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    NEPHROLOGY

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    Definition and classification/staging system for acute kidneinjury (AKI)

    AKI stage Creatinine criteria Urine output criteria

    • AKI stage I Increase of serum creatinine by≥ 0.3 mg/dl (≥ 26.4 μmol /L)

    orincrease to ≥ 150% – 200% from baseline < 0.5 ml/kg/hour for > 6 h

    -------------------------------------------------------------------------------------------------------------------• AKI stage II Increase of serum creatinine to

    > 200% – 300% from baseline < 0.5 ml/kg/hour for > 12

    -------------------------------------------------------------------------------------------------------------------• AKI stage III increase of serum creatinine to

    > 300% from baseline < 0.3 ml/kg/hour for > 24or or

    serum creatinine ≥ 4.0 mg/dl anuria for 12 hou≥ 354 μmol /L) after a rise of at least 44 μmol /L

    ortreatment with renal replacement therapy

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    ATN vs. Prerenal AzotemiaIndices Prerenal ATN

    UNa < 20 > 40

    FeNa < 1% > 4%

    U/PCreat > 40 < 20

    FeUN < 35% >70%

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    Urinary Sediment Findings in Intra-Renal AcuRenal Failure

    Intra-renal AcuteRenal Failure

    Dysmorphic Hematuria

    Red cell casts

    Oval fat bodies

    Fatty Casts

    Muddy brown casts

    Renal tubular epithelialcells and casts

    White cells

    White cell castsEosinophiluria

    GlomerulonephritisAtheroembolic diseaseThrombotic

    microangiopathy

    Minimal changediseaseFocal segmentalglomerulosclerosis

    Albuminuria Tubular proteinuria

    Tubular epithelialinjury

    -Ischemic-Nephrotoxic

    InterstitialnephritisUrinary tract

    infection

    D

    U

    Cc

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    Acute Renal failureIntroduction to casts

    Hyaline Cas

    • Better seewith low

    • Non-spec• Compose

    Tamm-Hmucoprot

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    Acute Renal Failure

    Waxy Casts:• Smooth app• Blunt ends.• May have a • Felt to be la

    degeneratinrepresentativdisease.

    Granular Casts:•

    Represent dcellular castprotein.

    • Nonspecific

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    Acute Renal FailureFatty Casts:

    • Seen in patients wsignificant protei

    • Refractile in app

    • May be associatefree lipid in the u

    • Can see also “ovbodies” – RTE’have ingested lip

    • Polarize – demo

    “Maltese cross”.

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    Acute Renal Failure

    Muddy • High

    of AT

    • Pigmgranuseen hypecan bfor th

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    Acute Renal Failure

    White Bloo• Raises co

    interstitia

    • Can be se

    other infldisorders

    • Also seenpyelonep

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    Acute Renal Failure• Hematuria

    Nonglomerular hematu

    • Urologic causes.

    • Bladder/Foley traum

    • Nephrolithiasis.

    • Urologic malignancy

    • May be “ crenatedupon age of urine, os

    – NOT dysmorphic.

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    Acute Renal Failure

    Red Blood Cell Cas

    • Essentially diagnvasculitis orglomerulonephri

    Dysmorphic Red Ce

    • Suggestive of glo

    bleeding as seen glomerulonephri

    • Blebs, buds, memloss.

    • Rarely reported iconditions – DM

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    Acute Renal FailureCrystals – Pretty and important.

    Uric acid crystals:• Seen in any setting of

    uric acid and an acidi• Seen with tumor lysis

    Calcium oxalate crystals• Monohydrate – du

    may be needle-like.• Dihydrate – envelop• Form independent of• Seen acutely in ethyl

    ingestion.

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    Conditions that Lead to Pre-renal Acute Renal Failure

    Generalizedor Localized Reduction in

    Renal Blood Flow

    IschemicAcute Renal Failure

    Intravascular Volume Depletion

    Decreased Effective Circulating VolumeCHF Cirrhosis Nephrosis

    MedicationsCYA, TacrolimusACE inhibitors NSAIDS

    Radiocontrast Amphotericin BAminoglycosides

    HepatorenalSyndrome

    Sepsis

    Large-vessel Renal VasRenal Artery ThrombRenal Artery EmboliRenal Artery Stenosi

    Small-vessel Renal VascVasculitis AtheroThrombotic MicroTransplant Reject

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    Common Causes of Drug Induced AIN• NSAIDS• Antibiotics

    – Penicillins• methacillin• Ampicillin, amoxacillin, carbenacillin, oxacillin• Cephalosporins

    – Quinolones (ciprofloxacin) – Anti-tuberculous medications (rifampin, INH, ethambutol) – Sulfonamides (TMP-SMX, furosemide, thiazides)

    • Miscellaneous – Allopurinol, cimetidine, dilantin

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    Acute Glomerulopathies• RPGN most commonly seen with:

    – Lupus nephritis (DPGN, class IV) – Pauci-immune GN (ANCA associated) – Anti-GBM disease – less commonly: IgA, post-infectious

    • Nephrotic presentations of ARF – Collapsing FSGS (HIV nephropathy) – Minimal change disease with ATN

    • Thrombotic microangiopathies (HUS, TTP, malignant hyperten

    scleroderma kidney, pre-eclampsia)

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    Hepatorenal Syndrome - Major Criteria• Chronic or acute liver disease with advanced hepatic failure and portal

    hypertension• Low GFR, as indicated by a serum creatinine >1.5 mg/dL or a creatinine

    clearance < 40 mL/min• Absence of shock, ongoing bacterial infection, fluid loss, and current or

    recurrent treatment with nephrotoxic drugs. Absence of gastrointestinal flosses (repeated vomiting or intense diarrhea) or renal fluid losses (asindicated by weight loss > 500 gm/d for several days in patients with ascwithout peripheral edema or > 100 gm/d in patients with peripheral edem

    • No sustained improvement in renal function (decrease in serum creatinin1.5 mg/dL or less or increase in creatinine clearance to 40 ml/min or moafter withdrawal of diuretics and expansion of plasma volume with 1.5 Lisotonic saline

    • Proteinuria < 500 mg/d and ultrasonographic evidence of obstructive uroor parenchymal renal disease.

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    Hepatorenal syndrome - Minor Criteria

    Urine volume < 500 mL/day• Urine sodium < 10 mEq/L• Urine osmolality > plasma osmolality• Urine red blood cells < 50 per high-pow

    field•

    Serum sodium concentration < 130 mEq CURRENT STAR MCQS

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    CURRENT STAR MCQS• Abdominal Compartment Syndrome

    – Presence of IAP >20 that is associated with a single or multiple organ system faCauses severe oliguric or anuric renal failure. Tx: surgical decompression.

    • Acute Phosphate Nephropathy – AKI from Nephrocalcinosis after use of oral sodium phosphate (phospho soda)

    colonoscopy.• Orlistat associated AKI

    – AKI from Oxalate nephropathy due to enhancing oxalate absorption with increaurinary excretion.

    • IVIG associated AKI – AKI from osmotic nephrosis from sucrose-containing formulation.

    • Herbal, Home remedies – Arsenal X, Chromium picolinate, Chineses Herb Xi Xin with aristolochic acid;

    Mouring Cypress, Snake gallbladder, Star fruit (oxalate), Ma Huang (ephedra),Juice

    D fi iti f

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    Definition ofCKD-Mineral and Bone Disorder

    A systemic disorder of mineral and bonmetabolism due to CKD manifested by eitheone or a combination of the following:

    • Abnormalities of calcium, phosphorus, PTH, vitamin D metabolism

    • Abnormalities in bone turnover, mineralizationvolume, linear growth, or strength

    • Vascular or other soft tissue calcification

    Moe S, et al. Kidney Int 69: 1945, 2006

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    Mechanism of Cyst Formation

    1. Mutation(s) leads to changes in epithelial cell behavior2. Tubule epithelial cells proliferate to form cyst3. Electrolytes and water accumulate in cyst lumen

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    Cystic diseases of kidney• ADPKD•

    ARPKD• VHL : AD,hemangioblastoma, RCC (40-70%)• TS: angiomyolipomas in CNS• MSK : AD, 3rd & 4 th decade, stones, recurrent hematu• NPH =3 types:juvenille,infantile,adolescent. AR.

    Cerebellar ataxia , hepatic fibrosis• MCK = AD. 3rd & 4 th decade.

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