status of the patient. Nutrient recommendations frequently provided for patients receiving renal replacement therapies (dialysis or transplantation).

CKD Stages 1 and 2 Specific nutrition goals for stages 1 and 2 have not been identified, however nutrition therapy should focus on the comorbid conditionsdiabetes, hypertension, and hyperlipidemiaand on slowing the progression of potential cardiovascular disease. Glucose control, blood pressure reduction, and lipid management . Nutrition counseling recommendations include regular assessment (at 13 month intervals) of the patients nutritional status. Interventions that maintain or improve nutritional status during the progression of kidney disease are associated with improved patient survival.

CKD Stages 3 and 4 The KDOQI clinical practice guidelines specifically for adults with CKD who are not on dialysis (Stage 4). These guidelines outline recommended: nutrition measures, protein intake, energy requirements, and nutrition counseling. Nutrition measures identified for individuals with GFR <20 mL/min include:
o Serum albumin and actual or percent standard body weight and/or subjective global assessment (SGA) every 1 to 3 months. o Dietary interviews and food intake records and/or normalized protein equivalent of nitrogen appearance (nPNA) every 3 to 4 months.

 Recommendations for nutrition intervention for patients with CKD (GFR <25 mL/min) who are not currently undergoing dialysis low-protein diets are associated with a slowed progression of renal disease and a delayed need for renal replacement therapy, but there is not aconsistent agreement regarding the level of protein restriction that is effective. The purpose of medical nutrition therapy (MNT) in Stages 3 and 4 is: To provide adequate kcal to prevent malnutrition To provide adequate protein to preserve muscle mass and serum proteins To treat abnormalities of vitamin and mineral absorption, utilization, and excretion present in CKD To normalize blood lipids.

 The ability of the kidney to excrete metabolic products of protein, regulate acid/base balance, produce adequate amounts of erythropoietin, activate vitamin D, and regulate calcium, phosphorus, potassium, sodium, and fluid excretion diminishes modifications in calcium, phosphorus, vitamins, minerals, and fluid are frequently necessary.

CKD Stage 5 The goals of nutrition therapy : prevent malnutrition minimize uremia and associated CKD complications (cardiovascular disease, anemia, secondary hyperparathyroidism) maintain blood pressure and fl uid status.

In general, the hemodialysis diet is high in protein and controls intake of potassium, phosphorus, fluids, and sodium. Based on nutritional requirements, additional modifi cations may be needed for fat, cholesterol, and triglycerides. Patients receiving peritoneal dialysis have a more liberalized diet than hemodialysis patientsthis diet is higher in protein, sodium, potassium (due to increased losses during the dialysis process), and fluid, but it is still limited in phosphorus.

Nutrient Recommendations for CKD

PROTEIN Factors relating to higher protein requirements include: (1) losses of approximately 10 to 12 grams free amino acids per day and 5 to 15 grams per day of albumin (2) altered albumin turnover (3) metabolic acidosis, which increases amino acid degradation (4) inflammation (5) infection. The NKF K/DOQI guidelines on nutrition 1.2 grams of protein/kg body weight for HD patients to ensure adequate intake of essential amino acids. At least 50% of the protein should be of high biological value. The protein requirements for PD are slightly higher than for HD. During episodes of peritonitis (inflammation of the peritoneum), even in mild cases, the dialysate protein losses increase by 50% to 100% to an average of 15 to 36 g/24 hours and have been reported to remain elevated for several weeks.

ENERGY Adequate energy intake is important in order to prevent catabolism and achieve optimal nutritional status. Sufficient kcal from carbohydrates and fat may help to prevent muscle and visceral protein from being utilized as energy. The energy recommendation from the K/DOQI Nutrition Guidelines is based on the finding that energy expenditure is similar to or slightly higher than that of healthy persons . A lower caloric requirement has been shown to be adequate for older persons who are more sedentary. Caloric requirements should be adjusted accordingly for those with higher activity levels, those who are underweight and those who display catabolic stress.

 There are adjusted edema-free body weight for Obese and Underweight patients to be used when calculating protein and energy requirements for underweight and obese patients.

FAT In general, patients on HD and PD are at increased risk for CAD (coronary artery disease) and stroke. Hemodialysis patients typically display normal low-density lipoprotein (LDL) cholesterol, low high-density lipoprotein (HDL) cholesterol, and elevated triglyceride levels. PD patients exhibit higher total serum cholesterol levels as well as LDL levels. Triglyceride levels are especially increased in PD patients due to the absorption of glucose in the dialysate. It is recommended that both PD and HD patients adhere to the nutrient composition guidelines of the therapeutic lifestyle changes (TLC) diet.

Therapeutic Lifestyle Changes for Patients with CKD

POTASSIUM The potassium restriction for HD and PD patients varies, depending on the degree of kidney function, serum potassium levels, modality, and drug therapy. For the most part, a diet that allows 50 to 70 mmol/day or approximately 2 to 3 g/day of potassium is commonly prescribed in HD. Those who are oliguric or anuric are at an increased risk for hyperkalemia and should have a more stringent dietary restriction. The target range for serum potassium is 3.56.0 mEq/L. Severe hyperkalemia (serum K greater than 7.0 mEq/L) may precipitate fatal arrhythmias.

FLUID AND SODIUM

Fluid and sodium allowances are highly individualized and based primarily on residual urine output and dialysis modality. Other considerations include blood pressure control, interdialytic weight gains in HD patients, presence of edema, and congestive heart failure. The interdialytic weight gain goal in HD patients should not exceed 5% of body weight. Higher fluid gains can lead to sudden changes in blood volume and hypotension during the hemodialysis treatment. If patients become oliguric or anuric within the first 12 months of hemodialysis 2 gram sodium diet with a fluid allowance of not more than 1 L (1000 mL) daily. If urine output is greater than 1 L per day, the sodium and fl uid allowance can be liberalized to approximately 2 to 4 g sodium per day and 2 L (2000 mL) of fluid per day.

 Fluid and sodium requirements for patients on PD therapy are highly individualized and largely based on ultrafiltration. Ultrafiltration can remove 2 to 2.5 kg of fluid per day. Fluid and sodium restriction for the PD patient includes a fluid allowance of 2 L per day and a sodium allowance between 2 and 4 g per day. Fluid overload shortness of breath, hypertension, congestive heart failure, and edema.

PHOSPHORUS In early CKD hyperphosphatemia is prevented by an adaptive increase in renal excretion and decreased phosphate reabsorption. If the GFR : 20 - 30 mL/min/1.73 m2 Hyperphosphatemia. Phosphorus restriction of 8001000 mg/day or <17 mg/kg of ideal body weight or standard body weight per day has been recommended for HD and PD patients.

CALCIUM Dietary calcium requirements are higher in CKD. Low serum calcium levels often accompany CKD due to alterations in vitamin D metabolism, decreased absorption of calcium from the gut, and elevated phosphorus levels. Foods high in calcium are restricted, because they tend to be high in phosphorus as well. Calcium supplements should be taken on empty stomachbetween meals or at bedtime) . The amount of calcium from the diet plus the amount found in supplements should not exceed 2,000 mg per day.

VITAMIN SUPPLEMENTATION Supplementation of water-soluble vitamins due to increased losses during dialysis, anorexia, and poor dietary intake is typically indicated for HD and PD patients. In general, the renal vitamin contains B vitamins, folic acid, and vitamin C. Fat-soluble vitamins and minerals are not included. Preparations containing vitamin A or high doses of vitamin C should be avoided. Serum levels of B1 (thiamin), B2 (ribofl avin), pantothenic acid, and biotin are typically normal. Biotin supplementation of 10 mg/day has been found to be helpful in treating patients with peripheral neuropathy, encephalopathy, and intractable hiccups.

 Vitamin C should be limited to no more than 100 mg per day. serum vitamin A levels are elevated in HD and PD patients supplementation is not necessary. Very little is known about the long-term effects of vitamin E Vitamin K supplementation may be needed for those patients receiving antibiotic therapy, since the antibiotics may destroy the bacteria found in the gastrointestinal tract (these bacteria are a primary source of vitamin K). Most HD patients receive anti-coagulation therapy caution must be taken due to vitamin Ks role in promoting clot formation.

MINERAL SUPPLEMENTATION
Magnesium is excreted by the kidneys. magnesium levels are usually normal to mildly elevated in dialysis patients and not generally supplemented. Iron deficiency is common , due to the kidneys inability to make adequate erythropoietin for production of red blood cells Most patients will require iron supplementation, which is individualized depending on serum markers of ferritin, iron, total iron binding capacity, and transferrin saturation. Some studies have indicated that impaired taste sensation, loss of appetite, and sexual dysfunction may be ameliorated with zinc supplementation. The allowance for zinc is the same as the RDA: 15 mg per day.

Nutritional Requirements of the Posttransplant Patient The goal in the acute posttransplant period is : - to manage the increased metabolic demands of transplant surgery, obesity, blood pressure, insulin resistance, diabetes, and hyperlipidemia - maintenance of electrolyte balance - maximized bone health. Nutrition therapy for kidney transplant patients differs between the acute phase (up to 8 weeks following transplant) and the chronic phase (beginning the ninth week following transplant).

Monitoring and Evaluation Outcome measures for MNT in the CKD population can be classified as clinical or patient behavioral outcomes see table

Acute Renal Failure

.

Definition: ARF is a disorder characterized by abrupt cessation or reduction in GFR an accumulation of nitrogenous wastes.

Epidemiology The prevalence of ARF is estimated at 1% for all hospitalized patients, 3% to 5% for general medical-surgical patients, 5% to 25% for those in intensive care units, 5% to 20% for open-heart surgery patients, 20% to 60% for those with severe burns. Death occurs in 40% of nonsurgical patients with severe ARF, 80% of surgical patients is associated with the degree of hypercatabolism and infection.

Etiology
The three major types of acute renal failure are : prerenal azotemia, intrinsic and obstructive. Prerenal azotemia : reduce perfusion to the kidney ( ex: severe dehydration, circulatory collapse, fluid losses from the GI tract or from extensive wounds such as seen in burns). Acute tubular necrosis (ATN) is the ischemia damages epithelial cells, causing necrosis of the kidney , potentially irreversible renal failure. Intrinsic ARF : refers to damage to the anatomical structure of the kidney occur after exposure to toxins such as antibiotics, chemotherapy, or contrast dyes used in various imaging tests, infection such as glomerulonephritis Obstructive failure results from a blockage of the ureter or neck of the bladder could result in obstruction include kidney stones, blood clots, or a tumor.

Pathophysiology
In prerenal ARF the lack of blood flow to kidneys reduction the filtrate pressure in the glomerulus uremic symptoms. If blood flow is not restored necrosis of the cells . Liu (2010) 4 phases of ARF: 1. Initiation (when GFR declines) 2. Extension (when ischemia and inflammatory damage continue) 3. Maintenance (when GFR is at its lowest level) 4. Recovery (when epithelial cells regenerate).

Clinical Manifestations Normal urine output: 1 to 1.5 L per day. GFR declines and reaches its lowest level: ARF patients may produce <500 mL of urine. ARF develop fluid and electrolyte disorders & azotemia, particularly if they are both oliguric and hypercatabolic . Serum levels of potassium, magnesium, and phosphorus are generally elevated because of decreased renal clearance and marked net protein breakdown.

 Decreased levels of serum potassium, magnesium, and phosphorus may also occur as a result of intracellular shifts associated with carbohydrate delivery and anabolism. Hypophosphatemia also occurs in the refeeding syndrome, malnutrition, and diuretic therapy. Serum levels of potassium, magnesium, and phosphorus should be monitored frequently to assess the need for additional supplementation.

 Nitrogen (BUN) and creatinine are elevated in ARF, although the ratio of BUN to creatinine may be normal (10:1 or higher). Insufficient dietary kcal and protein and altered blood levels of proteases contribute to high levels of protein catabolism. Dialysis may be required to remove metabolic wastes and excess water. When recovery of renal function is expected to take several weeks, or when wasting is severe, aggressive dialysis is often recommended. Medical and nutrition management typically aim to maintain BUN in the range of 80 to 100 mg/dL.

Treatment Treatment options and nutrition support should be based on ; - the underlying cause of renal failure, - the specific metabolic changes within each patient, - other complications associated with the illness. Generally, continuous renal replacement therapy (CRRT) is the mode of treatment for an individual with ARF. CRRT is the term for several different modes of providing dialysis over a continuous period that allow for a significant amount of fluid (12 L/hour) to be removed.

Nutrition Therapy for Acute Renal Failure It is common for the nutritional status of patients with ARF to decline within a short period of time, owing to :
nitrogen losses (up to 30 g per day), which lead to loss of lean body mass; toxicity-related symptoms (anorexia, nausea, vomiting, bleeding); loss of essential and nonessential amino acids loss of plasma proteins during intervention dialysis therapy; metabolic disturbances (impaired glucose utilization and protein synthesis) from uremia. Energy and protein

malnutrition

Nutrition Intervention
Energy and protein intake should meet the patients requirements depends on the patients nutritional status, catabolic rate, residual GFR, and medical and/or surgical interventions (e.g., type of dialysis therapy). Protein, amino acids, and energy substrates may not be utilized efficiently difficult to maintain or improve the nutrition status of these patients by enteral or parenteral support. When feasible, patients with ARF should receive oral nutrition. If a patient cannot eat adequately, other forms of nutrition support should be pursued. Enteral nutrition support with standard formulations should be considered first for patients with ARF. If necessary, specific formulas with lower electrolytes can be considered.

 General recommendations f or protein are 0.6 (no dialysis) to 1.4 (dialyzed) g/kg/d. Adequate kcal should also be provided (30 to 35 kcal/kg/d). Protein sources containing both essential and nonessential amino acids should be provided. The patients nutrition and metabolic status and the renal diagnosis determine the exact dose. For patients receiving acute hemodialysis, the recommendation is 1.2 to 1.4 g/kg of protein. For those on CRRT, protein requirements should be estimated at 1.5 to 2.0 g/kg.

 Traditional recommendations indicate that when energy requirements cannot be measured by indirect calorimetry, can be estimated using 25 to 35 kcal/kg. ASPEN guidelines: In all ICU patients receiving PN, mild underfeeding should be considered at least initially. After energy requirements are determined, 80% of these requirements should serve. The total fluid intake depends on the amount of residual renal function (i.e., whether the patient is oliguric or anuric) and f uid and sodium status. Fluid intake can be calculated by adding 500 mL (for insensible losses) to the 24-hour urine output. Fluid and mineral balance need to be carefully monitored in ARF to prevent over hydration and electrolyte disorders.

 Total fluid input is recommended to equal output from urine and all other measured sources (e.g., nasogastric aspirate or fistula drainage) plus 400 to 500 mL per day. If the patient is catabolic weight can be allowed to drop by 0.2 to 0.5 kg per day to avoid excessive accumulation of fluid. Records of daily intake and output, weight changes, serum electrolyte levels, and blood pressure for assessment of fluid tolerance and requirements. Supplementation of minerals, electrolytes, and trace elements monitoring serum and urine to prevent excess or deficiency states .

Nephrotic Syndrome
Definition NS is an abnormal condition that is marked by a deficiency of albumin in the blood and its excretion in the urine due to altered permeability of the glomerular basement membranes. Epidemiology About 2 : 10.000. The prevalence is difficult to establish in adults because the condition is usually a result of an underlying disease. NS may occur at any age but is more prevalent in children than in adults. In children it is most common between 1-4 y.o, males > females.

Etiology NS can occur with many diseases : - Primary glomerular disease glomerular dysfunction, including many conditions with a variety of genetic and environmental causes. - Focal segmental glomerulosclerosis (FSGS) - Diabetic nephropathy - an infection/drug toxic to the kidneys. - autoimmune diseases (IgA nephropathy or systemic lupus erythematosus(SLE)).

Nephrotic syndrome is characterized by: - proteinuria (urinary protein levels greater than 3.5 g per 1.73 m2 of body surface area per day), - hyperlipidemia, - hypoalbuminemia <3.5 g/dL - edema. Proteinuria is thought to occur through a functional derangement in the glomerular barrier that allows larger molecular weight proteins and sometimes red blood cells to leak into the urine. Sign & symptoms of NS is: - frothy urine due to proteinuria. - anorexia, malaise - puffy eyelids - abdominal pain - muscle wasting. - Anasarca with ascites and pleural effusions may occur. - Blood pressure may low, normal, or elevated depending on the degree of angiotensin II production

 Oliguria or acute renal failure may develop because of hypovolemia (a decrease in the volume of the circulating blood) and diminished renal perfusion. Orthostatic hypotension and even shock can be seen in pediatric patients. Protein losses in adults with NS average about 6 to 8 grams per day. Albumin is the principal protein lost in urine, accounting for between 75% and 90% of urinary protein. In adults, serum albumin levels may be less than 2 g/dL. Micronutrients lost in the urine include those bound to plasma proteins such as zinc, copper, vitamin D, and iron.

 Nephrotic syndrome has also been associated with increased risk of atherosclerosis due to altered lipid metabolism characterized : by cholesterol and triglycerides , LDL , HDL N or The reduction of lipoprotein lipase, an enzyme responsible for lipoprotein metabolism, is thought to be the reason for reduced clearance of these lipids. Atherogenic lipoprotein and fibrinogen levels due to increased hepatic synthesis cardiovascular risk. Hyperlipidemia alone can impair renal function . Reducing lipid levels can slow down the progression of renal injury.

Treatment Medical treatment of nephrotic syndrome focuses on identifying and treating the underlying cause, reducing high cholesterol, blood pressure, and protein in the urine diet and drugs ACE therapy reduces proteinuria and slows down the progression of CKD. ACE inhibitor and angiotensin receptor blockers (ARBs) therapy, including combination therapy reduce proteinuria in diabetic nephropathy and idiopathic nephritic syndrome. Proteinuria may also be decreased by lowering the patients mean arterial pressure to levels below 92 mm Hg . Potassium levels should be checked in those with moderate to severe renal dysfunction, because ACE inhibitors may exacerbate hyperkalemia

Nutrition Therapy for Nephrotic Syndrome The goals: - minimizing the effects of edema, proteinuria, and hyperlipidemia - replacing nutrients lost in the urine - reducing the risks of further renal progression and atherosclerosis.

Nutrition Assessment Evaluate biochemical measures of renal function (GFR, BUN, creatinine), acid-base balance, lipid profile, fluid and electrolyte balance, protein status, and vitamin/mineral status. energy and protein needs should be calculated using usual or ideal body weight, because anthropometrics will be skewed due to the presence of edema. Dietary assessment will focus on usual dietary intake with a careful evaluation of protein, phosphorous, calcium, potassium, and sodium consumption .

Nutrition Diagnosis Include: increased nutrient needs, inadequate protein intake, excessive sodium intake, and food/nutrition knowledge defi cit Nutrition Intervention The nutrition therapy prescription components for NS are summarized in Table . Minimize edema include sodium restriction and diuretics. A sodium restriction of 2000 mg or less per day Fluid intake is generally not restricted. Current protein recommendations are 0.8 to 1.0 g/kg/day. This level of intake is believed to decrease proteinuria without reducing serum albumin. Several studies have suggested that soy protein or flaxseed-based proteins may be more beneficial than high-quality proteins in reducing proteinuria, lowering lipid levels, and slowing down the progression of renal . There are no long-term studies to suggest the safety of low-protein diets that provide less than 0.8 g/kg/day.

Nephrolithiasis
Definition Kidney stones (renal lithiasis or nephrolithiasis) form as a result of abnormal crystallization of calcium, oxalate, struvite, cystine, hydroxyapatite, or uric acid that is unable to be excreted normally in the urine. Epidemiology Nephrolithiasis affects almost one million individuals in the United States each year. men > women , varies depending on ethnicity and geographic region. Ages : 20 - 30 years.77 Risk factors for kidney stones include family history, certain medical conditions (hypercalciuria, hyperuricosuria, hyperoxaluria); and low urine volume. Hypercalciuria is the cause of more than 50% of all kidney stones. Other causes of kidney stones include gout, excess intake of vitamin D, urinary tract infections and urinary tract blockages.

Pathophysiology
Kidney stones generally consist of calcium salts, cystine, uric acid, or struvite (a combination of magnesium, ammonium, and phosphate). Generally, the development of kidney stones is not directly related to any one cause. Multiple factors may contribute . Kidney stones typically do not cause any symptoms until a stone acutely blocks urine flow. The pain will migrate depending on the location of the stone. Other symptoms : hematuria, nausea ,vomiting, pain with urination, and an urgency to urinate.

Treatment
Depends on whether or not the patient can pass the stone on his or her own. Although most patients can pass the stone with plenty of fluids and pain medication, hospitalization may be required in some cases if the pain is severe. If the patient cannot pass the stone, there are several procedures available: extracorporeal shockwave lithotripsy (ESWL), percutaneous nephrolithotomy, and ureterorenoscopy.

Nutrition Therapy for Nephrolithiasis Nutrition therapy can assist with minimizing the factors that may contribute to kidney stone formation. A complete analysis of the stone composition is necessary for the development of appropriate nutrition interventions. Nutrition Assessment Dietary assessment should focus on nutrient intake that may affect the development of a specifi c stone composition. Assessment of fluid intake is also a critical factor in development of appropriate nutrition prescriptions and interventions. Nutrition Diagnosis Include : excessive mineral intake, inadequate fluid intake, or food and nutrition-related knowledge deficit.

Nutrition Intervention
The objectives of nutrition therapy are to minimize the supersaturation of urinary components associated with the formation of stones and to prevent stones from recurring. The most effective preventative treatment is to increase fluid intake by 3 L per day should be taken in divided doses, throughout the day and night -- > will ensure a minimum urine output of 2 L/day.

 a diet low in calcium would help prevent the formation of calcium stones. However, it has now been demonstrated that foods high in calcium, including dairy products, can actually prevent the formation of stones. A possible explanation for this is that a reduction in dietary calcium aids in the intestinal absorption of oxalate, thus increasing urinary super-saturation of calcium The goal with minimizing oxalate intake is to decrease the bioavailability of oxalate.

 The following foods should be avoided : beets, chocolate, cola, coffee/tea, nuts/nut butters, berries, wheat bran, spinach, and rhubarb. Avoidance of greater than 2 grams of vitamin C should also be advised. For stones that are composed of uric acid, avoidance of foods high in purine is recommended. Foods high in purine include: animal protein, seafood, meat extracts, consomme, gravies and organ meats.