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28 Cards in this Set
- Front
- Back
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Define the following terms as relating to glomerular nephropathy...
a. acute b. subacute |
1. glomerular injury occuring over days to weeks
2. (aka Rapidly Progressive) weeks to few months |
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Definitions:
Acute GN: Subacute (_________): Chronic: Focal: <____% Diffuse: >___% most common GN worldwide? |
acute - days/weeks
subacute, rapidly progressive - weeks to months chronic - months/years focal - <50% involved diffuse - >50% involved IGA nephropathy |
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Major S/S of acute GN? (6)
Proteinuria > 3.5 g/d, low albumin, high lipids, edema: |
hematuria
RBC casts proteinuria HTN edema decreased renal fxn (incresaed BUN, Cr) nephrotic syndrome |
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Defined the following terms as related to GN
a. focal b. diffuse |
a. <50% of glomeruli involved
b. >50% involved helps determine how it is distributed in the kidney |
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Inflammation of the kidney:
any kidney disease: Proteinura = 24 hr UA protein > _____ g/day. Blood work often shows high _____ and low ______. Treatment of post strep GN |
nephritis
nephrosis >3.5 g/day high lipids, low albumin treat infection and fluids |
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1. Case #1: 36 y/o f with hematuria x several days; LE swelling, feels "puffy", URI 2-3 weeks ago. D/d? and most likely agent of cause?
2. UA+ for blood,40-60 RBC's and casts found (meaning?) (test to find?), 3. throat cx negative, ASO+ (what does this mean?) 4. Explain S/S, UA, labs: 3 other causes of infectious GN? |
1. post URI - post strep GN Group A strep
2. UA RBC's - bleeding RBC casts - glom involved (need microscope) 3. throat cx -, (ASO= anti-streptolsis O an elevated titer means sub optimal clearing of infection): strep infection resolved, but not cleared 4. bacterial endocarditis, visceral abscesses, infected shunts |
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Case #2: 12 y/o sports physical, possible viral URI 1-2 weeks prior:
What drug generally given as renal protective? What else can be given to treat the HTN? |
IGA nephropathy
ACEI's fish oil |
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Case #3: 56 y/o m w/ proteinuria, pneumonia 5-6 wks prior, flank pain x 1 mo, bilat x 1 wk; mild leg edema, nocturia x 10, 10# wt loss:
PMH- HTN 1 year prior, high cholesterol, Father died renal failure, mother HTN SH- heavy metal miner, rancher with cows, alfalfa, construction worker Albumin 1.8 - normal? urine drip protein 4+ - normal? |
idopathic nephrotic syndrome- characterized by proteinuria and hypoalbuminemia, edema, and hyperlipdemia
albumin is low - (N ~ 3.5) protein shouldn't be in urine |
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systemic causes of nephrotic syndrome?
drugs that can cause nephrotic syndrome? infections causing nephrotic syndrome? Common cancers that cause? |
DM, SLE, amyloidosis, HIV
gold, penicillamine, probenecid, captopril, NSAIDs, heroin bacterial endocarditis, Hep B, shunts, syphilis, malaria Hodkins, breast, GI |
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comprises 40% of idiopathic GN:
complications of nephrotic syndrome? why incresaed risk of drug interactions? |
MGN (membranous GN)
renal vein thrombosis infection susceptibility Vitamin D deficiency protein malnutrition decreased protein to bind with |
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1. 15% of nephrotic syndromes, sediment usually neg, HTN/renal insuff. rare, no CKD: Normal glomeruli by light microscopy
2. Should consider what diseases if does not get better with prednisone? 3.Active urine sediment, changes over weeks-months, often post viral illness, crescentic Gn on biopsy: (most common clinical presentation? 4. Tx for RPGN? |
1. MCD (minimal change disease)
2. Hodgkin's, non-Hodgkin's lymphoma 3. RPGN (rapidly progressive glomerulonephritis)- severe oliguria and proteinuria 4. 50-75% respond to high pulse steroids, cyclophosphamide for extrarenal dx may progress to dialysis |
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Describe the following for focal and segmental glomerulosclerosis...
a. pt population b. histo pic c. treatment d. prognosis |
a. older people
b. slide says fusion of foot processes c. no set treatment d. slow progression to ckd |
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56 y/o m to ER, polydipsia, polyuria, BP 130/86, +1 edema on LE's:
Two major causes of ESRD? proteinuria, hematuria, edema; histo similar to FSGS, common in IVD users, may respond to Zibuvidine: |
DM
GN, diabetic nephropathy HIV GN |
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subset of RPGN, crescentic:
if the above has both Lung and renal involvement: irreversible changes in kidney, poor response to therapy, glom sclerosis, tubular atrophy, interstitial fibrosis: |
Anti-GBM disease
Goodpasture's disease SLE |
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52 y/o m, 2 days post CABG: urine output <15ml/hr, Bun, Cr, K increasing, Fe(Na) > 1, developing pulmonary congestion:
What's happening? Fe(Na) formula (fractional excretion of sodium)? Fe(Na) > 1 = ? |
compromised fluid removal from kidneys
P= plasma, U= urine Fe(Na) = (Na first, UP/PU) U(Na) x P(Cr) ------------- P(Na) x U(Cr) Fe(Na) > 1 = intrinsic renal failure possibly prolonged post renal failure |
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Case #1 cont:
UA has muddy brown casts - significant? elevated BUN/Cr = ? most common form of renal failure in hospitalized pt? |
significant - tubules sloughing off (Acute tubular necrosis)
elevated BUN/Cr = renal failure Acute tubular necrosis (ATN)- due to ischemia, drugs, toxins |
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1. 1st tx for ATN? 2nd option?
2. Most common cause of ATN? 3. 3 other causes of ATN? |
1. furosemide (a loop diuretic), if unresponsive, then temporary dialysis
2. Most common cause ischemia 3. a. sickle cell nephropathy b. hypercoagulable state c. arteriolar sclerosis |
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Case #2: 58 y/o f w/ RLL pneumonia; on ranitidine, put on levofloxacin abx, develops fine diffuse rash, fever, arthralgia.
CBC: elevated WBC, left shift, eosinophils UA: hematuria, pyuria Dx? |
AIN Acute "allergic" interstitial nephritis (AIN)- wont show red cell casts, actual term is "Acute Interstitial Nephritis"
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Some typical drugs that cause AIN? (CHAN PQRS)
Other exogenous causes? |
Most common- PND penicillins, NSAIDS, diuretics
H2 blockers Allopurinol Rifampin Quinolones Sulfa , acetominophen, lead, cyclosporine, radiocontrast, heavy metals |
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Endogenous (metabolic) causes of AIN?
Glucocorticoids are effective, but why should you be careful with infections? |
acute uric acid elevation
hypercalcemia hypokalemia Misc: hyperoxaluria, cystinosis, Fabry's disease glucocorticoids reduce immune fxn |
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Polycystic kidney disease:
S/S? usually show up at what age? Why should you do scans of the brain? |
ADPKD- autosomal dominant polycystic kidney disease
hematuria, multiple cysts, episodic flank pain, HTN, prone to UTI's- most end up on dialysis 30s, 40s risk of Berry aneurysm - intracranial hemorrhage |
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Renal tubular acidosis:
1. Type I: Where, problem? 2. Type II: Where, problem? 3. Type III: Where probelm? 4. Type IV: Problem? 5. RTA usually causes _______ metabolic acidosis. |
1. Type I: DCT - acid excretion defect
2. Type II: PCT - HCO3 reabsorption defect 3. Type III no longer used DCT w/ bicarb wasting in children but resolves with age 4. Type IV: defect in NH4+ excretion 5. non-AG |
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Myeloma, renal transplant, ifosphamide, L-lysine usually cause _______ RTA.
Sjogren's, sarcoid, urinary obstruction, amphotericin B, lithium usually cause: Hyperkalemia, low renin/aldos, cause: and defect? |
Type II - PCT
Type I - DCT Type IV - NH4+ excretion defect |
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Causes of Non-AG metabolic acidosis? (HARDUPS)
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Hyperalimentation
Addison's, Acetazolamide RTA Diarrhea Ureteral/sigmoid/ileal diversion Pancretaic fistula Spironolactone |
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3 conditions associated with Type IV RTA:
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DM
glomerulosclerosis Many forms of advanced CKD (chronic kidney disease w/ Tubulointerstitial involvement) |
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What is necessary to diagnose primary glomerular disease?
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biopsy needed to determine type of GN, but first rule out other sytstemic causes
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Describe minimal change diseases...
a. % of nephrotic syndromes b. sed? c. other negs? d. if not resolving? |
a. 15% of neph
b. sediment usually neg c. neg HTN, renal insuff, CKD unusual d. consider Hodgkin's and non-hodgkins |
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GN w/ nephrotic syndrome as primary presentations (5)
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MMFMM
1. membranous glomerulonephropathy MGN 40% 2. Minimal Change Disease (MCD) 15% 3. Focal segemental glomerulosclerosis (FSGS) 15% 4. Membranoproliferative glomerulonephritis (MPGN) 7% 5. Mesangioproliferative GN 5% |
