Joyce Anne Billedo Section1 D Case 1 1. What is the significance of the present condition?

APSGN is believed to be an immune-mediated disease, in which an immune complex containing a streptococcal antigen is deposited in the affected glomeruli. Immune complexes preformed by the combination of specific antibodies against streptococcal antigens, localize on the glomerular capillary wall and activate the complement system. The immunologic system may also be activated by streptococcal antigens that adhere to the glomerular structures and act as "planted antigens" or by alterations in endogenous antigens. The activation of the complement cascade then generates chemotactic plasma-activated complement 5 (C5a) and platelet-derived inflammatory mediators. Various cytokines and other cellular immunity factors initiate an inflammatory response manifested by cellular proliferation and edema of the glomerular tuft. Only a few strains of streptococci produce acute glomerulonephritis. Studies performed approximately 50 years ago led to the identification of certain strains of group A streptococci that are nephritogenic. More recently, non-group A streptococci, particularly group C, have also been demonstrated to produce glomerulonephritis. Tea-colored urine – This is often the first clinical symptom. This is caused by the hemolysis of RBC that have penetrated the glomerular basement membrane and have passed into the tubular system. • Periorbital edema – The onset is sudden, it is a result of a defect in renal excretion of salt and water. • Bipedal edema – Compromised intraglomerular blood flow due to glomerular hypercellularity results in progressive encroachment on the cross-sectional area of the glomerular capillaries. This leads to reduced blood flow that manifests as low fractional excretion of sodium and concentrated urine. This salt and water retention leads to edema. • Hypertension – It is thought to be as a result of excessive salt and water retention. In not very severe cases, hypertension is transient. It normalizes after the restoration of GFR, loss of edema and normalization of plasma volume. 2. What is the significance of the past medical history? A history of sorethroat, fever and pyoderma which is suggestive of preceding streptococcal infection is a sine qua non for the diagnosis of APSGN. The past medical history is significant in the diagnosis of the kind of glomerulonephritis the child has. Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci, designated as nephritogenic. The offending organisms are virtually always Group A Streptococci. Acute poststreptococcal glomerulonephritis (APSGN) follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12. 3. Describe the histologic changes particularly in the glomerulus in this condition? APSGN is characterized histologically by diffuse proliferation of glomerular cells, associated with influx of leukocytes. These lesions are typically caused by immune complexes. Hypercellularity of the glomeruli is the classic diagnostic picture which is caused by infiltration of leukocytes, both neutrophils and onocytes, and the proliferation of endothelial and mesangial cells, and in many cases, epithelial cells. The •

ASO titers are frequently used to document streptococcal infection. How does this pathology affect glomerular filtration? When the immune complex has deposited in the glomeruli. By immunofluorence microscopy. Many of the glomeruli become blocked by the inflammatory reaction. there are granular deposits of immunoglobulins and C3 in the mesangium and along the basement membrane. that is. 5. Can RBC be found in the urine without any pathology in the filtering membrane? . large numbers of WBC become entrapped in the glomeruli. serum C3. Small deposits of fibrin within capillary lumens and mesangium can be demonstrated in most cases. Turbidity: The haziness is a result of the white blood cells in the urine. In addition. and the combination of proliferation. but many mesanglial cells that lie between the endothelium and the epithelium. The activation of the alternative pathway of the complement system is thought to be responsible for the hypocomplementemia. Interpret the findings in the urinalysis. Deposits on the epithelial side of the membrane often have the appearance of “humps” presumed to represent the antigenpantibody complexes at the epithelial cell surface. and the tubules contain red cell casts. WBC: They become entrapped in the glomruli and is also able to penetrate the glomerular capillary membrane. swelling. many of the cells of the glomeruli begin to proliferate.proliferation and leukocyte infiltration are diffuse. involving all lobules of all glomeruli. Proteinuria indicates an alteration in the permeability of the glomerular capillary membrane. and ASO titer. and leukocyte infiltration obliterates the capillary lumens. 4. they are often focal and sparse. SERUM C3: Low serum complement levels indicative of an antigen-antibody interaction are a universal finding in the acute phase of APSGN. There may be interstitial edema and inflammation. allowing both proteins and RBC to leak from the blood of the glomerular capillaries into the glomerular filtrate. Protein: Proteins are normally not excreted in the urine since they are not able to pass through the glomerular membrane. 6. The level of reduction of serum complement levels does not have any prognostic significance. URINALYSIS: Color: Tea colored urine is caused by hemolysis of red blood cells that have penetrated the glomerular basement membrane and have passed into the tubular system. excessive permeability allows protein to leak from the blood into the glomerular filtrate. RBC: Caused by hemolysis of red blood cells that have penetrated the glomerular basement membrane and have passed into the tubular system. and those that are not blocked by this inflammatory reaction become excessively permeable. Although universally present. There is also swelling of the endothelial cells. ASO TITER: Antibody titers to extracellular products of streptococci are positive in more than 95% of patients with pharyngitis and 80% of patients with skin infections. As a result.

so as trauma to prostate or any components of the urinary tract. fever )  Poor intake of fluids  Medication. for example. the transport system for glucose becomes saturated resulting to spilling of glucose in the urine. Examples of prerenal causes are:  Hypovolemia (low blood volume) due to blood loss  Dehydration from loss of body fluid (vomiting. Kidney and bladder stones can cause irritation or abrasion of the urinary tract leading to bleeding.  Loss of blood supply to the kidney due to obstruction of the renal artery or vein b) GFR The GFR filters creatinine from our body system. Prerenal causes (pre=before + renal=kidney) are due to decreased blood supply to the kidney. This can also stem from hematologic disorders involving the clotting system of the body and cancer. their effect on . Creatinine is produced naturally by the body (creatinine is a break-down product of creatine phosphate. Medications such as aspirin. This margin of error is acceptable considering the ease with which creatinine clearance is measured. dissolved compounds have an osmotic pressure. kidney function is lost rapidly and can occur from a variety of insults to the body. in cases of increased plasma glucose concentration beyond the renal threshold of glucose (160-200 mg%). ureters. How will this condition affect the following? a) Renal Blood Flow Acute renal failure. which is found in muscle). due to poor filtration rate of the patient. 7. but also actively secreted by the peritubular capillaries in very small amounts such that creatinine clearance overestimates actual GFR by 10-20%. However. The list of causes is often categorized based on where the injury has occurred. it is clear that the creatinine is not fully filtered in the kidneys. Case 2 1. bladder or urethra). diuretics ("water pills") may cause excessive water loss. warfarin. Unlike precise GFR measurements involving constant infusions of inulin.Bleeding anywhere along the urinary tract can cause gross and microscopic hematuria and this cannot be distinguished as to origin (kidneys. Creatinine clearance or estimates of creatinine clearance based on the serum creatinine level are used to measure GFR. It is freely filtered by the glomerulus. Because large plasma proteins cannot easily cross through the capillary walls. sweating. c) Plasma Colloidal Osmotic Pressure Throughout the body. clopidogrel may also lead to bloody urine. Do you expect to find glucose in the urine if the filtration barrier is damaged? Glucose is not expected to be found in the urine even if the filtration barrier is damaged because it is always reabsorbed in the renal tubules. however. diarrhea. creatinine is already at a steady-state concentration in the blood and so measuring creatinine clearance is much less cumbersome.

in effect. often markedly so. opposes the hydrostatic pressure coming from the glomerulus. from being lost in the urine (proteinuria) or from malnutrition. glomerular filtration persists for some time because the filtrate subsequently diffuses back into the renal interstitium and perirenal spaces. That is.5mL/kg/hour.) What is the significance of 5cc/kg/hr urine output? The expected urine output for an adult is > 0. the fluid there also exerts a hydrostatic pressure and it. Renal Blood Flow Efferent arteriolar constriction also reduces renal blood flow. d) Bowman’s Capsule Pressure The glomerulus is surrounded by the Bowman's capsule. Because of this continued filtration. 2. the oncotic pressure tends to pull fluid into the capillaries. Fluid exchange in the Bowman's capsule is governed by the same Starling’s forces operating in the glomerulus. the effect of efferent arteriolar constriction depends on the severity of the constriction. e.g. It may be useful in the differential diagnosis of azotemia and in monitoring renal disease when protein-restricted diets are being given. where it ultimately returns to the lymphatic and venous systems. 3) What is the significance of Creatinine and blood Urea Nitrogen Determination of blood creatinine and blood urea nitrogen (BUN) and the relationship between them is an additional assessment of renal function. the affected calyces and pelvis become dilated. Comparing the 5cc/kg/hr is higher than the normal urine output. this can suggest Dehydration of the patient. the result of low oncotic pressure can be excess fluid buildup in the tissues (edema). the expected urine output is closer to 1ml/kg/hour. so an average adult of 70kg would be expected to produce 35-40ml/hour of urine. For children. the filtration fraction and glomerular colloid osmotic pressure increase as efferent arteriolar resistance increases. The high pressure in the pelvis is transmitted back through the collecting ducts into the cortex. b. modest efferent constriction raises GFR.the osmotic pressure of the capillary interiors will. In other words. and filtrate is forced into the Bowman's capsule. causing renal atrophy. How does the presence of the ureteral stone affect the following? a. CASE 3 1. but it also . However. also possible as a symptom for diabetes mellitus. to some extent. balance out the tendency for fluid to leak out of the capillaries. but severe efferent constriction (more than a threefold increase in resistance) tends to reduce GFR. Tubular Pressure and Pressure in the pelvic-calyceal system Hydronephrosis is the term used to describe dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction to the outflow of urine. Even with complete obstruction. In conditions where plasma proteins are reduced. c. Glomerular Filtration Constriction of the efferent arterioles increases the resistance to outflow from the glomerular capillaries.

What is the significance of the RBC in the urine? The presence of blood (RBC and/or hemoglobin) is clinically significant. 2. what structural changes do you expect in the: a. the initial functional alterations are largely tubular. leading eventually to interstitial fibrosis. kidney stones. glomerulonephritis. thrombocytopenia. catabolize it to hemosiderin and ferritin. poisoning. visible with the naked eye or under the microscope (macroscopic or microscopic hematuria) due to damage to the lining of the urinary tract. Evaluation is important to determine if the problem is pathological or non-pathological. parasite infections. There can be blood in the urine. True hemoglobinuria is an uncommon occurrence. obstruction will lead to medullary functional disturbances. pyelonephritis. 3. Hematuria is characterized by a cloudy. The resulting obstruction causes dilation or stretching of the upper ureter and renal pelvis (the part of the kidney where the urine collects before entering the ureter) as well as muscle spasm of the ureter. The medullary vascular defects are reversible. Ureter b. hemophilia. anticoagulants. trying to move the stone. The use of Prussian blue stain will confirm the presence of hemosiderin. Major causes of hematuria are trauma. and trauma. most commonly felt in the flank. leukemia. manifested primarily by impaired concentrating ability. then this would strongly suggestive of hemoglobinuria. Hemoglobinuria may be the result of intravascular hemolysis because of a transfusion reaction or hemolytic anemia. acute febrile episodes. If the urine is transparent and red. cystitis. Blood can enter the urinary tract at any point in the urinary system. malaria. appendicitis. proximal cold hemoglobinuria. Other causes of this problem are burns. The presence of RBC's in urine may be an indicator of early renal disease and requires medical follow-up. exhausting and intense physical activity. and exposure to toxic chemicals. tumors. Renal pyramids If stones grow to sufficient size before passage—on the order of at least 2-3 millimeters—they can cause obstruction of the ureter. proximal nocturnal hemoglobinuria. Renal colic can be associated with nausea and vomiting. catheterization. If hemoglobin is crossing the glomerulus. Accordingly. This leads to pain. renal tubular cells will reabsorb some of the hemoglobin. Only later does the GFR begin to diminish. Obstruction also triggers an interstitial inflammatory reaction. Most hemoglobin in the urine is the consequence ofhemolysis.compresses the renal vasculature of the medulla. and excrete it a few days later into the urine. The presence of a . smokey colored urine. Renal tubular epithelial cells containing hemosiderin can be observed in the urine sediment as-well-as hemosiderin granules. If the ureterolithiasis persists. Pelvic-calyceal system c. exhausting and intense physical activity. but if they are protracted. lower abdomen and groin (a condition called renal colic). causing a diminution in inner medullary plasma flow.

few (very few) RBC's in urine is generally considered to be normal. If RBC’s are present. look for RBC casts. .

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