Glomerular Diseases Flashcards
Prerenal Proteinuria
Caused by conditions affecting the plasma prior to reaching the kidney this is caused by increased levels of low molecular weight plasma proteins such as hemoglobin, myoglobin, and acute phase reactants; reagent test strips primarily detect albumin so this is usually missed in routine urinalysis
Glomerular Proteinuria
Conditions that present the glomerular membrane with abnormal substances are major causes of proteinuria due to glomerular damage, proteinuria that occurs during the latter months of pregnancy may indicate a preeclamptic state
Tubular Proteinuria
Increased albumin is also present in disorders affecting tubular reabsorption because albumin can no longer absorbed, causes of tubular dysfunction include exposure to toxic substances and heavy metals severe viral infections and Fanconi syndrome (A group of disorders marked by renal tubular dysfunction associated with some inherited and acquired conditions)
Microalbuminuria
Detects onset of renal complications in persons with both type one and type two diabetes mellitus
Glomerular Disorders
Most result from immunologic disorders, immune complexes formed from immunologic reactions or increased serum immunoglobulins, such as immunoglobulin A (IgA), circulate in the bloodstream and are deposited on the glomerular membranes. Components of the immune system, including complement, neutrophils, lymphocytes, monocytes, and cytokines, are then attracted to the area, producing changes and damage to the membranes. Nonimmunologic causes of glomerular damage include exposure to chemicals and toxins or disruption of the electrical membrane charges as occurs in the nephrotic syndrome
Overflow Disorders
Result from disruption of a normal metabolic pathway causing increased plasma concentrations of the nonmetabolized substances. Either override the reabsorption ability or are not normally reabsorbed.
Glomerulonephritis
A sterile, inflammatory process that affects the glomerulus and is associated with the finding of blood, protein, and casts in the urine, predominant casts will be RBC
Acute Glomerulonephritis (AGN)
Disease marked by the sudden onset of symptoms from damage to the glomerular membrane: edema (most noticeably around the eyes), fatigue, hypertension, oliguria, and hematuria.
Symptoms usually occur in children and young adults following respiratory infections caused by certain strains of group A streptococcus that contain M protein in the cell wall.
Streptococci form immune complexes and become deposited on the glomerular membranes.
Primary urinalysis findings include marked hematuria, proteinuria, and oliguria, accompanied by red blood cell (RBC) casts, dysmorphic RBCs, hyaline and granular casts, and white blood cells (WBCs).
Rapidly Progressive (Or Crescentic) Glomerulonephritis
Has a poor 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 glomerulonephritis or an immune systemic disorder such as systemic lupus erythematosus (SLE). Lab results include markedly elevated protein levels and very low glomerular filtration rates.
Goodpasture Syndrome
Morphologic changes to the glomeruli like those in rapidly progressive glomerular nephritis are seen in conjunction with this autoimmune disorder. Attachment of autoantibodies (antiglomerular basement membrane antibody) to the basement membrane, followed by complement activation, produces the capillary destruction. The autoantibody can be detected in patient serum.
Lab results include proteinuria, hematuria, and the presence of RBC casts. Progression to chronic glomerulonephritis and end-stage renal failure is common.
Wegener granulomatosis
Causes a granuloma-producing inflammation of the small blood vessels of the kidney. Antineutrophilic cytoplasmic antibody (ANCA) in the patient’s serum. Binding of these autoantibodies to the neutrophils located in the vascular walls initiate the immune response and the resulting granuloma formation. If the neutrophils are fixed in ethanol, the antibodies form a perinuclear pattern called p-ANCA.
Henoch-Schönlein Purpura
Occurs primarily in children after upper respiratory infections. Mild to heavy proteinuria and hematuria with RBC casts. Complete recovery with normal renal function is seen in more than 50% of patients.
Membranous Glomerulonephritis
A pronounced thickening of the glomerular basement membrane resulting from the deposition of IgG immune complexes. Found in patients with systemic lupus erythematosus, Sjögren syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, and malignancy. Nephrotic syndrome symptoms frequently develop. There may also be a tendency toward thrombosis.
Membranoproliferative Glomerulonephritis (MPGN)
Type 1: displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman’s capsule), causing thickening of the capillary walls; progress to the nephrotic syndrome
Type 2: displays extremely dense deposits in the glomerular basement membrane, experience symptoms of chronic glomerulonephritis.
Hematuria, proteinuria, and decreased serum complement levels are usual findings.
Chronic Glomerulonephritis
Symptoms include fatigue, anemia, hypertension, edema, and oliguria.
Urine reveals hematuria, proteinuria, glucosuria as a result of tubular dysfunction, and varieties of casts, including broad casts. A markedly decreased glomerular filtration rate is present in conjunction with increased BUN and creatinine levels and electrolyte imbalance.
