| Sample Case Report |
Case Report on Patient
Anna Baxter Introduction to the Patient Anna Baxter an eleven year old girl, first came into her family doctor, concerned about a blister on her left foot which had become redder, more painful, and began to weep fluid. Initially the thought was that it was caused by her roller skates that she had received a week prior to the development of the blister. She was also slightly ill, with a mild sore throat. About a week later, Anna’s symptoms progressed, she became tired, had headaches, and vomited, although she had no fever. Anna had only voided twice in two days, and her urine was dark and smokey, her face became puffy and she gained nine pounds. Test Results and Explanations Her blood urea nitrogen (BUN) measured at 69 mg/dl, and she was hospitalized. The first apparent concern was that her urine was an abnormal color and her BUN level was elevated. The normal level for a person her age is about 5-18 mg/dl. The dark and smokey urine could suggest that red blood cells (RBCs) oxidized to methemoglobin (Fischbach, 2000, p.199). The methemoglobin is a transformation product of oxygen and hemoglobin (red blood cells) as a result of the oxidation of normal iron II and III ions (Spraycar, 1995). This smokey color of urine could also be associated with blood in the urine, if not related to the pH, a urinary tract infection, a kidney infection or disease, and more generally hemoglobin. The type of tests that are useful in this type of symptom are a urine test (urinalysis) to test red blood cells or hematuria. If hematuria is found in the urine by the use of the dipstick method, it suggests that there are disorders associated with the renal (kidney) or the genital organs (Fischbach, 2000, p. 202). The three glass test which shows where in the stream of urine is the problem, if the dark color shows up towards the beginning that means that the problem is lower in the body, and if the dark color shows up towards the end that means that the problem is higher in the body (Tierney, 2002, p. 919). The BUN
level is a metabolic by-product in the liver from the breakdown of
blood, muscle and protein (see figures 1-2). Abnormal elevation of
the blood urea nitrogen can indicate several things: renal disease,
bleeding internally (gastrointestinal bleeding), or severe dehydration.
The liver, which controls metabolism, digestion and helps to eliminate
substances from the body is an important factor in the BUN levels,
either showing a high or low value. The blood is a circulating “tissue”
composed of a fluid portion (plasma) with suspended formed elements
of red blood cells, white blood cells, and platelets (see figure 3-10).
Blood is the means
by which oxygen and nutrients are transported to tissues. Gastrointestinal
bleeding describes any bleeding that may occur along the GI tract
(Spraycar, 1995). When Anna
was admitted to Holmes General Hospital, her vital signs were blood
pressure of 140/100 mm/Hg, temperature was 99 degrees Fahrenheit,
her pulse was 74 beats/min, and her respiration's were 16/min. When
she was physically examined, there was no rash on her skin, her head,
eyes, ears, nose, and throat were normal, chest was clear, her abdomen
showed that her liver and spleen were not palpable, no tenderness,
there was a tender 2 cm ulcer (see figure 11) on her left medial instep
with a dry yellow crusty surface surrounded by a red rim, and normal
cranial nerves and deep tendon reflexes. The serum creatinine level helps to determine kidney function (see figure 12). Creatinine is a protein produced by muscle and released into the blood. The amount produced is relatively stable in a given person. The creatinine level in the serum is therefore determined by the rate it is being removed, with is roughly a measure of the kidney function. If kidney function falls, the creatinine level will rise. Normal is about 0.5-1.0 for an average child. Serum creatinine only reflects renal function in a steady state. The rate of how fast the level rises depends on creatinine production, which is related to how much muscle one has. A child may need dialysis when the creatinine reaches 3.0-7.0. The anti-streptolysin O titer (ASO), is used to detect antibodies to enzymes produced by organisms. Group A B-hemolytic streptococci (are associated with streptococcal infections or illness) produce several enzymes including streptolysin O. The ASO test is a serologic detection of streptococcal antibodies which helps to establish prior infection but are not of any value for diagnosing a cure streptococcal infections. Acute infections should be diagnosed by direct streptococcal cultures or the presence of streptococcal antigens (Fischbach, 2000, p.587). With increased ASO the chance of the illness to be Acute Poststreptococcal Glomerulonephritis is 70% (Tierney, 2002). The erythrocyte sedimentation rate (ESR+), should not be used to screen patients for disease, but rather the sedimentation rate is an indication that a disease process is ongoing and must be investigated. The ESR is the rate at which erythrocytes settle out of the blood in one hour. This test is based on the fact that inflammatory and necrotic (the death of one or more cells, or tissue, or organs) processes cause an alteration in blood proteins, which causes an a change among the red blood cells. This makes the red blood cells heavier and more likely to fall rapidly when placed in a special vertical test tube. The faster the settling of the cells, the higher the ESR (Fischbach, 2000, p. 89). In looking at her urinalysis, the color was smokey brown, there were many red cells and red cell castes, few leucocyte casts, her protein was at 2+, her specific gravity was 1.030, and the pH was 5.0. The pH of 5.0 shows that her urine is more acidic, (neutral is 7.0). Urine specific gravity is a measurement of the kidney’s ability to concentrate urine (see figure 13). Urine specific gravity for a normal concentrated urine should be 1.025-1.030+. The test compares the density of urine against the density of distilled water, water has a density of 1.000. Urine is made up of minerals, slats, and compounds dissolved in water, and the specific gravity is a measure of the density of the dissolved chemicals in a specimen of the urine solution. The range on the urine specific gravity is due to how hydrated a person is and also varies with urine volume and the amount of solids that are excreted under standardized conditions. When fluid intake is restricted or increased, the specific gravity measures the concentrating and diluting functions of the kidney. Loss of these functions is an indication of renal dysfunction (Fischbach, 2000, p.191). Background on Kidney Function The most common problems in acute renal failure (nephrosis) are positive sodium and water balance causing weight gain and edema. Kidney pain is usually uncommon. Although serum creatinine and urea nitrogen rise at a steady pace, their ratio should remain at 10:1 (creatinine:BUN). If the renal function is stable, the several possibilities that exist can be further investigated with urinalysis and a 24-hour urine collection. The 24-hour urine collection, which is a more precise estimate of kidney function than the serum creatinine since it does not depend on the amount of muscle one had, should show the excretion of urea nitrogen. This is useful because it will be less than the nitrogen intake. If this is not the case, the extra nitrogen must have come from gastrointestinal bleeding (Drazen, 2000, p. 569). The nephron is the functional unit of the kidney (see figure 14-15), responsible for the actual purification and filtration of the blood. About one million nephrons are in the cortex of each kidney, and each one consists of a renal corpuscle and a renal tubule which carry out the functions of the nephron. The renal tubule consists of the convoluted tubule and the loop of Henle. The blood goes in through the afferent arteriole and goes out though the efferent arteriole. The afferent arteriole is larger than the efferent, and this is due to the involvement of increased pressure. With the high pressure and the small amount of leaking that occurs, large proteins and cells do not get out, but the fluid is forced out. Fluid is forced out around the glomerulus, and then goes into the proximal tubules. The water can then be reabsorbed depending on hormones present in the body. The nephron
is part of the homeostatic mechanism of your body. This system helps
regulate the amount of water, salts, glucose, urea and other minerals
in your body. The nephron is a filtration system located in your kidney
that is responsible for the reabsorption of water, salts. This is
where glucose eventually is absorbed in your body. The glomerulus
is the main filter of the nephron and is located within the Bowman's
capsule (see figure 16). The glomerulus resembles a twisted mass of
tiny tubes through which the blood passes. The glomerulus is semi
permeable, allowing water and soluble wastes to pass through and be
excreted out of the Bowman's capsule as urine. The filtered blood
passes out of the glomerulus into the efferent arteriole to be returned
through the medullary plexus to the intralobular vein. The kidneys play a critical role in overall health. Acting like a water filter that separates out harmful minerals and chemicals, the kidneys process about 200 quarts of blood in an adult every day to produce about 1 to 2 quarts of urine, which is made up of waste products and extra water. Urine leaves the kidneys (almost all people are born with two) through tubes called ureters, which empty into the bladder. Without the kidneys, waste products would build up in the blood and damage the body. The filtration process occurs in microscopic units inside the kidneys called nephrons; each kidney has about a million nephrons. As they remove waste products and extra water, the nephrons return chemicals the body needs (such as sodium, phosphorus, and potassium) to the blood. Each chemical is vital to overall health and must be in proper balance. Too much or too little can be harmful. The kidneys also produce three important hormones: erythropoietin, which stimulates the bone marrow to make red blood cells; renin, which helps regulate blood pressure; and the active form of vitamin D, which helps control the calcium balance in the body and maintain healthy bones. When something goes wrong with the hormones or filtering process, it could indicate a kidney disease. Anna's Kidneys and More Background on Blood Pressure and Immune Function In Anna’s body, her kidney has antibodies (see figure 17) attaching themselves to streptococcus, and they are large enough to get trapped in the kidney, which stops normal filtration of blood and protein. They are not big enough to be eaten by macrophages but are big enough to be trapped. Usually what is supposed to happen is that antibodies breakdown bacteria and anything that is foreign. Macrophages come in and recognize antibodies and eat them and get rid of the bacteria. Complements make holes triggered by antibody-antigen complexes. The complements make holes and pores in the bacteria cell and the cell begins to leak and die. The complements will begin to lay down on the basement membrane of the kidney and start eating though tissue and the membranes. This is a problem and should not be occurring. Inflammation in the kidney, where the nephrons are inflamed, is called nephrosis. Poststreptococcal infection could lead to heart failure when the kidney shuts down. High blood pressure is a very common feature of IgA nephropathy. IgA stands for immunoglobin A which is one class of structurally related proteins consisting of two pairs of polypeptide chains, the chains can be of light molecular weights or heavy. IgA is a type of structure based upon the amount of protein present in the normal human serum, for IgA there is 10-15% protein. Antibodies are Ig’s. IgA nephropathy often is present as episodic gross hematuria following upper respiratory tract and other infections or exercise, as seen in children (Drazen, 2000, p.590). It often appears suddenly and for many is the means by which their IgAN disease is first detected. High blood pressure is defined by medical professionals as being several readings of blood pressure using a arm cuff showing pressure of 140 (systolic) / 90 (diastolic) mmHg or above. Since there is considerable variation of blood pressure in any individual both over daily and longer cycles it is necessary to confirm several readings over a period of days to confirm high blood pressure (Fauci, et al. 1998, p.203). High blood pressure itself is a potentially serious disorder and can result in a number of complicating conditions. When a person's kidneys begin to lose some of their filtering function the body's regulatory system notices this fact and signals the circulatory system to flush more blood through the kidneys by causing blood vessels throughout the body to constrict increasing blood pressure and flow rate. In a normal healthy person with lots of excess kidney capacity this blood pressure strategy of the human body helps to deal with short term chemical imbalances. But when the chemical imbalances are not short term, such as in those with kidney disease, the high blood pressure will be sustained perhaps forever. This higher pressure can and often does damage the sensitive filtering structures in the kidney. In the case of kidney disease patients who have little reserve kidney function this body response turns out to be the wrong way to help the body. Fortunately we can monitor blood pressure and intervene with appropriate treatment to reduce blood pressure. In time, the uncontrolled high blood pressure will surely cause further damage to the kidney, producing a vicious cycle (Fauci, et al. 1998, p.1384 & 1558). One of the first signs is edema of swelling of the feet, legs, hands, or a puffy face. This is caused by retention of fluids in those parts of the body where reduced blood flow results in a build up of fluids. Generally the farther from the heart the lower the less the blood flow and the greater the edema but this is modified by individual characteristics. Headaches and tintinitus (ringing or a persistent noise) sometimes accompany high blood pressure. More serious complications include strokes, heart problems, and arterial disease (Fauci, et al. 1998, p.210). Immune complexes (see figure 16) are clusters of interlocking antigens and antibodies. Under normal conditions immune complexes are rapidly removed from the bloodstream by macrophages in the spleen and Kupffer cells in the liver. In some circumstances, however, immune complexes continue to circulate. Eventually they become trapped in the tissues of the kidneys, lung, skin, joints, or blood vessels. Just where they end up probably depends on the nature of the antigen, the class of antibody-IgG, for instance, instead of IgM-and the size of the complex. There they set off reactions that lead to inflammation and tissue damage. As a side note, immune complexes work their damage in many diseases. Sometimes, as is the case with malaria and viral hepatitis, they reflect persistent low-grade infections. Sometimes they arise in response to environmental antigens such as the moldy hay that causes the disease known as farmer's lung. Frequently, immune complexes develop in autoimmune disease, where the continuous production of auto antibodies overloads the immune complex removal system. Post-streptococcal glomerulonephritis (PSGN) is an immune complex disease in its acute phase and its characterized by the formation of antibodies against streptococcal antigens and the localization of immune complexes with complement in the kidney. PSGN occurs only after infection with certain nephritogenic trains of group A B-hemolytic streptococci. Most cases of PSGN are diagnosed by detecting hematuria and hypertension, depending on the length of time which is longer for a streptococcal skin infection. More than 85% of patients with streptococcal skin infections have positive antibody titers. The serum total hemolytic complement levels and C3 levels are decreased in more than 90% of patients during the time of the acute glomerulonephritis (Drazen, 2000, p.590). In most patients PSGN is a self-limited disease with recovery of renal function and disappearance of hypertension in several weeks. Hematuria may resolve more slowly over months. Therapy may be recommended and directed at controlling the hypertension and fluid retention. Type III hypersensitivity develops when immune complexes are formed in large quantities and cannot be cleared adequately by the system, leading to serum-sikness type reactions. Antibodies of the IgG or IgM isotype can form complexes with the allergen, be deposited in tissues, and activate the complement cascade. With similar concentrations of both allergen and antibody, the Arthur reaction, a localized cutaneous injection of antigen was shown to initiate within hours, acute local inflammation. With this inflammation, it was ultimately shown to require immune complexes. The deposition of immune complexes in local tissue with resultant inflammation is common is rheumatic diseases. Rheumatic diseases are those characterized by various conditions with pain or other symptoms of articular origin or related to other elements of the musculoskeletal system (Tierney, 2002, p.807). When large amounts of antigen enter the circulation, a serum sickness reaction may result. As antibody is produced, antigen-antibody complexes are formed. Such complexes may localize to small vessels, resulting in local inflammation. Deposition of immune complexes in the glomerular basement membrane can lead to glomerulitis. Diseases resulting from immune complex formation can be placed broadly into three groups: first, the combined effects of a low-grade persistent infection (such as occur with -haemolytic Streptococcus, or with a parasite as in a viral hepatitis), together with a weak antibody response, leads to chronic immune complex formation with the eventual deposition of complexes in the tissues. Second, the immune complex disease is a frequent complication of autoimmune disease where the continued produced of antibody to a self-antigen leads to prolonged immune complex formation. The mononuclear phagocyte, erythrocyte, and complement systems (which are responsible for the removal of complexes) become overloaded and the complexes are deposited in the tissues. Third, immune complexes may be formed at body surfaces, seen in the lungs following repeated inhalation of antigenic material from moulds, plants or animals. This is known to occur after repeated exposure to the antigen (Tierney, 2002, p.814). Children with blood and protein in their urine or who have kidney insufficiency may require a kidney biopsy. The procedure of a kidney biopsy is used to further identify problems when your kidney function is decreasing for unknown reasons, you have blood in your urine, or to much protein in your urine. A biopsy is done, with the doctor taking a sample of your kidney to test it in the lab. Usually a biopsy is reserved for patients that prerenal and postrenal failure have been excluded and the cause of intrinsic renal azotemia is unclear. Azotemia is the nitrogen retention resulting from something other than primary renal disease (Fauci, et al. 1998, p.1510). As seen in Anna’s biopsy results (see figure 18-19), by method of light microscopy looking at the glomerulus, the glomerular capillary loops are not defined and the glomerulus itself is unremarkable. The capillaries that exist are not thin or arranged throughout the kidney. The endothelial and mesangial cells are not abundent as there may be in a normal looking kidney. The surrounding tubules are globed together without shape or formation, there seems to be only slight segmental prominence. There is no siginificant interstitial infiltratinon by the leukocytes. The glomerulus seen with the immunofluorescence micrograph, shows that Anna’s glomerular basement membrane of her kidney is abnormal and no significant expansion is taking place. The capillary loops of the glomerulus are thick and appear flattened. No capillary wall or immune complex-type deposits are present, in Anna’s kidney either. The immunofluorescence microscopy revealed no staining of glomeruli with specifics for IgG or C3 (Jennette, 1995). Differential Diagnosis of Anna Baxter Upon first
reading Anna Baxter’s case, our possible diagnoses that were
considered were thyroid disease, diabetes, liver disease, kidney stones,
(sickle cell) anemia, and a urinary tract infection. The reason that the diagnosis of hypothyroidism was not considered to be right for Anna, was because she did not have a common symptom that usually characterizes hypothyroidism: dry, cold, pale skin. There was no note of hair loss or an absence of sweating, no brittle thick nails, and she did not become puffy on her hands. To rule this diagnosis out completely the * may be low or low normal, and the serum TSH (Thyroid Stimulating Hormone) is usually increased. Free thyroxine immunoassay * is a direct measurement of the serum concentration of free unbound thyroxine *. * is only about 0.025% of the serum concentration total, and is only the metabolically active fraction from the total of * which freely enters cells to produce its effects. The serum thyroid test of thyroid-stimulating hormone TSH immunoassay, points in the direction of hypothyroidism. TSH is secreted by the pituitary and stimulates several steps of thyroid hormone production. Increased serum cholesterol, liver enzymes, and anemia are apparent (Tierney, 2002, p.1135-1147). Kidney stones (nephrolithiasis) can be caused by substances in the urine, uric acid and calcium in particular, which can crystallize within the kidney and form rocklike particluld called stones. Some stones stay in the kidney and produce no symptoms, and others break loose and travel down the urinary tract. The stones are in many different shapes, sizes, and textures. Symptoms of kidney stones, are nausea, vomiting, fever, elevated blood pressure. The other common symptom is having blood in the urine (hematuria), therefore a color of dark and of being smokey could be present. The blood does not have to exist in the urine, by seeing blood with the naked eye, but it could be visible with a microscopic examination. The diagnosis of kidney stones was eliminated because Anna did not have discomfort when sitting or lying still. She did not urinate frequently or have a burning sensation during urination. To fully diagnose kidney stones tests could be done through imaging to confirm if a stone was causing the symptoms, X-ray or ultrasound can help locate the stone and determine its size and shape. Blood and urine analyses is used to identify the presence of infection (Urology Channel, 2001). A urinary
tract infection was also a first diagnosis, it is an acute infection
of the urinary tract. Infections at various sites along the tracts
may occur together or independently. Urinary tract infections exist
when pathogenic microorganisms are detected in the urine, urethra,
bladder, or kidney. Under normal functioning circumstances, bacteria
in the bladder are rapidly cleared. They are cleared through the flushing
and dilution effects of voiding, and also because of antibacterial
properties of urine and the bladder mucosa. This was thought to be
a possible diagnosis because Anna, was not voiding as much as she
usually did, maybe it was painful. She had a low-grade fever, she
experienced nausea and vomiting. The final diagnosis is that the red blister, which was caused by her roller skates, was the start of Anna Baxter’s problem. The progression of her blister to produce weeping fluid, was a site of infection for streptococcus. At this point streptococcus could be indicated by her elevated anti-streptolysin O titer level. Anna then developed into acute poststreptococcal, known as glomerulonephritis. Acute renal failure or nephrosis was the next stage of her poststreptococcal. Acute renal failure in her case was suggested by her elevated specific gravity in her urine. The part of her kidney that was failing, was the glomeruli, which are responsible for the filtering protein and blood. Anna’s blood urea nitrogen and creatinine levels could clearly indicate the diagnosis, even though there were many things along the line that played a factor in producing her symptoms and illness. Glomerulonephritis, acute poststreptococcal, is a relatively common bacterial inflammation of the renal glomeruli. It follows a streptococcal infection of the respiratory tract, but in Anna’s case, it was a skin infection. The main cause of acute poststreptococcal glomerulonephritis (APSGN) is from the collection and trapping of antigen-antibody in the glomerular capillary membranes. The antibody that was being produced was an aid in response to the immunological mechanism of streptococcus. With the collection of antigen-antibody, it causes inflammatory damage and inhibits the glomerular function (Goldberg et al., 2000). Treatment The treatment we recommend for Anna Baxter for her acute poststreptococcal glomerulonephritris, is to have a diet high in calories low in protein, sodium, potassium, and fluids. Rest during its acute phase, and as symptoms decrease resume normal activity, providing good nutrition, good hygiene, and preventing contact with infected persons will help any secondary infection. A follow up exam, to detect if any chronic renal failure. The use
of penicillin or moxicillin, or another antibiotic to treat the streptococcus.
Antibiotics will kill antibodies, which are toxic to bacteria(??).
Penicillin inhibits the cell wall biosynthesis, so that the cell can
not become a bacteria in the body. Antigen-antibody complexes should
be treated with dialysis, which will help with the shutting down of
the kidneys, and the buildup of toxic substances, without filtering.
With the use of dialysis, the hope is that macrophages will come in
and clean the antibodies up. If that is not successful, a kidney transplant
may be needed, especially is the infection is very bad (Abbas et al.,
1994). References Abbas, Abulk, Andrew H. Lichtman, and Jordan S. Pober. Cellular and Molecular Immunology. 2nd ed. London: W.B. Saunders Co. 1994. DeGowin, Richard, and Donald D. Brown. Diagnostic Examination. 17th ed. New York: McGraw Hill Co. 2000. Drazen, Jeffrey, Gordon N. Gill, Robert C. Griggs, Juha P. Kokko, Gerald L. Mandell, Don W. Powell, Andrew I. Schafer. Cecil Textbook of Medicine. 21st ed. New York: W.B. Saunders Company. 2000. Fauci, Anthony S., Eugene Braunwald, Kurt J. Isselbacher, Jean D. Wilson, Joseph B. Martin, Dennis L. Kasper, Stephen L. Hauser, Dan L. Longo (eds.). Harrison’s Principles of Internal Medicine. 14th ed. New York: McGraw Hill Co. 1998. Fischbach,
Frances. A Manual of Labratory & Diagnostic Tests. 6th
ed. New York: Lippincott, 2000. Jennette, Charles. J. Renal Biopsy Case Reports. Renalnet. Gamewood Data System, Inc. 31 Mar. 1995. http://ns.gamewood.net/pathcase/395/395-case.html Reddy, Vinay N. Dr. Reddy’s Pediatric Office on the Web. 16 Aug. 1996 http://www.drreddy.com. Spraycar, Marjory. PDR Medical Dictionary. 1st ed. Baltimore: William Wood and Co, 1995. Starr, Cecie, and Beverly McMillan. Human Biology. 4th ed. United States: Wadsworth Group, 2001. Tierney, Lawrence M., Stephen J. McPhee, Maxine A. Papadakis (eds.). Medical Diagnosis and Treatment. 41st ed. New York: McGraw Hill Co. 2002. Urology Channel. Kidney Stones. http://urologychannel.com/kidneystones/index.shtml 2001. |
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