A. Brief Description of the Disease Condition Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss of renal function over a period of months or years in which the bodys ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia. In this condition, the GFR falls below 10% of the normal rate. Chronic Kidney Disease (CKD) affects 26 million Americans. Early detection can help to prevent progression of the disease which ultimately can lead to kidney failure and death. However, early detection can be difficult because the signs and symptoms of kidney disease, and even acute kidney failure, are often overlooked. The prevalence of CKD has steadily increased over the past two decades, and was reported to affect over 13% of the U.S. population in 2004. In 2009, more than 570,000 people in the United States were classified as having end-stage renal disease (ESRD), including nearly 400,000 dialysis patients and over 17,000 transplant recipients. A patient is determined to have ESRD when he or she requires replacement therapy, including dialysis or kidney transplantation. The rise in incidence of CKD is attributed to an aging populace and increases in hypertension (HTN), diabetes, and obesity within the U.S. population. CKD is associated with a host of complications including electrolyte imbalances, mineral and bone disorders, anemia, dyslipidemia, and HTN. It is well known that CKD is a risk factor for cardiovascular disease (CVD), and that a reduced GFR and albuminuria are independently associated with an increase in cardiovascular and all-cause mortality. Local Statistics: MORTALITY: TEN LEADING (10) LEADING CAUSES Number and rate/100,000 Population Philippines 5-Year Average (2000-2004) & 2005 Cause 5 Year Average (2000-2004) 2005* Number Rate No. Rate 1. Diseases of the Heart 66,412 83.3 77,060 90.4 2. Diseases of the Vascular system 50,886 63.9 54,372 63.8 3. Malignant Neoplasm 38,578 48.4 41,697 48.9 4. Pneumonia 32,989 41.4 36,510 42.8 5. Accidents 33,455 42.0 33,327 39.1 6. Tuberculosis, all forms 27,211 34.2 26,588 31.2 7. Chronic lower respiratory diseases 18,015 22.6 20,951 24.6 8.Diabetes Mellitus 13,584 17.0 18,441 21.6 9. Certain conditions originating in the perinatal period 14,477 18.2 12,368 14.5 10. Nephritis, nephrotic syndrome and nephrosis 9.166 11.5 11,056 3.6 Note: Excludes ill-defined and unknown causes of mortality (R00-R99) n=23,235
* reference year ** External Causes of Mortality Last Update: September 29, 2011
TEN LEADING (10) CAUSES OF MORTALITY AMONG MALES Number and Rate/100,000 Population Philippines, 2005
Cause No. Rate 1. Diseases of the Heart 43,809 102.1 2. Diseases of the Vascular system 30,531 71.2 3. Accidents 27,281 63.6 4. Malignant Neoplasms 21,993 51.3 5. Tuberculosis, all forms 18,229 42.5 6. Pneumonia 18,145 42.3 7. Chronic lower respiratory diseases 14,450 33.7 8. Diabetes Mellitus 8,912 20.8 9. Certain conditions originating in the perinatal period 7,385 17.2 10. Nephritis, nephrotic syndrome and nephrosis
6,548 15.3 Last Update: September 28, 2011
TEN LEADING (10) CAUSES OF MORTALITY AMONG FEMALES Number and Rate/100,000 Population Philippines, 2005 Cause No. Rate 1. Diseases of the Heart 33,251 78.5 2. Diseases of the Vascular system 23,841 56.3 3. Malignant Neoplasms 19,704 46.5 4. Pneumonia 18,365 43.3 5. Diabetes Mellitus 9,529 22.5 6. Tuberculosis, All Forms 8,359 19.7 7. Chronic lower respiratory diseases 6,501 15.3 8. Accidents 6,046 14.3 9. Certain conditions originating in the perinatal period 4,983 11.8 10. Nephritis, nephrotic syndrome and nephrosis 4,508 10.6 Note: Excludes ill-defined and unknown causes of mortality (R00-R99) for males (n=11,840) and females n=11,395 ** External Causes of Mortality Last Update: September 28, 2011 (http://www.doh.gov.ph/node/198)
The tables show that diseases of the vascular system are second to the highest cause of morbidity and mortality in the Philippines in both male and female. It can also be seen that males have higher rates than female. It is a must that people would cautiously monitor their health and practice healthy living to avoid diseases that could lead to death. And people should prioritize their health more than anything else.
B. GENERAL OBJECTIVES: The general objective of the case study is to gain the comprehensive knowledge about the disease to gain the practical exercise about the Adult Health Problem and also to gain Practical experience working with a patient having chronic kidney disease and to give holistic patient care according to their need.
II. ANATOMY AND PHYSIOLOGY Function of the Urinary System The major functions of the urinary systems are performed by the kidneys and the kidneys plays the following essentials roles in controlling the composition and volume of body fluids: 1. Excretion. The kidneys are the major excretory organs of the body. They remove waste products, many of which are toxic, from the blood. Most waste products are metabolic by- products of cells and substances absorbed from the intestine. The skin, liver, lungs, and intestines eliminate some of these waste products, but they cannot compensate if the kidneys fail to function. 2. Blood volume control. The kidneys play an essential role in controlling blood volume by regulating the volume of water removed from the blood to produce urine. 3. Ion concentration regulation. The kidneys help regulate the concentration of the major ions in the body fluids. 4. pH regulation. The kidneys help regulate the pH of the body fluids. Buffers in the blood and the respiratory system also play important roles in the regulation of pH 5. Red blood cell concentration. The kidneys participate in the regulation of red blood cell production and therefore, in controlling the concentration of red blood cells in the blood. 6. Vitamin D synthesis. The kidneys. Along with the skin and the liver, participate in the synthesis of vitamin D.
Kidneys The kidneys balance the urinary excretion of substances against the accumulation within the body through ingestion or production. Consequently, they are major controller of fluid and electrolyte homeostasis. The kidneys also have several non-excretory metabolic and endocrine functions, including blood pressure regulation, erythropoietin production, insulin degradation, prostaglandin synthesis, calcium and phosphorus regulation and Vitamin D metabolism. The kidneys are located retroperitoneally, in the posterior aspect of the abdomen. On either side of the ventral column. They lie between the 12 th thoracic and third lumbar vertebrae. The left kidney is usually positioned slightly higher than the right. Adult kidneys are average approximately 11 cm in length, 5 to 7.5 cm in width, and 2.5 cm in
thickness. The kidney has a characteristic curved shape, with a convex distal edge and a concave medial boundary.
Ureters, Urinary Bladder and Urethra The ureters are small tubes that carry urine from the renal pelvis of the kidney to the posterior inferior portion of the urinary bladder. The urinary bladder is a hollow muscular container that lies in the pelvic cavity just posterior to the pubic symphysis. It functions to store urine, and its size depends on the quantity of urine present. The urinary bladder can hold from a few milliliters to a maximum of about 1000 mL of urine. When the urinary bladder reaches a volume of a few hundred mL, a reflex is activated, which causes the smooth muscle of the urinary bladder to contract and most of the urine flows out of the urinary bladder through urethra. The urethra is a tube that exits the urinary bladder inferiorly and anteriorly. The triangle-shaped portion of the urinary bladder located between the opening of the ureters and the opening of the urethra is called trigone. The urethra carries urine from the urinary bladder to the outside of the body. Renal Blood flow and Glomerular Filtration The kidney receive 20% to 25% of the cardiac output under resting conditions, averaging more than 1 L of arterial blood per minute. The renal arteries branch from the abdominal aorta at the level of he second lumbar vertebra, enter the kidney, and progressively branch into lobar arteries. Blood flows from the interlobular arteries through the afferent arteriole, the glomerular capillaries, the efferent arteriole and the peritubular capillaries. Some of the peritubular capillaries carry a small amount of blood to the renal medulla in the vasa recta before entering the venous drainage. The blood leaves the kidney in venous system closely corresponding to the arterial system: interlobular veins, arcuate veins, interlobar veins, and the renal vein. The renal circulation then empties into the inferior vena cava. Physiology Characteristics of Urine Urine is a watery solution of nitrogenous waste an inorganic salts that are removed from the plasma and eliminated by the kidneys. It is 5% water and 5% dissolved solids and gases. The amount of these dissolved substances is indicated by it specific gravity. The specific gravity of pure water, used as a standard is 1.000. Because of the dissolved materials it contains, urine has a specific gravity that normally varies from 1.010 to 1.040. When the kidneys are diseased, they lose the ability to concentrate urine, and the specific gravity no longer varies as it does when the kidneys function normally. Urine formation The chief function of the kidneys is to produce urine. Each part of the nephrons performs a special function. There are three important processes by which urine is formed. They are glomerular filtration, tubular reabsorption and tubular secretion. What do the kidneys do? The kidneys remove wastes and extra water from the blood to form urine. Urine flows from the kidneys to the bladder through the ureters. Your kidneys are bean-shaped organs, each about the size of your fist. They are located near the middle of your back, just below the rib cage. The kidneys are
sophisticated reprocessing machines. Every day, your kidneys process about 200 quarts of blood to sift out about 2 quarts of waste products and extra water. The waste and extra water become urine, which flows to your bladder through tubes called ureters. Your bladder stores urine until you go to the bathroom. The wastes in your blood come from the normal breakdown of active tissues and from the food you eat. Your body uses food for energy and self-repair. After your body has taken what it needs from the food, waste is sent to the blood. If your kidneys did not remove these wastes, the wastes would build up in the blood and damage your body. The actual filtering occurs in tiny units inside your kidneys called nephrons. Every kidney has about a million nephrons. In the nephron, a glomeruluswhich is a tiny blood vessel, or capillaryintertwines with a tiny urine-collecting tube called a tubule. A complicated chemical exchange takes place, as waste materials and water leave your blood and enter your urinary system. At first, the tubules receive a combination of waste materials and chemicals that your body can still use. Your kidneys measure out chemicals like sodium, phosphorus, and potassium and release them back to the blood to return to the body. In this way, your kidneys regulate the bodys level of these substances. The right balance is necessary for life, but excess levels can be harmful. The kidneys remove wastes and extra water from the blood to form urine. Urine flows from the kidneys to the bladder through the ureters. In addition to removing wastes, your kidneys release three important hormones: Erythropoietin (eh-RITH-ro- POY-eh-tin), or EPO, which stimulates the bone marrow to make red blood cells Renin (REE-nin), which regulates blood pressure Calcitriol (kal-suh-TRY-ul), the active form of vitamin D, which helps maintain calcium for bones and for normal chemical balance in the body What is renal function? Your health care team may talk about the work your kidneys do as renal function. If you have two healthy kidneys, you have 100 percent of your renal function. This is more renal function than you really need. Some people are born with only one kidney, and these people are able to lead normal, healthy lives. Many people donate a kidney for transplantation to a family member or friend. Small declines in renal function may not cause a problem.
III. PATIENT AND HIS ILLNESS A. Definition of the disease Chronic or irreversible, renal failure is a progressive reduction of functioning renal tissue such that the remaining kidney mass can no longer maintain the bodys internal environment. Chronic Renal failure can develop insidiously over many years,
or it may result from an episode of acute renal failure from which the client has not recovered. Progressive loss of renal function over time; based on a gradual decline in the GFR and creatinine clearance. The diagnosis of CKD requires the following: 1. Decline of kidney function for 3 months or more AND 2. Evidence of kidney damage (e.g. albuminuria or abnormal biopsy) OR GFR <60 mL/min/1.73 m 2
Each patient is classified into one of the following 5 stages of CKD because management and prognosis varies according to the progression of damage. Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m 2 ) Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m 2 ) Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m 2 ) Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m 2 ) Stage 5: Kidney failure (GFR <15 mL/min/1.73 m 2 or dialysis) B. Precipitating Factors Chronic glomerular disease such as glomerunephritis Chronic infections such as chronic pyelonephritis or tuberculosis Congenital anomalities such as polycystic Vascular diseases, such as renal nephrosclerosis or hypertension Hypertension Glomerular and vascular changes: o Elevated systemic blood pressures cause a hypertrophic response leading to intimal thickening of the large and the small vasculature. o The mechanisms are compensatory at first, but later lead to glomerular damage Global sclerosis ischemic injury to the nephrons causes death Focal segmental sclerosis glomerular enlargement for compensation of the loss of nephrons in other areas of the kidney. Interstitial nephritis: o The vascular and glomerular disease lead to tubular atrophy and an intense chronic interstitial nephritis The intense chronic interstitial nephritis is thought be secondary to immunologic processes against ischemia-mediated antigen changes on the tubular epithelial cell surface. Chronically these changes lead to tubular and glomerular loss causing nephrons loss. o With the death of some nephrons, less are available to maintain the GFR. o Gradual decline in the GFR is noticed as the nephrons continue to die. Obstructive processes such as calculi nephrotoxic agents such as long-term aminoglycoside endocrine diseases such as diabetic neuropathy Such conditions gradually destroy the nephrons and eventually cause irreversible renal failure. Similarly, acute renal failure that fails to respond to treatment becomes chronic renal failure. Blockages Scarring from infections or a malformed lower urinary tract system (birth defect) can force urine to back up into the kidney and damage it. Blood clots or plaques of cholesterol that block the kidneys blood vessels can reduce blood flow to the kidney
and cause damage. Repeated kidney stones can block the flow of urine from the kidney and are another kind of obstruction that can damage the kidneys. Overuse of Painkillers and Allergic Reactions to Antibiotics Heavy use of painkillers containing ibuprofen (Advil, Motrin), naproxen (Aleve), or acetaminophen (Tylenol) have been linked to interstitial nephritis, a kidney inflammation that can lead to kidney failure. A new study suggests that ordinary use of painkillers (e.g., one pill per day) is not harmful in men who are not at risk for kidney disease. Allergic reactions toor side effects ofantibiotics like penicillin and vancomycin may also cause nephritis and kidney damage. Drug Abuse Use of certain nonprescription drugs, such as heroin or cocaine, can damage the kidneys, and may lead to kidney failure and the need for dialysis. Inflammation Certain illnesses, like glomerulonephritis (inflammation of the filtering units of the kidneys), can damage the kidneys, sometimes enough to cause CKD. Some glomerulonephritis is inherited, and some may be an immune response to infections like strep throat. C. Predisposing Factors Sex- both sexes are affected by chronic renal failure. But in 1998, based on United States Renal Data System, a higher total number of males with ESRD was found Age- CRF can be found in people of any age, from infants to the very old. The elderly population also is the most rapidly growing ESRD population in the United States. Note that age 30 years progressive physiological glomerulosclerosis. Aging also results in concomitant progressive physiological decrease in muscle mass such that daily urinary creatinine excretion also decreases. High risk groups for chronic kidney disease (CKD) include those with a family history of kidney disease. One inherited disease, polycystic kidney disease, causes large, fluid-filled cysts that eventually crowd out normal kidney tissue. African Americans, Hispanics, Pacific Islanders, and Native Americans are also at increased risk. D. Clinical Manifestations The clinical manifestations of CRF are present throughout the body. No organ system is spared. Electrolyte imbalances Electrolyte balance may be upset by impaired excretion and utilization in the kidney. Although many clients maintain normal serum sodium level, the salt- wasting properties of some failing kidneys, in addition to vomiting and diarrhea, may cause hyponatremia. Because the kidneys are efficient at excreting potassium, potassium levels usually remain within normal limits until late in the disease. Several mechanisms contriburte to hypocalcemia. Conversion of 25- hydroxycholecalciferol to 1,25-dihyroxycholecalciferol (necessary to absorb calcium) is decreased, which results in reduced intestinal absorption of calcium. At the same time, phosphate is not excreted, which causes hyperphosphatemia. Because calcium and phosphate are inversely related, a high phosphate level results in a reduced calcium level.
Metabolic changes In advancing renal failure, BUN and serum creatinine rise as waste products of protein metabolism accumulate in the blood. The serum creatinine level is the most accurate measure of renal function. The proteinuria accompanying renal disease and sometimes inadequate dietary intake of proteins cause hypoproteinuria, which lowers the intravascular oncotic pressure. Metabolic acidosis occurs because of the kidneys inability to excrete hydrogen ions. Decrease reabsorption of sodium bicarbonate and decreased formation of dihydrogen phosphate and ammonia contribute to this problem. Acidosis accentuates hyperkalemia and the reabsorption of calcium from the bones. Hematologic changes The primary hematologic effect of renal failure is anemia, usually normochromic and normocytic. It occurs because the kidneys are unable to produce erythropoietin, a hormone necessary for red blood cell production. Frequently, the fatigue, weakness, and cold intolerance accompanying the anemia lead to a diagnosis of renal failure. Gastrointestinal changes The entire gastrointestinal system is affected. Transient anorexia, nausea, vomiting are almost universal. Clients often experience a constant bitter , metallic, or salty taste, and their breath commonly smells fetid, fishy or ammonia-like. Stomatitis, parotitis and gingivitis are common problems because of poor oral hygiene and the formation of ammonia from salivary urea. Accumulations of gastro may be a major cause of ulcer disease. Esophagitis, gastritis, colitis, gastrointestinal bleeding, and diarrhea may be present. Serum amylase level may be increased, although they do not necessarily indicate pancreatitis. Immunologic changes Impairment of the immune system makes the client more susceptible to infection. Several factors are involved, including depression of humoral antibody formation, suppression of delayed hypersensitivity and decreased chemotactic function of leukocytes. Immunosuppression is an important part of the medical management of renal diseaes such as glomerulonephritis. Cardiovascular changes The most common clinical manifestation is hypertension, produced through: mechanism of volume overload, stimulation of the renin-angiotensin system, sympatheically mediated vasoconstriction, absence of prostaglandins. Respiratory changes Some of the respiratory effects such as pulmonary edema can be attributed to fluid overload. Metabolic acidosis causes a compensatory increase in respiratory rate as the lungs try to eliminate excess hydrogen ions. Musculoskeletal changes The etiologic mechanism involves the kidney-bone-parathyroid and calcium- phosphate-vitamin D connections. As the GRF decreases, the phosphate excretion decreases and calcium elimination increases. Abnormal levels of calcium and phosphate stimulate the release of parathyroid hormone that mobilizes calcium from the bones and facilitates phosphate excretion. Integumentary changes
The skin is also often very dry because of atrophy of the sweat glands. Severe and intractable pruritus may result from secondary hyperparathyroidism and calcium deposits in the skin. The pallor of anemia is evident. 1. Changes in Urination Because your kidneys are tasked with making urine, and thereby eliminating waste, any changes in the frequency, color, or appearance of urine should be taken seriously. Some common types of changes include: Urinating more frequently during the night or in greater amounts Urinating less often or in smaller amounts Having foamy or bubbly urine or blood in your urine Difficulty urinating 2. Swelling If your kidneys are unable to remove extra fluid from your body, you will likely experience swelling in your legs, ankles, feet, face, or hands. Water retention due to a loss of GFR leading to sodium and fluid retention. Fluid moves into the extravascular space, due to increased hydrostatic pressure, causing pitting edema in the lower extremity (fluid movement could also be due to hypoalbuminemia, in some diseases, leading to a low oncotic pressure). 3. Skin Rash / Itching If your kidneys are unable to remove waste from the bloodstream, the buildup can cause rashes and severe itching. 4. Leg, Back or Side Pain Kidney problems can lead to pain in the back, side or even in the leg. Kidney cysts (large, fluid-filled sacs) resulting from polycystic kidney disease that form on kidneys and occasionally on the liver can also cause back and leg pain. 5. Metallic Taste in Mouth/Ammonia Breath When waste builds up in the bloodstream, it can cause bad breath, a metallic taste in the mouth, and affect how food tastes. You may also have a change in appetite that results in weight loss. 6. Nausea and Vomiting Waste buildup in the blood can also cause nausea and vomiting. 7. Feeling Cold Healthy kidneys make the hormone known as erythropoietin, which prompts the body to make oxygen-carrying red blood cells. Kidney disease can interrupt the healthy production of this hormone and cause a decrease in red blood cells, a condition known as anemia. Anemia and kidney disease can result in a variety of symptoms, including constantly feeling cold and shortness of breath. 8. Shortness of Breath Kidney disease can cause extra fluid to build up in the lungs, leading to shortness of breath. Anemia, a common side-effect of kidney disease which starves your body of oxygen, can also cause you to feel winded or short of breath. Fluid accumulation causes pulmonary edema and loss of air space causing ventilation-perfusion mismatch. This leaves less area for oxygen diffusion form the blood vessels.
9. Dizziness and Trouble Concentrating When you suffer from anemia related to kidney failure, both your body and your brain will be lacking the proper amount of oxygen. The result can be dizziness, trouble with concentration, and memory-related issues. 10. Fatigue When kidneys fail, and side effects like anemia set in, you may experience tired muscles, weakness, and overall fatigue. Erythropoietin (EPO), the major erythropoiesis stimulator, is released from the kidneys; with renal failure, there is loss of EPO release
V. MEDICAL MANAGEMENT The goal of management is to maintain kidney function and homeostasis for as long as possible. Because of the great deterioration of renal function, the duration of management may vary from months to years. Nothing can be done to prevent or delay the fatal outcome. Control of urinary volume: fluids are forced since kidney has lessened ability to concentrate solids. more fluids about 2litres is needed to excrete waste. Sometimes frusemide may be required to increase urine production. Control of nausea and vomiting: anorexia, nausea and vomiting tend to develop when the cretinine clearance falls below 5ml/min. so reduction in protein is required to improve nausea. Blood: 0.8-1.4 mg/dL is the normal. Due to impaired kidney function, creatinine in the blood elevates. Creatinine clearance rate was 10.g mg/dl on 4/2, 8.5 mg/dl on 068/4/6, 9.7mg/dl on 068/4/9. Antiseizure agents Antihypertensive agents: hypertension is managed by intravascular volume control and a variety of anti- hypertensive agents. Control of hyperkalaemia will be treated with I/V glucose and insulin in a ratio of 3 gm Glucose to 1 unit soluble insulin. Control of anemia: blood transfusion are frequently required. Accurate record of input and output chart should be maintained Other therapy: dialysis It is usually initiated when the patient cannot maintain a reasonable lifestyle with conservative treatment. VI. Nursing Management: Nursing care is directed toward assessing fluid status and identifying potential source of imbalance Implement a dietary program to ensure proper nutritional intake within the limits of the treatment regimen. Promote positive feelings by encouraging increased self care Provide explanations and information to the patient and family concerning ESRD, treatment options and potential complications Nurse must be familiar with various drugs and their side effects Provide emotional support to the patient and his family because of the numerous changes experienced. Cardiovascular disease (CVD)is the leading cause of death in patients with CKD. o Reducing risk factors for development of CVD is beneficial. E.g. treatment of hyperlipidemia, lifestyle and dietary changes Tight blood pressure control: o Reducing damage due to the end organ effects of hypertension on the kidney as well as the heart. o Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers(ARBs) block the effects of angiotensin II on (i) sodium and fluid retention, (ii) vasoconstriction, (iii) stimulating ADH release, (iv) stimulating aldosterone release, and (v) inducing a sympathetic response.
ACEIs and ARBs also slow down progression of proteinuria in patients with diabetic CKD. Diabetes management: o Tight glucose management slows the progression of vascular and heart disease. Avoidance of IV contrast, NSAIDs, and nephrotoxic drugs: o These agents can potentially induce an acute kidney injury (AKI) on the underlying kidney disease and therefore exacerbate the baseline CKD. Diet: o Mixed evidence exists whether dietary protein restriction is beneficial in slowing disease progression. o Proteins affect the renal hemodynamics, raising the GFR, in hypothesized 2 ways. Hormonal effects proteins cause secretion of glucagon, IGF-1 and kinins, all of which have been shown to raise the GFR. Tubuloglomerular effects high amino acid (AA) filtration leads to increased AA and hence the sodium uptake in the proximal convoluted tubule. A decreased sodium delivery to the distal convoluted tubule leads to the rennin-angiotensin system activation via the macula densa and these work to raise the GFR (mechanisms above) o Controlling hyperphosphatemia: Protein restriction also limits phosphorus consumption. Hyperphosphatemia plays a major role in the progression of renal osteodystrophy. Phosphate binders are used to reduce phosphate absorption through the GI tract. VII. Surgical Management Kidney transplantation: it involves transplanting a kidney from a living donor to a recipient who has ESRD. The success rate increases if kidney transplantation from a living donor is performed before dialysis is initiated. VIII. REFERENCES 1. Coresh J, Selvin E, Stevens LA, et al. Prevalence of chronic kidney disease in the United States. 2007. 2. Collins AJ, Foley RN, Chavers B, et al. U.S. renal data system 2011 annual data report. Am J Kidney Dis. 2012. 3. Matsushita K, van der Velde M, Astor BC, et al. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Lancet. 2010. 4. Rashidi A, Sehgal AR, Rahman M, O'Connor AS. The case for chronic kidney disease, diabetes mellitus, and myocardial infarction being equivalent risk factors for cardiovascular mortality inpatients older than 65 years. Am J Cardiol. 2008. 5. Rao MV, Qiu Y, Wang C, Bakris G. Hypertension and CKD: Kidney Early Evaluation Program (KEEP) and National Health and Nutrition Examination Survey (NHANES), 19992004. Am J Kidney Dis. 2008. 6. Botdorf J, Chaudhary K, Whaley-Connell A. Hypertension in cardiovascular and kidney disease. Cardiorenal Med. 2011.
7. Segura J, Ruilope L. Hypertension in moderate-to-severe nondiabetic CKD patients. Adv Chronic Kidney Dis. 2011. 8. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. 2003.
Chronic Kidney Disease. Retrieved from http://www.medscape.com/viewarticle/766696_6.
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TEN LEADING (10) CAUSES OF MORTALITY (2011). Retrieved from http://www.doh.gov.ph/node/198.
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