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21 Cards in this Set
- Front
- Back
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Nephrotic syndrome |
-abnormal filtration NO inflammation -normal bowman space -big damage in glomerular structure Alterations: hypoalbuminemia, generalized edema (can become edema in the whole body), proteinuria more than 3,5g, hypertrigliceridyemia, hypercolesterolemia, deep vein thrombosis, frothy urine=big amount of protein in urine |
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Causes of nephrotic syndrome |
Podocytes damage= alterations in the barrier: podocytopahy -genetic alteration in nephrin (present in slit diaphragm)= dramatic proteinuria |
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Pathophysiology of nephrotic syndrome |
Severe damage to barrier=saturation=patient develops proteinuria -estimation of proteinuria: 24h urinary collection or protein to creatinine ratio in urine -nephrotic proteinuria can occur without syndrome If patient left untreated: reduction in oncotic pressure =edema formation=lots of fluid in interstitial space. Reduction in plasma volume=reduction in GFR =activation of RAAS with secondary hyperaldosteronism= vasoconstriction + Na and H2O retention=increased edema formation -in the liver: increase in lipoprotein synthesis= increase in cholesterol and serum triglycerides=lipiduria -treatment is complex: furosemide has to be filtered and linked to albumin in blood and we should expect RAAS activation Treatment: ACE inhibitors -reduced GFR and proteinuria, increased BP |
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Nephrotic syndrome symptoms |
High mortality, low BP, high triglycerides, hyper-coagulability (caused by clotting inhibitors, zymogens, plasminogen), increased liver activity linked to increase production in fibrinogen and coagulation cofactors Dramatic sign of this condition is found in the renal vain due to a high concentration of coagulation factors, thrombosis oh renal vain = high mortality -platelet aggregation: increase in platelets, hemoglobin and leukocytes due to decreased blood volume |
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Electrolytes in nephrotic syndrome |
-Na decreases thanks to brain sensors which detect low blood flow and try to increase water reabsorption but Na continues to pass through barrier -K is almost normal, case of secondary hyper-aldosteronism (angiotensin 2 is high, decreased GFR), ANGIOTENSIN 2 moves ROMK from luminal to basolateral space even if u have activation of aldosterone u can compensate for the hypokalemia |
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Diagnoses of nephrotic syndrome |
1.clinical diagnoses: 24h urine collection or protein to creatinine in ration -blood sample: detect albumin, renal function, electrolytes, cholesterol, coagulation factor and hormones 2.investigation of possible causes and decide if renal biopsy is needed -urine microscopy: performed and examined after centrifugation, observe cells and casts due to coagulation of proteins, hyaline casts with no cells inside |
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TYPES OF PROTEINS THAT CAN PASS DURING NEPHROTIC SYNDROME |
Depends on damage: - normal urine: small amount of albumin and tubular proteins as uromodulin produced by distal tubular convoluted cells -selective proteinuria: albumin and immunoglobulins + dramatic immunodeficiency due to loss of immunoglobulins -non selective proteinuria due to severe damage:bigger proteins found as well |
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Treatment of nephrotic syndrome |
Management of symptoms Edema: low salt diet, diuretics Proteinuria: ACE inhibitors Hypoalbuminemia: high protein diet not recommended Management of complications: Hyperlipidemia, thromboembolic risk, infections due to immunodeficiency |
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Nephritic syndrome |
Inflammatory condition with abnormal filter: reduction in glomerular filtration space due to increased cellularity=passage of RBC and leukocytes in urine Active urinary sediment: presence of dysmorphic RBC in urine+ small amount of protein=formation of granular casts + edema Hypertension Hematuria (even macro hematuria ) Cylinduria: renal casts in urine Oligoanuria: due to reduction in GFR Asothemia: abnormally high levels of nitrogen compounds Modest proteinuria: not nephrotic |
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Is nephritic syndrome the same as glomerulonephritis? |
Yes. An example of GN, is acute GN a typical condition in which there is inflammation with an increase in cellularity and in filtration of WBC |
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Clinical presentation of nephritic syndrome |
Decrease in urinary output Alteration in color of urine due to free hemoglobin after the break of RBC (brown urine) Blood in urine: macrohematuria that can be detected with dipstick. Other conditions in which we have macrohematuria: urological diseases, tumors, alteration in coagulation Reduction in GFR due to increased pressure in bowman space= increased creatinine and blood pressure -edema due to reduction in GFR, no severe proteinuria because there is no damage in podocytes and electric charge is preserved. We do not expect hypoalbuminemia -alteration is cellularity= chronic damage due to fibrosis development |
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Nephritic spectrum |
Asymptomatic glomerular hematuria: small alteration in glomerular structure, micro or macroscopic hematuria -nephritic syndrome: acute kidney injury, hematuria, RBC casts, edema, hypertension, proteinuria 1-3g/day -RPGN: ACUTE kidney injury, hematuria, RBC casts, systemic symptoms, protein urea 1-3g/day -chronic glomerular disease: chronic kidney disease, hematuria, proteinuria, hypertension, late stage GN, burned out disease |
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Main causes of acute GN |
Post-infectious streptococ., Vasculitis, IGA nephropathy, genetic conditions |
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Primitive GN presenting with nephritic syndromes are |
1.Acute GN post-infections: condition linked to systemic infection 2.GN rapidly progressive: sudden progression in ESRD 3.GN with mesangial deposits of IGA (Berger) due to alteration in mesangial cells 4.mixed syndromes: focal segmental glomerulo sclerosis: nephritic + nephrotic syndromes |
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Glomerular diseases |
-primary glomerulopathys: specific and rare disease -secondary glomerulopathys: systemic disease which can have renal involvement. Th most common cause is diabetes and other causes like SLE, R. Arthritis, vasculitis, myeloma, cryoglobulimenia The outcome is influenced by genetic predispositions |
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Acute glomerulonephritis |
-asymptomatic glomerular hematuria due to small alterations in glomerular structure -typical nephritic syndrome -rapidly progressive glomerulonephritis a more severe form Characteristics: hematuria with RBC casts, proteinuria (1-3g/dl), edema due to reduction in GFR AND NOT DUE TO DECREASE IN ONCOTIC PRESSURE (NEPHROTIC), SEVERE hypertension |
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Ethiopathogenesis of acute GN |
In kids: first post infections GN, since upper respiratory tract infections are frequent In adults: suspect first BERGER disease or membranous proliferative GN |
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Acute GN post-infectious |
-Develops after respiratory bacterial or viral infections -kids are most involved -increasing in elderly due to immunodeficiency and is more severe due to general state of patients since an increase in BP and Na retention can lead to heart failure |
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Etiology of acute GN |
Mechanism developed after strepcoc. Infection, presence of nephritogenic strain similar to protein present in glomerular barrier -glomerular damage through 2 different mechanisms: 1.mimic mechanism= formation of immune complexes inside glomerulus 2.trapping of circulating immuno-complexes in glomerular barrier. This mechanism distinguishes acute GN from Bergers diseases that presents IGA and works without complement activation in which we have the involvement of the first immunological response. Both mechanism lead to activation of complementary system in kidney. -formation of humps = deposition of immuno-complexes in sub-epithelial sites= podocyes detachment + cytokine activation =WBC migration + damage to glomerular barrier |
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Immuno-complex deposition in kidney |
Complement activation + leukocytes recruitment Platelet aggregation= thrombosis in vessels of glomerular structure -activation of factors = fibrosis -inflammation and increased cellularity = reduction in GFR + PROLIFERATION of mesangial cells -kidney has to reactivate remaining nephrons to try to compensate |
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Diagnoses of acute GN |
1.Throat swab: presence of pharyngeal injury and beta hemolytic strep group A 2.Immunological response: presence of isoenzymes of strep 3.transient decrease in serum C3: signal that smt is wrong in glomerular cells -in urine glomerular casts are formed by dysmorphic RBC -at biopsy with optical microscopy: increase in mesangial cells and endothelial cells, sub epithelial humps due to deposition of immuno-complexes -immunostaining: IGG, IGM and C3 -timing =2 weeks |
