SGD Gross Anatomy Renal Pediatrics

Viola, Luis Alfredo B. E2

1. Describe the location and position of the kidneys. The kidneys are a pair of organs found along the posterior muscular wall of the abdominal cavity. The left kidney is located slightly more superior than the right kidney due to the larger size of the liver on the right side of the body. Unlike the other abdominal organs, the kidneys lie behind the peritoneum that lines the abdominal cavity and are thus considered to be retroperitoneal organs. The ribs and muscles of the back protect the kidneys from external damage. Adipose tissue known as perirenal fat surrounds the kidneys and acts as protective padding. The kidneys are located in the abdominal cavity, near the middle of the back, just below the rib cage. There is one kidney located on either side of the spine. To find your kidneys, put your hands on your hips, then slide your hands up until you can feel your ribs. If you put your thumbs on your back, your kidneys are directly between that area and the area below your ribs. The right kidney sits just below the diaphragm behind the liver, while the left is below the diaphragm, behind the spleen. Because the abdominal cavity is not symmetrical, the right kidney is usually slightly lower than the left. Both kidneys are about 4 inches long and about 2 1/2 inches wide. This size allows them to be small enough sit comfortably within the abdominal cavity, but large enough to effectively filter waste from your body. 2. Describe the gross external features of the kidney. a. Weight: The average weight of an adult human kidney is approximately one-quarter pound. b. Dimensions: Each kidney is approximately 4 inches long, 2.5 inches wide, and 1.5 inches thick. c. Surfaces:

d. Boarders: The medial border is indented at the hilus, where blood vessels enter and leave, and there the ureter emerges. Each kidney is composed of a paler cortex and a darker medulla. The kidneys lie obliquely along the vertebral column, abutting the psoas major muscles. e. Poles: The upper poles are normally oriented more medially and posteriorly than the lower poles. 3. Give the blood supply of the kidney. Trace the branching up to the afferent arteriole. The renal arteries normally arise off the side of the abdominal aorta, immediately below the superior mesenteric artery, and supply the kidneys with blood. Each is directed across the crus of the diaphragm, so as to form nearly a right angle with the aorta. The renal arteries carry a large portion of total blood flow to the kidneys. Up to a third of total cardiac output can pass through the renal arteries to be filtered by the kidneys. The arterial supply of the kidneys is variable and there may be one or more renal arteries supplying each kidney. It is located above the renal vein. Supernumerary renal arteries (two or more arteries to a single kidney) are the most common renovascular anomaly, occurrence ranging from 25% to 40% of kidneys. Afferent arteriole to the glomerulus into the Bowman's capsule into the proximal convoluted tubule. Most of its companion water molecules would be reabsorbed into the blood in the PCT. Water molecules would then go through the descending loop of Henle to the ascending loop of Henle and into the distal convoluted tubule. What is not absorbed in the distal convoluted tuble the water moves into the papilarry duct that drains into the minor calyx. 4. Trace the venous drainage. (from within outward). The renal veins are veins that drain the kidney. They connect the kidney to the inferior vena cava. They carry the blood purified by the kidney. It is usually singular to each kidney, except in the condition "multiple renal veins". It also divides into 2 divisions upon entering the kidney: the anterior branch which receives blood from the anterior portion of the kidney and, the posterior branch which receives blood from the posterior portion. 5. Describe the gross features as seen in coronal section. The renal pelvis is the point of convergence of two or three major calyces. Each renal papilla is surrounded by a branch of the renal pelvis called a calyx. The major function of the renal pelvis is to act as a funnel for urine flowing to the ureter. The renal pelvis is the location of several kinds of kidney cancer. Its mucous membrane is covered with transitional epithelium, and an underlying lamina propria of loose to dense connective tissue. 6. Trace the flow of urine from the kidneys to urethra. Blood flows to the kidney through the renal artery. Once in the kidney the blood flows through a series of smaller and smaller arteries until it gets to the glomerulus. The glomerulus filters blood and to be very simplistic creates a filtrate of the blood or

"urine". This urine then flows through a series of progressively bigger tubules and ducts until it gets to the renal pelvis. flows out of the bladder and into the urethra. The urethra connects the bladder to the outside of the body. As blood passes through the renal artery, it also passes through certain complexes that im not going to name. Those complexes are responsible for filtering out all un-needed components in blood. Those fluids flow down renal tubes at the mercy of diffusion. When it reaches the ureter, reabsorbtion takes place where its the body's last chance to make any changes. Once it passes the ureter, it collects in the bladder. All the blood that was passed through the kidney gets returned to the heart via the renal vein. 7. Name the specific structure in the kidney affected in glomerulonephritis. Describe briefly. Glomerulonephritis is the name given to a range of conditions that can affect the kidney, specifically the glomeruli of the kidney. The glomeruli become damaged, commonly because of a problem with the body's immune system. Many people with glomerulonephritis may not notice any symptoms initially. However, salt and excess fluid can build up in the body if the glomeruli and kidneys are not working normally. This can lead to complications such as high blood pressure and, in some cases, chronic kidney disease, which may lead to end-stage kidney failure. 8. Enumerate the clinical manifestations of an acute glomerulonephritis. -Pink or cola-colored urine from red blood cells in your urine (hematuria) -Foamy urine due to excess protein (proteinuria) -High blood pressure (hypertension) -Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen -Fatigue from anemia or kidney failure 9. Describe the anatomical correlations of each manifestation. Primary - glomerulonephritis develops on its own and is not related to another preexisting disease or condition in the body. Secondary - glomerulonephritis develops because of another pre-existing disease or condition in the body. Examples of diseases that can lead to glomerulonephritis in some people are systemic lupus erythematosus (SLE) and polyarteritis nodosa. See separate leaflet called Systemic lupus erythematosus for more details. When a sample of tissue is taken from a kidney affected by glomerulonephritis (when a kidney biopsy is taken), the glomerulonephritis can be classified according to the changes that can be seen when the tissue sample is examined under a microscope. For example, glomerulonephritis can be: Focal and segmental glomerulosclerosis - the glomeruli are sclerosed or scarred. Focal means that only some of the glomeruli are affected and segmental means that only parts of a glomerulus (and not the whole glomerulus) may be affected. IgA glomerulonephritis - IgA is one of the antibodies produced by the immune system to fight infection. In IgA glomerulonephritis, IgA becomes deposited (settles) in the kidneys leading to inflammation, scarring and damage.

IgM glomerulonephritis - the glomeruli become damaged by IgM antibody settling in them. Membranoproliferative glomerulonephritis - a glomerulus is made up of a membrane (the tiny blood vessels that filter the blood) and the mesangium which provides support to the glomerulus structure. In membranoproliferative glomerulonephritis, the membrane and the mesangium are both affected and damaged. Membranous glomerulonephritis - just the membrane of the glomerulus is damaged and the mesangium is not affected in this type of glomerulonephritis. Minimal change nephropathy - if a sample of kidney tissue (a biopsy) is examined under the microscope in this type of glomerulonephritis, it looks essentially normal - there is minimal change - but symptoms of glomerulonephritis can still be present. This is a common type of glomerulonephritis in children. 10. State the age group commonly affected by acute glomerolunephritis. This problem is most common in people between the ages of 15 and 35 or after age 55. It is not contagious and it is more common in men and Caucasians.

SGD Biochemistry Renal Pediatrics

Viola, Luis Alfredo B. E2
1. What are the different etiologic agents in the development of acute glomerulonephritits. A variety of conditions can cause glomerulonephritis, ranging from infections that affect your kidneys to diseases that affect your whole body, including your kidneys. Sometimes the cause is unknown. Here are some examples of conditions that can lead to inflammation of the kidneys' glomeruli: a. Infections a.1. Post-streptococcal glomerulonephritis. Glomerulonephritis may develop a week or two after recovery from a strep throat infection or, rarely, a skin infection (impetigo). An overproduction of antibodies stimulated by the infection may eventually settle in the glomeruli, causing inflammation. Symptoms usually include swelling, reduced urine output and blood in the urine. Children are more likely to develop post-streptococcal glomerulonephritis than are adults, and they're also more likely to recover quickly. a.2. Bacterial endocarditis. Bacteria can occasionally spread through your bloodstream and lodge in your heart, causing an infection of one or more of your heart valves. Those at greatest risk are people with a heart defect, such as a damaged or artificial heart valve. Bacterial endocarditis is associated with glomerular disease, but the exact connection between the two is unclear. a.3. Viral infections. Among the viral infections that may trigger glomerulonephritis are the human immunodeficiency virus (HIV), which causes AIDS, and the hepatitis B and hepatitis C viruses. b. Immune diseases b.1. Lupus. A chronic inflammatory disease, lupus can affect many parts of your body, including your skin, joints, kidneys, blood cells, heart and lungs. b.2. Goodpasture's syndrome. A rare immunological lung disorder that may mimic pneumonia, Goodpasture's syndrome causes bleeding (hemorrhage) into your lungs as well as glomerulonephritis. b.3. IgA nephropathy. Characterized by recurrent episodes of blood in the urine, this primary glomerular disease results from deposits of immunoglobulin A (IgA) in the glomeruli. IgA nephropathy can progress for years with no noticeable symptoms. The disorder seems to be more common in men than in women.

c. Vasculitis c.1. Polyarteritis. This form of vasculitis affects small and medium blood vessels in many parts of your body, such as your heart, kidneys and intestines. c.2. Wegener's granulomatosis. This form of vasculitis affects small and medium blood vessels in your lungs, upper airways and kidneys. d. Conditions that are likely to cause scarring of the glomeruli d.1. High blood pressure. Damage to your kidneys and their ability to perform their normal functions can occur as a result of high blood pressure. Glomerulonephritis can also cause high blood pressure because it reduces kidney function. d.2. Diabetic kidney disease. Diabetic kidney disease (diabetic nephropathy) can affect anyone with diabetes. Diabetic nephropathy usually takes years to develop. Good control of blood sugar levels and blood pressure may prevent or slow kidney damage. d.3. Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli, this condition may result from another disease or occur for no known reason. d.4. Chronic glomerulonephritis sometimes develops after a bout of acute glomerulonephritis. In some people there's no history of kidney disease, so the first indication of chronic glomerulonephritis is chronic kidney failure. Infrequently, chronic glomerulonephritis runs in families. One inherited form, Alport syndrome, may also involve hearing or vision impairment. 2. Discuss the pathophysiology of Acute Glomerulonephritis. Glomerular lesions in acute GN are the result of glomerular deposition or in situ formation of immune complexes. On gross appearance, the kidneys may be enlarged up to 50%. Histopathologic changes include swelling of the glomerular tufts and infiltration with polymorphonucleocytes. Immunofluorescence reveals deposition of immunoglobulins and complement. Except in PSGN, the exact triggers for the formation of the immune complexes are unclear. In PSGN, 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. Structural and functional changes, Acute GN involves both structural changes and functional changes. Structurally, cellular proliferation leads to an increase in the number of cells in the glomerular tuft because of the proliferation of endothelial, mesangial, and epithelial cells. The proliferation may be endocapillary (ie, within the confines of the glomerular capillary tufts) or extracapillary (ie, in the Bowman space involving the epithelial cells). In extracapillary proliferation, proliferation of parietal epithelial cells leads to the formation of crescents, a feature characteristic of certain forms of rapidly progressive GN. Leukocyte proliferation is indicated by the presence of neutrophils and

monocytes within the glomerular capillary lumen and often accompanies cellular proliferation. Glomerular basement membrane thickening appears as thickening of capillary walls on light microscopy. On electron microscopy, this may appear as the result of thickening of basement membrane proper (eg, diabetes) or deposition of electron-dense material, either on the endothelial or epithelial side of the basement membrane. Electron-dense deposits can be subendothelial, subepithelial, intramembranous, or mesangial, and they correspond to an area of immune complex deposition. Hyalinization or sclerosis indicates irreversible injury. These structural changes can be focal, diffuse or segmental, or global. Functional changes include proteinuria, hematuria, reduction in GFR (ie, oligoanuria), and active urine sediment with RBCs and RBC casts. The decreased GFR and avid distal nephron salt and water retention result in expansion of intravascular volume, edema, and, frequently, systemic hypertension. Poststreptococcal glomerulonephritis Streptococcal M-protein was previously believed to be responsible for PSGN, but the studies on which this belief was based have been discounted. Nephritis-associated streptococcal cationic protease and its zymogen precursor (nephritis-associated plasmin receptor [NAPlr]) have been identified as a glyceraldehyde-3-phosphate dehydrogenase that functions as a plasmin(ogen) receptor. Immunofluorescence staining of the renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in earlyphase acute PSGN, and glomerular plasmin activity was almost identical to NAPlr deposition in renal biopsy tissues of acute PSGN patients. These data suggest that NAPlr may contribute to the pathogenesis of acute PSGN by maintaining plasmin activity. Antibody levels to NAPR are elevated in streptococcal infections (of group A, C, and G) associated with GN but are not elevated in streptococcal infections without GN, whereas anti-streptolysin-O titers are elevated in both circumstances. These antibodies to NAPR persist for years and perhaps are protective against further episodes of PSGN. In a study in adults, the 2 most frequently identified infectious agents were streptococci (27.9%) and staphylococci (24.4%). 3. Discuss the different types of hypersensitivity reaction? Explain and give example of each. Hypersensitivity refers to excessive, undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. Hypersensitivity reactions can be divided into four types: type I, type II, type III and type IV, based on the mechanisms involved and time taken for the reaction. Frequently, a particular clinical condition (disease) may involve more than one type of reaction.

TYPE I HYPERSENSITIVITY Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 - 12 hours). Immediate hypersensitivity is mediated by IgE. The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils. A biopsy of the reaction site demonstrates mainly mast cells and eosinophils. The mechanism of reaction involves preferential production of IgE, in response to certain antigens (allergens). IgE has very high affinity for its receptor on mast cells and basophils. A subsequent exposure to the same allergen cross links the cell-bound IgE and triggers the release of various pharmacologically active substances. Cross-linking of IgE Fc-receptor is important in mast cell triggering. Mast cell degranulation is preceded by increased Ca++ influx, which is a crucial process; ionophores which increase cytoplasmic Ca++ also promote degranulation, whereas, agents which deplete cytoplasmic Ca++ suppress degranulation. TYPE II HYPERSENSITIVITY Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples. The reaction time is minutes to hours. Type II hypersensitivity is primarily mediated by antibodies of the IgM or IgG classes and complement. Phagocytes and K cells may also play a role (ADCC). The lesion contains antibody, complement and neutrophils. Diagnostic tests include detection of circulating antibody against the tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence. The staining pattern is normally smooth and linear, such as that seen in Goodpasture's nephritis (renal and lung basement membrane) and pemphigus (skin intercellular protein, desmosome). Treatment involves anti-inflammatory and immunosuppressive agents. TYPE III HYPERSENSITIVITY Type III hypersensitivity is also known as immune complex hypersensitivity. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis),

lungs (e.g., aspergillosis), blood vessels (e.g., polyarteritis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms. The reaction may take 3 - 10 hours after exposure to the antigen (as in Arthus reaction). It is mediated by soluble immune complexes. They are mostly of the IgG class, although IgM may also be involved. The antigen may be exogenous (chronic bacterial, viral or parasitic infections), or endogenous (non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE). The antigen is soluble and not attached to the organ involved. Primary components are soluble immune complexes and complement (C3a, 4a and 5a). The damage is caused by platelets and neutrophils. The lesion contains primarily neutrophils and deposits of immune complexes and complement. Macrophages infiltrating in later stages may be involved in the healing process. The affinity of antibody and size of immune complexes are important in production of disease and determining the tissue involved. Diagnosis involves examination of tissue biopsies for deposits of Ig and complement by immunofluorescence. The immunofluorescent staining in type III hypersensitivity is granular (as opposed to linear in type II such as seen in Goodpasture's syndrome). The presence of immune complexes in serum and depletion in the level of complement are also diagnostic. Polyethylene glycol-mediated turbidity (nephelometry), binding of C1q and Raji cell test are utilized to detect immune complexes. Treatment includes anti-inflammatory agents. TYPE IV HYPERSENSITIVITY Type IV hypersensitivity is also known as cell mediated or delayed type hypersensitivity. The classical example of this hypersensitivity is tuberculin (Montoux) reaction which peaks 48 hours after the injection of antigen (PPD or old tuberculin). The lesion is characterized by induration and erythema. TYPE IV HYPERSENSITIVITY Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, histoplasmosis, toxoplasmosis, leishmaniasis, etc.) and granulomas due to infections and foreign antigens. Another form of delayed hypersensitivity is contact dermatitis (poison ivy), chemicals, heavy metals, etc.) in which the lesions are more papular. Type IV hypersensitivity can be classified into three categories depending on the time of onset and clinical and histological presentation. Mechanisms of damage in delayed hypersensitivity include T lymphocytes and monocytes and/or macrophages. Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes and macrophages, which cause the bulk of the damage. The delayed hypersensitivity lesions mainly contain monocytes and a few T cells. Major lymphokines involved in delayed hypersensitivity reaction include monocyte chemotactic factor, interleukin-2, interferon-gamma, TNF alpha/beta, etc.

4. Explain the following symptoms came about the in the patient. a. Proteinuria: is the medical term for excess protein in the urine. When healthy, the kidneys filter most protein out of the urine, but this process can be disrupted by injury to the kidneys filtering mechanism. As the filters of the kidneys, glomeruli can filter the blood and make urine. In normal condition, macro-molecules like proteins, cells such as red blood cells do not pass through the filter and are retained within the blood as they are essential for health. Due to immune disorder, there will be massive immune complexes deposited in the kidneys and lead to inflammation of the glomeruli. In this case, substances which are normal preserved in the circulation escape into the urine through the filtration mechanism. Consequently, protein and red blood cells appear in the urine. The amount of protein can be measured by collecting urine for a 24 hour period. b. Hypertension: can damage the kidneys and subsequently their normal functioning. Glomerulonephritis itself can cause hypertension because kidney function is undermined - the kidneys play a vital role in regulating our blood pressure. Isn order to treat the hypertension and halt or slow down kidney function decline, the doctor may prescribe diuretics, Angiotensin-converting enzyme (ACE) inhibitors, and Angiotensinconverting enzyme (ACE) inhibitors, which help to relax the blood vessels, reducing the workload of the heart. Hypertension can cause further kidney decline and other health problems and needs to be controlled. c. Hematuria: is the presence of red blood cells in the urine. If there are enough red cells, the urine can become bright red, pink or cola colored. Often, however, the urine appears completely normal because there is not enough blood to cause a color change. In this case, the condition is called "microscopic" hematuria. Glomerulonephritis is a family of illnesses that are characterized by inflammation of the glomeruli, the filtering units of the kidneys. Glomerulonephritis is a rare complication of certain viral and bacterial infections (including strep throat). It can also occur in people with certain autoimmune diseases, systemic lupus erythematosus (lupus or SLE) and vasculitis. Sometimes there is no identifiable cause. If glomerulonephritis is not severe, it may not cause any symptoms. If symptoms appear, they can include swelling, especially in the lower extremities, reduced urination, and high blood pressure. d. Edema: is a nephritic syndrome; therefore, it causes edema through an increase in hydrostatic pressure and fluid overload secondary to inflammatory damage. Examples of nephritic syndrome include: DPGN, IgA nephropathy, lupus nephritis, and MPGN. Hypoalbuminemia is the cause of edema in nephrotic syndrome (characterized by heavy proteinuriagreater than 3.5 g/day). Examples include: minimal change disease (MCD), membranous glomerulonephritis (MGN), focal segmental glomerulosclerosis (FSGS), lupus, amyloidosis, and diabetes.

5. What are the different diagnostic laboratories to request? Urinalysis and sediment examination are crucial in the evaluation of patients with acute nephritic syndrome. Look for protein, blood, red blood cells (RBCs), white blood cells (WBCs), dysmorphic RBCs, acanthocytes, cellular (ie, RBC, WBC) casts, granular casts, and oval fat bodies. In some instances, marked sterile pyuria is present. The presence of RBC casts is almost pathognomonic of glomerulonephritis (GN). Urine electrolyte, urine sodium, and fractional excretion of sodium (FENa) assays are needed to assess salt avidity. Other tests should include the following: - Complete blood count (CBC) - Blood urea nitrogen (BUN), serum creatinine, and serum electrolytes (especially serum potassium) - Erythrocyte sedimentation rate (ESR) - Complement levels (C3, C4, CH50) A CBC is performed. A decrease in the hematocrit may demonstrate a dilutional anemia. In the setting of an infectious etiology, pleocytosis may be evident. Electrolyte levels are measured (particularly the serum potassium), along with BUN and creatinine (to allow estimation of the glomerular filtration rate [GFR]). The BUN and creatinine levels will exhibit a degree of renal compromise. The ESR is usually increased. Differentiation of low and normal serum complement levels may allow the physician to narrow the differential diagnosis. Results are not readily available to the emergency physician but may be useful to the consultant. Low serum complement levels suggest the following systemic diseases: cryoglobulinemia, systemic lupus erythematosus (SLE), bacterial endocarditis, and shunt nephritis. Under the same conditions, renal diseases characteristic of membranoproliferative GN (MPGN) or poststreptococcal GN (PSGN) also may be considered. Normal serum complement levels suggest a visceral abscess, polyarteritis nodosa, Goodpasture syndrome, or Henoch-Schnlein purpura. In addition, normal complement levels suggest renal diseases such as immune complex disease, idiopathic rapidly progressive GN, and immunoglobulin G (IgG) or immunoglobulin A (IgA) nephropathy. Low C3 levels are found in almost all patients with acute poststreptococcal nephritis; C4 levels may be slightly low. Hypocomplementemia is noted in 73.9% of adult patients. Type III cryoglobulinemia may be present. If methicillin-resistant S aureus (MRSA) is the inciting agent, then hypocomplementemia is usually not present, but plasma immunoglobulins, especially IgA, are markedly elevated. The urine is dark. Its specific gravity is greater than 1020. RBCs and RBC casts are present. Proteinuria is observed. With the qualitative estimation of proteinuria, determination of high-molecular-weight (HMW) protein (eg, fractional excretion of IgG [FEIgG]) and low-molecular-weight (LMW) protein (eg, alpha-1-microglobulin), may help predict the clinical outcome and may help in guiding steroid and immunosuppressive therapy, especially in patients with primary glomerular diseases with nephrotic syndrome. The 24-hour urine protein excretion and creatinine clearance, though not

indicated in the emergency department (ED) setting, may be helpful to document the degree of renal dysfunction and proteinuria. With this test, it is important to remember that creatinine clearance is a steady-state measurement. Because of rapidly changing renal function, the creatinine clearance may not reveal the true picture; therefore, it is better to wait until renal function has stabilized before performing creatinine clearance. Blood culture is indicated in patients with fever, immunosuppression, intravenous (IV) drug use history, indwelling shunts, or catheters. Blood culture may indicate hypertriglyceridemia, decreased glomerular filtration rate, or anemia. Cultures of throat and skin lesions to rule out Streptococcus species may be obtained. 6. How will you manage this patient? Pharmacologic Therapy Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts. Antimicrobial therapy does not appear to prevent the development of GN, except if given within the first 36 hours. Antibiotic treatment of close contacts of the index case may help prevent development of PSGN. Other agents Loop diuretics may be required in patients who are edematous and hypertensive in order to remove excess fluid and to correct hypertension. Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present. Glucocorticoids and cytotoxic agents are of no value, except in severe cases of PSGN. Diet and Activity Sodium and fluid restriction should be advised for treatment of signs and symptoms of fluid retention (eg, edema, pulmonary edema). Protein restriction for patients with azotemia should be advised if there is no evidence of malnutrition. Bed rest is recommended until signs of glomerular inflammation and circulatory congestion subside. Prolonged inactivity is of no benefit in the patient recovery process.

Long-Term Monitoring Long-term studies on children with PSGN have revealed few chronic sequelae. Results of such studies are controversial because homogenous populations suitable for proper epidemiologic analysis have not been assembled. Long-term studies show higher mortality rates in elderly patients, particularly those on dialysis. Patients may be predisposed to crescent formation.