chronickidneydisease 2

7/28/2019 ChronicKidneyDisease 2

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Chronic Kidney Disease

MOHAMAD S. RABABAH , MDConsultant Nephrologist , Head of Renal Unit, KAUH_Jordan


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Prevalence

1 in 5 diabetics

1 in 6 hypertensives

1 in 5 of all elderly > 80 without

HTN and DM


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Definition of CKD

Structural or functional abnormalities ofthe kidneys for >3 months, asmanifested by either:

1. Kidney damage, with or withoutdecreased GFR, as defined by

pathologic abnormalities

markers of kidney damage, includingabnormalities in the composition of the bloodor urine or abnormalities in imaging tests

2. GFR


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Definition

For greater than 3 months

Kidney damage

Abnormal structure by imaging

Abnormal function by urine/bloodwork

OR

GFR < 60


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Classification of CKD by Diagnosis

Diabetic Kidney Disease

Glomerular diseases (autoimmunediseases, systemic infections, drugs, neoplasia)

Vascular diseases (renal artery disease,hypertension, microangiopathy)

Tubulointerstitial diseases(urinary tractinfection, stones, obstruction, drug toxicity)

Cystic diseases(polycystic kidney disease)

Diseases in the transplant(Allograftnephropathy, drug toxicity, recurrent diseases,

transplant glomerulopathy)


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Screening

Screen all high risk and age > 55

HTN, DM, recurrent UTI

Systemic illness that affects kidney(NNS = 8.7)

Screen with

Creatinine to calculate GFR

ANDurine protein analysis


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Glomerular Filtration

You MUST calculate the GFR!

Use an equation MDRD or C-G

Use a 24 hr urine in special cases


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Prevalence of Abnormalities at each level of GFR

0

10

20

30

40

5060

70

80

90

15-29 30-59 60-89 90+

Estimated GFR (ml/min/1.73 m2)

P

roportionofpopu

lation(%)

Hypertension* Hemoglobin < 12.0 g/dL

Unable to walk 1/4 mile Serum albumin < 3.5 g/dL

Serum calcium < 8.5 mg/dL Serum phosphorus > 4.5 mg/dL

*>140/90 or antihypertensive medication p-trend < 0.001 for each abnormality


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Screening

Screen all high risk and age > 55

HTN, DM, recurrent UTI

Systemic illness that affects kidney

Screen with

Creatinine to calculate GFR

ANDurine protein analysis


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Proteinuria

Good evidence for screening withannual micro-albumin in DM

Consider screening in HTN, age> 55

WHAT to use?

- urine microalbumin- urine micro for casts


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Proteinuria

Protein in urine is associated with amore rapid decline in renal function

This decline can be slowed by ACE-Ior ARB even without diabetes

Can be helpful in diagnosis if not DM


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Causes of CKD

Diabetes

Hypertension??

Transplant

Non-diabetic

Glomerular Tubulointerstitial

Vascular

Cystic


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Non-DM Causes of CKD

Glomerular

Lupus or vasculitis

Hepatitis or HIV

Endocarditis Amyloidosis

Medications

Lithium

Ratio of protein:creatinine is high

Tubulointerstitial

Myeloma

Pyleonephritis

Obstruction BPH

Tumor

Chronic reflux

Sarcoidosis


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Non-DM Causes of CKD

Cystic and otherhereditary renaldiseases

Transplant

Chronic rejection

Medications

Chronic disease

Vascular

Hypertension

Renal artery

stenosis Renal vasculitis

Sickle cell

HUS

Low-flow states

Cirrosis, CHF, etc.


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CKD and no diabetes?

Medications? Family history?

Risks of HIV and Hepatitis

Rashes, joints, renal bruit Screen again for diabetes

Look at urine micro for clues

Consider ESR, SPEP, ANA, ANCA Renal ultrasound


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CKD Stages

Stage 1 GFR > 90

Damage but normal or elevated GFR

Stage 2 GFR 60-90

Stage 3 GFR 30-60

Stage 4 GFR 15-30

Stage 5 GFR < 15


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Goals of Care

1. Slow decline in renal function

2. Prevent cardiovascular disease

3. Detect and manage complications Anemia

Hyperparathyroidism

Bone disease

Electrolyte abnormalities

Vascular complications


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Bone Disease in Renal

Failure


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Resorptionosteoclasts Formationosteoblasts matrix

MineralisationQuiescence

Normal Bone

Remodelling Cycle


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Pathogenesis

Kidney failure disrupts systemic calciumand phosphate homeostasis and affects thebone, GIT and parathyroid glands.

In kidney failure there is decreased renalexcretion of phosphate and diminishedproduction of calcitriol (1,25-dihydroxyvitamin D) Calitriol increases serum calcium levels

The increased phosphate and reducedcalcium, feedback and lead to secondaryhyperparathyroidism, metabolic bonedisease, soft tissue calcifications and othermetabolic abnormalities


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GFR

PO4

1,25 DHCC

Ca

PTHCalcitriol


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econ aryhyperparathyroidism

In renal failure driven by

Hypocalcaemia

Decreased vitamin D

hyperphosphataemia


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Clinical manifestations of bonedisease

Most with CKD and mildlyelevated PTH are asymptomatic

When present classified as either1. Musculoskeletal

2. Extra-skeletal


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Resorptionosteoclasts Formationosteoblasts matrix

Accelerates:High PO4 or

Low Ca2+

, calcitriol,HCO3, oestrogen

Retards:Calcitriol*, Age,

Diabetes, Al3+, PTHx

Mineralisation

*Acts via

osteoblasts

Quiescence

Uraemic Bone

Remodelling

CycleVia PTH*,IL-1,6 & TNF

t


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g turn over onedisease

Due to excess PTH

Increased bone turnover activity(greater number of osteoclasts and

osteoblasts) and defectivemineralization.

Associated with bone pain andincreased risk of fractures.

Severe symptomatic disease iscurrently uncommon with moderntherapy.


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Osteomalacia

Formally linked to aluminiumtoxicity

From aluminium based phosphatebinders

From contamination of water indiasylate solutions


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xe uraem c onedisease

Mixture of high turn over bonedisease and osteomalacia


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Adynamic bone disease

Characterized by low osteoblastic activityand bone formation rates

Seen in up to 40% HD and 50% PD

May be due to excess suppression of theparathyroid gland with therapies,particularly calcium-containing phosphatebinders and vitamin D analogues.

Typically maintain a low serum intact PTH

concentration, which is frequentlyaccompanied by an elevated serum calciumlevel.

Felt to represent a state of relativehypoparathyroidism
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To slow decline

Low salt diet (for HTN)

Low protein diet in CKD 4 & 5 Nutrition consult!

Avoid nephrotoxic agents Contrast dye, NSAIDs, gentamicin


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To slow decline

Diabetes control HA1c ~ 7.0 7.5

Metformin?

Glipizide v. Glyburide

Blood pressure control - < 130/80

ACE-I or ARB

Diuretics thiazide for GFR > 30

- furosemide for GFR < 30


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To slow decline

Prescribe an

ACE-I or ARB

for proteinuria + CKD

even in the ABSENCE of

diabetes


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Goals of Care




Hyperparathyroidism

Bone disease




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Prevent CV disease

Most common cause of death is CV diseaseand not renal failure.

Smoking cessation

Diabetes and Blood pressure control

Lipids No evidence that tx affects renal fxn

Guidelines: ATP3 -> LDL goal < 100


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Goals of Care




Hyperparathyroidism

Bone disease




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When to refer

Proteinuria > 3.5 gm in 24 hours

Nephritis

Hematuria, proteinuria and HTN Diabetes & CKD but no retinopathy

GFR decline of 50% in one year

Stage 3 or 4 CKD


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Key Points

Think about CKD and screen

Creatinine AND urine protein

Calculate the GFR!

Look for reversible cause if no DM

Get to know the KDOQI guidelines &think about the complications

chronickidneydisease 2

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