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bacterial endocarditis, visceral abscesses, andventriculoperitoneal shuntinfections can also lead to
thisimmunecomplex–mediateddisease.
Low complementlevelsare usuallyseen.ASOtitersmaybe elevatedserially,as mayanti-DNaseB
antibodiesinstreptococcal-associateddisease.
DIAGNOSIS
Kidneybiopsyrevealshump-shapedsubepithelialdepositsonelectronmicroscopycorrespondingtothe
depositsonimmunofluorescence(C3dominant,orC3andIgGco-dominantstaining).Thereis
widespreadmesangialproliferationandinfiltrationofpolymorphonuclearneutrophils.
TREATMENT
Treatmentisprimarilysupportive.Resolutionoftheunderlyinginfectiontypicallyleadstorenalrecovery
in2–4weeks,evenincasesrequiringdialysis.Abriskdiuresisshouldbeanticipatedintherecovery
periodandelectrolytesshouldbecarefullymonitored.
LupusNephritis
GENERALPRINCIPLES
Lupusnephritis(LN)canmanifestasproteinuriaofvaryingdegreeswithdysmorphicRBCsandRBC
castsandrenalinsufficiency.Positivelupusserology(e.g.,ANA,anti–double-strandedDNAantibodies,
anti-histoneantibodies,anti-Smithantibodies)andhypocomplementemia(especiallylowC3)areoften
presentduringacuteflares.Theanti-SmithantibodyisspecificforSLE.
DIAGNOSIS
Renal biopsy can provide diagnostic and prognostic information. The International Society of
Nephrology/Renal Pathology Society classification has six major categories based on histologic
appearance.
32
Class I (minimal mesangial LN) does not show mesangial hypercellularity, though mesangial
depositsmaybeseeninimmunofluorescenceandelectronmicroscopy.
Class II(mesangial proliferativeLN)ischaracterizedbymesangial hypercellularity(fouror more
nuclei in nonhilar region) or matrix expansion, primarily with mesangial deposits on
immunofluorescenceandelectronmicroscopy.
Class III (focal LN) shows glomerular lesions (including endocapillary or extracapillary
hypercellularity, necrosis, crescents)withmesangial andsubendothelial deposits, involving<50%
ofglomeruli.
Class IV (diffuse LN) shows glomerular lesions (including endocapillary or extracapillary
hypercellularity,necrosis,crescents)withmesangialandsubendothelialdepositsinvolving≥50%of
glomeruli.
Class V (membranous LN) has features resembling MN with >50% of glomeruli showing
subepithelial deposits with or without mesangial hypercellularity. This may occur in conjunction
withclassIIIorclassIVdisease.
ClassVI(advancedsclerosisLN)with≥90%globallysclerosedglomeruli.
Immunofluorescence is usually positive for IgG, IgA, IgM, C1q, and C3, for the “full-house”
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fluorescence pattern. It is also important to note that these classes could switch, and biopsy is
necessarytoclassifyLNpatientspriortotreatment.
TREATMENT
Aggressivenessoftherapytakesintoconsiderationtherenalandextrarenalmanifestationsofthedisease.
ClassILNrarelyrequiresspecifictreatment,andtherapyisdirectedattheextrarenalmanifestations.
Thereareusuallynolong-termadverseeffectsonkidneyfunction.
For class II LN, therapy depends on the amount of proteinuria and the degree of extrarenal
manifestations.Whenproteinuriais<1g/d,routinemanagementandmonitoringistypicallysufficient.
However, if there is significant proteinuria >3 g/d, treatment with corticosteroids or calcineurin
inhibitorsmayberequired.
For class III, IV, or V LN, treatment can be divided into initial induction therapy and maintenance
therapy.
Initial inductiontherapyfor aggressive disease is with corticosteroids (IV methylprednisolone5–10
mg/kgfor3daysfollowedbyoralprednisone0.5–1.0mg/kg/dtaperedover6–12monthsaccordingto
patient’sclinicalresponse)PLUSeithercyclophosphamideormycophenolatemofetil.
Cyclophosphamide canbe given IV or PO, though more recentstudies utilize the IV route due to a
lower cumulative dose. Astandard regimen is 0.5–1.0 g/m2 monthly for 6 months, althougha more
recentstudyinEuropeanpatientsfoundcomparable efficacywithalower cumulativedose,givenas
500mgIVevery2weeksfor3months
33
Mycophenolate mofetil (2–3 g daily in divided doses) was compared to cyclophosphamide for
inductiontherapy,withnosignificantdifferenceintheresponserateat6months
34
For maintenance therapy, mycophenolate mofetil (1–2 g/d in divided doses) with low-dose
corticosteroids(lessthan10mg/dayofprednisone)wasshowntobesuperiortoazathioprine(1.5–2.5
mg/kg/d)combinedwithcorticosteroids.
35
Rituximab therapy has also been shown to have treatment efficacy in lupus nephritis refractory to
standardtherapy.Whencombinedwithcorticosteroidsandmycophenolatemofetil,however,itdidnot
showimprovedclinicaloutcomesafter1year.
36
Treatment course should be closely followed to ensure remission by monitoring renal function,
proteinuria,hematuria,complementlevels,andauto-antibodylevels.
Pulmonary–RenalSyndromes
GENERALPRINCIPLES
Severaldistinctclinicalentitiesmakeupthepulmonary–renalsyndromeswithvasculiticinvolvementof
thealveolarandglomerularcapillaries.Typically,thisresultsinrapidlyprogressiverenalfailurewith
concurrentpulmonaryinvolvementintheformofalveolarhemorrhage.Anephriticpicturepredominates,
withdysmorphicRBCsandRBCcastsintheurine.Arthralgias,abdominalpain,andfevermayrepresent
othersystemicmanifestations.
DIAGNOSIS
In anti-GBMantibodydisease, circulating antibody tothe α-3 subunit of the noncollagenous (NCI)
domainof typeIV collagen is deposited inthebasement membraneofglomeruli, resulting inlinear
staining on immunofluorescence. Goodpasture syndrome includes pulmonary involvement with
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damagetothealveolarbasementmembraneandcanpresentwithlife-threateningalveolarhemorrhage.
Thepresenceofanti-GBMantibodyintheserumsupportsthediagnosis,and10%–30%ofpatientswill
also haveapositiveANCAserology.ThisdiseaseismorecommoninCaucasianpatients,with peak
ageof20–30yearsandanotherpeakat60–70years.
Ingranulomatosiswithpolyangiitis(GPA),vasculiticlesionsinvolvethesmallvesselsofthekidneys
and may also involve the lungs, skin, and gastrointestinal tract. As in anti-GBM antibody disease,
pulmonary hemorrhage may be life-threatening. Biopsyfindings include small-vessel vasculitis with
noncaseatinggranulomaformationinthekidneys,lungs,orsinuses.
GPA is part of a group of diseases known as ANCA-associated vasculitis, or pauci-immune
glomerulonephritis (referring to the absence of immunostaining deposits), which includes
eosinophilicgranulomatosiswithpolyangiitis(EGPA)andmicroscopicpolyangiitis(MPA).
In GPA, there is a positive cytoplasmic ANCA (c-ANCA) directed against serine proteinase-3
(PR3)in80%–90%ofcases,whereasinMPAandEGPA,thereisapositiveperinuclearANCA(pANCA)directedagainstmyeloperoxidase(MPO)in60%ofcases.
TREATMENT
Inanti-GBMantibodydisease,thegoaloftherapyistoclearandsuppressproductionofthepathogenic
antibodies.Treatmentiswithdailytotalvolume(4L)plasmapheresisforapproximately14daysPLUS
oral cyclophosphamide2 mg/kg/dfor3months PLUSglucocorticoids(IV methylprednisolone500 to
1000 mg/d IV for 3 days followed by oral prednisone, 1 mg/kg/d based on ideal body weight not
exceedingatotalof80mg/daywithaslowtaperoffby6months).Serialmeasurementoftheanti-GBM
antibodylevelisusefultomonitortherapy;thetreatmentgoalistoachieveanundetectablelevel.
Poor response to therapy is predicted by the presence of oliguria, Cr >5.7 mg/dL, or dialysis
dependence on presentation. Evenifthe likelihoodof renal recoveryis low,evidence ofpulmonary
involvementwarrantsaggressivetherapy.
ManagementofANCA-associatedvasculitisincludescorticosteroids(IVmethylprednisolone1g/dfor
3daysfollowedbyprednisone1mg/kg/dnotexceedingatotalof80mg/d,taperedover3–6months),
andeithercyclophosphamide(15mg/kgIVevery2weeksforthreedosesthenevery3weeksfor3–6
months, or as 1.5–2 mg/kg/d PO for 3–6 months) or rituximab (either as 375 mg/m2 weekly for 4
weeks,oras1 gwith two doses14 daysapart)toinduceremission.Azathioprinecanbesubstituted
onceremissionis achieved(2mg/kg/d).Methotrexate(15–25mg/wk)was notfoundtobesaferthan
azathioprine.37Mycophenolatemofetil(1.5–3g/dindivideddoses)waslessefficaciousinmaintaining
remission than azathioprine.38 Maintenance therapy is continued for a duration dictated by the
individual patient’sclinical course, though a typical course may extend 12–24 monthsafter a stable
remissionhasbeenachieved.
Inarecentstudy,therewasnobenefitwiththeadditionofplasmaexchange.39Thisstudyalsoreported
noninferiority of a reduced dose of prednisone (0.5 mg/kg/d not exceeding a total of 40 mg/d) as
comparedtothestandardregimen.
Double-strengthsulfamethoxazole–trimethoprimgiventwicedailyhasbeenshowntoreduceextrarenal
relapses and to prevent Pneumocystis (carinii) jirovecii infection in patients on high-dose
immunosuppression.
PolycysticKidneyDisease
GENERALPRINCIPLES
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Autosomal dominantpolycystic kidney disease (ADPKD) is a hereditary disorder resulting in cystic
enlargement of the kidneys. The incidence is estimated to be 1 in 500 to 1000 live births.
Approximately20%ofpatientswithADPKDdonothaveapositivefamilyhistory.ADPKDcurrently
accountsforupto10%ofpatientswithESRD.
There aretwowell-described mutationsinthepolycystingenes, PKD1andPKD2whichencodefor
polycystin(PC)1and2, respectively.PKD1is morecommon,accountingforapproximately85% of
ADPKD.PKD2isassociatedwithlaterprogressionofdisease.
Themechanismbywhichcystsformisunclear;aproposed“two-hit”hypothesisimplicatesa second
somaticmutationthatinactivatesthewild-typealleleinindividualcells.Thepolycystingeneproducts
localizeto the primarycilium oftheapical membraneoftubular cells.Disordered cell divisionand
aberrantplanar cell polarity may lead toovergrowth ofthe tubular segment,eventuallypinching off
fromtherestofthecollectingsystemandformingdiscretecysts.Inabnormalcells,cyclicAMPimparts
aproliferativephenotypeaswellasinducingchlorideextrusionintothecystlumen.
DIAGNOSIS
ClinicalPresentation
Hypertension is an early feature of ADPKD and occurs even prior to a reduction in the GFR in
approximately 60% of patients. As the affected tubules enlarge, they impinge on the blood flow to
neighboring glomeruli, renderingthem ischemic. This inturnleadstoRAASactivationandsystemic
hypertension.Onsetofkidneyfailureishighlyvariable,withhalfofpatientsreachingESRDbytheage
of60.
Kidneystonesdevelop inapproximately25% ofpatientswithADPKD, with a higher proportionof
uricacidcompositionascomparedtothegeneralpopulation.
Cerebral aneurysms, hepatic cysts, mitral valve prolapse, and colonic diverticula are found in
associationwithADPKD.Ascystsenlarge,theymayresultinapalpableflankmass.Grosshematuria
andpainmay indicatecysthemorrhageintothe collectingsystem.Flank painmayalso be caused by
cystinfectionorstretchingoftherenalcapsule.
DiagnosticTesting
Differentiation from other renal cystic diseases (acquired cystic kidney diseases, medullary sponge
kidney,medullarycystickidneydisease,glomerulocystickidneydisease)canbemadebythepresence
ofenlargedcystickidneysratherthanshrunkenornormal-sizedcystickidneys.
Ultrasonography reveals multiple cysts. In the setting of a positive family history, a diagnosis of
ADPKDcanbemadefromultrasoundfindings,withcriteriadifferingaccordingtoage.Threeormore
cysts (unilateral or bilateral) are required for diagnosis in patients between the ages of 15 and 39.
Fromages40to59,twoormorecystsineachkidneyarerequired.Fromage60andolder,morethan
fourcystsineachkidneyarerequiredtomakethediagnosis.
Patients with a family history of cerebral aneurysms or with symptoms attributable to a cerebral
aneurysmshouldundergoevaluationwithbrainMRI/MRA;imagingcanbeperformedwithouttheuse
ofgadoliniumcontrast.
Genetictestingmaybeconsideredifpatientshaveequivocalimagingresultsoradefinitivediagnosis
isrequired.
TREATMENT
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Treatment of hypertension consists of reduction in sodium intake and pharmacologic therapy when
indicated. A large randomized controlled trial of patients with ADPKD suggested improved
preservationofrenalfunctionatbloodpressuretargetsof95–110/60–75,buttolerabilitywaslimited
bysymptomatichypotension.40Thus,guidelinesforbloodpressurecontrolinpatientswithADPKDare
similar to those in other patients with CKD, targeting a systolic pressure of <120 mm Hg using
standardizedofficemeasurements.
In 2018, tolvaptan was approved in the United States for treatment of ADPKD. Blockade of the
vasopressin-2 receptor inhibits cyclic AMP production. Large randomized controlled trials of
tolvaptan have revealed a reductionofthecystgrowth rate anda decreased rateofGFRdeclineas
comparedtoplacebo.
41,42
Treatment canbe offeredtopatientswith a GFRabove25mL/min/1.73m
2
andevidence of disease progression (e.g.,GFR decline, enlarged kidney volume, increased kidney
length).Ofnote,subjectsbetweentheagesof56and65whowereenrolledintheclinicaltrialdidnot
showabenefitbeyondthatofplacebo.Polyuriaandpolydipsiaarefrequentlyexperiencedbypatients
onthismedication,anditmaylimitdoseescalationtothegoalof90mginthemorningand30mginthe
afternoon. Close monitoring of hepatic enzymes is mandatory, with measurements at baseline, at 2
weeks,4weeks,monthlythroughthefirst18months,thenevery3monthsafterward.
Grosshematuriafromcysthemorrhagecanusuallybemanagedwithbedrest,hydration,andanalgesia.
Resolutionmaytake5–7days.
Cyst infections are generally treated with antibiotics that achieve good penetration into the cysts.
Sulfamethoxazole–trimethoprim and ciprofloxacin are the antibiotics of choice. The absence of
bacterial growth in the urine does not rule out infection as the cystic fluid does not necessarily
communicatewiththerestofthecollectingsystem.
Pain that persists without an obvious hemorrhagic or infectious cause may respond to targeted cyst
drainageorcystreductionsurgery.Drainedcystsdotendtorecur,limitingthelong-termefficacyofthis
procedure.
Nephrolithiasis
GENERALPRINCIPLES
Nephrolithiasisismorecommoninmenthanwomenbya2:1ratio,withapeakageatthethirdtofourth
decade.Therearecertainmedicalconditionsthatpredisposepatientstokidneystones,includingdiabetes
mellitus,hypertension,metabolicsyndrome,distalrenaltubularacidosis,gout,andADPKD.
Calcium-based stones are the most common type of kidney stones (80%). Among these, the most
commontypeismixedcalciumoxalateandcalciumphosphatefollowedbycalciumoxalatealone,and
thencalcium phosphatealone.These stones are radiopaque.Calcium oxalatestones canbe found in
acidic or alkalineurine and canbe dumbbell shapedor appear as paired pyramids (giving theman
envelopeappearancewhenviewedonend).Calciumphosphatestonescanappearaselongated,blunt
crystalsandforminalkalineurine.
Uricacidstones(10%)developinconditionsthatpromoteanacidicurine,suchaswhatisobserved
inpatientswith the metabolic syndrome.Hyperuricosuric states such as goutandmyeloproliferative
disorders are also associated with uric acid stones, though the predominant risk factor for their
precipitation is an acidic environment. These stones are radiolucent, and the crystals can exhibit a
varietyofshapes,withneedlesandrhomboidformsbeingthemostcommon.
Struvitestones(10%)arealsoknownas“triplephosphate”stones,withphosphatebeingpresentinits
trivalent form and combining with three cations, ammonium, magnesium, and calcium. They are
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radiopaqueandcanextendtofilltherenalpelvis,takingonastaghornconfiguration.Onmicroscopy,
struvitecrystalshaveacharacteristiccoffin-lidshape.Theydevelopinalkalineurineassociatedwith
urea-splitting organisms (e.g., Proteus, Klebsiella, Serratia, Haemophilus, Pseudomonas) and are
morecommonlyseeninpatientswithanatomicabnormalities(e.g.,vesicoureteralreflux,obstructionof
thepelviuretericjunction,ureteralstricture).
Cystinestones(<1%)areuncommonandformasaresultofanautosomalrecessivedisorder,inwhich
the renal epithelium has a decreased ability to reabsorb the dibasic amino acids cystine, ornithine,
lysine,andarginine.Among these, onlycystineishighlyinsolubleandprecipitatestoform stonesin
acidicurine.Thesestoneshaveanintermediateradiolucencyandappearashexagonalcrystalsinthe
urine.
DIAGNOSIS
ClinicalPresentation
Theclinicalpresentationofkidneystonesvariesbasedonthelocationandthesizeofthestone.Some
stonesarecompletelyasymptomatic,andothersmaypresentwithflankpainatthecostovertebralangle
radiatingtothegroin,genitals,orsuprapubicarea.Patientsmayalsopresentwithhematuria,dysuria,and
urinaryurgency.NondysmorphicRBCsmaybenotedunderurinemicroscopy.OliguriaandAKIare
uncommonbutcanresultifthereisbilateralobstructionorifasolitaryfunctioningkidneyisaffected.
DiagnosticTesting
Basiclaboratoryinvestigationsincludeurine(culture,pH,microscopy)andserum(calcium,phosphate,
parathyroidhormone[PTH],magnesium,uricacid)studies.Urineshouldbestrainedandpassedstones
analyzedforcomposition.
Akidneyultrasoundissafe,relativelyinexpensive,andreadilyavailablebutmaymissstonesthatare
<3mm.Plainabdominal filmsmayreveal radiopaquestonescomposedofcalcium salts,struvite,or
cystine,butmaymisssmallstones,thosethatareobscuredbyotherstructures,orradiolucenturicacid
stones. Noncontrast CT scanning has replaced other imaging modalities as the study of choice for
suspectednephrolithiasisinanacutepresentation.
Certainpatientsmayrequireamoreextensiveevaluation,includingadetaileddietaryhistoryanda24hoururinecollectionforvolume, calcium,sodium,phosphate,uricacid,citrate,oxalate,andcystine,
andpHmeasurement.Ahistoryofrecurrentstoneorbilateralstonediseases,familyhistoryofstones,
andpresenceofinflammatoryboweldiseasesorothermalabsorptiveprocessesshouldpromptamore
detailed evaluation. This collection should not be done during an acute episode in a hospitalized
patientbutratherreservedforwhenthepatientisontheirusualoutpatientdiet.
TREATMENT
Generaltreatmentofanacuteeventconsistsofvolumeexpansiontoincreaseurineoutputaswellas
analgesia. Ifthestoneis obstructingoutflowor accompaniedbyinfection,removalis indicatedwith
urgenturologicorradiologicintervention.
Afterpassageofastone,treatmentisdirectedatpreventionofrecurrentstoneformation.Regardless
ofstonetype,thefoundationoftherapyismaintenanceofhighurineoutput(2–3L/d)andalow-sodium
diet(2–2.3g/dor80–100mmol/d).
For calcium oxalate stones, an age-appropriate dietary calcium intake with no added calcium
supplementsis recommended. Ifhypercalciuria ispresent,adherencetoalow-sodium dietshouldbe
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ensured,withtheadditionofathiazidediureticasthenextstep.Ifhypocitraturiaispresent,potassium
citrate (10–60 mEq/d individed doses) canbe started;lemonjuice (4 ounces mixed with a liter of
water) is analternatestrategythathasbeenstudied, thoughconsistentlong-term benefithasnotbeen
proven.Oxalate-richfoods(e.g.,spinach,rhubarb)shouldbeavoidedifhyperoxaluriaispresent.
Uric acid stones can be prevented or reduced in size by urinary alkalinization, preferentially with
potassiumcitrate10–60 mEq/dindivideddoses totargetaurinepHof6–6.5. Alow-proteindietis
advised. Inpatients who do not respond to urine alkalinization with potassium citrate, reduction in
uricosuriacanbetargetedwithxanthineoxidaseinhibitors(allopurinolorfebuxostat).
Struvitestonesfrequentlyrequiresurgicalinterventionfortheirremoval.Monthlyurineculturesshould
beobtained,andifpositive,aggressiveantibiotictreatmentis indicated.Anyanatomicalabnormality
identifiedasacausativefactorforstruvitestonesshouldbecorrectedwhenpossible.
Cystine stones require extensive urinary alkalinization to a pH of 7.0–7.5 to induce solubility,
aggressive sodium restriction (<2 g/d), and high fluid intake of 3.5–5 L/d. Tiopronin can further
increasesolubilitythroughbreakageandexchangeofdisulfidebonds.Sideeffectsincludelossoftaste,
fever,rash,arthritis,proteinuria,myelosuppression,andhepatotoxicity.
ManagementofChronicKidneyDisease
GENERALPRINCIPLES
CKD is classified based on the GFR and albuminuria. Based on the GFR (Figure 13-1), it can be
dividedintofivestages:G1(GFR≥90mL/min/1.73m2),G2(GFR60–89),G3(subdividedintoG3a
withaGFR45to59andG3bwithaGFR30–44),G4(GFR15–29),andG5(GFR<15notonrenal
replacementtherapy).ForG1andG2,additionalevidenceofrenaldisease,suchasproteinuria,needs
tobe presentforatleast 3 months. Definitionsfor albuminuria are based ontheurinaryalbumin-tocreatinineratioasdescribedearlierinthechapter.GFR,degreeofalbuminuria,etiologyofCKD,and
otherriskfactorsshouldbeconsideredtogetherasthesepredictclinicaloutcomesandhelpinplanning
forrenalreplacementtherapy.
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Figure13-1 Stages of chronic kidneydisease. CKD, chronic kidneydisease; GFR,glomerular filtration rate.(Reprinted
from Summary of recommendation statements. Kidney Int Suppl (2011). 2013;3(suppl):5–14. Copyright © 2013
InternationalSocietyofNephrology.Withpermission.)
Patientsare usuallyasymptomaticuntilsignificantrenalfunctionislost(latestageG4andstageG5).
However, complications including hypertension, anemia, and mineral bone disorders (renal
osteodystrophyandsecondaryhyperparathyroidism)oftendevelopduringstageG3andthusshouldbe
investigatedandaddressedbeforepatientsbecomesymptomatic.
In thesetting of CKD,initiationof dialysis basedsolelyona target GFRhas not showna mortality
benefit.43 Dialysis should be started before the worsening of the patient’s metabolic or nutritional
status.
RiskFactors
DecreasedrenalperfusioncanleadtoadeclineinGFR.Thiscanoccurwithtruevolumedepletionor
diminished effective circulatingvolume (e.g., congestive heart failure, liver cirrhosis with ascites).
NSAIDs can be particularly deleterious in this setting because they block renal autoregulatory
mechanismswhichpreserve GFR.ACEinhibitors or ARBs also producea reversible decrement in
GFRthroughalterationsinhemodynamics.
Uncontrolled hypertension leads to hyperfiltration, which may lead to worsening proteinuria and
furtherdamagetotheglomeruli.
Albuminuriahas also been identifiedas a riskfactorfor progressionofrenal disease. Aprognostic
scale has been developed incorporating both the GFR and degree of albuminuria to predict the
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likelihoodtorenalfailure(seeFigure13-1).
Nephrotoxicagents,suchasiodinatedcontrastagentsandaminoglycosides,shouldbeavoidedwhen
possible. Careful attention to drug dosing is mandatory, frequently guided by the estimated GFR or
CKDstage.Druglevelsshouldbemonitoredwhereappropriate.
Patients undergoing coronary angiography are at particular risk for worsening CKD. Contrast
nephropathyandatheroembolicdiseasearepotentialcomplicationsofcoronaryangiography,andthe
risksandbenefitsoftheproceduremustbeweighedwiththepatientbeforeproceeding.
UTIorobstructionshouldbeconsideredinallpatientswithanunexplaineddropinrenalfunction.
Worseningrenalarterystenosis may also lead to a more rapid declineinGFRas well as sudden
worseningofpreviouslycontrolledhypertension.
RenalveinthrombosismayoccurasacomplicationofnephroticsyndromeandcanexacerbateCKD.
Hematuriaandflankpainmaybepresent.
TheAPOL1genehasbeenlinkedtoamajorhealthdisparityinpatientswithAfricanancestry,witha
cumulative lifetime risk of reaching ESRD approximately 7.5% compared to 2% in patients with
European ancestry. The high-risk genotypes include homozygous G1/G1, homozygous G2/G2, and
compoundheterozygousG1/G2.AfricanAmericanpatientswithorwithoutdiabetesmellituswithtwo
APOL1 riskalleles have a faster rate of CKD progression and increased likelihood of developing
ESRD.
44
OtherriskfactorsincludehighBMI,historyofcardiovasculardisease,andsmoking.
TREATMENT
TreatmentofCKDisfocusedonaddressingtheriskfactorsmentionedabove:dietarymodification,blood
pressurecontrol,adequatetreatmentofassociatedconditions,andultimately,preparationforrenal
replacementtherapy.
Dietaryrecommendations
Sodiumrestrictionto<2g/disrecommendedforpatientswithCKDandhypertension.Restriction
to<2g/dshouldalsobeusedifheartfailureorrefractoryhypertensionispresent.
Fluidrestriction isgenerally notrequired in CKDpatients and,ifexcessive, maylead to volume
depletionandhypernatremia.Restrictionisappropriateinpatientswithdilutionalhyponatremia.
Thereiscurrentlynobenefittoshowthatstrictdietaryproteinrestrictionisindicatedasatreatment
toslowprogressionofCKD.
Potassium should be restricted to 60 mEq/d in individuals with hyperkalemia. Tomato-based
products,bananas,potatoes,andcitrusdrinksarehighinpotassiumandshouldbeavoidedinthese
patients.
Dietaryphosphate restriction shouldbeto800–1000 mg/d.Dairyproducts,darkcolas,nuts,and
processed meat should be avoided in hyperphosphatemia. Oral binders (calcium carbonate or
acetate,lanthanumcarbonate, sevelamer carbonate) canbe takenwithmeals ifdietaryrestrictions
areunabletocontrolphosphatelevels.
Smoking accelerates CKD progression and patients should be counseled about the importance of
tobaccocessation.
Hypertension
Uncontrolled hypertension accelerates the rate of decline of renal function. The 2021 KDIGO
guidelinesrecommendtargetingasystolicbloodpressureof<120mmHgusingstandardizedoffice
measurementsforpatientswithCKD.
45
ACE inhibitors or ARBs should be used preferentially in the CKD population. They lower
intraglomerular pressure and possess renal protective properties beyond their antihypertensive
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effect,particularlyinproteinuricstates.Becauseoftheireffectsonintrarenalhemodynamics,a30%
rise in serum Cr should be anticipated and tolerated; a further rise should prompt a search for
possiblerenalarterystenosis.TheCrandserumpotassiumshouldbecheckedapproximately1week
after a dose adjustment. Combined therapy with ACE inhibitors and ARBs is not recommended
becauseofanincreasedriskofhyperkalemiaandAKIwithoutstatisticalbenefitinmortalityorlong-
termrenalprotection.
46
Diuretics are also beneficial in achieving euvolemia in hypertensive CKD patients. Thiazide
diuretics becomeless effective as the GFR falls below 30 mL/min, whereas loop diuretics retain
theirefficacy,althoughhigherdosesmayberequiredforthedesiredeffect.
Albuminuriaandproteinuria
Blood pressure control, and RAAS inhibition specifically, has been shown to decrease
albuminuriaandCKDprogression.
Metabolicacidosis
As renal function deteriorates, the kidneys are unable to appropriately excrete sufficient acid,
resultinginmetabolicacidosis(mixedhighandnormalaniongap).Tocompensate,alkalinebufferis
releasedfrombonebutcanultimatelyworsenbonemineraldisease.
Oral bicarbonate tablets (650 or 1300 mg twice or three times daily) tokeepserum bicarbonate
levelof≥22mEq/LhavebeenshowntoslowCKDprogression.
47
Hyperlipidemia
Therapywithstatins combinedwithezetimibehasshownimprovedcardiovascularoutcomeswith
fewer major atherosclerotic events in patients with moderate to severe CKD and in the dialysis
population,althoughthe benefitinpatientsondialysiswasless.48Useoflipid-loweringtherapyis
appropriateinpatientswithatheroscleroticdiseaseatallstagesofCKD.
In2014,KDIGOclinicalpracticeguidelinesrecommendedastatinwithezetimibeinadultsaged50
and older with a GFR <60 mL/min/1.73 m2, but not for patients receiving dialysis or transplant
recipients. An escalating statin dose in those not meeting LDL cholesterol targets was not
recommended.
49
Diabetesmellitus
KDOQIguideline recommends a target HbA1Cof 7% toprevent progressionof CKDas well as
micro-andmacrovascularcomplications.
SGLT2inhibitorshavebeenextensivelystudiedandnowreportedtohavereno-protectiveoutcomes
as well as cardiovascular benefits in patients with or without albuminuria with a GFR of ≥30
mL/min/1.73m2.
25
Anemia
A normocytic anemia is common in CKDandshould be evaluated once the GFR falls below 60
mL/min/1.73.
Alternatecausesforananemiashouldbesoughtintheappropriatesettingandironstoresassessed.
Ifthetransferrinsaturationis≤30%andthereisnoevidenceofironoverload(ferritin<500ng/mL),
consideration should be given to iron repletion with an intravenous preparation of iron. Options
includeirondextran(1000mgoncewithtestdoseof25mg),ferricgluconate(125mg,eightdoses),
or iron sucrose (200 mg, five doses). IV iron use should be avoided in patients with active
infections.
Erythropoiesis-stimulating agents(ESAs), suchas epoetin anddarbepoetin,can effectivelyreduce
but do not prevent the need for RBC transfusions. ESA therapy increases the risk of stroke,
thromboticandcardiovascularevents,andcanworsenoutcomesinpatientswithmalignancy.These
agentsshouldnotbestartedinCKDunlessthehemoglobinis<10g/dL,othercausesofanemiasuch
as iron deficiencyare addressed, and reductionintransfusions is a goal. The minimum dose that
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