ࡱ> ~Root Entry  Fi4@ 1Table%&'()*+,-./56789[@WordDocumentPUVWXYZ[\]`SummaryInformationlmno(z{|}   !"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOZ[\]^_`abcde{|} [(@(NormalCJmH 8@8 Heading 1 $$@&5CJ8@8 Heading 2 $$@&5CJ4@4 Heading 3 $$@&CJ8`8 Heading 4$ & F@&>*>`> Heading 5$ & F@& >*<A@<Default Paragraph Font,>@,Title$ 5>*CJ$*B@* Body TextCJ@C`@Body Text Indent@ , @",Footer  !&)@1& Page Number0J`B0Subtitle$6CJBUh55?٨Us !!!!  ! ! ! BUM^ {%*H/h55 (rs$5  %ey} '(;u 2`mn9:>?BJ`m}x'()*PQefty%  J c ^ _ ( 9 P Q s  - [ c %(+./OPcdst  opN-.Qy&Epq.CHIJKLMNOPQRUtm<Xi0 x LiNf,Z82DS*Os| 'Ci  = ^ s !'!K!a!~!!!"c""#e#x######"$A$\$l$w$$$$$$%=%R%|%}%%%&H&\&&& 'X'''''((g(x((())"))*8*f**** +`++*,,,-?--B.v.....//*/4/F/I/^///e00000@1n111J2|222M3h33!4>4k444445I5V5h555!!<ositsMinimal Change (Lipoid nephrosis)Nephrotic SyndromeUnknownChildren w/ massive proteinuria, renal function remains good, Tx: corticosteroidsNormalNegativeLoss of foot processesFocal Segmental glomerulo sclerosisNephrotic syndrome, non-nephrotic proteinuriaUnknownCompared to Minimal change disease: inc hematuria, red GFR, inc HTN, poor steroid response, many progress to chronic GN, IF shows deposits. Rare spontaneous remission.Hallmark is degeneration and focal disruption of visceral epithelial cells. Focal and segmental sclerosis, collapse of BM, inc mesangial matrix and hyalinosisFocal IgM and C3Loss of foot processes, epithelial denudationDiseaseClinical PresentationPathogenesisClinical CourseLMIFEMMembranoproliferative GN Type I Nephrotic Syndrome Immune complex Older children, young adults. Some patients develop crescents, and RPGN, 50% develop CRF. Tx of steroids, immunosuppressive agents not very effective. Large hypercellular glomeruli, Mesangial proliferation, GBM thickening, splitting, some crescents IgG, C3, C1, C4 Subendothelial depositsMembranoproliferative GN Type II Hematuria, CRF AutoAb, alternative complement pathway Older children, young adults. Some patients develop crescents, and RPGN, 50% develop CRF. Tx of steroids, immunosuppressive agents not very effective. Recurrence is common in Type II Large hypercellular glomeruli, Mesangial proliferation, GBM thickening, splitting, some crescents C3, some IgG Dense depositsIgA Nephropathy (Bergers disease)Recurrent hematuria and /or proteinuriaUnknownAffects children/young adults in 1-2 days of mucosal infections of Resp, GI or urinary tracts, slowly progressive diseaseFocal proliferative GN; mesangial wideningIgA, IgG, IgM, C3 in mesangiumMesangial and paramesangial dense depositsChronic glomerulonephritisCRFVariableInsidious development slowly progresses to death in uremia. Most patients have HTN, manifested by cerebral or cardio symptoms. Hyalinized glomeruliGranular or negativenone Chronic renal failure: Major Causes of CRF Glomerulopathies Hypertension Obstructive uropathy Interstitial nephritis Hereditary (PCKD) Intact Nephron hypothesis nephrons in damaged kidneys operate at a higher functional level so that gross kidney function is preserved Discrimination between ARF and CRF H & P- Previous serum Creatinine, nocturia, history of foray urine, edema, orthostatic HTN, muscle tenderness, etc Kidney size small, CRF Renal Osteodystrophy yes- CRF Carbamylated HgB yes- CRF Anemia no- ARF Stages of renal failure Decreased renal reserve excretory regulatory capacity intact, GFR dec. but labs normal Renal insufficiency mild azotemia, impaired concentrating ability, nocturia, anemia Renal failure anemia inc, hypocalcemia, hyperphosphatemia, hyponatremia, impaired concentrating ability, nocturia, isothenuria, metabolic acidosis Uremia constellation of signs/symptoms Signs and symptoms of uremia: Nervous- stupor, coma, fatigue, malaise, insomnia, memory, speech slurred, tics, dementia, headache, cramps GI hiccup, parotitis, gastritis, anorexia, pancreatitis, ulcer, nausea/vomiting Hematology anemia, bleeding Immunology inc infection/ cancers Cardio pericarditis, atheromatosis, edema HTN, cardiomyopathy Pulmonary pleuritis, edema Skin pruritus, nail atrophy, melanosis Endocrine glucose intolerance, hyperlipidemia, hyperPTH, hypogonadism, growth retardation Bone renal osteodystropy, amyloidosis Misc thirst, weight loss, uremic fetor, hyperthermia Functions of the Kidney Fluid-electrolyte balance, acid/base homeostasis Types of filtrate products Non regulated plasma concentration falls w/GFR (creatinine, BUN) Partial regulation balanced until GFR < 30-40 ml/min (Hydrogen ion, uric acid, phosphate, calcium) Complete regulation balance maintained until GFR < 10-15 ml/min (Na+, K+, H20) CRF loss of renal concentrating ability At max urine output, CRF patients make less urine than normal and at higher osmolaritymore Na+ loss At min urine output, CRF patients make more urine than normaland at less osmolarityunable to excrete enough Na+ Signs of abnormal fluid balance Abnormal concentration Nocturia Volume depletion/hypernatremia w/o access to H20 or impaired thirst Abnormal dilution Hyponatremia Greater susceptibility to H20 intoxication Na+ excretion with CRF CRF patients excrete same amount of Na+ as normal patients, but they have dec GFR, so they lose higher % of Na+ Regulation of Na+ by CRF patients Adaptation occurs in distal tubule Aldosterone levels normal to high ANP inc Uremic symptoms from abnormal Na+ Hypernatremia-- edema, CHF, hypertension Hyponatremiavolume contraction, ARF e. K+ excretion with CRF i. K+ regulation with CRF Maintained until GFR <10% Less flexibility in handling loads Kidney and colon adapt to inc K+ secretion ii. Factors that allow serum K+ to remain normal inc Na+ delivery to distal nephron inc flow/nephron inc Na/K ATPase up to 35% of K+ can be colon excreted uremic symptoms from abnormal K+ cardiac arrhythmia flaccid paralysis f. Metabolic acidosis in CRF decreased NH3 production decrease titratable acid production HCO3- loss (equivalent to H+ gain) Characteristics of renal acidosis i. Normal or high anion gap ii. acidic urine pH Treatment of uremic acidosis i. use of HCO3- (Na bicarbonate, calcium carbonate, Na citrate) ii. Adverse effects of acidosis Metabolicprotein wasting, altered triglyceride metabolism Hormonal inc catecholamines, inc aldosterone, inc corticosteroids Hemodynamicsaltered contractility, arteriolar dilatation, peripheral venoconstriction, inc pulmonary vasc. Resistance, ventricular arrhythmia GI nausea, vomiting, gastric atony Skeletal inc bone resorption, dec bone formation, enhanced PTH action Excretion of waste Uremic toxicity i. ameliorated by dietary protein restriction ii. limited by possible negative N balance Hormone production As GFR dec, PTH inc trade off hypothesis Treatment of hyperphosphatemia i. Dietary Pi restriction ii. Pi binders Ca binders Renal production of EPO and 1,25 D i. EPO loss anemia ii. 1,25 Dsecondary anemia Hormone catabolism Treatment for CRF Focus on ACEIs Reduce MAP while also lowering glomerular capillary pressure Decrease proteinuria Tend to be grown inhibitor of fibrosis Secondary Hypertension: I. Conditions causing secondary Hypertension Renal parenchymal disease (acute/chronic GN, nephritis, PCKD) Systemic Vasculitis/glomerulitis (Wegners, Henoch-Schonlein purpura) Oral contraceptives a. causes HTN, esp with cigarette smoking Renal vascular disease Renovascular hypertension stenonic lesion results in dec perfusion of kidney, inc renin secretion, high AgII diagnosed by ultrasound, captopril radionucleotide renography, angiography Mineralocorticoid excess (hyperaldosteronism, Liddles, licorice) hypertension with hypokalemia metabolic acidosis aldosterone secreting tumor i. elevated 24hr urinary aldosterone after 3 days high salt diet ii. renin is low (as opposed to secondary hyperaldosteronism) Pheochromocytoma a. adrenomedullary tumor tachy, HTN, palpitations, headache Hypothyroidism associated with inc total peripheral resistance, higher sympathetic tone Tubular Disorders: Acute Tubular Necrosis results in coagulative necrosis, desquamation of cells in lumen to form granular and cellular casts, RBCs in lumina, ATN usually heals by resolution Nephrotoxic injury affects much of the PCT only drugs aminoglycosides, sulfonamides, methoxyflurane Metals mercury, silver, arsenic, lead, gold Diagnostic agents radiocontrast dyes Organic compoundscarbon tet, ethylene glycol, CH3OH Ischemic lesions are patchy in distribution Interstitial Disorders: Acute interstitial nephritis rapid onset, morphologic finding of interstitial edema Direct bacterial neutrophils a plenty Drug hypersensitivity clinically most important, limits pharmacologic agents, findings of patchy inflammatory cells, inc. eosinophils, rare granuloma formation Common drugs: methicillin, ampicillin, rifampicin, phenindione, sulfonamides, NSAIDs Cell mediated immunitysuggested by monocytes, or granulomas Anti tubular BM Antibodiesdrug acts as hapten and combines with BM rendering them antigenic Allergin-reagin systemelevated IgG Chronic interstitial nephritis- interstitial fibrosis and tubular atrophy, with some inflammation, glomerular and vascular changes Chronic pyelonephritis not really consequence of longstanding bacterial infection, may or may not have reflux or obstruction large segmental areas of scarring, at poles usually dilated pelvis lymphocytes and plasma cells beneath transitional epithelium large clusters of atrophic tubules Obstruction Vesico-ureteral reflux Chronic infection Analgesic abuse Radiation Other nephropathy Acute Renal Failure: Definitionsudden decline in renal function w/ rise in serum creatinine, azotemia, normal or decreased urine output Causes of ARF Pre-renal dec. volume by blood loss, diarrhea, vomiting, diuretic, CHF, shock, prostaglandin inhibitors in susceptible individuals orthostatic changes in BP Post-renal- obstruction by prostatic hypertrophy, nephrolithiasis, tumor inc. BUN/Cr ratio Parenchymal ARF Acute glomerulonephritis (AGN)HTN, edema, proteinuria, RBCs, RBC casts in urine look for history of sore throat, strep, SLE proteinuria, RBC casts in urine ii. Vasculitis inflammatory involvement of blood vessels, HTN, proteinuria iii. Acute interstitial nephritis (AIN) allergic rxn in kidney after drug exposure, eosinophils in urine History of nephrotoxic drugs, skin rash, fever RBCs in urine, proteinuria, and eosinophiluria iv. Acute tubular necrosis (ATN) severe hypo-perfusion after toxins Poorly concentrated urine, rich in Na+, muddy brown casts, renal tubular cell casts III. Complications of ARF Similar to CRF, including metabolic, neurological cardio, GI symptoms Also hematologicalanemia, platelet dysfunction (bleeding) and inc. infections (most common cause of death in ARF) Treatment of established ARF Measure weight as indicator of volume status Restrict fluid intake, give high calorie, low protein diet to minimize catabolism 3. 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Cgd<0g;,2?ܺ#ܴPNS changes9 a 4>9jbjb j5]D===<>X>X??(??????VVVVVVV,XZW?????W,@??p?&,@,@,@?(??Vhh?V,@,@,D RV?lI!=?FVbKENdensed Renal Pathophysiology Notes I Glomerular diseases: Histologic Alterations Glomerular hypercellularity cellular proliferation, leukocytic infiltration Basement Membrane thickening- thickening of BM, deposition of electron dense material (most common thickening is by extensive subepithelial deposition, as in membranous glomerulonephritis) Hyalinization- accumulation of material that is homogenous, and eosinophilic by LM Sclerosis- Loss of structural detail of Glomerular tuft by increased BM or mesangial matrix, other alterations include fibrin deposition, amyloid, lipid The Clinical Syndromes: SyndromeClinical FindingsCausesAcute Nephritic SyndromeHematuria, azotemia, variable proteinuria, oliguria, edema, HTNPost streptococcal SLE Polyarteritis nodosaRapidly progressive GNAcute nephritis, proteinuria, ARFPostinfectious Systemics: SLE Goodpastures Vasculitis Henoch-Schonlein purpuraNephrotic SyndromeProteinuria, hypoalbuminemia, hypercholesterolemia, edemaMembranous GN Minimal Change Disease (Lipoid nephrosis) FS glomerulosclerosis Membranoproliferative GN IgA Nephropathy Sytemics: DM Amyloidosis SLE Drugs ( Gold, penicillamine) Infectious (malaria, syphilis, Hep B, HIV) CarcinomaChronic Renal FailureAzotemia progressing to uremiaAlmost any glomerulopathy!Asymptomatic heamturia or proteinuriaGlomerular hematuria, subnephrotic proteinuria(incidental finding in routine exam) DiseaseClinical PresentationPathogenesisClinical CourseLMIFEMPoststrep glomerulonephritis Acute nephritis  Ab mediated, circulating or planted Ag Case: young child w/ malaise, fever, nausea, oliguria, hematuria after sore throat. RBC casts in urine, mild proteinuria, periorbital edema, some HTN. Labs: ASO titer, serum C3 Tx: 95% recover w/ conservative Na/H20 balance therapy  Enlarged, hypercellular bloodless glomeruli, Diffuse proliferation, leukocytic infiltration  Granular IgG, C3 in GBM and mesangium Subepithelial humpsGoodpasturesRPGNAnti GBM AgRBC casts in urine, moderate proteinuria, variable HTN, edema Tx: intensive plasmapheresis, steroids, cytotoxic agents (these also relieves pulmonary failure)Crescents, formed by proliferation of parietal cells and by monocyte/macrophage migration into Bowmans spaceGranular immune depositsDistinct ruptures in GBM, some subepithelial depositsIdiopathic RPGNRPGNAnti GBM immune complexTherapy as with Goodpastures, but results not as dramaticProliferation, crescentsLinear IgG, C3 or granular, or noneDeposits or noneMembranous GlomerulonephritisNephrotic SyndromeAb mediated, in situMajor cause of Nephrotic syndrome in adults: Tumor, ALE, gold, mercury, Drugs, Hep B, syphilis, schisto, malaria, idiopathic. Case: insidious nephrotic syndrome, hematuria, HTN, w/ increasing sclerosis of glomeruli, rising BUN notoriously variable courseUniform, Diffuse capillary wall thickening, BM spikes between depositsGranular IgG, C3subepithelial dep2223334744444$5F55626e6677d77 & F-p & Fp & F, & F+ & F+ $d%d&d'd77!8s88888 99!9"9-9.9/9:9;9<9=9>9&`#$ & Fp & F. & F+s88888 99!9"9-9.9/9:9;9<9=9>9gi |    ,9-9/90969798999:9>90JmH j0JU0J/ =!"#$%0= /!"#$%|,, ` }!(,, ` ,-^&'d/ =!"#$%|,, ` } #(,, `,-^&'d/ =!"#$%|,, ` } #(,, `,-^&'dsevere CNS change7 Glomerular disease thru Acute Renal Failure pgs 62-130 in Renal PPD notes 10 ppo(.ppo(.o(.ppo(.o(.ppo(.ppo(.0o(.o(.ppo(.0o(.o(.ppo(.o(.ppo(.0o(.o(.DDo(.o(.ppo(.88o(.0  !"$%&'()*+,-./01.@//r// 56>*CJ & FF & FGCJOJQJmH (^qrsV5^5f5g5h5}5~5555`@aal``P@`R@aaa`zr@`Dr@a`pr@`xr@`zr@GTimes New Roman5Symbol3 Arial3Times"phC"E"V\ , ]g !4d6g5+'KENdensed Renal Pathophysiology Notes IKen LinKen Lin&{00020857-0000-0000-C000-000000000046}AddIn\\ BaseInterface&&{00020400-0000-0000-C000-000000000046}44  NumMethod7\\ProxyStu FMicrosoft Word DocumentNB6WWord.Document.8ʣk=X!{i0*Ȋ2=bI$WnC ՜.+,D՜.+,T hp|  'en]6 (KENdensed Renal Pathophysiology Notes I Title 6> _PID_GUID'AN{DE847080-A07E-11D1-9CB6-C97145A755F2}νޥ Oh+'0t  0 < HT\dl'(KENdensed Renal Pathophysiology Notes IENdKen Linen NormalKen Lin86 Microsoft Word 8.0h@(s0@Y4@jF4  ,0@0ʄ蘽PX%d@0aJ@9&OLˆޔ \M l؀feOLnDWIH$2;|HJnbh,Nz R%)OVZg0l\IKS'᪇I~C (G8:X'tL[R\s܅ale- h (ɕ9!Gc "h5y/[X`yW7} q ~Of?'4H9 g d(4Ȃj$aFP."Ԑ@mӁ #fP>kv D5tD!}񅔶?Q3R=l1e H#"$ ~y Q phg5CBt [j^hyMmi3. Cgd<0g;,2?ܺ#ܴPe9 a D>9jbjb h5]4r=r=r=h==W4?4?(\?\?\?\?\?\?xVzVzVzVzVzVzV,X|ZV\?\?\?\?\?V?\?\??&???\?(\?\?xV^f^\?xV??C RRxV>lo!r=?:VbKENdensed Renal Pathophysiology Notes I Glomerular diseases: Histologic Alterations Glomerular hypercellularity cellular proliferation, leukocytic infiltration Basement Membrane thickening- thickening of BM, deposition of electron dense material (most common thickening is by extensive subepithelial deposition, as in membranous glomerulonephritis) Hyalinization- accumulation of material that is homogenous, and eosinophilic by LM Sclerosis- Loss of structural detail of Glomerular tuft by increased BM or mesangial matrix, other alterations include fibrin deposition, amyloid, lipid The Clinical Syndromes: SyndromeClinical FindingsCausesAcute Nephritic SyndromeHematuria, azotemia, variable proteinuria, oliguria, edema, HTNPost streptococcal SLE Polyarteritis nodosaRapidly progressive GNAcute nephritis, proteinuria, ARFPostinfectious Systemics: SLE Goodpastures Vasculitis Henoch-Schonlein purpuraNephrotic SyndromeProteinuria, hypoalbuminemia, hypercholesterolemia, edemaMembranous GN Minimal Change Disease (Lipoid nephrosis) FS glomerulosclerosis Membranoproliferative GN IgA Nephropathy Sytemics: DM Amyloidosis SLE Drugs ( Gold, penicillamine) Infectious (malaria, syphilis, Hep B, HIV) CarcinomaChronic Renal FailureAzotemia progressing to uremiaAlmost any glomerulopathy!Asymptomatic heamturia or proteinuriaGlomerular hematuria, subnephrotic proteinuria(incidental finding in routine exam) DiseaseClinical PresentationPathogenesisClinical CourseLMIFEMPoststrep glomerulonephritis Acute nephritis  Ab mediated, circulating or planted Ag Case: young child w/ malaise, fever, nausea, oliguria, hematuria after sore throat. RBC casts in urine, mild proteinuria, periorbital edema, some HTN. Labs: ASO titer, serum C3 Tx: 95% recover w/ conservative Na/H20 balance therapy  Enlarged, hypercellular bloodless glomeruli, Diffuse proliferation, leukocytic infiltration  Granular IgG, C3 in GBM and mesangium Subepithelial humpsGoodpasturesRPGNAnti GBM AgRBC casts in urine, moderate proteinuria, variable HTN, edema Tx: intensive plasmapheresis, steroids, cytotoxic agents (these also relieves pulmonary failure)Crescents, formed by proliferation of parietal cells and by monocyte/macrophage migration into Bowmans spaceGranular immune depositsDistinct ruptures in GBM, some subepithelial depositsIdiopathic RPGNRPGNAnti GBM immune complexTherapy as with Goodpastures, but results not as dramaticProliferation, crescentsLinear IgG, C3 or granular, or noneDeposits or noneMembranous GlomerulonephritisNephrotic SyndromeAb mediated, in situMajor cause of Nephrotic syndrome in adults: Tumor, ALE, gold, mercury, Drugs, Hep B, syphilis, schisto, malaria, idiopathic. Case: insidious nephrotic syndrome, hematuria, HTN, w/ increasing sclerosis of glomeruli, rising BUN notoriously variable courseUniform, Diffuse capillary wall thickening, BM spikes between depositsGranular IgG, C3subepithelial dep2223334744444$5F55626e6677d77 & F-p & Fp & F, & F+ & F+ $d%d&d'd77!8s88888 99!9"9-9.9/9:9;9<9=9>9&`#$ & Fp & F. & F+s88888 99!9"9-9.9/9:9;9<9=9>9gi |    ,9-9/90969798999:9>90JmH j0JU0J/ =!"#$%0= /!"#$%|,, ` }!(,, ` ,-^&'d/ =!"#$%|,, ` } #(,, `,-^&'d/ =!"#$%|,, ` } #(,, `,-^&'dsevere CNS change7 Glomerular disease thru Acute Renal Failure pgs 62-130 in Renal PPD notes 10 NS changes9