nephrology Flashcards
diagnostic method of kidney
most chronic diseases r asx so picked up incidently on urine analysis or abnormal renal aprameters (creatinine, uric acid, BUN). blood test (ESR,anemia, proteinuria). deranged electrolyte balance.
history of patient
good history outlines: questioning & evaluating sx, Socrates to evaluate PAIN (SITE, ONSET, CHARACTERISTICS ,RADIATION, association Factor, time, exacerbating and relieving factors.
pMH, RF’s, FMhx and social hisotry.
hsigns and symptoms of kidney dsiease
urination changes (poly/oligo or anuria). foamy/ hematuria.
peripheral oedema -> fluid overload, nephrotic syndrome, hypercholesterlimenia / hypoalbunisim.
hypertension (increased intravascular pressure due to renin). dyspnea (fluid in chest)/ angina.
other signs: difficulty sleeping / fatigue (increased toxin, secondary anaemia).
muscle spasm/twitching: electrolyte imbalance, low Ca 2+,high phosphates (erythropoetin-> stimulate RBC production).
uremia: in R-> uremic pericarditis, uremic encepalopathy (ALS< confusion), asterixis (tremor flap bilateral), pruritis (dry skin).
N+ V (anoreixa, Wt loss)- decreased appetitie
platelet dysfunction (thrombocotyopenia, gingivial bleeds, cutaenous bleeds, epistaxis, petechiae/ purpura, easy bruising).
physical exam
inspect for bruises, edema, uremic tinge, vasculitis rash (indicitive for autoimmune vasculitis HSH) . plpation (PCKD enlarged), percuss (R. kidney below 12th ICS-> liver ). pain indicate urolithiasis and pelonephirits (flank P).
ascultation- renal bruits (RA stenosis).
CVAT- tenderness if pain reported on hit).
kidney: 5-6 cm, 125-10 g. from t12 to L3.
uroanalysis/ quality of urine.
painless hematuria (malignancy!), hemogloinuria (severe intravascular hemolysis) polyuria (DM, DI, overhydration), persistent hematuria (vesicular or supra/vesicular cause), hematuria on 1st or last part of voiding (urethral damage).
terminology:
polyuria > 2 L/ day in adults.
oliguria (< 500/ ML day) indicate obstrution, renal parenchymal disease).
anuria < 100 ml (stones/ tumor, HTN).
* HTN causes poly/anuria*.
isosthenuria - loss of ability to concentrate / dilute urine-> CKD. specifci grvity 1.010 SG
glycosuria - DM.
proteinuria -1/3 g/l AGN (acute GN) (light) 0.3- 1.5 g/L , mild = 1.5-4 g/l & severe > 4 g/L.
SG: 1.005-1.030 (dehydrated-> 1.030) and lots of fluid (1.001).
urinalysis : presence of blood, protein, glucose, ketone, nitrate, leukocyte, pH, osmolarity- dipstick.
urinalysis continued
urine microscope or flow cytometry detect Er (dysmorphic RBC nephritis), RBC casts -> glomerular disease. crystals -> urolithiasis.
leucocytes+ bacteria + white casts-> pyelonephritis.
urine pH (RT acidosis).
collect urine over 24 hrs-> assess calcium oxalate+ urate (renal stone disease) e.g catheterization.
blood values -> serum creatinine ( 53-106 normal) only rises if eGFR < 50% (indirect indicator).
creatinine clearance -80-180 mL/min
U+V/P
if 700-800 begin dialysis.
BUN >/= 20:1 prerena (dehydration).</=10:1 (renal damage.
10:1-2: 1 (normal or post renal cause).
uric acid: metabolite of purine bases.
other investigations for diagnosing kidney diseases
USS and biopsy -> nature and extend of disease.
imaging: X ray-> renal size, diff b/w tumors/ casts. dilution of UT.
IVU-. x ray taken via IV bolus injection-> visualise renal parenchyma-> stones, papillae, urothelial malignancy.
CT- lesions, stones.
radionuclide-> cortex, size, function of each kidney
nephritic syndrome/AGN
inflammation to glomerulus. microscopic/ macro hematuria, proteinuria, glycosuria (sterile), HTN. extra -renal _> alveolar hemorhage, rash.
AGN causes nephritic syndrome.
damage to bowman capsule causes leaks-> RBC (acanthocytes/ dysmorphic)
podocytes cause proteinuria (<3.5 g/24 hr).
Neu recruited and leak (sterile pyouria).
inflammation reduces eGFR -> oliguria and AKI creatinine increase).
azotemia (increase urea).
RAAS activation (HTN)- Na+ and water retention.
nephrotic if >3.5 g/24 hr.
compexes: rapidly progressive GN, anti GBM antibody (good pasutre), ANCA ( vasculitis), imune complex mediated GN (IgA nephropathy, SLE, PSA), membranoproliferative GN.
rapidly progressive GN
aka crescenteric GN. its caused by other GN disease - anca, immune complex or anti GBM.
loss of 50 % GFR.
ruptured capilary wall-> accumulate immune complex, fibrin and fibroblasts, paritetal epithelial cells & leak. proliferate paritetal cell (severe injury)
on biopsy see crescenteric shape on MS.
trx: treat underlying cause.
anti GBM ( good pasture)
Ab-Ag mediated inflammation against GBM.
crescent formation and 90% have RPGN.
targets NC1 domain of alpha 1 chai of type 4 collagen (also present in lungs). linear deposition along the GBM. on immunoflourescent.
alveolar haemorrhage (seen 60%) or sometimes isolated.
anti GBM -> plasma phoresies, corticosteroids, cyclophosphamide (immune suppressant agent)
ANCA-> no immune deposit on electron MS and immunofluorescent. account for majority of cases .
pANCA and cANCA against myeloperoxidase and proteinase 3 Neu-> lysosomes and Neu granules activated-> vasculitis.
systemic: prodrome of flu like sx and AKI sx manifest, myalgia, malaise, arthalgia.
Neu-> infiltrate, cause inflammation & necrosis.
monocyte infiltrate-> scarring/ fibrosis.
Trx: steroids, immunosuppressant, azithroprim (12 month till stability).
immune complex-> immunofluorescent seen deposit in GM. histological and
IgA nephropathy. (mesangial and GC IgA deposits)
post strep-> sub-epithelial hum, anti strep Ab.
lupus nephritis: full house IgG, IgA, c3, c1q,
- pathophysiology: activate classical complement pathway (inflammation) associated with low c3, c4 levels.
Membrano-proliferative GN
immune complex ediated MPGN and complement mediated mPGN.
causes -idiopathic and secondary is autoimmune, paraproteinaemoa, infection.
complement- decreased serum c3+c4. genentic (complement dysregulation) activates alt. pathway. low c3 and normal c4 levels.
changs: mesanglial expansion, thick BM, tram tracking of BM.
extra notes
divided into KD: glomerulopathies (bilateral) and interstitial disease. AGN (post strep 90%) affects children.
primary classification: AGN, CGN, rapid, minimal change GN, membranous and igA nephropathy.
secondary: systemic/ hereditary ( lupus, DM, amyloidosis, wegener’s (angitis), good pastures.
etiology: B-hemolytic infection (most strains r nephritogenic).
other agents include staph, pneumococcus, ricketssia. virus (mumps, small pox, hepatitis.
ma: kidney symmetrically enlarged, petechaie on surface ‘flex-bitten kidney’.
mi- diffused endcapilayr GN.
exudative: cells present, glomeruli hyperaemia-leaky.
proliferative:l structural changes.
sg urine increases 1.001-1.040.
isosthenuria reflects damage to tubules/medulla.
triad of volhard complex (IMPORTANT)
edema (face/periorbital) , slight HTN, haematuria (macroscopic).
urinary syndromes: oliguria/anuria, proteinuria, duiresus, sediment (hematuria).
edematous syndrme: nephrotic?
HTN + CVS syndrome=> retention.
neurological: brain edema seizures.
normal urine protein (1-3 g/L).
associated real function loss with AGN
low Egfr, brief azotaemia (BUN elevated).
high Sg.
dx: hx (previous infections, sore throat), bloods (elevated wbc, anemia, increased protein aplha 2 and sigma, fibrinogen increase.
immunological test: ast, decreased complement, increased circulating immune complex.
treatment of AGN
penicillin (3-4 ml) 10-14 days.
ampicillin 3-4 g/ 24 hrs.
special cases: erythromycin, cephalosporin.
prophylaxis= benzacillin 200,000 iu.
calcium gluconium 10% twice day.
vit c : 500 mg/2x daily.
diureitcs, anti -hTN (nifedipine) , cardiac failure and treat brain edema’s.
extra notes: nephritic (edema, mild proteinuria, hematuria).
chronic GN
progresive GN lasting for more than 3 months. slow cumultative damage and scarring (inflammation) result in nerotic/ neprhtic syndrome. its irreversible.
tubulointersitial fibrosis small size kidney, scarring. reductin in GFR, retention of uremic toxin, electorlyte imbalance, protein, anameia, calcium imbalance.
idiopathic cause, strep, viral hep B,C , HIV/aids, autoimmune disease SLE and oter vasculitis. most commmon in RPGN
focal glomueruloscrlosis is high.
CGN (hardening of arteries)-> scarring/contracted-> severe damage-> RF.
sx: foamy+ cola like hematuria urine, edema, face, legs edema, ascites, PE, anemia, dyspnoea, decreased alertness (uremic).
malaise, HTN secondary, oliguria, uric seizures, cramps, N+ V (electrolyte imbalance/ cerebro-edema).
urameic frost (sweating out stinky crystal uremic).
heavy proteinuria: DM, amylodiosis, membranous, focal sclerosis, minimal changes.
+hematuria: memrbanoproliferative, endocarditis, HSP, lupus.
predominantly haematuria: acute strep, RPGN, HUS.
AGN disappear and re-appear as CGN.
AGN-> CGN-> RF.
investigations of CGN
history, systemic investigation (PE),
blood test; thrombocytopenia, high BUN, CK high, HB, pancytopneia, leukopenia, cast present, proteinuria, hypocalcemia, Na,K,ph changes as disease progresses.
KUB, CT, USS- see size of kidney.
biospy-> etiology (few case)
antibody (immunoflorescence) suppress immune system, hep C+ B.
CXR (pericardium check).
abdomen, IVP, urinalysis, HCO3 checked and increased PTH.
managemnet: symptomatic, immunosuppression (teroid, MTX, cyclophsophamide, treat complication, blood transfusion, EPO IV, protein intake, phosphate levels decreased and calcium supplement,
trx: renal replacement, pharmacological, diet and activity (physiotheraphy-> BMI, exercise).
diuretics (furosemide -> fluid, HTN treated.
lifestyle-> restrict na+ and water intake, restrict potassium, po4-, mg2+, cut down protein (uric cut down), maintain weight.
CGN
acidosis is common.
end stage-> high mortality.
idioapthoc nephrotic syndrme: minimal change, focal segmental and mesangial prolif.
-BM intact, epithelial foot changes, deposit of IgM.
-all share nephrotic syndrome.
immune- humoral/cell mediated (cytokine GF), complement/ alt pathway.
humoral- insitu (ab-ag complex localised to tissue).
CIC-> trapped and cause glomerulus injury (no specificity).
cell mediated once localised can release ROS, and other harmful metabolite (amplify exisiting immune response)- direct injiry or denature glomerular proteins.
classifications (bulgarian)
INS (mentioned above)
mebraneous prolfierative:
mesanglial igG, igM, C3 depsoits
mix of both
acute pyelonephritis
RF same as lower UTI (obstruction, female,catheter, sex,DM). upper (kidney and ureter.
VUR-> retrograde urine, failure of orifice - congenital or bladder outlet obstruction.
urinary stasis.
ascending- e.coli, proteus, enterobacter (bowel flora).
hematogenous- disseminated (less common)
staph, ecoli.
unilateral - acteria adhere to tubular epith-> neu attracted-> interstitial disease.
urinalysis-wbc (casted in shape of tubule).
leukocytosis, fever, chills, N+ V-> costovertebral angle pain.
systemic.
trx;# hydrated, antibiotic-> renal abscess. recurrent-> chronic-> papillary necrosis (poor prognosis).
chronic pyelonephritis
chronic- tubulointerstitial tissue leading to scarring of pelvis, renal parenchyma and calyces.
-causes ESRD.
- congenital VURS, superimposed urinary infection.
uni/ bilateral
chronic obstructive pyelonephritis-> recurrent infx superimposed on obstructive lesion-> inflammation, atrophy and scarring.
gross- atrophy (scar-> upper/lower lobes) well defined and coarse scar.
calcyx irregular and thickened, papillae flattened.
tubules-.chronic infiltrates-> atrophy, hypetrophy and dilution.
thryoidization-> diluted-> esophilinic hyaline material resembles thryoid colloid,
hyaline arteriosclerosis, endoarteritis obliterians.
xanthogranulomatous -> unusual, rare form, proteus infx.
gross: cut surface, large orange nodules.
stag horn calculi. confused with RCC
foamy macrophage, plasma, lymp
c/f: back/ flank pain, fever, bacteriuric, pyuris.
honeymoon cystitis- frequent vaginal intercourse
endocrinological distubrnace-low EPO, vit D , low calcium, low PO4-.
classification: non symptomatic bacteriuria, acute and chronic pyelonephritis.
treatment: gentacmin or aminoglycosides. tobramycin (1-2 mg/kg. ) for 10 days
aid in regimen, diet and treat in hospital. diet rich in protein.
features of CPN
asx or w/ headache, wekanes,s dry mouth, dysuria, polyuria (2L/ 24 hr), nocturia, fever, wt loss, uti n childhood. additiona sx (palpable pain anemia, HTN).
labs: low spg, proteinuria, decreased tubular clearanc (acidosis), USS changes.
xray- low size, salt loosing, haemuatric .
features of CPN
asx or w/ headache, wekanes,s dry mouth, dysuria, polyuria (2L/ 24 hr), nocturia, fever, wt loss, uti n childhood. additiona sx (palpable pain anemia, HTN).
labs: low spg, proteinuria, decreased tubular clearanc (acidosis), USS changes.
xray- low size, salt loosing, haemuatric .
treatment of CPN
scheme-> etiolgical treat-» abx (10 days), suphonamide- biseprol-tmp/smx (10 ) & quinolone- 10 days.
abx ( 10 days) clarithromycin, aminoglycosides, gentamicin (2mg/kg), no strep.
b-lactam-cephalo.
RPGN
most severe, cellular proliferation of BC._> crescent shape.
RF shortly after.
rapid GFR via 50%.
nephrotic syn, HTN, sclerosis -> filtered-> RF.
post strep.
classification- type 1 - anti GMB detected (good pasture/ idiopathic).
type 2: immunw complex -1gA nephropahty (1) and 2 type -SLE< HSP.
immunoflorescent pattern-> granular sub.epi/endothelial deposit of c3 and ig3.
type 3: non mediated, 60 %.
ANCA (Ab against eutrophils.
1- idiopathic
2- wegener, polyangitis, churg straus syndrome/
pathophysiology-bm damange, protein, inflammaotry, cytokines (fever, inflammation), fibrin clots, hematuria, other immune component.
check C-anca and p - anca (p-anca -> mciroscopic polyangitis whereas C-anca associated with wegener).
CF: proteinuira, nephrotic or nephritic, rbc cast edema, HTN, myalgia, arthalgia, N+V.
dx: resistant HTN treatment, rapid CRF, pulmo hemorhage seen, biopsy confirms.
lower salt and fluid intak. corticosteroids. methylpredisone 10.g/kg.
suppress
plasmapheresis-> remove circulating Ab, blood TFN.
notes for analgesic nephropathy
tubular dysfunction, w. electrolyte, proteinuria mod, renal impairement.
classification: if chronic then anlagesic nephropaty, balkan endemic disease, metal and radioation nephritis, chronic PN, gout.
PG; edema, compress vessels-> hypoperfusino of intersititum->ishcmeia-> dysfunction.
toxic: polyuria, hyosthenuria, high BUN if ischemia (papillae necrosis)
CF: weight gain (retention), hematuria, oliguria (sometimes) .
usually non-oliguric.
cause: hypersensitivty to drugs like sulfonamide, floroquionolones, rifampicin, nsaid, phenytoin etc.
infection- ecoli, strep, cmv, trep pallidium, (fever) if drug then rash.
immune- lupus, sarcoidiosis, sjoren syndrome.
anti-tubular BM disease, TINU (anti.uveitits infection w/ AKI).
drug and microbes depost and immune reaction.
asx or systemic (malaise, NV , flank).
sterile pyruria, wbc cast, subneprhtoci range, esophinilia, microscopic hematuria.
trx: dialysis, urinalysis , bloods, biopsy (definitive), clinical. corticosteroid key, remove offending age.
ddx:
2-2.5 g/L proteinuria, creatine 0.6-1.2 mg/dl.
USS (enlarged), biopsy (inflammatin).
hx.
2-3 mg/kg then reduce to 0.8 mg/kg. high dose start of methypredisolone.
chronic IN: intoxication chronic, acute IN.
CF: CKD< HTN, small kidney, moderate-> hyperkalaemia, acidosis (stage 3).
salt losing nephropahty- hypotension, polyuria, dehydration, impaired urine conc ability.
chech volume + sg of urine (zimnitsky test (3hr for 24 hr). 1020 normal
if no oedema, HTN, advanced CRF, pregnant then volhard concer test (dry food , no fluid for 36 hr-> conc should reach 1028 sg).
trx: vit C 2-3 x /day and calcium gluconate, correct defciit
analgesic nephrophaty: chronic IN after excssive analgesic + NSAIDS>
if >6 / day for 3 years (phenacetin source)-> papillary necrosis.
pieces in urine seen , dark/ brown urine, pain in bavk.
same dx as IN, HTN, urinalysis.
tx: anemia reliefed, treat acidosis, dialysis if severe, HTN treat, lower analgesic.
myeloma manifestatin of kidney
IG: labda and kappa free chain 9light ) and heavy chain.
myeloma-> produe mix , whole or just ligt chain.
-500 mg normal, normal to see in urine, catalizd via PT.
bens johns protein if myeloma persists in excess. 40-50 % affected, dialysis.
depost in glomerulus.
light chai deposition disease or amyloidosis.
if in DT-> cast nephropahty-obstructive (myeloma kidney), fanconi syndrome.
volume depletion- dehydration, sepsis (suppressed), hypocalcemia, meds toxicity, infection related, nsaid related.
CRAB - hypercalciu,, rneal disease, anemia, lesions (npehrotic impaired function, micro hematuria,tubular dysfunction).
do ESR, FBC -anaemia , serum ablumin blood picture, BJP urinalysis, lytic lesions, hypercalcemia.
dx: biospy.
high cut off dialysis- membranr to reduce FLC clearance.
HTN / diseasee
uncontrolled HTN cause CKD an HT can be 2 to kidney.
hTN-> thicken and reduce lume-> ischmeia-> fibrosis and changes.
malignant HTN -> more damage since presure recieved directed va glomerulus (hyaline arteriosclerosis).
management: low salt diet, control BP WELL.
stenosis RA: renin-> angiotensin-> aldosteorne-> h20 and salt retnetion-> fluid overload.
Diabetic nephropahty
poorly controlled diabetes (check retinopahthy)
type of nephrotic syndrome (lupus and amylodisos also causes it).
lose oncotic-> oedema.
hyperproteinemia > 4 g/day in urine and hypoproteinemia in serum.
nephrotic-MCD, FSGC, SLE,MM, HSP, good pasture.
diabetes destroy efferent arteriole then afferent and cause hyperfiltration injury (mesangial sclerosis), nodular glomerulosclerosis.
affect papillae-necrosis.
renal pelvis -P PN.
glucose damage protein, fat-> BM destroyed.
ace I destroy angio 2 -> decrease GFR, decrease injury.
hyaline arterioscloeriss.
trx: manage DM.
aceI-> HSP, DM and scleroderma (contraindicated in preg)
lupus nephritis
SLE: 1/2 patients -> nephritis.
anti-nuclear ab attack , poor clearance-> attack and deposit-> inflammaton (type 3 hypersensitivity)
deposit in capillary wall, mesngial, BS, BM space.
can be focal or diffuse.
nephrotic syndrome.
hypoalbumenia.
hyperlipidemia and lipiduria.
can present a nephritic: hematuria.
location of lesion and extent of AKI determiens which 1.
dx: biospy, wire loop and crescent shaped swelling, BM.
immune maekers, complement and iG markers-> stain.
corticosteroid, suppress.
damage to mesangium secrete cytokine.
nephropathies in pregnancies and multiple myelomas.
CF of DM nephropathies
sevre tiredness, headache, N+ V , appetite reduced, pruritis, leg swelling.
DM is 1 of CKD complciation.
dx;urinalysis, screening -> urine albumin; creatine ratio. USS-> hypertrophy.
nodula wimmelstial wilsons disease (type II DM)
stage:
stage 1: v early signs of GFR (normal).
2: microalbuminemia (30-300 mg/24 hrs)
3. clinical proteinuria
4.nephortic syn+ HTN -> (5) renal impairement-> stage 6 final (ESRF).
lupus: skin UV damage-> DNA damage-> attack immune-> deposit in organs -> inflammation.
CF of lupus
etiologiy: genetic susceptibility+ environmental triggers (autoimmune) complexes deposit.
fever, wt loss, LN, malar rash, SCLE (erythema cutaneous), arthritis, raynauds, , CVS manifestaion,
LN: nephrotic manifestation or nephritis (microscopic hematuria)
mesangial and sub-epithelial damage->inflammation + nephritic synd.
stages:
class 1:minimal mesanglial lupus nephritis-> no change in biopsy, few deposits
class 2: proliferation.
class 3: focal LN-> sclerosis + necrosis.
class 4: diffuse LN, hyper cellularity, necrosis, proliferation changes etc.
class 5: membraneous LN - expansion , deposit in sub-epithelial area.
6: advanced sclerosing LN - glomerulosclerosis.
dx: immunofluorescent-> C3, IgG, m, A seen, lumps and bumps. ANA detected, esr, anemia, leukocytopenia/ thrombocytopenia.
Trx: normal renal function. analgesic, NSAIDS, hydroxychloroquine (200-40- mg/day).
corticosteroids+ immunosuppressant.
acei?ARBS.
pregnancies and renal disease
egfr picks up 80% in 1st trimester and little bit in 3rd trimester.
pre-eclampsia-> HTN and proteinuria.
susceptible to UTI, pyelonephritis due to stasis, VURS etc.
ARF: hypoperfusion? HEELPS, eclampsia, haemorrhage delivery.
CF: v. young vs older, multiple preg, DM.
L. platelets, vision disturbance, epigastric P, LDL low. hallmark (swollen intra-capillary endothelial CELLS in glomerus)
trx: MDT -abx= vancomycin, sulfonamide.
pyelonephritis: treat w/ ceftriaxone +hospitalization.
-severe: iv ticarcillin -clavulante or piperacillin tazobactam (oliguria/ immunocompromised).
end stage= infrequent cycle, ovulation, hormone imbalance.DM: use CCB instead like nifedipine.
Asx: UTI high, more nutrient in urine.
microvasculature fibrin aggregate.
1- HUS (post partum)-damage to SV in kidney (damaged RBC clog kidney filtration).
thrombocytopenia, neurological disturbance- (small clots all over)> thrombocytopenia purpura (antepartum).
acute fatty liver -> hepatocytes infiltrated.
MM: hypercalcemia - kidney damage.
uromodulin (abdundant uroprotein), hyperuricemia due to obstruction.
- Tamm-horsfall proteins (reno -original and in thick ascending limb).
monoclonal Ig deposit -> other organs-> nodular GS.
CF systemic: fever, fatigue, night sweat, wt loss, anemia.
tubular pathology-acidosis-> inability to concentrate (cannot acidify-> accumulate).
Fanconi syndrome- disorder of tubes-> faulty genes or kidney damage, 0 reabsorption.
CF
hypercalcameia-> falconi. inadequate reabsorption in proximal tubule.
clinical form
1.ARF 2. CRF.
3. falconi.
dx: bone scans, BJ urinalysis etc.
Trx: transplant, Dialysis doesn’t WORK unless special.
maintain diuresis.
deranged electrolytes: hypercalcaemia, hypercaluria, hyperphosphaturia, glycosuria.
amyloidosis
irregular misfolded protein-> deposit in organs.in tubule, glomeruli,
localised vs systemic (poorer prognosis).
primary-> MM (AL )
2nd-> familiar meditterea disease, RA< TB, MM, chronic sepsis (CHONIC INFLAMMATIODN)
classificaition based on precursor protein->
Ig light chain (AL)- MM.
serum Amyloid-> 2 to inflammation e.g RA.
manifestation: nephrotic, nephrotogenic DI, retro-peritoneal fibrosis.
cf; nephrotic syn (2-20 g/24hr), biospy to dx, glycosuria, t.acidosis, uremicemia.
Congo red and immunofluorescent, ben-johns protein, eosinophilic, apple green bifringence in plane polarised light.
proteasomes should remove it, faulty genes-> amyloidosis.
Trx: diuretic, cs, dialysis, transplant, immunosuppressant in fmf -colchine-> prevention.
find it: arteries, glomerular tuft, capillary wall, mesangial, interstitium.
gout
primary: meat and purine consumption.
secondary: to CKD.
clinical
1. after chemo-. crystallisation-> obstruction-> AKF.
2.chronic interstitial nephritis- salts in tubule-> deposit in joints, interstitial etc.
CF: conc urine polyuria, nocturia, anemia early), acid base disbalance.
nephrolithiasis-uric calculi-chronic pyelonephritis-> CRF.
CF: H. creatinine, oliguria.
acute: malignant hemopathies and tumors.
cellular disease-> hyperaemia, tubular damage + obstruction.
chornic nephto-> obese (hyperlipidemia), HTN, polydispia, micro hematuria.
dx: renal stones, joint pain (clinical)
allpurinol inhibits hypoxanthine-> xanthine-> UA metabolism, diuretic-> clear urine, diet (low red meat).
PKD
genetic autosomal (adult- PC affected)/ recessive disease (infant/ neonates-> fibrocystein affected)
tubular epith expand-> calcium influx-> water follow-> cyst enlarge-> compress vessel-> ischemia.
RAA activated-> HTN (2nd).
autosomal on cellular elvel becomes recessive (guarantee faulty in healthy protein for polycystin).
copy 1- severe, earlier onset.
copy 2: later, less severe.
see cyst in seminal vesicle, liver fibrosis-> PTN -> varices/bleeds/ hemorrhoids etc.
choestasis->cholangitis.u
potters sequence due to oligohydraminosis (oliguria intrauterine)-> pulmo hypoplasia, RF, deformities (uterine wall compress),clubbed feets, flattened nose.
berry anuerysm-> subarachnoid hemorrhage, pancrease, aortic root dilution-> CHF.
trx: urosodiol for bile issues, portocaval shunt,liver and kidney transplant.
cf: hematuria, flank pain, RF insufficiency.
more
> 5 cysts bilateral kidney.
50% chance of having it.
polycystein 1: ca2+ transport.
polycystein 2: voltage-linked ca2+ channel.
neoplastic theory= cysts due to embryological deficit, nephron don’t connect-> blind ends-> filtrate accumulate-> distend and cyst forms.
associated with diverticular disease, hernia/ abnormal vascular.
normal kidney-15-.170 g. PKD 1-5kg.
pregnancy: nerphopathia gravidum UTI’s.
dx: >5 cysts, bilateral, fhx.
2nd: complciation: cyst in liver, enlarged kidney, USS cyst >4mm. IV pyelography, other imaging techniques.
polydipseabalkan endemic nephropathy
balkan countreis-,acedonia, bulgaria, romania, serbia.#chroic bilateral fibrosis of kidneys w/ atrophy.
intersitital nephritis.
etiology: genetic-> small kidney 3-4 cm and weight 50g.
40-50 years,
terminal and slow RF.
fibrotic CT, intersistial fibrosis, flattened PT. glomerulosclerosis.
polydipsia, polyuria, nocturia, anemia,HTN, porteinuria, glucosuria, urothelial tumors?
functional: impaired concentration, clearance etv
4 stages 1. latnt (asx)-biopsy only.
2. mid and subclinical
3. clinical, fatigue, headahce, dizziness, tumor redce weight, renal colic, hematuria, backpain
clinical / decomensaption-terminal.
xathochromoia-> copper in palms and poles (red).
trx: same , reduce portien, dialysis, furosemide, tumor removal.
nephrolithiasis
kidney stone.
85% calcium-hypercalcuria, hypocituria since ccitriate inhibit calcium being free.
10% uric acid-acidic (pH<55)
2% cystin
struvite-bacteria, proteus, klebisella.
sx: severe colic pain lasting for 20 min cyclic.
N+V. flank pain cannot sit still-> shifting, diaphresis.
dx: urinalysis to exclude other test CT abdo, hx since remission high.
imaging (not x-ray since most stone are radio-luscent).
obtain- analysis (chemical composition - prevention and treatment).
Trx: analgesia (morphine).
medical expulsive therapy -> a receptor blocker like Tamsulosin to dilute.
calculus removal.
1. non-invasive-> lithotripsy.
invasive- endoscope surgery (larger than 1 cm).
meds: ca2+ (resorption-> thiazide diuretic).
chornic kidney disease
acute< 3 months kidney decrease Egfr.
chronic> 3 month.
age, diseases and co-morbidities reduce Egfr
100-120 ml/ min, les in females
make hormones, regulte, remove water.
hypertension: walls thicken-> narrow lumen-> ischemic injury- foam cells-> growth facotrs-> mesangial - mesangioblasts-> glomeruloscleroiss-> ckd.
diabetes: excess glucose to porteins - efferent stiff+ narrow (Hyaline)- hyperinfiltration-> structural matrix increaes to support-> glomerulosclerosis.
other causes: systemic disase, infection (HIV), tobacco, nsaids.
urea-> axotemia (blood, nausea/loss of appeitite)-> encepalopathy-> coma & death-> pericarditis-> decrease in platelet aggregation-> uremic frost in skin.
eletrolyte deficiency.
hyperkalemia- cardiac arrythmia.
less vitamin D- ca2+ absorption-_> PTH rleeased-> resorbed from bone-> bone weakens.
renin released-> secondary HTN.
erythropoetin-> reduction in RBC-> anemia.
dx; 90 ml/min.
irreversible if <60ml.
biospy to assess hisoltogy changes.
trx: symptomatic, transplant, dialysis.
CKD notes
etiology: GN, PN, AKD, nephropathies, DM, gout, amylodiosis, systemc diseases, esential HTN.
pathogenesis=> decrease in mass-> hyeprtrophy compensatory of surviving nephrons-> undergo sclerosis.
intia; increase of EGFR then decrease. oliguria/anuria.
fluid retention-> increase BP+ oedema.
not to use k+ sparing diuretic since k+ increase causes muscle weakness.
distal failure of na/k+ pmp-> K+ retention.
metaboloc acidosis->bone decalficiation
decrease calcitorl.
uremia-> headahche, hicupds, headache, peripheral neuropahty.
reproduction-impotent.
skin changes-> pruritis > depost urea. kussmauld breathing, melanosis
CV system-> edema, HTN.
anemia- hematuria.
classification: normal 70-120 lower in females. urea is 2.5-8. ceatinine clearance 75-125.
grade 1
2: 150-350, 8-15 urea levels, 40-20
3: 350-700, 15-30, 20-16
4:00-1300,30-50, 10-5
5>1300, >50, <5.
goes fro hyposthenuria-> isothenuria.
from excess osmalitariy and low spg to either high or lowe rthna protein free plasma 1.008-1.012..
diuresis: polyuria-> anuria.
labs
abnormal hyperphosphatemia, hypocalcmeia, anaemia, proteinuria.
USS-> small kidneys bilateral.
<400 mg/day- oliguria
<100 g/day: anuria
hosphatemia-> ectoic calcification (depost ca2+ in tissues).
increase Mg-> confusion.
haematuria
ckd: stage 1 (normal ranges)
stage 2: mild loss rf < 60, proteinuria.
stage 3: mild-seere loss 30-59.
stage 5: < 15 ml/min. ESRF.
trx: increase fluid.
decrease sodium, protein. maintian 500 Ml of na 2+ and water.
furosemide.
correct acidoiss. insulin dextrose and bicarbonate infusion.
allopurinol to control gout
gie ca2+ and vit D supplements
anemia-recombinant EPO humans.
HTN-> ace I combination.
