Mejia, Kirsten Hazel M.

2:00-3:00 AUBF LECTURE MWF R206 Glomerular Disorders Etiology Deposition of immune complexes, formed in conjunction with group A Streptococcus infection, on the glomerular membranes Deposition of immune complexes from systemic immune disorders on the glomerular membrane Attachment of a cytotoxic antibody formed during viral respiratory infections to glomerular and alveolar basement membranes Antineutrophilic cytoplasmic autoantibodybinds to neutrophils in vascular walls producing damage to small vessels in the lungs and glomerulus Occurs primarily in children following viral respiratory infections; a decrease in platelets disrupts vascular integrity

Disorder Acute glomerulonephritis

Clinical Course Rapid onset of hematuria and edema Permanent renal damage seldom occurs Rapid onset with glomerular damage and possible progression to end-stage renal failure Hemoptysis and dyspnea followed by hematuria Possible progression to endstage renalfailure Pulmonary symptoms including hemoptysis develop first followed by renal involvement and possible progression to end stage renal failure Initial appearance of purpura followed by blood in sputum and stools and eventual renal involvement Complete recovery is common, but may progress to renal failure Slow progression to the nephrotic syndrome or possible remission

Rapidly progressive glomerulonephritis

Goodpasture syndrome

Wegeners granulomatosis

Henoch-Schnlein purpura

Membranous glomerulonephritis

Membranoproliferative glomerulonephritis

Chronic glomerulonephritis

Thickening of the glomerular membrane following IgG immune complex deposition associated with systemic disorders Cellular proliferation affecting the capillary walls or the glomerular basement membrane, possibly immune-mediated Marked decrease in renal function resulting from

Slow progression to chronic glomerulonephritis or nephrotic syndrome Noticeable decrease in renal function progressing

IgA nephropathy

glomerular damage precipitated by other renal disorders Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA Disruption of the electrical charges that produce the tightly fitting podocyte barrier resulting in massive loss of protein and lipids Disruption of the podocytes occuring primarily in children following allergic reactions and immunizations Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and AIDS Genetic disorder showing lamellated and thinning of glomerular basement membrane

to renal failure

Nephrotic syndrome

Recurrent macroscopic hematuria following exercise with slow progression to chronic glomerulonephritis Acute onset following systemic shock Gradual progression from other glomerular disorders and then to renal failure Frequent complete remission following corticosteroid treatment May resemble nephrotic syndrome or minimal change disease Slow progression to nephrotic syndrome and end-stage renal disease

Minimal change disease

Focal segmental glomerulosclerosis Alport Syndrome

Disorder Acute tubular necrosis

Metabolic and Tubular Disorders Etiology Damage to the renal tubular cells caused by ischemia or toxic agents Inherited in association with cystinosis and Hartnup disease or acquired through exposure to toxic agents Inherited defect of tubular response to ADH or acquired from medications Inherited autosomal recessive trait

Clinical Course

Fanconi syndrome

Acute onset of renal dysfunction usually resolved when the underlying cause is corrected Generalized defect in renal tubular reabsorption requiring supportive therapy Requires supportive therapy to prevent dehydration Benign disorder

Nephrogenic diabetes insipidus Renal glucosuria

Disorder Cystitis

Interstitial Disorders Etiology Ascending bacterial infection of the bladder Infection of the renal tubules and interstitium related to interference of urine flow to the bladder, reflux of urine from the bladder, and untreated cystitis Recurrent infection of the renal tubules and interstitium caused by structural abnormalities affecting the flow of urine

Clinical Course Acute onset of urinary frequency and burning resolved with antibiotics Acute onset of urinary frequency, burning, and lower back pain resolved with antibiotics

Acute pyelonephritis

Chronic pyelonephritis

Acute interstitial nephritis

Frequently diagnosed in children; requires correction of the underlying structural defect Possible progression to renal failure Allergic inflammation of the Acute onset of renal renal interstitium in response dysfunction to certain medications often accompanied by a skin rash Resolves following discontinuation of medication and treatment with corticosteroids