Module 9: Fluids & Electrolytes in Renal Disorders PDF

Republic of the Philippines TARLAC STATE UNIVERSITY COLLEGE OF SCIENCE DEPARTMENT OF NURSING Lucinda Campus, Brgy...

Republic of the Philippines TARLAC STATE UNIVERSITY COLLEGE OF SCIENCE DEPARTMENT OF NURSING Lucinda Campus, Brgy. Ungot, TarlacCityPhilippines 2300 Tel.no.: (045) 493-1865 Fax: (045) 982-0110 website: www.tsu.edu.ph Awarded Level 2 Status by the Accrediting Agency of Chartered Colleges and Universities in the Philippines Inc (AACCUP) -------------------------------------------------------------------------------------------------------------------- INSTRUCTIONAL MODULE:9 COURSE: NCM 112: CARE OF CLIENTS WITH PROBLEMS IN FLUIDS AND ELECTROLYTES Developer and their Background: Prof. Merlie Q. Espiritu,RN,MAN Email add: merlieespiritu04@gmail [email protected] … COURSE DESCRIPTION: This course deals with concepts, principles, theories and techniques of nursing care management of at risk and sick adult clients in any setting with alteration/problems in oxygenation, fluid and electrolytes, infectious, inflammatory and immunologic responses, cellular aberrations, acute and chronic. The learners are expected to provide nursing care plan to at risk and sick adult clients utilizing the nursing process. COURSE OUTLINE: Week 10 & UNIT II: Fluid and Electrolyte Imbalances in Renal Disorders 12 Week 13 &14 UNIT III. : Fluid and Electrolytes Imbalances of Patient with Burn Injury Week 15 & 17 UNIT IV: Fluid and Electrolytes Imbalances of Patient with Neurogenic Disorders Week 18 Final Examination WEEK 10 and 12: UNIT II: A. Introduction: Structure and Functions of Urinary system B. Fluids and Electrolytes Imbalances in Renal Disorders - Acute and Chronic Glomerulonephritis - Nephrotic Syndrome - Renal Failure - Chronic Renal Failure –End Stage Renal Disease - Dialysis; Peritoneal dialysis and Hemodialysis RATIONALE: This module will help the students to learn the concepts, theories, and principles of fluid and electrolyte imbalances in caring for patients with renal disorders. It will also guide and equip student nurses to apply their knowledge and skills in the formulation of a comprehensive plan of care. 1. MQE INSTRUCTIONS TO THE USERS: The student(s) will answer the given activities; preparatory activities entail assessment of the student's understanding and knowledge about the concepts, theories, and principles of fluid and electrolyte imbalances in caring for patients with renal disorders. Developmental activities comprise applications, discussions, and analysis based on the concepts learned. Closure activities consist of case studies, critical thinking exercises, and evaluation examinations. Learning objectives: At the end of this module, the nursing student will be able to: 1. Describe the structure and function of the renal and urinary systems. 2. Explain the role of the kidneys in regulating fluid and electrolyte. 3. Identify the diagnostic studies used to determine upper and lower urinary tract function and related nursing implications. 4. Describe the key factors associated with the development of kidney disorders. 5. Differentiate between the causes of chronic kidney disease (CKD) and acute kidney injury (AKI). 6. Explain the pathophysiology, clinical manifestations, laboratory and diagnostic procedures, medical management, and nursing management for patients with kidney disorders. 7. Apply the nursing process to caring for patients with renal disorders. 8. Formulate a comprehensive plan of care and health education for patients with renal disorders. 9. Ensure completeness of documentation of the client's responses based on the nursing care rendered with integrity, safety, accessibility, and security of information. CONTENT: A. PREPARATORY ACTIVITIES: ACTIVITY 1: 1. Describe the location and gross structure of the kidney. 2. Describe the structure and function of the glomerulus and tubular components of the nephron in terms of regulating the composition of the extracellular fluid compartment. 3. Explain the function of sodium in terms of tubular transport mechanisms. A. STRUCTURE AND FUNCTIONS OF THE KIDNEY  Kidneys are paired, bean-shaped organs that lie outside the peritoneal cavity in the back of the upper abdomen, one on each side of the vertebral column at the level of the 12th thoracic to 3rd lumbar vertebrae.  Right kidney - situated lower than the left (position of the liver)  Adult, each kidney - 10 to 12 cm long, 5 to 6 cm wide, and 2.5 cm deep; weight- 113 to 170 g.  Medial border of the kidney is indented by a deep fissure called the hilus - blood vessels and nerves enter and leave the kidney.  Ureters- connect the kidneys with the bladder; enter the kidney at the hilus.  Kidney is a multilobular structure, composed of up to 18 lobes.  Each lobe is composed of nephrons, which are the functional units of the kidney. 2. MQE   Each nephron- glomerulus that filters the blood and a system of tubular structures that reabsorb material from the filtrate back into the blood and secrete materials from the blood into the filtrate as urine is being formed. TWO DIVISION 1. Cortex -is reddish-brown, contains the glomeruli and convoluted tubules of the nephron and blood vessels. 2. Medulla - light colored, cone-shaped masses—the renal pyramids—that are divided by the columns of the cortex (columns of Bertin) that extend into the medulla.  Each pyramid, topped by a region of cortex, forms a lobe of the kidney.  Apices of the pyramids form the papillae ( 8 to 18 per kidney, corresponding to the number of lobes) - perforated by the openings of the collecting ducts.  Renal pelvis is a wide, funnel-shaped structure at the upper end of the ureter. It is made up of the calyces or cuplike structures that drain the upper and lower halves of the kidney. INTERNAL STRUCTURE:  Kidney is sheathed in a fibrous external capsule and  surrounded by a mass of fatty connective tissue at its ends and borders.  Adipose tissue protects the kidney from mechanical blows and assists, together with the attached blood vessels and fascia, in holding the kidney in place. Figure 53-1 A. Kidneys, ureters, and bladder. B. Internal structure of the kidney. Redrawn with permission from Porth, C. M., & Matfin, G. (2009). Pathophysiology: Concepts of altered health states (8th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. Source: Brunner & Suddarth, 2018; 14 ed. RENAL BLOOD SUPPLY 3. MQE   Each kidney is supplied by a single renal artery that arises on either side of the aorta.  Renal artery - divides into five segmental arteries that enter the hilus of the kidney.  Segmental artery branches into several lobular arteries that supply the upper, middle, and lower parts of the kidney.  Lobular arteries – subdivide: - interlobular arteries at the level of the corticomedullary junction. - arcuate arteries - arch across the top of the pyramids. - intralobular arteries radiate from the arcuate arteries to supply - the cortex of the kidney. - afferent arterioles that supply the glomeruli arise from the - intralobular arteries.  Blood flow to the kidneys passes through the cortex, less than 10% is directed to the medulla and only approximately 1% goes to the papillae.  Decreased perfusion or increased sympathetic nervous system stimulation, blood flow is redistributed away from the cortex toward the medulla--blood flow decreases glomerular filtration while maintaining the urine concentrating ability of the kidneys during shock. Source: Porth’s Pathophysiology, Concepts of Health States, NEPHRON:  Each kidney - more than 1 million tiny, functional units called nephrons.  Glomerulus - blood is filtered  Proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting duct- water, electrolytes, and other substances needed to maintain the constancy of the internal environment are reabsorbed into the bloodstream while other, unneeded materials are secreted into the tubular filtrate for elimination. COMPONENTS: NEPHRON  Vascular component- connects to the circulatory system.  Two arterioles associated with two capillary beds: 4. MQE  1. Glomerulus - where water-soluble nutrients, wastes, and other small particles are filtered from the blood. 2. Peritubular capillaries- which surround the tubular structures.  Tubular component-connects to both the circulatory system and the elimination functions of the kidney.  Processes the glomerular filtrate (urine), facilitating the reabsorption of substances from the tubular fluid into the peritubular capillaries and the secretion of substances from the peritubular capillaries into the urine filtrate. CATEGORIES: 1. Cortical nephrons- approximately 85% of the - nephrons originate in the superficial part of the cortex. - short, thick loops of Henle that penetrate only a short distance into the medulla. 2. Juxtamedullary nephrons -15%, originate deeper in - the cortex and have longer and thinner loops of Henle that penetrate the entire length of the medulla. - largely concerned with urine concentration. Nephrons are supplied by two capillary systems: 1. Glomerulus- is a unique, high-pressure capillary  Filtration system located between two arterioles:  afferent and efferent.  Two arterioles are high resistance vessels and the afferent arteriole has a larger diameter than the efferent arteriole, - the blood pressure in the glomerulus is extraordinarily high for a capillary bed and easily forces fluid and - solutes out of the blood into the glomerular capillary along its entire length. 2. Peritubular capillary - originate from the efferent arteriole.  Low-pressure vessels that are adapted for reabsorption rather than filtration.  Surround all portions of the tubules, an arrangement that permits rapid movement of solutes and water between the fluid in the tubular lumen and the blood in the capillaries.  In the deepest part of the renal cortex, the efferent arterioles serving the juxtaglomerular glomeruli also continue into long, thin-walled looping vessels called the vasa recta.  Vasa recta accompany the long loops of Henle in the medullary portion of the kidney to assist in exchange of substances flowing in and out of that portion of the kidney.  Rejoin to form the venous channels by which blood leaves the kidney and empties into the inferior vena cava. 5. MQE GLOMERULUS  Consists of a compact tuft of capillaries encased in a thin,double-walled capsule - Bowman’s capsule.  Blood flows into the glomerular capillaries from the afferent arteriole and flows out of the glomerular capillaries into the efferent arteriole, which leads into the peritubular capillaries.  Fluid and particles from the blood are filtered through the capillary membrane into a fluid-filled space in Bowman’s capsule - Bowman’s space.  Portion of the blood that is filtered into the capsule space - filtrate.  Mass of capillaries and its surrounding epithelial capsule - renal corpuscle Glomerular capillary membrane is composed of three layers: - capillary endothelial, basement membrane, and single-celled capsular epithelial layer. 1. Endothelial layer lines the glomerulus and interfaces with blood as it moves through the capillary. - contains many small perforations, called fenestrations. - covers the glomerulus is continuous with the epithelium that lines Bowman’s capsule. - cells of the epithelial layer have unusual octopus-like structures that possess a large number of extensions, or foot processes (podocytes), which are embedded in the basement membrane - foot processes form slit pores through which the glomerular filtrate passes. 2. Basement membrane consists of a homogeneous acellular meshwork of collagen fibers, glycoproteins, and mucopolysaccharides 6. MQE  - determines the permeability of the glomerular capillary membrane. - Spaces between the fibers that make up the basement membrane represent the pores of a filter and determine the size-dependent permeability barrier of the glomerulus. - Size of the pores in the basement membrane- prevents red blood cells and plasma proteins from passing through the glomerular membrane into the filtrate. - Alterations in the structure and function of the glomerular basement membrane are responsible for the leakage of proteins and blood cells into the filtrate that occurs in many forms of glomerular disease 3. Mesangial cells produce an intercellular substance -covers the endothelial cells. - possess or develop phagocytic properties and remove macromolecular materials that enter the intercapillary spaces. - exhibit contractile properties in response to neurohumoral substances and are thought to contribute to the regulation of blood flow through the glomerulus. NOTE: In normal glomeruli, the mesangial area is narrow and contains only a small number of cells. Mesangial hyperplasia and increased mesangial matrix occur in a number of glomerular diseases. TUBULAR COMPONENTS OF THE NEPHRON:  Four segments: 1. Proximal convoluted tubule - a highly coiled segment which drains Bowman’s capsule. 2. Loop of Henle - a thin, looped structure 3. Distal convoluted tubule distal coiled portion 4. Collecting tubule- final segment, which joins with several tubules to collect the filtrate. - The filtrate passes through each of these segments before reaching the pelvis of the kidney. - Proximal tubule is a highly coiled structure that dips toward the renal pelvis to become the descending limb of the loop of Henle. - Ascending loop of Henle returns to the region of the renal corpuscle, where it becomes the distal tubule. - Distal convoluted tubule, which begins at the juxtaglomerular complex, is divided into two segments: - - diluting segment and late distal tubule. - Late distal tubule fuses with the collecting tubule.  Distal tubule, the collecting duct is divided into two segments: cortical collecting tubule and inner medullary collecting tubule.  Tubule is composed of a single layer of epithelial cells resting on a basement membrane.  Structure of the epithelial cells varies with tubular function.  Cells of the proximal tubule have a fine, villous structure that increases the surface area for reabsorption;  Rich in mitochondria- support active transport processes.  Epithelial layer of the thin segment of the loop of Henle has few mitochondria - indicates minimal metabolic activity and re-absorptive function. 7. MQE Figure 53-2 Representation of a nephron. Each kidney has about 1 million nephrons of two types: cortical and juxtamedullary. Cortical nephrons are located in the cortex of the kidney; juxtamedullary nephrons are adjacent to the medulla. Source: Brunner & Suddarth,2018; Textbook in Medical- Surgical Nursing, 14 ed. FUNCTIONS OF KIDNEYS:  Urine formation  Excretion of waste products  Regulation of electrolytes  Regulation of acid–base balance  Control of water balance  Control of blood pressure  Renal clearance  Regulation of red blood cell production  Synthesis of vitamin D to active form  Secretion of prostaglandins I. URINE FORMATION: PROCESS  A. Filtration of blood by the glomerulus to form an ultrafiltrate of urine. - water and solutes smaller than proteins are forced through the capillary walls and pores of the glomerular capsule into the renal tubule.  B. Tubular reabsorption of electrolytes and nutrients needed to maintain the constancy of the internal environment. - water, glucose, amino acids and needed ions are transported out of the filtrate into the tubule cells and then enter the capillary blood. 8. MQE   C. Secretion- eliminating waste materials. - H, K, creatinine and drugs are removed from  the peritubular blood and secreted by the tubule cells into the filtrate. Figure 53-3: Urine is formed in the nephrons in a three-step process: filtration, reabsorption, and secretion. Water, electrolytes, and other substances, such as glucose and creatinine, are filtered by the glomerulus; varying amounts of these substances are reabsorbed in the renal tubule or excreted in the urine. Approximate normal volumes of these substances during the steps of urine formation are shown at the top. Wide variations may occur in these values depending on diet. Source: Hinkle & Cheeve (2022); Brunner & Suddarth’s,Textbook of Medical Surgical Nursing, 15ed, THREE-STEP PROCESS OF URINE FORMATION: (Brunner & Suddarth, 2018) 1. Glomerular filtration, 2. Tubular reabsorption, 3. Tubular secretion  Each nephron functions independently from other nephrons because each has its own blood supply (Eaton & Pooler, 2013).  Substances normally filtered by the glomerulus, reabsorbed by the tubules, and excreted in the urine include sodium, chloride, bicarbonate, potassium, glucose, urea, creatinine, and uric acid.  Within the tubule, some of these substances are selectively reabsorbed into the blood. Others are secreted from the blood into the filtrate as it travels down the tubule. 9. MQE   Amino acids and glucose are usually filtered at the level of the glomerulus and reabsorbed so that neither is excreted in the urine.  Normally, glucose does not appear in the urine.  Renal glycosuria (excretion of glucose in the urine) occurs if the amount of glucose in the blood and glomerular filtrate exceeds the amount that the tubules are able to reabsorb. - occur on its own as a benign condition (Hall, 2016). - occurs in poorly controlled diabetes—the most common condition that causes the blood glucose level to exceed the kidney’s reabsorption capacity.  Protein molecules also are not usually found in the urine; low– molecular-weight proteins (globulins and albumin) may periodically be excreted in small amounts. Protein in the urine is referred to as proteinuria (Eaton & Pooler, 2013). 1. Glomerular Filtration- normal blood flow through the kidneys is between 1000 and 1300 mL/min (Grossman & Porth, 2014). - As blood flows into the glomerulus from an afferent arteriole, filtration occurs. - The filtered fluid, also known as filtrate or ultrafiltrate, then enters the renal tubules. - Normal conditions- about 20% of the blood passing through the glomeruli is filtered into the nephron, amounting to about 180 L/day of filtrate (Eaton& Pooler, 2013). - Filtrate normally consists of water, electrolytes, and other small molecules, because water and small molecules are allowed to pass, whereas larger molecules stay in the bloodstream. - As blood enters the glomerulus from the afferent arteriole, filtration depends on adequate blood flow that maintains a consistent pressure through the glomerulus called hydrostatic pressure. Alterations of blood flow and pressure: - hypotension, decreased oncotic pressure in the blood, and increased pressure in the renal tubules from an obstruction (Eaton & Pooler, 2013; Grossman & Porth, 2014). 2. Tubular Reabsorption and Tubular Secretion- occur in the renal tubules. - a substance moves from the filtrate back into the peritubular capillaries or vasa recta. 3. Tubular secretion- a substance moves from the peritubular capillaries or vasa recta into tubular filtrate of the 180 L (45 gallons) of filtrate that the kidneys produce each day, 99% is reabsorbed into the bloodstream, resulting in the formation of 1 to 2 L of urine each day. - occurs when substances move from the peritubular capillary blood plasma (blood) into the tubular lumen (filtrate). It helps with the elimination of potassium, hydrogen ions, ammonia, uric acid, some drugs, and other waste products (Headly, 2015). - Filtrate becomes concentrated in the distal tubule and collecting ducts under hormonal influence and becomes urine, which then enters the renal pelvis. In the absence of tubular reabsorption, volume depletion would rapidly occur (Headly, 2015). NOTE: Reabsorption and secretion in the tubule frequently involve passive and active transport and may require the use of energy. Antidiuretic hormone (ADH) - known as vasopressin, is a hormone that is secreted by the posterior portion of the pituitary gland in response to changes in osmolality of the blood. 10. MQE  - With decreased water intake, blood osmolality tends to increase, stimulating ADH release. ADH then acts on the kidney, increasing reabsorption of water and thereby returning the osmolality of the blood to normal. - With excess water intake, the secretion of ADH by the pituitary is suppressed; therefore, less water is reabsorbed by the kidney tubule, leading to diuresis (increased urine volume). NOTE: A dilute urine with a fixed specific gravity (about 1.010) or fixed osmolality (about 300 Osm/L) indicates an inability to concentrate and dilute the urine - common early sign of kidney disease (Skorecki et al., 2015). Osmolarity - to the ratio of solute to water. - regulation of salt and water is paramount for control of the extracellular volume and both serum and urine osmolarity.. - Osmolarity and ionic composition are maintained by the body within very narrow limits. - As little as a 1% to 2% change in the serum osmolarity can cause a conscious desire to drink and conservation of water by the kidneys (Skorecki et al., 2015). Osmolality - degree of dilution or concentration of the urine is measured. - number of osmoles; ( standard unit of osmotic pressure) dissolved per kilogram of solution). -filtrate in the glomerular capillary normally has the same osmolality as the blood— 280 to 300 mOsm/kg. II. Regulation of Water Excretion  Regulation of the amount of water excreted is an important function of the kidney.  With high fluid intake, a large volume of dilute urine is excreted.  Low fluid intake, a small volume of concentrated urine is excreted.  A person normally ingests about 1300 mL of oral liquids and 1000 mL of water in food per day.  Approximately 900 mL - lost through the skin and lungs (insensible loss), 50 mL -sweat, and 200 mL - feces.  Fluid gained and lost when evaluating total fluid status.  Daily weight measurements are a reliable means of determining overall fluid status.  One pound (1 lb) equals approximately 500 mL, so a weight change of as little as 1 lb could suggest an overall fluid gain or loss of 500 mL (Grossman & Porth, 2014). III. Regulation of Electrolyte Excretion  Volume of electrolytes excreted per day is equal to the amount ingested  Regulation of sodium volume excreted depends on aldosterone, a hormone synthesized and released by the adrenal cortex.  With increased aldosterone in the blood, less sodium is excreted in the urine, because aldosterone fosters renal reabsorption of sodium.  Release of aldosterone from the adrenal cortex is largely under the control of angiotensin II.  Angiotensin II levels are in turn controlled by renin, an enzyme that is released from specialized cells in the kidneys. 11. MQE   complex system is activated when pressure in the renal arterioles falls below normal levels, as occurs with shock, dehydration, or decreased sodium chloride delivery to the tubules.  Activation of this system increases the retention of water and expansion of the intravascular fluid volume, thereby maintaining enough pressure within the glomerulus to ensure adequate filtration Figure 53-4 The renin–angiotensin system. GFR, glomerular filtration rate; ADH, antidiuretic hormone. IV. Regulation of Acid–Base Balance  Normal serum pH is about 7.35 to 7.45 and must be maintained within narrow range for optimal physiologic function (Grossman & Porth, 2014).  Kidney performs major functions to assist in this balance. 1. to reabsorb and return to the body’s circulation any bicarbonate from the urinary filtrate; 12. MQE  2. to excrete or reabsorb acid, synthesize ammonia, 3. excrete ammonium chloride (Headly, 2015).  Bicarbonate is a small ion, it is freely filtered at the glomerulus.  Renal tubules actively reabsorb most of the bicarbonate in the urinary filtrate.  To replace any lost bicarbonate, the renal tubular cells generate new bicarbonate through a variety of chemical reactions.  Newly generated bicarbonate is then reabsorbed by the tubules and returned to the body.  Body’s acid production is the result of catabolism, or breakdown, of proteins- produces acid compounds; phosphoric and sulfuric acids.  Normal daily diet - certain amount of acid materials. Unlike carbon dioxide (CO2), phosphoric and sulfuric acids cannot be eliminated by the lungs - accumulation of acids in the blood lowers pH (making the blood more acidic) and inhibits cell function, they must be excreted in the urine. If the hydrogen ions are low, they will be reabsorbed.  Normal kidney function- excretes about 70 mEq of acid each day. - able to excrete acid directly into the urine until the urine pH reaches 4.5, which is 1000 times more acidic than blood (Grossman & Porth, 2014).  Excess acids- bound to chemical buffers so that they can be excreted in the urine.  Two Chemical buffers: Phosphate ions and Ammonia (NH3).  When buffered with acid, ammonia becomes ammonium (NH4). Phosphate is present in the glomerular filtrate, and ammonia is produced by the cells of the renal tubules and secreted into the tubular fluid.  Through the buffering process- the kidney is able to excrete large quantities of acid in a bound form without further lowering the pH of the urine. V. Autoregulation of Blood Pressure  Regulation of blood pressure is an important function of the kidney.  Specialized vessels of the kidney, called the vasa recta, constantly monitor blood pressure as blood begins its passage into the kidney.  When the vasa recta detect a decrease in blood pressure, specialized juxtaglomerular cells near the afferent arteriole, distal tubule, and efferent arteriole, secrete the hormone renin.  Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II—the most powerful vasoconstrictor known; angiotensin II causes the blood pressure to increase (Hall, 2016).  Adrenal cortex secretes aldosterone in response to stimulation by the pituitary gland, which occurs in response to poor perfusion or increasing serum osmolality.  The result is an increase in blood pressure. When the vasa recta recognize the increase in blood pressure, renin secretion stops.  Failure of this feedback mechanism is one of the primary causes of hypertension VI. RENAL CLEARANCE:  refers to the ability of the kidneys to clear solutes from the plasma.  A 24-hour collection of urine is the primary test of renal clearance used to evaluate how well the kidney performs this important excretory function. Renal clearance depends on several factors: 1. how quickly the substance is filtered across the glomerulus, 2. how much of the substance is reabsorbed along the tubules, 13. MQE  3. how much of the substance is secreted into the tubules.  Creatinine is an endogenous waste product of skeletal muscle that is filtered at the glomerulus, passed through the tubules with minimal change, and excreted in the urine.  Creatinine Clearance- to measure the renal clearance of any substance. - measure of the Glomerular Filtration Rate (GFR), the amount of plasma filtered through the glomeruli per unit of time. - - To calculate creatinine clearance, - a 24-hour urine specimen is collected. Midway through the collection, the serum creatinine level is measured. The following formula is then used to calculate the creatinine clearance: Glomerular Filtration Rate (GFR)- amount of plasma filtered through the glomeruli per unit of time Adult GFR can vary from a normal of approximately 125 mL/min (1.67 to 2 mL/sec) to a high of 200 mL/min (Grossman & Porth, 2014). NOTE: Creatinine clearance is the best approximation of renal function. As renal function declines, both creatinine clearance and renal clearance (the ability to excrete solutes) decrease. VII. REGULATION OF RED BLOOD CELL PRODUCTION:  When the kidneys detect a decrease in the oxygen tension in renal blood flow, because of anemia, arterial hypoxia, or inadequate blood flow, they release erythropoietin.  Erythropoietin is a glycoprotein from the kidney that stimulates the bone marrow to produce red blood cells (RBCs), which carry oxygen throughout the body (Eaton & Pooler, 2013). VIII. VITAMIN D SYNTHESIS:  Kidneys are also responsible for the final conversion of inactive vitamin D to its active form, 1,25-dihydroxycholecalciferol.  Vitamin D is necessary for maintaining normal calcium balance in the body. IX. SECRETION OF PROSTAGLANDINS AND OTHER SUBSTANCES  Kidneys also produce prostaglandin E (PGE2) and prostacyclin (PGI2), thromboxanes and leukotrienes, which have vasoactive effects.  Substances help the afferent and efferent arterioles maintain renal blood flow by causing selective vasodilation or vasoconstriction (Headly, 2015). Note: PGs- vasodilatory effects increase renal blood flow and GFR under conditions associated with decreased actual or effective circulating volume, resulting in greater tubular flow and secretion of potassium. - Thromboxanes –(produced by platelet cells) are vasoconstrictors and facilitate platelet aggregation. - L eukotrienes – mediators of renal diseases and drug nephrotoxicity. 14. MQE X: EXCRETION OF WASTE PRODUCTS  Kidneys eliminate the body’s metabolic waste products.  Major waste product of protein metabolism is urea, of which about 25 to 30 g are produced and excreted daily (Grossman & Porth, 2014).  Urea must be excreted in the urine  Other waste products of metabolism that must be excreted are creatinine, phosphates, and sulfates.  Uric acid, formed as a waste product of purine metabolism, is also eliminated in the urine.  kidneys serve as the primary mechanism for excreting drug metabolites. URINE STORAGE:  Bladder is the reservoir for urine. Both filling and emptying of the bladder are mediated by coordinated sympathetic and parasympathetic nervous system control mechanisms involving the detrusor muscle and the bladder outlet.  Conscious awareness of bladder filling occurs as a result of sympathetic neuronal pathways that travel via the spinal cord to the level of T10 through T12, where peripheral, hypogastric nerve innervation allows for continued bladder filling.  As bladder filling continues, stretch receptors in the bladder wall are activated, coupled with the desire to void.  Information from the detrusor muscle is relayed back to the cerebral cortex via the parasympathetic pelvic nerves at the level of S1 through S4 (Grossman & Porth, 2014).  Overall bladder pressure remains low due to the bladder’s compliance (ability to expand or collapse) as urine volume changes.  Bladder compliance is due in part to the smooth muscle lining of the bladder and collagen deposits within the wall of the bladder, as well as to neuronal mechanisms that inhibit the detrusor muscle from contracting (specifically, adrenergic receptors that mediate relaxation).  To maintain adequate kidney filtration rates, bladder pressure during filling must remain lower than 40 cm water (H2O).  This low pressure allows the urine to freely leave the renal pelvis and enter the ureters.  The sensation of bladder fullness is transmitted to the central nervous system when the bladder has reached about 150 to 200 mL in adults, and an initial desire to void occurs (Hall, 2016).  Sense of fullness and discomfort with a strong desire to void usually occurs when the bladder reaches its functional capacity of 400 to 500 mL of urine. NOTE: Neurologic changes to the bladder at the level of the supraspinal nerves, the spinal nerves, or the bladder wall itself can cause abnormally high volumes (up to 2000 mL) of urine to be stored due to a decreased or absent urge to void. - Under normal circumstances with average fluid intake of approximately 1 to 2 L/day, the bladder should be able to store urine for periods of 2 to 4 hours at a time during the day (Hall, 2016). - At night, the release of vasopressin in response to decreased fluid intake causes a decrease in the production of urine and makes it more concentrated. - Bladder to continue filling for periods of 6 to 8 hours in adolescents and adults, making them able to sleep for longer periods before needing to void. - In older adults, decreasing bladder compliance and decreased vasopressin levels often cause nocturia (awakening during the night to urinate). 15. MQE BLADDER EMPTYING:  Micturition normally occurs approximately eight times in a 24-hour period.  Activated via the micturition reflex arc within the sympathetic and parasympathetic nervous systems, which causes a coordinated sequence of events.  Initiation of voiding occurs when the efferent pelvic nerve, which originates in the S1 to S4 area, stimulates the bladder to contract, resulting in complete relaxation of the striated urethral sphincter.  This is followed by a decrease in urethral pressure, contraction of the detrusor muscle, opening of the vesicle neck and proximal urethra, and flow of urine. GERONTOLOGIC CONSIDERATIONS  GFR decreases, starting between 35 and 40 years of age, and a yearly decline of about 1 mL/min continues thereafter.  Older adults are more susceptible to acute and chronic kidney injury due to the structural and functional changes in the kidney.  More prone to develop hypernatremia and fluid volume deficit, because increasing age is also associated with diminished osmotic stimulation of thirst.  Sense of thirst is so protective that hypernatremia almost never occurs in adults younger than 60 years.  Structural or functional abnormalities that occur with aging may also prevent complete emptying of the bladder - due to decreased bladder wall contractility; secondary to myogenic or neurogenic factors; or related to bladder outlet obstruction, such as in BPH or after prostatectomy.  Vaginal and urethral tissues atrophy (become thinner) in aging women due to decreased estrogen levels - causes decreased blood supply to the urogenital tissues, resulting in urethral and vaginal irritation and urinary incontinence. B. MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCES IN KIDNEY DISORDERS ACTIVITY 2: 1. Describe the key factors associated with the development of kidney disorders. 2. Differentiate between the causes of chronic kidney disease (CKD) and acute kidney injury (AKI). 3. Explain the pathophysiology, clinical manifestations, medical management, and nursing management for patients with kidney disorders. 4. Understand the nursing management of patients with chronic kidney disease and acute kidney injury. I. CHRONIC KIDNEY DISEASE (CKD)  is an umbrella term that describes kidney damage or a decrease in the glomerular filtration rate (GFR) lasting for 3 or more months.  associated with decreased quality of life, increased health care expenditures, and premature death.  Untreated CKD can result in end-stage kidney disease (ESKD), which is the final stage of CKD ESKD results in retention of uremic waste products and the need for renal replacement therapies, dialysis, or kidney transplantation 16. MQE RISK FACTORS:  Cardiovascular disease,  Diabetes mellitus,  Hypertension,  Obesity. PATHOPHYSIOLOGY:  Early stages of CKD, there can be significant damage to the kidneys without signs or symptoms.  Pathophysiology of CKD is not yet clearly understood, but the damage to the kidneys is thought to be caused by prolonged acute inflammation that is not organ specific and thus has subtle systemic manifestations. STAGES OF CHRONIC KIDNEY DISEASE  Stage 5 results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions; thus, renal replacement therapies are required to sustain life.  Increased risk for CVD- leading cause of morbidity and mortality (Kane-Gill, Sileanu, Murugan, et al., 2015). TREATMENT;  hypertension, anemia, and hyperglycemia and detection of proteinuria all help to slow disease progression and improve patient outcomes (Lewis, 2013). 17. MQE CLINICAL MANIFESTATIONS:  Elevated serum creatinine levels indicate underlying kidney disease; as the creatinine level increases, symptoms of CKD begin.  Anemia, due to decreased erythropoietin production by the kidney, metabolic acidosis, and abnormalities in calcium and phosphorus herald the development of CKD (Taal, 2013).  Fluid retention, evidenced by both edema and congestive heart failure, develops. As the disease progresses, abnormalities in electrolytes occur, heart failure worsens, and hypertension becomes more difficult to control. ASSESSMENT AND DIAGNOSTIC FINDINGS:  Glomerular filtration rate (GFR) is the amount of plasma filtered through the glomeruli per unit of time.  Creatinine clearance is a measure of the amount of creatinine the kidneys are able to clear in a 24-hour period. Normal values differ in men and women. MEDICAL MANAGEMENT 1. Treatment of the underlying causes. 2. Regular clinical and laboratory assessment is important to keep the blood pressure below 130/80 mmHg (Klein-Kauric, 2015). 3. Early referral for initiation of renal replacement therapies as indicated by the patient’s renal status. 4. Prevention of complications is accomplished by controlling cardiovascular risk factors; - treating hyperglycemia; - managing anemia; - smoking cessation, - weight loss, - exercise programs as needed; - reduction in salt and alcohol intake. GERONTOLOGIC CONSIDERATIONS:  Changes in kidney function with normal aging increase the susceptibility of older patients to kidney dysfunction and kidney disease (Kane-Gill et al., 2015).  Incidence of systemic diseases, such as atherosclerosis, hypertension, heart failure, diabetes, and cancer, increases with advancing age, predisposing older adults to kidney disease associated with these disorders. Therefore, acute problems need to be prevented if possible or recognized and treated quickly to avoid kidney damage.  Alterations in renal blood flow, glomerular filtration, and renal clearance increase the risk of medication-associated changes in renal function, precautions are indicated with all medications.  When older patients undergo extensive diagnostic tests or when new medications ( diuretic agents) are added, precautions must be taken to prevent dehydration, which can compromise marginal renal function and lead to kidney disease (Kane-Gill et al., 2015). II. NEPHROSCLEROSIS  Nephrosclerosis (hardening of the renal arteries) is most often due to prolonged hypertension and diabetes.  Major cause of CKD and ESKD secondary to many disorders. 18. MQE PATHOPHYSIOLOGY  Two forms of Nephrosclerosis: 1. Malignant (accelerated) nephrosclerosis - associated with significant hypertension (diastolic blood pressure higher than 130 mmHg). - occurs in young adults and twice as often in men compared to women (Klein- Kauric, 2015). - Damage is caused by decreased blood flow to the kidney resulting in patchy necrosis of the renal parenchyma. - Over time, fibrosis occurs and glomeruli are destroyed. - disease process progresses rapidly. - Without dialysis, more than half of patients die of uremia (an excess of urea and other nitrogenous waste products in the blood) in a few years. 2. Benign nephrosclerosis - can be found in older adults, associated with atherosclerosis and hypertension. ASSESSMENT AND DIAGNOSTIC FINDINGS - Urine usually contains protein and occasional casts. - Renal insufficiency and associated signs and symptoms occur late in the disease. MEDICAL MANAGEMENT: 1. Aggressive antihypertensive therapy. An angiotensin-converting enzyme (ACE) inhibitor, alone or in combination with other antihypertensive medications, significantly reduces its incidence. III. PRIMARY GLOMERULAR DISEASES  Diseases that destroy the glomerulus of the kidney are the third most common cause of stage 5 CKD.  Glomerular capillaries are primarily involved.  Antigen–antibody complexes form in the blood and become trapped in the glomerular capillaries (the filtering portion of the kidney), inducing an inflammatory response.  Immunoglobulin G (IgG)—the major immunoglobulin (antibody) found in the blood—can be detected in the glomerular capillary walls. MAJOR CLINICAL MANIFESTATIONS OF GLOMERULAR INJURY:  proteinuria, hematuria, decreased GFR, decreased excretion of sodium, edema, and hypertension TERMS TYPICALLY USED WHEN DESCRIBING GLOMERULAR DISEASE - Primary: Disease is mainly in glomeruli - Secondary: Glomerular diseases that are the consequence of systemic disease - Idiopathic: Cause is unknown - Acute: Occurs over days or weeks - Chronic: Occurs over months or years Rapidly progressing: Constant loss of renal function with minimal chance of recovery - Diffuse: Involves all glomeruli - Focal: Involves some glomeruli - Segmental: Involves portions of individual glomeruli - Membranous: Evidence of thickened glomerular capillary walls 19. MQE  - Proliferative: Number of glomerular cells involved is increasing IV. ACUTE NEPHRITIC SYNDROME - type of kidney disease with glomerular inflammation (Grossman & Porth, 2014). - - Glomerulonephritis is an inflammation of the glomerular capillaries that can occur in acute and chronic forms. PATHOPHYSIOLOGY:  Primary glomerular diseases include post-infectious glomerulonephritis, rapidly progressive glomerulonephritis, membrane proliferative glomerulonephritis, and membranous glomerulonephritis.  Post-infectious causes are group A beta-hemolytic streptococcal infection of the throat that precedes the onset of glomerulonephritis by 2 to 3 weeks.  Follow impetigo (infection of the skin) and acute viral infections (upper respiratory tract infections, mumps, varicella zoster virus, Epstein–Barr virus, hepatitis B, and human immune deficiency virus [HIV] infection).  In some patients, antigens outside the body (medications, foreign serum) initiate the process, resulting in antigen–antibody complexes being deposited in the glomeruli. In other patients, the kidney tissue itself serves as the inciting antigen. Figure 54-1: Sequence of events in acute nephritic syndrome. 20. MQE CLINICAL MANIFESTATIONS  Hematuria, edema, azotemia (an abnormal concentration of nitrogenous wastes in the blood), and proteinuria (excess protein in the urine) (Grossman & Porth, 2014).  Hematuria – microscopic or macroscopic  Urine - cola colored because of red blood cells (RBCs) and protein plugs or casts; RBC casts indicate glomerular injury.  Glomerulonephritis - mild and the hematuria discovered incidentally through a routine urinalysis, or the disease may be severe, with AKI and oliguria.  Degree of edema and hypertension  Marked proteinuria due to the increased permeability of the glomerular membrane, with associated pitting edema, hypoalbuminemia, hyperlipidemia, and fatty casts in the urine.  Blood urea nitrogen (BUN) and serum creatinine levels may increase as urine output decreases.  Anemia may be present.  More severe form of the disease, patients also complain of headache, malaise, and flank pain.  Older patients - circulatory overload with dyspnea, engorged neck veins, cardiomegaly, and pulmonary edema.  Atypical symptoms- confusion, somnolence, and seizures, which are often confused with the symptoms of a primary neurologic disorder. ASSESSMENT AND DIAGNOSTIC FINDINGS  Acute nephritic syndrome, the kidneys become large, edematous, and congested.  All renal tissues- glomeruli, tubules, and blood vessels, are affected to varying degrees.  Elevated serum IgA and low to normal complement levels.  Electron microscopy and immunofluorescent analysis help identify the nature of the lesion;  Kidney biopsy may be needed for definitive diagnosis.  If the patient improves, the amount of urine increases and the urinary protein and sediment diminish.  Severe uremia (an excess of urea and other nitrogenous wastes in the blood) within weeks and require dialysis for survival. COMPLICATIONS:  Hypertensive encephalopathy, heart failure, and pulmonary edema.  Hypertensive encephalopathy - directed toward reducing the blood pressure without impairing renal function.  Acute nephritic syndrome or preeclampsia with chronic hypertension of greater than 140/90 mmHg.  Rapidly progressive glomerulonephritis is characterized by a rapid decline in renal function. MEDICAL MANAGEMENT: 1. Primarily of treating symptoms, attempting to preserve kidney function, and treating complications promptly. 2. Prescribing corticosteroids, managing hypertension, and controlling proteinuria. 3. Pharmacologic therapy depends on the cause of acute glomerulonephritis. - streptococcal infection = penicillin is the agent of choice 4. Dietary protein is restricted when renal insufficiency and nitrogen retention (elevated BUN) develop. 21. MQE  5. Sodium is restricted when the patient has hypertension, edema, and heart failure. NURSING MANAGEMENT 1. Carbohydrates are given liberally to provide energy and reduce the catabolism of protein. 2. I&O is carefully measured and recorded. 3. Fluids are given based on the patient’s fluid losses and daily body weight. Insensible fluid loss through the lungs (300 mL) and skin (500 mL) is considered when estimating fluid loss. 4. If treatment is effective, diuresis will begin, resulting in decreased edema and blood pressure. 5. Proteinuria and microscopic hematuria may persist for many months; in fact, 20% of patients have some degree of persistent proteinuria or decreased GFR 1 year after presentation (Grossman & Porth, 2014). 6. Patient education about the disease process, explanations of laboratory and other diagnostic tests, and preparation for safe and effective self-care at home. Promoting Home, Community-Based, and Transitional Care 1. Educating Patients About Self-Care a. Patient education is directed toward managing symptoms and monitoring for complications. b. Fluid and diet restrictions must be reviewed with the patient to avoid worsening of edema and hypertension. c. Instruct the patient verbally and in writing to notify the primary provider if symptoms of kidney disease occur (fatigue, nausea, vomiting, diminishing urine output) or at the first sign of any infection. 2. Continuing and Transitional Care a. Follow-up evaluations of blood pressure, urinalysis for protein, and BUN and serum creatinine levels to determine if the disease has progressed is stressed to the patient. b. provides an opportunity for careful assessment of the patient’s progress and detection of early signs and symptoms of renal insufficiency. C. If corticosteroids, immunosuppressant agents, or antibiotic medications are Prescribed - review the dosage, desired actions, and adverse effects of medications and the precautions to be taken. V. CHRONIC GLOMERULONEPHRITIS  due to repeated episodes of acute nephritic syndrome, hypertensive nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis.  Secondary glomerular diseases that can have systemic effects include systemic lupus erythematosus, Good pasture syndrome (caused by antibodies to the glomerular basement membrane), diabetic glomerulosclerosis, and amyloidosis. PATHOPHYSIOLOGY:  Kidneys are reduced to as little as one fifth their normal size (consisting largely of fibrous tissue).  Cortex layer shrinks to 1 to 2 mm in thickness or less. Bands of scar tissue distort the remaining cortex, making the surface of the kidney rough and irregular. 22. MQE   Numerous glomeruli and their tubules become scarred, and the branches of the renal artery are thickened.  The resulting severe glomerular damage can progress to stage 5 CKD and require a renal replacement therapy. CLINICAL MANIFESTATIONS  hypertension or elevated BUN and serum creatinine levels are detected.  loss of weight and strength, increasing irritability, and an increased need to urinate at night (nocturia).  Headaches, dizziness, and digestive disturbances  Chronic glomerulonephritis progresses, signs and symptoms of CKD =. poorly nourished, with a yellow-gray pigmentation of the skin and periorbital and peripheral (dependent) edema. = Blood pressure may be normal or severely elevated. = Retinal findings - hemorrhage, exudate, narrowed tortuous arterioles, and papilledema. = Anemia causes pale mucous membranes. = Cardiomegaly, a gallop rhythm, distended neck veins, and other signs and symptoms of heart failure = Crackles can be heard in the bases of the lungs. = Peripheral neuropathy with diminished deep tendon reflexes and neurosensory changes. = confused and demonstrates a limited attention span. = pericarditis with a pericardial friction rub and pulsus paradoxus (difference in blood pressure during inspiration and expiration of greater than 10 mmHg). ASSESSMENT AND DIAGNOSTIC FINDINGS  Urinalysis reveals a fixed specific gravity of about 1.010, variable proteinuria, and urinary casts (proteins secreted by damaged kidney tubules).  GFR falls below 50 mL/min,  Hyperkalemia due to decreased potassium excretion, acidosis, catabolism, and excessive potassium intake from food and medications  Metabolic acidosis from decreased acid secretion by the kidney and inability to regenerate bicarbonate  Anemia secondary to decreased erythropoiesis (production of RBCs)  Hypoalbuminemia with edema secondary to protein loss through the damaged glomerular membrane  Increased serum phosphorus level due to decreased renal excretion of phosphorus  Decreased serum calcium level (calcium binds to phosphorus to compensate for elevated serum phosphorus levels)  Mental status changes  Impaired nerve conduction due to electrolyte abnormalities and uremia  Chest x-rays - cardiac enlargement and pulmonary edema.  ECG - normal or may indicate left ventricular hypertrophy associated with hypertension and signs of electrolyte disturbances, such as tall, tented (or peaked) T waves associated with hyperkalemia.  Computed tomography (CT) and magnetic resonance imaging (MRI) scans - decrease in the size of the renal cortex. 23. MQE MEDICAL MANAGEMENT:  Hypertension, efforts are made to reduce the blood pressure with sodium and water restriction, antihypertensive agents, or both.  Weight is monitored daily, and diuretic medications are prescribed to treat fluid overload.  Proteins of high biologic value (dairy products, eggs, meats) are provided to promote good nutritional status. Adequate calories are provided to spare protein for tissue growth and repair.  Urinary tract infections (UTIs) must be treated promptly to prevent further kidney damage.  Dialysis is initiated early in the course of the disease to keep the patient in optimal physical condition, prevent fluid and electrolyte imbalances, and minimize the risk of complications of kidney disease. NURSING MANAGEMENT 1. Observes the patient for common fluid and electrolyte disturbances in kidney disease. 2. Changes in fluid and electrolyte status and in cardiac and neurologic status are reported promptly to the primary provider. 3. Gives emotional support by providing opportunities for the patient and family to verbalize their concerns, have their questions answered, and explore their options (Ahmad & Al Nazly, 2015). 4. Educating the patient and family about the prescribed treatment plan and the risks associated with noncompliance. 5. Instructions to the patient include explanations and scheduling for follow up evaluations: blood pressure, urinalysis for protein and casts, and laboratory studies of BUN and serum creatinine levels. 6. If long-term dialysis is needed, educates the patient and family about the procedure, how to care for the access site, dietary restrictions, and other necessary lifestyle modifications. 7. Assess the patient’s progress and continued education about changes to report to the primary provider (worsening signs and symptoms of kidney disease, such as nausea, vomiting, and diminished urine output). 8. Explain about recommended diet and fluid modifications and medications (purpose, desired effects, adverse effects, dosage, and administration schedule). 9. Periodic laboratory evaluations of creatinine clearance and BUN and serum creatinine levels are carried out to assess residual renal function and the need for dialysis or transplantation. 10. If dialysis is initiated, the patient and family require considerable assistance and support in dealing with therapy and its long-term implications. 11. Remind patient and family are reminded of the importance of participation in health promotion activities, including health screening. 12. Instruct to inform all health care providers about the diagnosis of glomerulonephritis so that all medical management, including pharmacologic therapy, is based on altered renal function. 24. MQE VI. NEPHROTIC SYNDROME  type of kidney disease characterized by increased glomerular permeability and is manifested by massive proteinuria (Grossman & Porth, 2014). CLINICAL FINDINGS:  marked increase in protein (albumin) in the urine (proteinuria), a decrease in albumin in the blood (hypoalbuminemia), diffuse edema, high serum cholesterol, and low-density lipoproteins (hyperlipidemia).  condition that seriously damages the glomerular capillary membrane and results in increased glomerular permeability to plasma proteins.  Although the liver is capable of increasing the production of albumin, it cannot keep up with the daily loss of albumin through the kidneys. Figure 54-2: Sequence of events in nephrotic syndrome. Reprinted with permission from Grossman, S. C., & Porth, C. M. (2014). Pathophysiology: Concepts of altered health states (9th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. PATHOPHYSIOLOGY  Occurs with many intrinsic kidney diseases and systemic diseases that cause glomerular damage. 25. MQE   It is not a specific glomerular disease but a constellation of clinical findings that result from the glomerular damage. CLINICAL MANIFESTATIONS  Edema – soft and pitting and commonly occurs around the eyes (periorbital), in dependent areas (sacrum, ankles, and hands), and in the abdomen (ascites).  Irritability, headache, and malaise. ASSESSMENT AND DIAGNOSTIC FINDINGS  Proteinuria (albumin) exceeding 3.5 g/day is the hallmark of the diagnosis of nephrotic syndrome.  Protein electrophoresis and immunoelectrophoresis- urine to categorize the type of proteinuria  Increased white blood cells (WBCs) - granular and epithelial casts.  Needle biopsy of the kidney- histologic examination of renal tissue to confirm the diagnosis. COMPLICATIONS:  Infection (due to a deficient immune response), thromboembolism (especially of the renal vein), pulmonary embolism, AKI (due to hypovolemia), and accelerated atherosclerosis (due to hyperlipidemia). MEDICAL MANAGEMENT:  Treatment is focused on the underlying disease state causing proteinuria, slowing progression of CKD, and relieving symptoms.  Typical treatment- diuretic agents for edema, ACE inhibitors to reduce proteinuria, and lipid-lowering agents for hyperlipidemia. NURSING MANAGEMENT  Adequate instruction about the importance of following all medication and dietary regimens so that their condition can remain stable as long as possible. VII. POLYCYSTIC KIDNEY DISEASE (PKD):  genetic disorder characterized by the growth of numerous fluid-filled cysts in the kidneys, which destroy the nephrons.  PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure.  PKD can cause cysts in the liver and problems in other areas, such as blood vessels in the brain and heart.  Number of cysts and the resulting complications help distinguish PKD from the usually harmless cysts that can form in the kidneys in later years of life.  Two major inherited forms of PKD exist: 1. Autosomal dominant PKD is the most common inherited form. - Symptoms- develop between 30 and 40 years of age, but they can begin earlier, even in childhood. - About 90% of all PKD cases are autosomal dominant PKD. 2. Autosomal recessive PKD is a rare inherited form. - Symptoms of autosomal recessive PKD begin in the earliest months of life or in 26. MQE  utero. - causes kidneys to fail, which usually happens after many years, the patient requires dialysis or kidney transplantation.  Approximately one half of individuals with autosomal dominant PKD progress to stage 5 CKD, requiring renal replacement therapy. CLINICAL MANIFESTATIONS:  loss of renal function and the increasing size of the kidneys as the cysts grow.  hematuria, polyuria (excessive urine production), hypertension, development of renal calculi and associated UTIs, and proteinuria.  growing cysts are noted with reports of abdominal fullness and flank pain (back and lower sides). ASSESSMENT AND DIAGNOSTIC FINDINGS  Palpation of the abdomen will often reveal enlarged cystic kidneys.  Ultrasound imaging of the kidneys MEDICAL MANAGEMENT 1. PKD has no cure, treatment is largely supportive and includes blood pressure control, pain control, and antibiotic agents to resolve infections. 2. Genetic linkage studies and counseling, particularly when screening family members for potential kidney donation (Grossman & Porth, 2014). C. MANAGEMENT OF PATIENT WITH KIDNEY DISEASES  results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions.  Substances normally eliminated in the urine accumulate in the body fluids as a result of impaired renal excretion, affecting endocrine and metabolic functions as well as fluid, electrolyte, and acid–base disturbances.  Systemic disease and a final common pathway of many different kidney and urinary tract diseases I. ACUTE KIDNEY INJURY:(AKI) - is a rapid loss of renal function due to damage to the kidneys. - a wide range of potentially life-threatening metabolic complications can occur, including metabolic acidosis as well as fluid and electrolyte imbalances (Vritis, 2013). Note: Treatment is aimed at replacing renal function temporarily to minimize potentially lethal complications and reduce potential causes of increased kidney injury with the goal of minimizing long-term loss of renal function. - A widely accepted criterion for AKI is a 50% or greater increase in serum creatinine above baseline (normal creatinine is less than 1 mg/dL) (Vritis, 2013). Urine volume may be normal, or changes may occur. Possible changes include nonoliguria (greater than 800 mL/day), oliguria (less than 0.5 mL/kg/hr), or anuria (less than 50mL/day) (Vritis, 2013). 27. MQE PATHOPHYSIOLOGY: - Pathogenesis of AKI and oliguria is not always known, many times there is a specific underlying cause. - Factors may be reversible if identified and treated promptly, before kidney function is impaired. - Conditions that reduce blood flow to the kidney and impair kidney function: 1. hypovolemia; 2. hypotension; 3. reduced cardiac output and heart failure; 4. obstruction of the kidney or lower urinary tract by tumor, blood clot, or kidney stone; 5. bilateral obstruction of the renal arteries or veins. - Hereditary stone diseases, primary struvite stones, and infection-related urolithiasis associated with anatomic and functional urinary tract anomalies and spinal cord injury may cause recurrent bouts of obstruction as well as crystal-specific damage to tubular epithelial cells and interstitial renal cells. CLASSIFICATIONS OF ACUTE KIDNEY INJURY  Classification criteria for AKI include assessment of three grades of severity and two outcome-level classifications.  This 5-point system is known as the RIFLE classification system (Davies & Leslie, 2012).  RIFLE stands for risk, injury, failure, loss, and ESKD (Vrtis, 2013).  Risk, injury, and failure are considered grades of AKI severity, whereas loss and ESKD are considered outcomes of loss that require some form of renal replacement therapy, (Dring & Hipkiss, 2015). 28. MQE Source: Brunner & Suddarth, 2018, Textbook in Medical-Surgical Nursing, 14ed. CATEGORIES OF ACUTE KIDNEY INJURY: 1. Prerenal (hypoperfusion of kidney)- occurs in 60% to 70% of cases  result of impaired blood flow that leads to hypoperfusion of the kidney commonly caused by volume depletion (burns, hemorrhage, GI losses), hypotension (sepsis, shock), and renal artery stenosis, ultimately leading to a decrease in the GFR (Vritis, 2013). 2. Intrarenal (actual damage to kidney tissue)- is the result of actual parenchymal damage to the glomeruli or kidney tubules.  Acute tubular necrosis (ATN), or AKI in which there is damage to the kidney tubules, is the most common type of intrinsic AKI. Characteristics of ATN; a. intratubular obstruction, tubular back leak (abnormal reabsorption of filtrate and decreased urine flow through the tubule), b. vasoconstriction, and c. changes in glomerular permeability. = These processes result in a decrease of GFR, progressive azotemia, and fluid and electrolyte imbalances. CKD, diabetes, heart failure, hypertension, and cirrhosis can lead to ATN. 29. MQE 3.Postrenal (obstruction to urine flow)- usually results from obstruction distal to the kidney by conditions such as renal calculi, strictures, blood clots, benign prostatic hypertrophy, malignancies, and pregnancy.  Pressure rises in the kidney tubules, and eventually the GFR decreases. CAUSES OF ACUTE KIDNEY INJURY 1. Prerenal Failure  Volume depletion resulting from:  Gastrointestinal losses (vomiting, diarrhea, nasogastric suction)  Hemorrhage  Renal losses (diuretic agents, osmotic diuresis)  Impaired cardiac efficiency resulting from:  Cardiogenic shock, Dysrhythmias, Heart failure, Myocardial infarction  Vasodilation resulting from Anaphylaxis  Antihypertensive medications or other medications that cause  Vasodilation and Sepsis 2. Intrarenal Failure  Prolonged renal ischemia resulting from: - Hemoglobinuria (transfusion reaction, hemolytic anemia) - Rhabdomyolysis/myoglobinuria (trauma, crush injuries, burns) - Pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures)  Nephrotoxic agents such as: - Aminoglycoside antibiotics (gentamicin, tobramycin), Angiotensin-converting enzyme inhibitors - Heavy metals (lead, mercury) - Nonsteroidal anti-inflammatory drugs - Radiopaque contrast agents - Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic)  Infectious processes such as: - Acute glomerulonephritis - Acute pyelonephritis 3. Postrenal Failure  Urinary tract obstruction, including: - Benign prostatic hyperplasia, blood clots, calculi (stones), strictures and tumors PHASES OF ACUTE KIDNEY INJURY There are four phases of AKI: initiation, oliguria, diuresis, and recovery. 1. Initiation period begins with the initial insult and ends when oliguria develops. 2. Oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids, and the intracellular cations [potassium and magnesium]). - The minimum amount of urine needed to rid the body of normal metabolic waste products is 400 mL in 24 hours or 0.5 mL/kg/hr. In this phase, uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop. 3. Diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. 30. MQE  - Laboratory values stabilize and eventually decrease. - volume of urinary output - reach normal or elevated levels, renal function may be markedly abnormal. - Patient must be observed closely for dehydration; if dehydration occurs, the 4.Recovery period signals the improvement of renal function and may take 3 to 12 months. - Laboratory values return to normal level. - A permanent 1% to 3% reduction in the GFR may occur, it is not clinically significant. - Some patients have decreased renal function with increasing nitrogen retention but actually excrete normal amounts of urine (1 to 2 L/day). NOTE: Nonoliguric form of kidney injury and occurs predominantly after exposure of the patient to nephrotoxic agents (any substance, medication, or action that destroys kidney tissue), burns, traumatic injury, and the use of halogenated anesthetic agents. CLINICAL MANIFESTATIONS  critically ill and lethargic.  skin and mucous membranes are dry from dehydration.  CNS signs and symptoms - drowsiness, headache, muscle twitching, and seizures. Table 54-3 COMPARING CLINICAL CHARACTERISTICS OF ACUTE KIDNEY INJURY Source: Brunner & Suddarth, 2018; Textbook in Medical Surgical Nursing, 14ed. ASSESSMENT AND DIAGNOSTIC FINDINGS  Urine - low specific gravity (compared with a normal value of 1.010 to 1.025).  Earliest manifestations of tubular damage is the inability to concentrate the urine (Vritis, 2013).  Prerenal azotemia- decreased amount of sodium in the urine (less than 20 mEq/L) and normal urinary sediment. 31. MQE   Intrarenal azotemia - urinary sodium levels greater than 40mEq/L with urinary casts and other cellular debris.  Ultrasonography  A renal sonogram or a CT or MRI scan  BUN level increases at a rate that depends on the degree of catabolism (breakdown of protein), renal perfusion, and protein intake.  Serum creatinine levels - monitoring kidney function and disease progression and increase with glomerular damage.  Decline in the GFR, oliguria, and anuria - high risk for hyperkalemia.  Protein catabolism results in the release of cellular potassium into the body fluids, causing severe hyperkalemia (high serum potassium levels).  Hyperkalemia may lead to dysrhythmias- ventricular tachycardia and cardiac arrest.  Sources of potassium - normal tissue catabolism, dietary intake, blood in the GI tract, or blood transfusion and other sources (e.g., IV infusions, potassium penicillin, and extracellular shift in response to metabolic acidosis).  Progressive metabolic acidosis - cannot eliminate the daily metabolic load of acid-type substances produced by the normal metabolic processes.  Decreased serum carbon dioxide (CO2) and pH levels.  Blood phosphate concentrations - increase;  Calcium levels - low due to decreased absorption of calcium from the intestine and as a compensatory mechanism for the elevated blood phosphate levels.  Anemia- result of reduced erythropoietin production, uremic GI lesions, reduced RBC lifespan, and blood loss from the GI tract. PREVENTION  AKI has a high mortality rate that ranges from 40% to 90%.  Factors that influence mortality include increased age, comorbid conditions, and preexisting kidney and vascular diseases and respiratory failure (Vritis, 2013). PREVENTING ACUTE KIDNEY INJURY 1. Continually assess renal function (urine output, laboratory values) when appropriate. 2. Monitor central venous and arterial pressures and hourly urine output of critically ill patients to detect the onset of kidney disease as early as possible. 3. Pay special attention to wounds, burns, and other precursors of sepsis. 4. Prevent and treat infections promptly. Infections can produce progressive kidney damage. 5. Prevent and treat shock promptly with blood and fluid replacement. 6. Provide adequate hydration to patients at risk for dehydration,including:before, during, and after surgery 7. Patients undergoing intensive diagnostic studies requiring fluid restriction and contrast agents (e.g., barium enema, IV pyelograms), especially older patients who may have marginal renal reserve 8. Patients with neoplastic disorders or disorders of metabolism (e.g., gout) and those receiving chemotherapy 9. Patients with skeletal muscle injuries (e.g., crush injuries, compartment syndrome) 10. Patients with heat-induced illnesses (e.g., heat stroke, heat exhaustion) 11. Take precautions to ensure that the appropriate blood is given to the correct patient in order to avoid severe transfusion reactions, which can precipitate kidney disease. 32. MQE  12. To prevent infections from ascending in the urinary tract, give meticulous care to patients with indwelling catheters. Remove catheters as soon as possible. 13. To prevent toxic drug effects, closely monitor dosage, duration of use, and blood levels of all medications metabolized or excreted by the kidneys. - Nonsteroidal anti-inflammatory drugs (NSAIDs), may cause interstitial nephritis (inflammation within the renal tissue) and papillary necrosis. 14. Treat hypotension promptly. GERONTOLOGIC CONSIDERATIONS  Etiology of AKI in older adults - prerenal causes such as dehydration, intrarenal causes such as nephrotoxic agents ( medications, contrast agents), and complications of major surgery (Elliott, 2012).  Suppression of thirst, enforced bed rest, lack of access to drinking water, and confusion all contribute to the older patient’s failure to consume adequate fluids and may lead to dehydration - compromising already decreased renal function.  Older adults - All medications need to be monitored for potential side effects that could result in damage to the kidney either through reduced circulation or nephrotoxicity.  Outpatient procedures - require fasting or a bowel preparation may cause dehydration and therefore require careful monitoring. MEDICAL MANAGEMENT:  Objectives of treatment: To restore normal chemical balance and prevent complication. 1. Eliminating the underlying cause; maintaining fluid balance; avoiding fluid excesses; and, providing renal replacement therapy. 2. Prerenal azotemia - optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. 3. Intrarenal azotemia - removal of causative agents, aggressive management of prerenal and postrenal failure, and avoidance of associated risk factors. 4.Shock and infection, if present, are treated promptly. 5. Presence of myoglobin in the urine ( myoglobinuria) in the patient who has had a crush injury, compartment syndrome, or heat-induced illness is treated for rhabdomyolysis. 6. Maintenance of fluid balance is based on daily body weight, serial measurements of central venous pressure, serum and urine concentrations,fluid losses, blood pressure, and the clinical status of the patient. 7. Parenteral and oral intake and the output of urine, gastric drainage, stools, wound drainage, and perspiration are calculated and are used as the basisfor fluid replacement. 8. Insensible fluid produced through the normal metabolic processes and lost through the skin and lungs is also considered in fluid management. 9. Fluid excesses can be detected by the clinical findings of dyspnea, tachycardia, and distended neck veins. - patient’s lungs are auscultated for moist crackles; pulmonary edema may be caused by excessive administration of parenteral fluids, extreme caution must be used to prevent fluid overload. 10. Development of generalized edema is assessed by examining the presacral and pretibial areas several times daily. 11. Mannitol (Osmitrol), furosemide (Lasix), or ethacrynic acid (Edecrin) may be prescribed to initiate diuresis (Walton, 2015). 33. MQE  12. Adequate renal blood flow in patients with prerenal causes of AKI may be restored by IV fluids or transfusions of blood products. 13. Hypovolemia secondary to hypoproteinemia, an infusion of albumin 14. Dialysis - to prevent complications such as hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema. - Dialysis corrects many biochemical abnormalities; allows for liberalization of fluid, protein, and sodium intake; diminishes bleeding tendencies; and promotes wound healing. - Hemodialysis - aprocedure that circulates the patient’s blood through an artificial kidney [dialyzer] to remove waste products and excess fluid, - Peritoneal dialysis (PD; a procedure that uses the patient’s peritoneal membrane [the lining of the peritoneal cavity] as the semipermeable membrane to exchange fluid and solutes), - Continuous renal replacement therapies (CRRTs) -methods used to replace normal kidney function by circulating the patient’s blood through a hemofilter PHARMACOLOGIC THERAPY 1. Monitor for hyperkalemia through serial serum electrolyte levels (potassium value greater than 5.0 mEq/L [5 mmol/L]), ECG changes (tall, tented, or peaked T waves), and changes in clinical status. 2. Kayexalate works by exchanging sodium ions for potassium ions in the intestinal tract. - Sorbitol may be given in combination with Kayexalate to induce a diarrhea-type effect (it induces water loss in the GI tract). - If a Kayexalate retention enema is given (the colon is the major site of potassium exchange), a rectal catheter with a balloon may be used to facilitate retention if necessary. - Retain the Kayexalate for at least 30 to 60 minutes (preferable 6 to 10 hours) to promote potassium removal (Comerford, 2015). Afterward, a cleansing enema may be prescribed to remove remaining medication as a precaution against fecal impaction. 3. Hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia), IV dextrose 50%, insulin, and calcium replacement may be given to shift potassium back into the cells. 4. Many medications are eliminated through the kidneys; therefore, dosages must be reduced when a patient has AKI. - used agents that require adjustment are antibiotic medications (aminoglycosides), digoxin (Lanoxin), phenytoin (Dilantin), ACE inhibitors, and magnesium-containing agents. 5. Diuretic agents are often used to control fluid volume, but they have not been shown to improve recovery from AKI (Prentice, 2013). 6. Severe acidosis, the arterial blood gases and serum bicarbonate levels (CO2) must be monitored because the patient may require sodium bicarbonate therapy or dialysis. 7. If respiratory problems develop, appropriate ventilatory measures must be instituted. 8. Elevated serum phosphate level may be controlled with phosphate-binding agents (e.g., calcium or lanthanum carbonate) that help prevent a continuing rise in serum phosphate levels by decreasing the absorption of phosphate from the intestinal tract. 34. MQE NUTRITIONAL THERAPY:  AKI causes severe nutritional imbalances (because nausea and vomiting contribute to inadequate dietary intake), impaired glucose use and protein synthesis, and increased tissue catabolism.  Weigh daily and loses 0.2 to 0.5 kg (0.5 to 1 lb) daily if the nitrogen balance is negative (i.e., caloric intake falls below caloric requirements).  If the patient gains or does not lose weight or develops hypertension, fluid retention should be suspected.  Nutritional support is based on the underlying cause of AKI, the catabolic response, the type and frequency of renal replacement therapy, comorbidities, and nutritional status.  Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms.  Caloric requirements are met with high-carbohydrate meals, because carbohydrates have a protein-sparing effect (high carbohydrate diet, protein is not used for meeting energy requirements but is “spared” for growth and tissue healing).  Foods and fluids containing potassium or phosphorus ( bananas, citrus fruits and juices, coffee) are restricted.  Oliguric phase- last 10 to 14 days and is followed by the diuretic phase, at which time urine output begins to increase, signaling the patient is in the recovery phase (Prentice, 2013).  Results of blood chemistry tests are used to determine the amounts of sodium, potassium, and water needed for replacement, along with assessment for over- or underhydration.  Diuretic phase, the patient is placed on a high-protein, high-calorie diet and is encouraged to resume activities gradually. NURSING MANAGEMENT 1.Monitor for complications, participates in emergency treatment of fluid and electrolyte imbalances, 2. Assess the patient’s progress and response to treatment, and provides physical and emotional support. 3. Keep family members informed about the patient’s condition, helps them understand the treatments, and provides psychological support. 4. Continue to provide nursing care indicated for the primary disorder ( burns, shock, trauma, obstruction of the urinary tract). MONITORING FLUID AND ELECTROLYTE BALANCE 1.Monitor the patient’s serum electrolyte levels and physical indicators of these complications during all phases of the disorder. 2. IV solutions must be carefully selected based on the patient’s fluid and electrolyte status. 3.Cardiac function and musculoskeletal status are monitored closely for signs of hyperkalemia. QUALITY AND SAFETY NURSING ALERT  Hyperkalemia is the most immediate life-threatening imbalance seen in AKI. Parenteral fluids, all oral intake, and all medications are screened carefully to ensure that sources of potassium are not inadvertently given or consumed. 4. Monitor fluid status by paying careful attention to fluid intake (IV medications should be given in the smallest volume possible),urine output, apparent edema, distention of 35. MQE  the jugular veins, alterations in heart sounds and breath sounds, and increasing difficulty in breathing. 5. Accurate daily weights, as well as I&O records, are essential. 6. Indicators of deteriorating fluid and electrolyte status are reported immediately to the primary provider, and preparation is made for emergency treatment. 7. Severe fluid and electrolyte disturbances may be treated with hemodialysis, PD, or CRRT. REDUCING METABOLIC RATE 1. Bed rest to reduce exertion and the metabolic rate during the most acute stage of the disorder. 2. Fever and infection, both of which increase the metabolic rate and catabolism, are prevented or treated promptly. PROMOTING PULMONARY FUNCTION 1. Assist to turn, cough, and take deep breaths frequently to prevent atelectasis and respiratory tract infection. 2. Drowsiness and lethargy may prevent the patient from moving and turning without encouragement and assistance. PREVENTING INFECTION 1. Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism. 2. An indwelling urinary catheter is avoided whenever possible due to the high risk of UTI associated with its use but may be required to provide ongoing data required to accurately monitor fluid I&O. PROVIDING SKIN CARE 1. Skin- dry or susceptible to breakdown as a result of edema - meticulous skin care is important. 2. Excoriation and itching of the skin may result from the deposit of irritating toxins in the patient’s tissues. 3. Bathing the patient with cool water, frequent turning, and keeping the skin clean and well moisturized and the fingernails trimmed to avoid excoriation are often comforting and prevent skin breakdown. PROVIDING PSYCHOSOCIAL SUPPORT 1. Treatment with hemodialysis, PD, or CRRT. The length of time that these treatments are necessary varies with the cause and extent of damage to the kidneys. 2. Assist, explain and support family need- purpose of the treatment 3. Psychological needs and other concerns of the patient and family be 4. Continious assessment of the patient for complications of AKI and precipitating causes is essential (Davies & Leslie, 2012). II.: END-STAGE KIDNEY DISEASE OR CHRONIC KIDNEY DISEASE  When a patient has sustained enough kidney damage to require renal replacement therapy on a permanent basis, the patient has moved into the fifth or final stage of CKD, also referred to as ESKD. PATHOPHYSIOLOGY:  As renal function declines, the end products of protein metabolism 36. MQE  (normally excreted in urine) accumulate in the blood.  Uremia develops and adversely affects every system in the body.  Greater the buildup of waste products, the more pronounced the symptoms.  Rate of decline in renal function and progression of ESKD is related to the underlying disorder, the urinary excretion of protein, and the presence of hypertension.  Disease tends to progress more rapidly in patients who excrete significant amounts of protein or have elevated blood pressure than in those without these conditions. CLINICAL MANIFESTATIONS  Severity of the signs and symptoms depends in part on the degree of renal impairment, other underlying conditions, and the patient’s age.  Cardiovascular disease is the predominant cause of death in patients with ESKD (Walton, 2015).  Peripheral neuropathy, a disorder of the peripheral nervous system  Severe pain and discomfort.  Restless leg syndrome and burning feet can occur in the early stage of uremic peripheral neuropathy.  Accumulation of uremic waste products -probable cause. SYSTEMIC SIGNS AND SYMPTOMS: Assessing for End-Stage Kidney Disease A. Neurologic:  Asterixis, behavior changes, burning of soles of feet,  Confusion, disorientation, inability to concentrate  Restlessness of legs, seizures, tremors, weakness and fatigue B. Integumentary:  Coarse, thinning hair,dry, flaky skin  Ecchymosis, Gray-bronze skin color, puritus, purpura  Thin, brittle nails C. Cardiovascular:  Engorged neck veins, Hyperkalemia, Hyperlipidemia, Hypertension, Pericardial effusion, Pericardial friction rub, Pericardial tamponade, Pericarditis, Periorbital edema, Pitting edema (feet, hands, sacrum) D. Pulmonary:  Crackles, depressed cough reflex, kussmaul-type respirations  Pleuritic pain, shortness of breath, tachypnea, thick, tenacious sputum  Uremic pneumonitis E. Gastrointestinal  Ammonia odor to breath (“uremic fetor”),anorexia, nausea, and vomiting  Bleeding from gastrointestinal tract  Constipation or diarrhea  Hiccups,metallic taste, mouth ulcerations and bleeding F. Hematologic  Anemia, thrombocytopenia G. Reproductive:  Amenorrhea,decreased libido, infertility, testicular atrophy H. Musculoskeletal:  Bone fractures, bone pain, footdrop, loss of muscle strength 37. MQE   Muscle cramps,renal osteodystrophy ASSESSMENT AND DIAGNOSTIC FINDINGS  Glomerular Filtration Rate- decreases (due to nonfunctioning glomeruli), creatinine clearance decreases,  serum creatinine and BUN levels increase. NOTE: Serum creatinine is a more sensiti