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AUBF Group 1 Alioden, Jasmelainie Galang, Aiko Nia Jimenez, Nicole Lacaba, Christelle Mae Lagman, Bunny Panlaqui,

Verneleen Pastor, Charmaine Romero, John Reden Tejada, Christian Jules

Glomerular Disorder
The majority of the disorders associated with the glomerulus are of immune origin, resulting from immunologic disorders throughout the body, including the kidneys. Immune complexes formed as a result of immunologic reactions and increased serum immunoglobulins, which circulates in the blood stream and are deposited on the glomerular membrane. Depending on the immune system mediators involved, damage may consist of cellular infiltration or proliferation resulting in thickening of the glomerular basement membrane and complement-mediated damage to the capillaries and basement membrane. Nonimmunologic causes of causes of glomerular damage include: Exposure to chemical and toxins that also affect the tubules. Disruption of the electrical membrane charges occurs in the nephritic syndrome. Deposition of amyloid material from systemic disorders. Basement membrane thickening associated with diabetic nephropathy.

These may include the ff: Fever Edema Fatigue Hypertension Oliguria Hematuria

Symptoms are found in children, young adults and immune compromise persons following respiratory infection caused by certain strain of group A streptococcus that contains M protein in their cell wall. In the course of infection this strain form immune complexes with their antibody and becomes deposited in the glomerular membrane. Primary urinalysis findings include: Marked hematuria Protenuria Oliguria with RBCs and WBCs As toxicity subside, urinalysis results returns to normal, with the possible exception of microscopic hematuria that lasts until the membrane damage has been repaired. Blood Urea Nitrogen (BUN) may be elevated during the acute stages but also returns to normal. Demonstration of an elevated serum antisterptolysin O (ASO) titer or antigroup A streptococcal enzyme tests provide evidence that the disease is of streptococcal origin.

This term refers to a sterile, inflammatory process that affects the glomerolus and is associated with the finding of blood, protein and casts in urine.

Acute Glomerulonephritis


Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN)

A more serious form of acute glomerular with a poorer prognosis often terminating in renal failure Symptoms are initiated by deposition of immune complexes in the glomerulus, often as a complication of another form of

Acute glomeronepritis (AGN) is a disease marked by sudden onset of symptoms consistent with damage to the glomerular membrane.

glomerulonephritis or an immune systemic disorder such as systemic lupus erythematosus (SLE). Damage by macrophages to the capillary walls releases cells and plasma into Bowmans space. Crescentic formations contain macrophages, fibroblasts, and polymerized fibrin, which cause permanent damage to the capillary tufts. Initial laboratory results are similar to acute glomerulonephritis. As the disease progresses, more abnormal results are obtained including markedly elevated protein levels, very low glomerular filtration rates, increased fibrin degradation products, cryoglobulins, and the deposition of IgA immune complexes in the glomerulus.

This usually progress to chronic glomerulonephritis and end-stage renal failure.

Goodpasture Syndrome
An autoimmune disorder which resembles the morphologic changes of glomeruli in RPGN Cytotoxic autoantibody appears against the glomerular and alveolar basement membranes following viral respiratory infections. Capillary destruction occurs when this autoantibody attaches to the basement membrane and activates complement. This autoantibody known as antiglomerular basement membrane antibody can be detected in patient serum. Initial pulmonary complaints are hemoptysis and dyspnea, followed by the development of hematuria. Urinalysis results include proteinuria, hematuria, and the presence of RBC casts.

Wegeners Granulomatosis This causes a granuloma-producing inflammation of the small blood vessels of primarily the kidney and respiratory system. Diagnosis is through the demonstration of antineutrophilic cytoplasmic antibody (ANCA) in the patients serum. These autoantibodies bind to the neutrophils in the vascular walls and initiate the immune response and the granuloma formation. Initially, patients present pulmonary symptoms and later develop renal involvement, hematuria, proteinuria, RBC casts, and elevated serum creatinine and BUN.

Henoch-Schnlein Pupura A disease occurring primarily in children following upper respiratory infections. Initial symptoms include the appearance of raised, red patches on the skin. Respiratory and gastrointestinal symptoms, including blood in the sputum and stools, may be present. Renal involvement is the most serious complication of the disorder and may range from mild to heavy proteinuria and hematuria with RBC casts. More than 50% of patients with normal renal function completely recover. In some patients, the disease may progress to a more serious form of

glomerulonephritis and renal failure. Patients who recovered from the original symptoms must be monitor with urinalysis and renal function tests.

Membranous Glomerulonephritis
The predominant characteristics of membranous glomerulonephritis is a pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes Disorders associated with the development of membranous glomerulonephritis: Systemic Lupus Erythematosus Sjogren Syndrome Secondary Syphilis Hepatitis B Gold and Mercury Treatments Malignancy Disease progresses slowly, with possible remission. However, frequent development of nephrotic syndrome symptoms occurs. There may also be a tendency toward thrombosis. Laboratory findings include: Microscopic hematuria Elevated urine protein excretion that may reach concentration similar to those in the nephrotic syndrome Demonstration of one of the secondary disorders through blood tests can aid in the diagnosis.

Marked by two different alterations in the cellularity of the glomerulus and peripheral capillaries: Type 1 displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowmans capsule), causing thickening of the capillary walls Type 2 displays extremely dense deposits in the glomerular basement membrane Many of the patients are children Disease has poor prognosis with type 1 patients progressing to the nephrotic syndrome and type 2 patients experiencing symptoms of chronic glomerulonephritis. Hematuria, proteinuria and decreased serum complement levels are usual findings and appear to be an association with autoimmune disorders, infections and malignancies.

Chronic Glomerulonephritis
Progression to chronic glomerulonephritis and end-stage renal disease may occur depending on the amount and duration of the damage occurring to the glomerulus in the previously discussed glomerular disease. Gradually worsening symptoms include fatigue, anemia, hypertension, edema and oliguria. Examination of the urine reveals hematuria, proteinuria, glucosuria as a result of tubular dysfunction and many varieties of casts. Markedly decreased glomerular filtration rate is present in conjunction with increased BUN and creatinine levels and electrolyte imbalance.

Membranoproliferative Glomerulonephritis (MPGN)

Immunoglobulin A Nephropathy
Also known as Berger Disease; most common cause of glomerulonephritis. Disease in which immune complexes containing IgA are deposited on the glomerular membrane Patients have increased serum levels of IgA, which may be a result of mucosal infection Most frequently seen in children and young adults Patient usually present with an episode of macroscopic hematuria following an infection or strenuous exercise. A patient with the disorder may remain essentially asymptomatic for 20 years or more except for periodic episodes of macroscopic hematuria; however, there is a gradual progression to chronic glomerulonephritis and end-stage renal disease.

the basal lamina and podocytes, producing a less tightly connected barrier. This facilitates the passage of high-molecular-weight proteins and lipids into the urine. Albumin- is the primary protein depleted from the circulation. Hypoalbuminemia- stimulates the increased production of lipids by the liver. Edema- is produced by the lower oncotic pressure in the capillaries resulting from the depletion of plasma albumin increases the loss of fluid into the interstitial spaces accompanied by sodium retention. Other effects: Depletion of immunoglobulins and coagulation factors places patients at an increased risk of infection and coagulation disorders, Tubular damage, May progress to chronic renal failure. Urinalysis observations include: Marked proteinuria; Urinary fat droplets; Oval fat bodies; Renal tubular epithelial (RTE) cells; Epithelial, fatty, and waxy casts; and Microscopic hematuria Absorption of the lipid-containing proteins by the RTE cells followed by cellular sloughing produces the characteristic oval fat bodies seen in the sediment examination.

Nephrotic Syndrome
Greater than 3.5 g/d- The nephrotic syndrome is marked by massive proteinuria. Low levels of serum, albumin, high levels of serum lipids, and pronounced edema are observed. Acute onset of the disorder can occur in instances of circulatory disruption. Progression to the nephrotic syndrome may also occur as a complication of the previously discussed forms of glomerulonephritis. Increased permeability of the glomerular membrane is attributed to damage to the membrane and changes in the electrical charges in

Minimal Change Disease

Also known as lipid nephrosis It produces little cellular change in the glomerulus, although the podocytes appear to be less tightly fitting, allowing for the increased filtration of protein.

Patients are usually children who present with edema, heavy proteinuria, transient hematuria, and normal BUN and creatinine results. Although the etiology is unknown at this time, allergic reactions, recent immunization, and possession of the human leukocyte antigen-B12 (HLA-B12) antigen have been associated. The disorder responds well to corticosteroids, and prognosis is generally good, with frequent complete remissions.

Focal Segmental Glomerulosclerosis

It affects only certain numbers and areas of glomeruli, and the others remain normal. Symptoms may be similar to the nephrotic syndrome and minimal change disease owing to damaged podocytes. Immune deposits, primarily immunoglobulins M and C3, are a frequent finding and can be seen in undamaged glomeruli. Often seen in association with abuse of heroin and analgesics and with AIDS. Moderate to heavy proteinuria and microscopic hematuria are the most consistent urinalysis findings.

Alport Syndrome
Inherited disorder affecting glomerlar basement membrane Inherited as sex-linked disorder\autosomal genetic disorder Males are more severely frequently affected During Respiratory infections, males before the age of six may exhibit; Macroscopic hematuria to Microscopic hematuria. Abnormalities in hearing and vision

Diabetic Nephropathy
AKA Kimmelstiel Wilson disease Most common cause of end- stage renal disease. Damage to the Glomerular membrane results from: Glomerular membrane thickening Increased proliferation of mesangial cells Increased deposition of cellular and noncellular material=Accumulation of solid substances around the capillary tufts

Tubular Disorders
Disorders affecting renal tubules Tubular function is disrupted=actual damage to the tubules Metabolic or hereditary disorder affects tubules functions

Acute Tubular Necrosis (ATN)

Primary disorder associated with damage to the renal tubules

Damage to the renal tubular cells (RTE) may be produced by the decreased blood flow that causes a lack of oxygen presentation in the tubules (ischemia) or the presence of toxic substances in the urinary filtrate Disorders causing ischemic ATN Shock Trauma (such as crushing injuries) Surgical procedures Shock- a general term indicating a severe condition that decreases the flow of blood throughout the body Some conditions that may cause shock Cardiac failures Sepsis involving toxogenic bacteria Anaphylaxis Massive haemorrhage Contact with high-voltage electricity Exposure to a variety of nephrotoxic agents can damage and affect the function of the renal tubular cells Examples of nephrotoxic agents: Aminoglycoside antibiotics Antifungal agent amphotericin B Cyclosporine Radiographic dye Organic solvents such as ethylene glycol Heavy metals Toxic mushrooms Filtration of large amounts of haemoglobin and myoglobin is also nephrotoxic Urinalysis findings include mild proteinuria, microscopic hematuria, and most noticeably the presence of RTE cells and RTE casts containing

tubular fragments consisting of three or more cells As a result of tubular damage, a variety of casts may be present, including hyaline, granular, waxy and broad.

Hereditary and Metabolic Tubular Disorders

Fanconi syndrome disorder most frequently associated with tubular dysfunction consists of a generalized failure of tubular reabsorption in the proximal convoluted tubule Substances most noticeably affected glucose amino acids phosphorus sodium potassium bicarbonate water may be inherited in association with cystinosis and Hartnup disease or acquired through exposure to toxic agents, including heavy metals and outdated tetracycline, or as a complication of multiple myeloma and renal transplant Nephrogenic Diabetes Insipidus When the action of ADH is disrupted either by the inability of the renal tubules to respond to ADH (nephrogenic diabetes insipidus) or the failure of the hypothalamus to produce ADH (neurogenic diabetes insipidus) excessive amounts of urine is excreted. Can be inherited as a sex-linked recessive gene or acquired from medications including lithium and amphotericin B. It also may be seen as a complication of polycystic kidney disease and sickle cell anaemia

Urinalysis findings associated are Low specific gravity Pale yellow color Possible false-negative results for chemical tests Requires supportive therapy to prevent dehydration

Renal Glycosuria Affects only the reabsorption of glucose Benign disorder This disorder is inherited as an autosomal recessive trait Patients demonstrate increased urine glucose concentrations with normal blood glucose concentration The maximal tubular reabsorption capacity for glucose (TmG) is a blood level of approximately 160 to180 mg/dL. When the TmG is reached, glucosuria occurs. In inherited renal glucosuria either the number of glucose transporters in the tubules is decreased or the affinity of the transporters for glucose is decreased.

Interstitial Disorders
Tubulointerstitial disease - disorders affecting the renal interstitium and tubules. The most common renal disease is UTI. Infection may involve the lower urinary tract: urethra (urethritis) and bladder (cystitis), and the upper urinary tract (pyelonephritis; rarely seen): renal pelvis, tubules, and interstitium. Cystitis- most frequently encountered urinary tract infection Prone to this: women and children Symptoms of cystitis: urinary frequency, burning sensation in

the urethra when urine is released. resolved with antibiotics

Acute Pyelonephritis

Acute pyelonephritis
Occurs as a result of ascending movement of bacteria from the lower urinary tract to the upper urinary tract. Enhanced in the presence of decreased downward flow of urine and incomplete emptying of the bladder. Causes are: renal calculi, pregnancy, and reflux of urine from the bladder back to the ureters (visicoureteral reflux) Symptoms of acute pyelonephritis: urinary frequency, burning sensation, lower back pain (rapid onset); Presence of WBC casts in the urine differentiates it from cystitis resolved with antibiotics

Chronic Pyelonephritis

Acute interstitial nephritis

Mild proteinuria Increased pH Leukocyturia Bacteriuria WBC casts Bacterial casts Microscopic hematuria Proteinuria Leukocyturia Bacteriuria WBC casts Bacterial casts Granular, waxy, broad casts Hematuria Proteinuria Hematuria Proteinuria Leukocyturia WBC casts

Urine culture Blood cultures

Urine culture Blood cultures BUN Creatinine Creatinine clearance Urine eosinophils BUN Creatinine Creatinine clearance

Chronic pyelonephritis
Is the permanent damage to the renal tubules that may lead to renal failure. Congenital urinary structural defects producing a reflux nephropathy is the most common cause. Children are prone to this infection. Presence of granular, waxy, broad casts differentiates it from acute pyelonephritis Acute Interstitial Nephritis (AIN) It is marked by inflammation of the renal interstitium followed by inflammation of the renal tubules. Patients present with a rapid onset of symptoms relating to renal dysfunction, including: Oliguria Edema Decreased renal concentrating ability Possible decrease in the glomerular filtration rate

Table 8-5 SUMMARY OF LABORATORY RESULTS IN INTERSTITIAL DISORDERS Disorder Primary Urinalysis Results Cystitis Lekocyturia Urine Bacteriuria culture Microscopic hematuria

*Fever and the presence of skin rash are frequent initial symptoms.

AIN is primarily associated with an allergic reaction to medications that occurs within the renal interstitium, possibly caused by binding of the medication to the interstitial protein. Symptoms tend to develop approximately 2 weeks following administration of medication Medications commonly associated with AIN include: Penicillin Methicillin Ampicillin Cephalosphorins Sulfonamides NSAIDS Thaizide diuretics

Renal Failure Renal failure exists in both acute and chronic forms. The progression to end-stage renal disease is characterized by: Decrease in the glomerular filtration rate (less than 25 mL/min) Steadily rising serum BUN and creatinine (azotemia) electrolyte imbalance lack of renal concentrating ability producing an isothenuric urine proteinuria renal glycosuria abundance of granular, waxy, and broad casts (often referred to as a telescoped urine sediment)

Discontinuation of the offending medication and administration of steroids to control the inflammation frequently results in a return to normal renal function. Disorder Etiology Clinical Course Acute onset of renal dysfunction often accompanied by a skin rash Resolves following discontinuation of medication and treatment with corticosteroids

Acute Renal Failure (ARF) exhibits a sudden loss of renal function and is frequently reversible. Primary causes: Sudden decrease in blood flow to the kidney (prerenal) Acute glomerular and tubular disease (renal) Renal calculi and tumor obstructions (postrenal)

Acute Allergic interstitial inflammation nephritis of the renal interstitium in response to certain medications.

Supportive renal dialysis may be required to maintain patients until the inflammation subsides.

Patients may present with many different symptoms relating in the particular disorder involved. However, a decreased glomerular filtration rate, oliguria, edema and azotemia are general characteristics.

Causes of Acute Renal Failure Renal Post renal

Acute glomerulonep hritis Acute tubular necrosis Acute pyelonephritis Acute interstitial nephritis

Prerenal Decreased blood pressure/ cardiac output Hemorrhage Burns Surgery Septicemia

Renal calculi Tumors Crystallization of ingested substances

Clumps of crystals in freshly voided urine suggests that conditions may be right for calculus formation. Approximately 75% of renal calculi are composed of calcium oxalate or phospahate

Other primary calculi constituents: Magnesium ammonium

phosphate(stuvite) Uric acid Cystine Calcium calculi are associated with metabolic calcium, phosphate disorders and diet In Magnesium ammonium phosphate, urine pH is higher than 7.0 due to urea splitting bacteria. High purine diet content is associated with uric acid calculi. Cystine calculi are seen in hereditary disorders of cystine metabolism Primary urinalysis finding : hematuria resulting from irritation to the tissues by the moving calculus.

Renal Lithiasis Renal calculi (kidney stones) may form in the calyces and pelvis of the kidney, ureters and bladder. In renal lithiasis, the calculi vary in size from barely visible to large, staghorn calculi resembling the shape of the renal pelvis and smooth round bladder stones with diameters of 2 or more inches. Small calculi passed in the urine subjecting patient to severe pain (from lower back to the legs) Larger stones cannot be passed and only detected until patients develop symptoms of urinary obstruction Lithotripsy procedure using high-energy shock waves which can be used to break stones located in the upper urinary tract into pieces that can then be passed in the urine. Conditions favouring the formation of renal calculi: pH chemical concentration urinary stasis