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
HEREDITARY METABOLIC TUBULAR DISORDERS
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