Acute Glomerulonephritis
Prepared by:
Meninguito, Eyeriz Gold Modesto, Guiliano Joss Monghit, Shane Mary A. Oraa,Myza Ocampo,SHaula Panganiban, Marielle Jean G.
BSN4-C Group 10
Presented to:
Mrs.Rodeth Lopera RN.,MAN Clinical Instructor
Acute Glomerulonephritis/ Nephritis/ Nephritic Syndrome
Histologic appearance of acute glomerulonephritis. A, Normal glomerulus. B, Glomerulonephritis. The glomerulus appears hypercellular and the capillaries are narrowed or occluded. From Damjanov, 2000.
Each kidney contains about 1-3 million nephrons and they are the functional unit of the kidney. Each nephron contains a structure called the glomerulus through which the blood vessels pass and the waste products of the body get purified. Acute nephritic syndrome is a group of disorders that cause swelling or inflammation of the internal kidney structures (specifically, the glomeruli). Nephritic syndrome is a type of glomerulonephritis.
Glomerulonephritis /glomerulonephritis/ (glo-meru-lo-n-fritis) it is the inflammation of the capillary loops in the renal glomeruli. It is the term used to describe a group of diseases that damage the part of the kidney that filters blood. When the kidney is damaged, it cannot get rid of wastes and extra fluid in the body. If the illness continues, the kidneys may stop working completely. The kidneys appear enlarged, fatty, and congested. It is characterized by proteinuria, hematuria, decreased urine production, and edema. Kinds of glomerulonephritis are acute glomerulonephritis, chronic glomerulonephritis, and subacute glomerulonephritis. Also called membranous nephropathy. Different Kinds: acute glomerulonephritis -an acute form characterized by proteinuria, edema, hematuria, renal failure, and hypertension, sometimes preceded by tonsillitis or febrile pharyngitis.]
chronic glomerulonephritis -a slowly progressive glomerulonephritis generally leading to irreversible renal failure. diffuse glomerulonephritis - a severe form with proliferative changes in more than half the glomeruli, often with epithelial crescent formation and necrosis; often seen in advanced systemic lupus erythematosus. IgA glomerulonephritis - IgA nephropathy; a chronic form marked by a hematuria and proteinuria and by deposits of immunoglobulin A in the mesangial areas of the renal glomeruli, with subsequent reactive hyperplasia of mesangial cells. lobular glomerulonephritis , membranoproliferative glomerulonephritis -a chronic, slowly progressive glomerulonephritis in which the glomeruli are enlarged as a result of proliferation of mesangial cells and irregular thickening of the capillary walls, which narrows the capillary lumina. membranous glomerulonephritis - a form characterized histologically by proteinaceous deposits on the glomerular capillary basement membrane or by thickening of the membrane; clinically resembling chronic glomerulonephritis, occasionally with transient nephrotic syndrome.
Acute Glomerulonephritis
Acute glomerulonephritis is an inflammatory disease of both kidneys predominantly affecting children from ages two to 12. Chronic glomerulonephritis can develop over a period of 10-20 years and is most often associated with other systemic disease, including diabetes, malaria, hepatitis, or systemic lupus erythematosus. Acute poststreptococcal glomerulonephritis occurs predominantly in males and often completely heals.
Etiology: The exact cause of this infection is unknown. What is known is that a glomerulonephritis infection frequently follows other infections, especially those of the upper respiratory tract such as a streptococcal infection. Glomerulonephritis usually occurs in children about one to four weeks after a streptococcal infection of the throat. There is a latent period of five days to six weeks between an infection and the onset of nephritis (inflammation of the kidneys)
Agent: -Group A beta hemolytic streptococcal infection of the throat that precedes the onset of glomerulonephritis by 2 to 3 weeks
Acute nephritic syndrome is often caused by an immune response that is triggered by an infection or other disease. Frequent causes in children and adolescents include the following: IgA nephropathy Henoch-Schonlein purpura Hemolytic uremic syndrome Post-streptococcal glomerulonephritis Frequent causes in adults include: Abdominal abscesses Infective endocarditis Klebsiella pneumonia Goodpasture syndrome Hepatitis Membranoproliferative GN I Membranoproliferative GN II Rapidly progressive (crescentic) glomerulonephritis SLE or lupus nephritis Syphilis and other sexually transmitted diseases Typhoid fever Vasculitis Viral diseases such as mononucleosis, measles, mumps
Acute nephritic syndrome may be associated with the development of: High blood pressure Swelling of the spaces between the cells of the kidney tissue Acute kidney failure
Several syndromes related to glomerulonephritis have been described. Nephrotic syndrome: Proteinuria in excess of 3.5 grams in 24 hours, accompanied by edema, hypoalbuminemia, hyperlipidemia and lipiduria. Acute nephritis or the Nephritic syndrome: Hematuria, variable proteinuria, azotemia, and hypertension. Rapidly progressive glomerulonephritis: Hematuria, oliguria and acute renal failure.
Signs and Symptoms of Acute Glomerulonephritis. A patient with acuteglomerulonephritis may experience the following signs and symptoms: (1) Hypertension (high arterial blood pressure) - mild to severe from sodiumretention, water retention, or inappropriate renin release. (Renin is an enzyme releasedby the kidney into the blood stream, where renin has a part in raising blood pressurewhen blood pressure is low.)Edema (swelling because of the retention of fluid)--may be mild to severe. (2)Edema (swelling because of the retention of fluid)--may be mild to severe.
(3) Hematuria (discharge of red blood cells in the urine)--resulting in smokyor coffee-colored urine.Albuminuria--abnormal amount of albumin excreted each day in the (4)urine.Oliguria--abnormally low amount of urine excreted per day.
Proteinurias Hematuria Azotemia Oliguria or anuria Edema Hypertension
caused by altered permeability of capillary walls. caused by loss of capillary wall integrity. caused by impaired filtration of nitrogenous wastes. caused by reduced or absent urine production. caused by loss of intravascular oncotic pressure. caused by fluid retentionand altered renal regulation of blood pressure.
Others:
fatigue nausea and vomiting shortness of breath disturbed vision swelling, especially noted in the face, hands, feet, and ankles headache, loss of appetite increased body temperature heaviness or pain in the back waist pain
Anatomy and Physiology
Functions of the Kidney:
Maintaining balance Regulation of body fluid volume and osmolality Regulation of electrolyte balance Regulation of acid-base balance Excretion of waste products (urea, ammonia, drugs, toxins) Production and secretion of hormones Regulation of blood pressure
T he kidneys are essentially regulatory organs which maintain the volume and composition of body fluid by filtration of the blood and selective reabsorption or secretion of filtered solutes. The kidneys are retroperitoneal organs (ie located behind the peritoneum) situated on the posterior wall of the abdomen on each side of the vertebral column, at about the level of the twelfth rib. The left kidney is lightly higher in the abdomen than the right, due to the presence of the liver pushing the right kidney down. The kidneys take their blood supply directly from the aorta via the renal arteries; blood is returned to the inferior vena cava via the renal veins. Urine (the filtered product containing waste materials and water) excreted from the kidneys passes down the fibromuscular ureters and collects in the bladder. The bladder muscle (the detrusor muscle) is capable of distending to accept urine without increasing the pressure inside; this means that large volumes can be collected (700-1000ml) without high-pressure damage to the renal system occuring. When urine is passed, the urethral sphincter at the base of the bladder relaxes, the detrusor contracts, and urine is voided via the urethra.
How do the kidneys and urinary system work? The body takes nutrients from food and converts them to energy. After the body has taken the food that it needs, waste products are left behind in the bowel and in the blood. The kidney and urinary systems keep chemicals, such as potassium and sodium, and water in balance and remove a type of waste, called urea, from the blood. Urea is produced when foods containing protein, such as meat, poultry, and certain vegetables, are broken down in the body. Urea is carried in the bloodstream to the kidneys,where ii is removed. Other important functions of the kidneys include blood pressure regulation and the production of erythropoietin, which controls red blood cell production in the bone marrow
Kidney and urinary system parts and their functions: two kidneys - a pair of purplish-brown organs located below the ribs toward the middle of the back. Their function is to remove liquid waste from the blood in the form of urine; keep a stable balance of salts and other substances in the blood; and produce erythropoietin, a hormone that aids the formation of red blood cells. The kidneys remove urea from the blood through tiny filtering units called nephrons. Each nephron consists of a ball formed of small blood capillaries, called a glomerulus, and a small tube called a renal tubule. Urea, together with water and other waste substances, forms the urine as it passes through the nephrons and down the renal tubules of the kidney. two ureters - narrow tubes that carry urine from the kidneys to the bladder. Muscles in the ureter walls continually tighten and relax forcing urine downward, away from the kidneys. If urine backs up, or is allowed to stand still, a kidney infection can develop. About every 10 to 15 seconds, small amounts of urine are emptied into the bladder from the ureters. bladder - a triangle-shaped, hollow organ located in the lower abdomen. It is held in place by ligaments that are attached to other organs and the pelvic bones. The bladder's walls relax and expand to store urine, and contract and flatten to empty urine through the urethra. The typical healthy adult bladder can store up to two cups of urine for two to five hours. two sphincter muscles - circular muscles that help keep urine from leaking by closing tightly like a rubber band around the opening of the bladder. nerves in the bladder - alert a person when it is time to urinate, or empty the bladder. urethra - the tube that allows urine to pass outside the body. The brain signals the bladder muscles to tighten, which squeezes urine out of the bladder. At the same time, the brain signals the sphincter muscles to relax to let urine exit the bladder through the urethra. When all the signals occur in the correct order, normal urination occurs.
The nephron is the unit of the kidney responsible for ultrafiltration of the blood and reabsorption or excretion of products in the subsequent filtrate. Each nephron is made up of: Responsible for urine formation: Filtration Secretion Reabsorption A filtering unit- the glomerulus. 125ml/min of filtrate is formed by the kidneys as blood is filtered through this sieve-like structure. This filtration is uncontrolled. The proximal convoluted tubule. Controlled absorption of glucose, sodium, and other solutes goes on in this region. The loop of Henle. This region is responsible for concentration and dilution of urine by utilising a counter-current multiplying mechanism- basically, it is water-impermeable but can pump sodium out, which in turn affects the osmolarity of the surrounding tissues and will affect the subsequent movement of water in or out of the water-permeable collecting duct. The distal convoluted tubule. This region is responsible, along with the collecting duct that it joins, for absorbing water back into the body- simple maths will tell you that the
kidney doesn't produce 125ml of urine every minute. 99% of the water is normally reabsorbed, leaving highly concentrated urine to flow into the collecting duct and then into the renal pelvis.
THE GLOMERULUS
Components of plasma cross the three layers of the glomerular barrier during filtration Capillary endothelium Basement membrane (net negative charge) Epithelium of Bowmans Capsule (Podocytes filtration slits allow size <60kD) The ability of a molecule to cross the membrane depends on size, charge, and shape
Reabsorption Active Transport requires ATP Na+, K+ ATP pumps Passive Transport Na+ symporters (glucose, a.a., etc) Na+ antiporters (H+) Ion channels Osmosis Hormones Produced by the Kidney Renin: Released from juxtaglomerular apparatus when low blood flow or low Na+. Renin leads to production of angiotensin II, which in turn ultimately leads to retention of salt and water. Erythropoietin: Stimulates red blood cell development in bone marrow. Will increase when blood oxygen low and anemia (low hemoglobin). Vitamin D3: Enzyme converts Vit D to active form 1,25(OH)2VitD. Involved in calcium homeostasis.
Pathophysiology: Acute Glomerulonephritis
Antigen (group A betahemolytic streptococcus)
Antigen antibody product
Depositon of antigen- antibody complex in glomerulus
Increased production of epithelial cells linings the glomerulus
Leukocytes ifiltrate the glomerulus
Thickening of the glomrular filtration membrane
Scarring and loss of glomerular filtration membrane
Decreased glomerular fitration rate (GFR)
Exams and Tests Because symptoms develop gradually, the disorder may be discovered when there is an abnormal urinalysis during a routine physical or during an examination for another, unrelated disorder. It may be discovered as a cause of high blood pressure that is difficult to control. Laboratory tests may reveal anemia or show signs of reduced kidney functioning, including azotemia. Later, signs of chronic kidney failure may be apparent, including edema. Tests that may be done include: Chest x-ray Kidney or abdominal CT scan Kidney or abdominal ultrasound IVP Urinalysis A kidney biopsy may show one of the forms of chronic glomerulonephritis or scarring of the glomeruli.
This disease may also alter the results of the following tests: Albumin Abdominal MRI Anti-glomerular basement membrane BUN Complement component 3 Complement Creatinine clearance Renal scan Total protein Uric acid, urine Urine concentration test Urine creatinine Urine RBC Urine specific gravity Urine protein Treatment Treatment varies depending on the cause of the disorder, and the type and severity of symptoms. The primary treatment goal is control of symptoms. High blood pressure may be difficult to control, and it is generally the most important aspect of treatment. Various medications may be used to attempt to control high blood pressure. Corticosteroids, immunosuppressives, or other medications may be used to treat some of the causes of chronic glomerulonephritis.
Dietary restrictions on salt, fluids, protein, and other substances may be recommended to help control of high blood pressure or kidney failure. Dialysis or kidney transplantation may be necessary to control symptoms of kidney failure and to sustain life.
Nursing Management: 1. Review fluid and diet restrictions. 2. Measure and record intake and output. 3. Instruct patient to schedule follow-up evaluations of blood pressure, urinalysis for protein, and BUN and creatinine studies to determine if disease has worsened. 4. Instruct patient to notify physician if infection or symptoms of renal failure occur: fatigue, nausea, and vomiting, diminishing urinary output. 5. Refer to home care nurse as indicated for assessment and detection of early symptoms and follow-up evaluations.
Nursing Interventions: 1. Provide best rest during the acute phase. 2. Perform passive range of motion exercises for the patient on bed rest. 3. Allow the patient to resume normal activities gradually as symptoms subside. 4. Consult the dietician about a diet high in calories and low in protein, sodium, potassium, and fluids. 5. Protect the debilitated patient against secondary infection by providing good nutrition and hygienic technique and preventing contact with infected people. 6. Check the patients vital signs and electrolyte values. 7. Monitor intake and output and daily weight. 8. Report peripheral edema or the formation of ascites. 9. Explain to the patient taking diuretics that he may experience orthostatic hypotension and dizziness when he changes positions quickly. 10. Provide emotional support for the patient and his family. 11. If the patient is scheduled for dialysis, explain the procedure fully.