Acute GlomeruloNephritis Introduction: Acute glomerulonephritis (AGN) is a disease characterized by the sudden appearance of edema, hematuria, proteinuria, and

hypertension [1, 2]. It is essentially a dis-ease of child hood that accounts for approximately 90% of renal disorders in children. The group A beta-haemolytic streptococcus (GAS) is a common infective agent in children that causes the widest range of clinical disease in humans of any bacterium [3]. Glomeru-lonephritis is a disease of the low socioeconomic class [4]. Post-streptococcal acute glomerulonephritis (PSAGN) is still prevalent in the developing countries [5]. Burden of APSGN in underdeveloped countries is 9.3 cases per 100,000 populations. The main functional unit of the kidney is the nephron. There are approximately one million nephrons per kidney. The role of nephrons is to make urine by: Filtering blood of small molecules and ions such as water, salt, glucose and other solutes including urea. Large macromolecules like proteins are untouched. Recycling the required quantities of useful solutes which then reenter the bloodstream. (A process called reabsorption) Allowing surplus or waste molecules/ions to flow from the tubules/ureter as urine. Nephron Function The blood is filtered and urine formed by the actions of the nephrons. In each nephron, high pressure in the glomerulus pushes water and small dissolved materials into the extravascular space of the Bowmans capsule and into the tubule. The proximal tubule reabsorbs water, salts, glucose, and amino acids to maintain electrolyte levels in the body. The interstitium of, that is the tissue space surrounding, the loop of Henle concentrates salts that will be excreted in the urine, creating a concentration gradient in the medulla. The limbs of Henles loop are permeable to particular ions (descending, water and some urea; thin ascending, general ions; medullary thick ascending sodium, potassium, chloride), with the cortical thick ascending limb draining into the distal convoluted tubule. The distal tubule contains cells specialized in active transport and maintains urine and blood pH levels, particularly through the regulation of sodium and potassium. Fluid then passes from the distal tubule to the collecting ducts, a tubule system that can become permeable or impermeable to water depending on the bodys needs. Ultrafiltration also occurs in the cortex in the cortical

collecting ducts, which is regarded by some anatomy references as not being a portion of the nephron, and by others as being the final portion of the nephron. The urine then passes from the collecting ducts through the drainage system of the kidney to the ureters and bladder for urination. Causes Causes of acute glomerulonephritis include postinfectious, renal, and systemic etiologies. Each is described briefly. Postinfectious etiologies o The most common cause is postinfectious Streptococcus species (ie, group A, beta-hemolytic). Two types have been described as (1) attributed to serotype 12, poststreptococcal nephritis due to an upper respiratory infection occurring primarily in the winter months, and (2) attributed to serotype 49, poststreptococcal nephritis due to a skin infection usually observed in the summer and fall and more prevalent in southern regions of the United States. Causes In diffuse glomerulonephritis (GN), all of the glomeruli are aggressively attacked, leading to acute renal failure (ARF). Disorders that attack several organs and cause diffuse GN are referred to as secondary causes. Secondary causes of diffuse GN include the following: Cryoglobulinemia Goodpasteurs syndrome (membranous antiglomerular basement membrane disease) Lupus nephritis Schnlein-Henoch purpura Vasculitis (e.g., Wegener's granulomatosis, periarteritis nodosa) Primary diseases that solely affect the kidneys and cause AGN, include the following: Immunoglobulin A nephropathy (IgA nephropathy, Bergers disease) Membranoproliferative nephritis (type of kidney inflammation) Postinfectious GN (GN that results after an infection) Signs and Symptoms Periorbital and facial edema (more prominent in the morning),decreased urinary output, cloudy, smoky, and brown-colored urine, anorexia, pallor, irritability and lethargy, headaches, abdominal or

flank pain, dysuria, hypertension, proteinuria, azotemia, increased blood urea nitrogen and creatinine levels and Antistreptolysin O titer. Pathophysiology With the exception of poststreptococcal glomerulonephritis, the exact triggers for the formation of the immune complexes are unclear. In streptococcal infection, involvement of derivatives of streptococcal proteins has been reported. A streptococcal neuraminidase may alter host immunoglobulin G (IgG). IgG combines with host antibodies. IgG/anti-IgG immune complexes are formed and then collect in the glomeruli. In addition, elevations of antibody titers to other antigens, such as antistreptolysin O or antihyaluronidase, DNAase-B, and streptokinase, provide evidence of a recent streptococcal infection. System Inspection Integumentary system Respiratory system Central Nervous System Circulatory system Gastrointestinal system Vomiting Anorexia Abdominal pain Musculoskeletal system Weakness Fatigue Back pain Skin flushing diaphoresis Tachypnea Dyspnea Physical Assessment Auscultation Percussion Palpitation edema

Cardiovascular system

Increase HR Increase BP

Genitourinary system VI.

Oliguria

Nursing Management

Review fluid and diet restrictions. Measure and record intake and output. Instruct patient to schedule follow-up evaluations of blood pressure, urinalysis for protein, and BUN and creatinine studies to determine if disease has worsened. Instruct patient to notify physician if infection or symptoms of renal failure occur: fatigue, nausea, vomiting, diminishing urinary output. Refer to home care nurse as indicated for assessment and detection of early symptoms and follow-up evaluations. Provide low salt, low sodium, low potassium and high protein diet.

The goal of treatment is to stop the ongoing inflammation and lessen the degree of scarring that ensues. Depending on the diagnosis, there are different treatment strategies. Often the treatment warrants a regimen of immunosuppressive drugs to limit the immune systems activity. This decreases the degree of inflammation and subsequent irreversible scarring.
BLOOD CHEMISTRY REPORT December 28, 2009
PARAMETER NORMAL VALUES ACTUAL VALUES ANALYSIS

BUN/ Urea

1.7-8.3 Mmol/L

10.10

Increased BUN levels suggest impaired kidney function. This may be due to acute or chronic kidney

disease, damage, or failure. URINALYSIS REPORT PARAMETER Color Transparency Reaction Specific Gravity Sugar Protein Squamous Epithelial Cells NORMAL VALUES Yellow Amber Clear to slightly turbid 4.5-8 1.0051.030 Negative Negative Few ACTUAL VALUES Light yellow Slightly turbid 6.0 1.010 trace +2 Few ANALYSIS normal

Strep A-beta Infection with Streptococcus pyogenes, a beta-hemolytic bacterium that belongs to Lancefield serogroup A, also known as the group A streptococci (GAS), causes a wide variety of diseases in humans. A ubiquitous organism, S pyogenes is the most common bacterial cause of acute pharyngitis, accounting for 15-30% of cases in children and 5-10% of cases in adults.[1] During the winter and spring in temperate climates, up to 20% of asymptomatic schoolaged children may be group A streptococcus carriers. (See Pathophysiology, Etiology, and Epidemiology.)[2, 3] An understanding of the diverse nature of infectious disease complications attributable to this organism is an important cornerstone of pediatric medicine. In addition to infections of the upper respiratory tract and the skin, S pyogenes can cause a wide variety of invasive systemic infections. Along with Staphylococcus aureus, group A streptococcus is one of the most common pathogens responsible for cellulitis . Infection with this pathogen is also causally linked to 2 potentially serious nonsuppurative complications: acute rheumatic fever (ARF) and acute glomerulonephritis. In addition, infection with S pyogenes has reemerged as an important cause of toxic shock syndrome (TSS) and of life-threatening skin and soft-tissue infections, especially necrotizingfasciitis

normal normal normal Indicative of glucosuria Indicative of proteinuria Indicative of nephrotic syndrome Hematuria, indicative of possible glomerular damage Indicative of bacterial infection Normal Normal

Red Blood Cells

Few

2-7

Pus Cells Mucus Bacteria

Few Few Few

1-3 Few Few

LABORATORY EXAMINATIONS HEMATOLOGY REPORT December 24, 2009

PARAMETER NORMAL VALUES ACTUAL VALUES ANALYSIS

Segmenters

0.550.65

0.86

Lymphocytes

0.250.35

0.14

Increased; indicate high glucose level in the blood Increased; indicates infection