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50 Cards in this Set
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Glomerular disorders characteristics |
Most result from immunologic disorders throughout the body, including the kidney. Components of immune system migrate to an area which produces changes and damage to the membranes
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- exposure to chemicals and toxins that affect tubules, disruption of electrical membrane charges as occurs in nephrotic syndrome, deposition of amyloid material, and basement membrane thickening associated w/diabetic nephropathy
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What is glomerulonephritis? |
Refers to a sterile, inflammatory process that affects the glomerulus and is associated with the finding of blood, protein, and casts in the urine |
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Acute Poststreptococcal Glomerulonephritis characteristics |
Glomerular disorder. Disease marked by sudden onset of symptoms consistent w/damage to the glomerular membrane
Fever, edema (around eyes), fatigue, hypertension, oliguria, hematuria.
Usually occur in children and young adults following respiratory infections caused by group A strep (have M protein) --> immune complexes become deposited on glomerular membranes --> inflammation that affects glomerular function |
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Acute Poststreptococcal Glomerulonephritis urinalysis findings |
Macroscopic hematuria, proteinuria, RBC casts, granular casts
*Anti-group A streptococcal enzyme tests |
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Rapidly Progressive (Crescentic) Glomerulonephritis characteristics |
Glomerular disorder (poor prognosis), often terminating in renal failure
Symptoms initiated by deposition of immune complexes in glomerulus, often as a complication of another form of glomerulonephritis or immune systemic disorder (ex: system lupus erythematosus)
Damage by macrophages to capillary walls releases cells & plasma into Bowman's space --> causes permanent damage to capillary tufts |
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Rapidly Progressive (Crescentic) Glomerulonephritis urinalysis findings |
Initially similar to acute glomerulonephritis but become more abnormal with progression
Macroscopic hematuria, proteinuria, RBC casts
*BUN, creatinine, eGFR decreases |
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Goodpasture Syndrome characteristics |
Glomerular disorder. Rapidly progressive glomerular nephritis.
Cytotoxic auto can appear against glomerular and alveolar basement membranes after viral respiratory infections. Attachment to basement membrane --> complement activation --> capillary destruction (antiglomerular basement membrane ab)
Hemoptysis and dyspnea --> hematuria
Often results in chronic glomerulonephritis and end-stage renal failure |
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Goodpasture Syndrome urinalysis findings |
Macroscopic hematuria
*Antiglomerular basement membrane ab |
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Wegener Granulomatosis characteristics |
Glomerular disorder. Causes a granuloma-producing inflammation of the small blood vessels primarily of the kidney and respiratory system
Antineutrophilic cytoplasmic autoab binds to neutrophils in vascular walls producing damage to small vessels in lungs and glomerulus
Hemoptysis --> end-stage renal failure |
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Wegener Granulomatosis urinalysis findings |
Macroscopic hematuria, proteinuria, RBC casts, elevated serum creatinine and BUN
*Antineutrophilic peripheral or cytoplasmic ab (testing: incubating pt serum w/ethanol or formalin/formaldehyde-fixed neutrophils --> examining for perinuclear pattern called p-ANCA or c-ANCA) |
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Henoch-Schonlein Purpura characteristics |
Glomerular disorder. Occurs primarily in children after upper respiratory infections.
Decrease in platelets disrupts vascular integrity
Initial appearance of purport followed by blood in sputum and stools and eventual renal involvement
Complete recovery in more than 50% of patients |
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Henoch-Schonlein Purpura urinalysis findings |
Macroscopic hematuria, proteinuria, RBC casts
*Stool occult blood |
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Membranous Glomerulonephritis characteristics |
Glomerular disorder. Pronounced thickening of the glomerular basement membrane resulting from the deposition of IgG immune complexes
Associated w/SLE, Sjogren syndrome, secondary syphilis, hep B, Au & Hg treatments, and malignancy
Tendency towards thrombosis. Slow progression towards nephrotic syndrome |
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Membranous Glomerulonephritis urinalysis findings |
Microscopic hematuria, proteinuria
*Antinuclear ab, Hep B surface ag, FTA-ABS (for secondary syphilis) |
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Membranoproliferative Glomerulonephritis characteristics |
Glomerular disorder. Type 1- Displays increased cellularity in the sub endothelial cells of the mesangium (inserstitial area Bowman's capsule) --> thickening of capillary walls. Progress to nephrotic syndrome
Type 2- Extremely dense deposits in glomerular basement membrane. Experience symptoms of chronic glomerulonephritis
Many of the patients are children |
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Membranoproliferative Glomerulonephritis urinalysis findings |
Hematuria, proteinuria
*Serum complement levels decreased
Appears to be an association with autoimmune disorders, infections, and malignancies |
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Chronic Glomerulonephritis characteristics |
Glomerular disorder.
Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders
Renal failure |
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Chronic Glomerulonephritis urinalysis findings |
Hematuria, proteinuria, glucosuria, casts
*eGFR decreased, increased BUN, creatinine levels, and electrolyte imbalance |
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IgA Nephropathy characteristics |
Glomerular disorder. AKA Berger disease. Most common cause of glomerulonephritis
Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA
Recurrent macroscopic hematuria following exercise with slow progression to chronic glomerulonephritis
Most frequently seen in children and young adults
Asymptomatic for 20 years or more --> gradual progression to chronic glomerulonephritis and end-stage renal disease |
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IgA Nephropathy urinalysis findings |
Macroscopic or microscopic hematuria
*Serum IgA increased |
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Nephrotic Syndrome characteristics |
Glomerular disorder. Marked by massive proteinuria (greater than 3.5g/day), low levels of serum albumin, high levels of serum lipids, and pronounced edema
Disruption of the shield of negativity and damage to the tightly fitting podocyte barrier resulting in massive loss of protein and lipids
Acute onset following systemic shock. Gradual progression from other glomerular disorders and then to renal failure |
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Nephrotic Syndrome urinalysis findings |
Heavy proteinuria, microscopic hematuria, renal tubular cells, oval fat bodies, fat droplets, fatty and waxy casts
*Serum albumin decreased, cholesterol, triglycerides |
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Minimal Change Disease characteristics |
Glomerular disorder. AKA lipid nephrosis
Produces little change, but disruption of the podocytes primarily in children following allergic reactions and immunizations
Frequent complete remission following corticosteroid treatment |
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Minimal Change Disease urinalysis findings |
Heavy proteinuria, transient hematuria, fat droplets
*Serum albumin, cholesterol, triglycerides |
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Focal Segmental Glomerulosclerosis characteristics |
Glomerular disorder.
Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and AIDS
Immune deposits, primarily IgM and C3, are a frequent finding and can be seen in undamaged glomeruli.
May resemble nephritic syndrome or minimal change disease |
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Focal Segmental Glomerulosclerosis urinalysis findings |
Proteinuria, microscopic hematuria, macroscopic or microscopic hematuria
*Drugs of abuse, HIV tests |
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Alport Syndrome characteristics |
Glomerular disorder/inherited tubular disorder
Genetic disorder showing lamented and thinning glomerular basement membrane (inherited disorder of collagen production affecting the glomerular basement membrane)
Can be inherited as a sex-linked or autosomal genetic disorder. Males inheriting the X-linked gene are more severely affected than females inheriting the autosomal gene.
During respiratory infections, males younger than age 6 may exhibit macroscopic hematuria and continue to exhibit microscopic hematuria. Abnormalities in hearing or vision may also develop
Slow progression to nephrotic syndrome and end-stage renal disease
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Alport Syndrome urinalysis findings |
Microalbuminuria
*Genetic testing |
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What are tubular disorders? |
Disorders affecting the renal tubules include those in which tubular function is disrupted as a result of actual damage to the tubules and those in which a metabolic or hereditary disorder affects the intricate functions of the tubules |
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Acute Tubular Necrosis characteristics |
Tubular disorder. Caused by ischemia or the presence of toxic substances in the urinary filtrate
Can be caused by shock, trauma, and surgical procedures. Ex: cardiac failures, sepsis involving toxigenic bacteria, anaphylaxis, massive hemorrhage, and contact with high-voltage electricity
Toxic substances such as amino glycoside abx, anti fungal agent amphotericin B, cyclosporine, radiographic dye, organic solvents such as ethylene glycol, heavy metals, and toxic mushrooms
Also filtration of large amounts of Hb and Mb
Acute onset of renal dysfunction usually resolved when underlying cause is corrected |
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Acute Tubular Necrosis urinalysis findings |
Microscopic hematuria, proteinuria, RTE cells, RTE cell casts, hyaline, granular, waxy, broad casts
*Hb, Hct, cardiac enzymes |
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Hereditary and metabolic tubular disorders |
Disorders affecting tubular function may be caused by systemic conditions that affect or override the tubular reabsorptive maximum for particular substances normally reabsorbed by the tubules or by failure to inherit a gene or genes required for tubular reabsorption |
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Fanconi Syndrome characteristics |
Tubular disorder. Most frequently associated with tubular dysfunction
Generalized failure of tubular reabsorption in the proximal convoluted tubule --> substances most noticeably affected include glucose, amino acids, phosphorous, sodium, potassium, bicarb, and water
Reabsorption may be affected by dysfunction of transport of filtered substances across the tubular membranes, disruption of cellular energy needed for transport, or changes in the tubular membrane permeability
May be inherited in association w/cystinosis and Hartnup disease, acquired through exposure to toxic agents (heavy metals, outdated tetracycline), or seen as a complication of multiple myeloma and renal transplant
Requires supportive therapy |
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Fanconi Syndrome urinalysis findings |
Glucosuria, possible cystine crystals
*Serum and urine electrolytes, amino acid chromatography |
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Uromodulin-Associated Kidney Disease characteristics |
Tubular disorder. Primarily an inherited disorder caused by an autosomal mutation in the gene that produces uromodulin. The mutation causes a decrease in the production of normal uromodulin that is replaced by the abnormal form.
Abnormal uromodulin is still produced by the tubular cells and accumulates in these cells, resulting in their destruction, which leads to the need for renal monitoring and eventual renal transplantation
Causes an increase in serum uric acid, resulting persons developing gout as early as the teenage years before the onset of detectable renal disease |
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Uromodulin-Associated Kidney Disease urinalysis findings |
RTE cells
*Serum uric acid increases |
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Diabetic Nephropathy characteristics |
Tubular disorder. Currently the most common cause of end-stage renal disease
Damage to the glomerular membrane occurs not only as a result of glomerular membrane thickening but also because of the increased proliferation of mesangial cells and increased deposition of cellular and noncellular material within the glomerular matrix, resulting in accumulation of solid substances around the capillary tufts
Believed tot be associated with deposition of glycosylated proteins resulting from poorly controlled blood glucose levels
The vascular structure of the glomerulus also develops sclerosis |
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Nephrogenic Diabetes Insipidus characteristics |
Tubular disorder.
Nephrogenic: inability of the renal tubules to respond to ADH
Neurogenic: failure of the hypothalamus to produce ADH
Nephrogenic can be inherited as a sex-linked recessive gene or acquired from medications, including lithium and amphotericin B. May be seen as a complication of polycystic kidney disease and sickle cell anemia |
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Nephrogenic Diabetes Insipidus urinalysis findings |
Low specific gravity, polyuria
*ADH testing |
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Renal Glycosuria characteristics |
Tubular disorder.
Unlike Fanconi syndrome (can't absorb anything from the glomerular filtrate), renal glycosuria affects only the reabsorption of glucose
Inherited as an autosomal recessive trait
Either the number of glucose transporters in the tubules is decreased or the affinity of the transporters for glucose is decreased.
Pts have increased urine glucose concentrations with normal blood glucose concentrations |
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Renal Glycosuria urinalysis findings |
Glucosuria
*Blood glucose normal |
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Interstitial disorders |
Disorders that affect the interstitial that also affect the tubules.
Most common is the UTI and cystitis |
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Acute Polynephritis characteristics |
Infection of the upper urinary tract, including both the tubules and interstitial. Can occur in both acute and chronic forms.
Most frequently occurs as a result of ascending movement of bacteria from a lower UTI into the renal tubules and interstitium.
Related to interference of urine flow to the bladder, reflux of urine from the bladder, and untreated cystitis |
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Acute Polynephritis urinalysis findings |
Leukocyturia, bacteriuria, WBC casts, bacterial casts, microscopic hematuria, proteinuria
*Urine culture |
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Chronic Pyelonephritis characteristics |
Can result in permanent damage to the renal tubules and possible progression to chronic renal failure.
Structural abnormalities may cause reflux between bladder and ureters or within the renal pelvis, affecting emptying of the collecting ducts.
Often diagnosed in children and may not be suspected until tubular damage has become advanced. |
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Chronic Pyelonephritis urinalysis findings |
Leukocyturia, bacteriuria, WBC casts, bacterial casts, granular, waxy, broad casts, hematuria, proteinuria
*Urine culture, BUN, eGFR |
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Acute Interstitial Nephritis characteristics |
Marked by inflammation of the renal interstitial followed by inflammation of the renal tubules
Primarily associated with an allergic reaction to medications that occurs within the renal interstitial, possibly caused by the medication binding to the interstitial protein.
Symptoms tend to develop approximately 2 weeks following administration of medication
Medications: penicillin, methicillin, ampicillin, cephalosporins, sulfonamids, NSAIDs, and thiazide diuretics |
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Acute Interstitial Nephritis urinalysis findings |
Hematuria, proteinuria, leukocyturia, WBC casts
*Urine eos, BUN, creatinine, eGFR |
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Acute vs chronic renal failure |
Acute 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), and renal calculi or tumor obstructions (postrenal)
Renal failure: marked decrease in the glomerular filtration rate (less than 25mL/min); steadily rising serum BUN and creatinine values (azotemia); electrolyte imbalance; lack of renal concentrating ability producing an isosthenuric urine; proteinuria; renal glycosuria; an abundance of granular, waxy, and broad casts, often referred to as a telescoped urine sediment |
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Renal Lithiasis characteristics |
Calculi vary in size from barely visible to large, stag horn calculi resembling the shape of the renal pelvis and smooth, round bladder stones with diameters of 2 or more inches
Lithotripsy can be used to break stones in upper urinary tract |
