Renal diseases
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Renal diseases






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    Renal diseases Renal diseases Presentation Transcript

    • What is human but an ingenious machine designed to turn, with “infinite artfulness, the red wine of Shiraz into urine”? Storyteller in Isak Dinesen’s Seven Gothic Tales
    • ACUTE GLOMERULONEPHRITIS  Deposition of immune complexes formed in conjunction with group A Streptococcus infection  Macroscopic hematuria, proteinuria rbc and granular casts  Antistreptolysin O titer and Anti-group A streptococcal enzymes
    • RAPIDLY PROGRESSIVE (CRESCENTRIC) GLOMERULONEPHRITIS  Deposition of immune complexes from systemic immune disorders on the glomerular membrane (i.e. Systemic Lupus Erythematosus)  Macroscopic hematuria, proteinuria and rbc casts  BUN, Creatinine and Creatinine clearance  Possible progression of ESRF
    • This immunofluorescence micrograph of a glomerulus demonstrates positivitywith antibody to fibrinogen. With a rapidly progressive GN, the glomerulardamage is so severe that fibrinogen leaks into Bowmans space, leading toproliferation of the epithelial cells and formation of the bright crescent.
    • GOODPASTURE’S SYNDROME Cytotoxic antibody formed during viral respiratory infection attach to glomerular and alveolar basement membrane Hemoptysis and dyspnea followed by hematuria, proteinuria and rbc casts Antiglomerular basement membrane antibody
    • This immunofluorescence pattern shows positivity with antibody to IgGand has a smooth, diffuse, linear pattern that is characteristic fordeposition of antiglomerular basement membrane antibody withGoodpasture syndrome.
    • WEGENER’S GRANULOMATOSIS Antineutrophilic cytoplasmic antibody binds to neutrophils in vascular walls Pulmonary symptoms (hemoptysis) followed by hematuria, protenuria and rbc casts ANCA test Progress to ESRF
    • HENOCH-SCHONLEIN PURPURA  Occurs in children after viral respiratory infection  Initial appearance of purpura followed by blood in stool and sputum then renal involvement  Stool occult blood
    • IgA NEPHROPATHY/ Berger’s Disease Deposition of IgA on glomerular membrane resulting from increased levels of serum IgA Recurrent macroscopic hematuria following mucosal infection or strenuous exercise Slow progression to CGN
    • MEMBRANOUS GLOMERULONEPHRITIS Most common cause of Nephrotic Syndrome in Adult Thickening of glomerular basement membrane from deposition of IgG immune complexes Associated with SLE, Sjogrens syndrome, secondary syphilis, Hep B and malignancy ANA, HbS Ag and FTA-ABS
    • MEMBRANOPROLIFERATIVE GLOMEROLUNEPHRITIS Cellular proliferation affecting the capillary walls or glomerular basement membrane Double contour or “tram-track” appearance Subendothelial deposits of C3, IgG, C1, C4 Hematuria and proteinuria Slow progression to nephrotic syndrome or possible remission Serum complement level
    • Membranoproliferativeglomerulonephritis (MPGN).-glomerulus has increasedoverall cellularity- Silver stain “tram-tracking”characteristic
    • CHRONIC GLOMERULONEPHRITIS Marked decreased in renal function due to glomerular damage precipitated by other renal disorders Hematuria, proteinuria, glucosuria, urin e casts (cellular, granular, waxy and broad) BUN, Creatinine, Creatinine clearance, Electrolytes
    • NEPHROTIC SYNDROME Acute onset following systemic shock Gradual progression from other gromerular disorder to renal failure Massive proteinuria (>3.5), hypoalbuminemia, generalized edema, hyperlipidemia & lipidosis Microscopic hematuria, renal tubular cells, oval fat bodies and fat droplets, fatty and waxy casts Serum albumin, cholesterol and triglycerides
    • MINIMAL CHANGE DISEASE (Lipid Nephrosis) NS in children after allergic reactions and immunizations Heavy proteinuria, transient hematuria and fat droplets Complete remission following corticosteroid treatment Serum albumin, cholesterol and triglycerides
    • Thickened Basement Membrane Effaced foot processesMinimal change disease (MCD) characterized by effacement of the epithelial cell(podocyte) foot processes and loss of the normal charge barrier
    • FOCAL SEGMENTAL GLOMERULONEPHRITIS Disruption of podocytes in some areas of glomeruli associated with heroin, analgesic abuse and HIV May resemble nephrotic syndrome or minimal change disease Drugs of abuse and HIV test
    • An area of collagenous sclerosis runs across the middle of this glomerulusTrichrome stain of aglomerulus in a patient withfocal segmentalglomerulosclerosis (FSGS)demonstrates blue collagendeposition.
    • ALPORT SYNDROME Inherited sex linked or autosomal disorder Males before age 6 during a respiratory infection may exhibit macroscopic hematuria and continue to exhibit microscopic hematuria Abnormal vision and hearing may be present
    • DIABETIC NEPHROPATHY a.k.a. Kimmelstiel-Wilson disease Deposition of glycosylated proteins due to uncontrolled blood glucose level Early monitoring of px with microalbuminuria is important Most common cause of End Stage Kidney Disease.
    • ACUTE TUBULAR NECROSIS Damage to renal tubular cells caused by ischemia or toxic agents Reversible renal dysfunction Microscopic hematuria, proteinuria, RTE cells and casts (hyaline, granular, broad and waxy) Hemoglobin, hematocrit and cardiac enzymes
    • FANCONI’S SYNDROME Inherited or acquired through exposure to toxic agents, outdated tetracycline or complication of Multiple Myeloma. Generalized defect in renal tubular reabsorption in proximal convoluted tubules Glucosuria and possible cystine crystals Serum and urine electrolytes, amino acid chromatography
    • NEPHROGENIC DIABETES INSIPIDUS Inherited sex-linked recessive or acquired from medication or as complication of PCKD or sickle cell anemia Inability of renal tubules to respond to ADH causing polyuria Urine is pale yellow, and with low specific gravity
    • RENAL GLYCOSURIA Generalized failure to reabsorb substances from glomerular filtrate, affecting the reabsorption of glucose Increased urine glucose concentration with normal blood glucose.
    • CYSTITIS Ascending bacterial infection of the bladder Acute onset of urinary frequency and burning resolved with antibiotics Leukocytoria, bacteruria, microscopic hematuria, mild proteinuria and increased pH Urine culture
    • ACUTE PYELONEPHRITIS Renal tubulointerstitial infection related to interference of urine flow to the bladder, urine reflux or untreated cystitis Acute onset of urinary frequency and burning resolved with antibiotics Leukocytoria, bacteruria, Casts (WBC, bacterial, granular, waxy and broad) hematuria and proteinuria Urine and blood cultures
    • CHRONIC PYELONEPHRITIS Recurrent renal tubulointerstitial infection caused by structural abnormalities affecting urine flow Diagnosed in children and requires correction of structural defects Leukocytoria, bacteruria, Casts (WBC, bacterial, granular, waxy and broad) hematuria and proteinuria Urine and blood cultures, BUN, Creatinine and Creatinine clearance
    • ACUTE INTERSTITIAL NEPHRITIS Allergic inflammation of renal interstitium in response to certain medications Acute onset of renal dysfunction accompanied by skin rash Resolves with discontinuation of medication and treatment with corticosteroids Hematuria, proteinuria, leukocyturia and WBC casts Urine eosinophils, BUN, creatinine and creatinine clearance
    • VASCULAR DISORDER Renal ischemia and loss of functional renal tissue Disorders that affect integrity of renal blood vessels:- Autoimmune disorders- Vaculitis- Diabetes mellitus
    • RENAL LITHIASIS May form in calyces and pelvis of KUB Renal colic or flank pain Vary from barely visible to staghorn calculi 75% compose of calcium oxalate and phosphates Lithotripsy and surgery
    • RENAL FAILURE Exists in both acute and chronic forms Gradual progression from the original disorder to end-stage renal disease Renal insufficiency Acute Renal Failure Chronic Renal Failure
    • Acute Renal FailurePrerenal: decreased blood pressure and cardiac output, hemorrhage, burns, surgery and septicemiaRenal: Acute glomerulonephritis, Acute tubular necrosis, Acute pyelonephritis, Acute interstitial necrosisPostrenal: Renal calculi, Tumors and Crytallization of ingested substances Chronic Renal Failure
    • Chronic Renal Failure- marked decreased in GFR- rising BUN and creatinine (AZOTEMIA)- electrolyte imbalance- Isothenuria, proteinuria, glycosuria- Abundance of granular, wax and broad casts END-STAGE RENAL DISEASE
    • Thank You!