Predisposing Conditions, Management and Prevention of Chronic Kidney Disease..ppt

7/28/2019 Predisposing Conditions, Management and Prevention of Chronic Kidney Disease..ppt

1/52

Predisposing Conditions,

Management and Prevention ofChronic Kidney Disease

Dr FA Arogundade FMCP FWACP, ISN FellowConsultant Nephrologist,

Obafemi Awolowo University,Ile-Ife.


2/52


3/52


4/52


5/52


6/52


7/52


8/52


9/52


10/52

Definition of CKD

Progressive and persistent deterioration in

kidney structure and function, ultimately

resulting in accumulation of nitrogenous

waste and disruption of acid basehomeostasis.

In addition, CKD also leads to derangements

of the kidneys osmoregulatory, metabolic

and endocrine functions.

Now CKD can be staged (KDOQI)


11/52

Stage 5

Stage 4

GFR 15-29

Staging of CKD


12/52

Stages of Chronic Kidney Disease

Stage 1 Kidney damage withnormal or GFR

GFR 90 ml/min/1.73m2

Stage 2 Kidney damage withmild GFR

GFR 60-89

Stage 3 Moderate GFR GFR 30-59

Stage 4 Severe GFR GFR 15-29

Stage 5 Kidney failure GFR


13/52


14/52

CKD Risk Factors

Diabetes Mellitus

Hypertension

Cardiovascular

Disease

Obesity

Metabolic Syndrome

Age and Race Acute Kidney Injury

Malignancy

Family history of CKD

Kidney Stones

Infections like Hep C

and HIV

Autoimmune diseases

Nephrotoxics like

NSAIDS


15/52

CKD - Causes

Diabetic Non Diabetic

Glomerular

Nephritic: PIGN, IgA, MPGN Nephrotic: FSGS, Membranous, Amyloidosis

Tubulointerstitial: Analgesic, Reflux, Ch. Obs

Vascular: Vasculitis, HTN, RAS

Cystic: ADPKD

CKD in transplantation


16/52

Prevalence of CRF is largely unknown

Conceivably high due to the high

prevalence of diseases that cause

chronic renal failure:

HYPERTENSION: > 15% in adults

DIABETES MELLITUS:>2.5-4.0%

Chronic inflammation endemicity

of malaria, Hepatitis B,C, & HIV

Socio-cultural practices

Others

Prevalence of CKD in Nigeria


17/52

0

10

20

3040

50

60

%


18/52

47

110

0 134

0 7 0 00

20

40

60

%

nil trace 30 100 500

Male

Female

mg/dl

The grading of proteinuria in respondents

(19% had proteinuria)

Ulasi et al. Medical screening by NAN, 2005


19/52

NHANES III

16,800

US Population CKD Prevalence

Stage % number

1 GFR:>90 3.3 5.9 millions

2 89-60 3 5.3

3 59-30 4.3 7.6

4 29-15 0.25 400,000

5


20/52

AusDiab

11,247

Population-based cross-sectional study to determine

the prevalence of DM,Obesity,CVD Risk factors,and

Indicators of Kidney disease in Australian adults

11,247 Participants

Renal impairment 9.7%

Haematuria 3.7%

Albuminuria 6% Proteinuria 0.6 %

Total 16%

Chadban et al, Prevalence of kidney damage in Australian adults:The AusDiab Kidney Study. J Am Soc Nehrol 2003, 14: S131 S138.


21/52

CRF accounts for 812% of hospital

medical admissions

CRF is a leading cause of mortalityamong adults

Sentinel study: based on available

hospital data

Prevalence of 300-400 per million

population

Hospital Data

Akinsola, 1989; Kadiri et al 1997; Akinsola et al, 2004. Arogundade et al 2005


22/52

0

100

200

300

400

500

600

700

800

1989 1991 1993 1995 1997 1999 2001 2003

Total medical

admissionsCRF admissions


23/52

0

2

4

6

8

10

12

14

16

18

1989 1994 1999

CRF

admissions as

percentage of

Medical

admissions


24/52

NHANES

4%

NHANES

96%

Aus-Diab

9.7%

Aus-Diab

90.3%


25/52

Documented causes in Nigeria

Hypertension Benign

Malignant

Chronic glomerulonephritis Causes unknown in the majority Occurs post-infection

Parasite malaria;

Bacteria sore throat or skin infections;

Helminths Schistosoma, Filaria

Viruses - Hepatitis B, C, HIV Fungal

Toxins: Bleaching creams / soap


26/52

Other documented causes in Nigeria

Diabetes Mellitus Chronic urinary tract infection

Obstructive Uropathies

Drugs Analgesic abuse

Inherited kidney disease-ADPKD

Connective Tissue Disease - SLE, RA

Others


27/52

010

20

30

40

5060

70

1989-

1993

1994-

1998

1999-

2003

Hypertension

CGN

Diabetic Nephropathy

Obstructive Uropathy

TIN

Arogundade et al, 2005


28/52


29/52

Objectives of Clinical Evaluation

Establishing that there is CKD

Defining the likely aetiology

Determining occurrence/presence ofcomplications

Assessing prognosis and survival


30/52

Clinical Evaluation Hx & Examination

Polyuria & NocturiaFrothiness of urine

Oliguria

Symptoms of prostatism

Features of uraemia

Use of Analgesics, Hg containingcreams/soaps, other drugs, local herbs

Past Medical Hx HT, DM, Body Swelling etc.Family Hx Renal Ds,

Social Hx Alcohol, Smoking


31/52

Clinical Evaluation Hx & Examination

Presence of HT

Presence of oedema

Presence of Pallor

Presence of Uraemic features

Presence of heart failure

Presence of retinopathy


32/52

Investigations

Blood Chemistry

E/U/Cr

Ca, Po4,

Alb, Chol, lipid profile

Haemogram Blood cell counts

Serology

Clotting profile

Urine Microscopy

Chemistry Full urinalysis

24 Hour profile

Imaging USS

CXR

ECHO

ECG

Renal Biopsy


33/52

Management

Conservative

Control of risk factors

Modifiable

Non modifiable

RRT

PD

HD

Transplant


34/52

CKDHypertension

Proteinuria

Lipids

Smoking

alcohol

Weight

Risk Factors/Markers for progressive CKD

Cal-phos

Anaemia

Nutrition

Gender

Race

Ageing

Card.VD

CKDDM

Infectns


35/52

BP

Classificat.

SBP

mmHg

DBP

mmHg

Lifestyle

Modific.

Initial Drug Treatment

Without

Compelling

Indic.

With

Compel.

Indic.

Normal 100 Yes 2 drug

combination

JNC VII Classification and management of BP for adults


36/52

75.7% had hypoalbuminaemia ( mean SD for serum albumin; 29.5 7.2 g/L).

88.9% had anaemia (Packed Cell

Volume,PCV


37/52

Hypertension


38/52

Choice of Antihypertensives

Regimens that include angiotensin-

converting enzyme inhibitors (ACEIs)are more effective than regimens that

do not include ACEIs in slowing

progression of both diabetic and non-diabetic kidney disease.

Combination therapy of ACEI and

angiotensin receptor blocker (ARB)

slows progression of both diabetic and

non-diabetic kidney disease more

effectively than either single agent.


39/52

ACEIs appear to be more effective than beta-

blockers and dihydropyridine calcium

channel blockers in slowing progressive

kidney disease.

Beta-blockers may be more effective in

slowing progression than dihydropyridine

calcium channel blockers, especially in the

presence of proteinuria.

Choice of Antihypertensives


40/52

RRT AVAILABILITY AFFORDABILITY USEFULNESS LIMITATIONS

PD Not readily Not Affordable 1. Diff. vasc.Access

2. Uncotr. HDHT.

3. Low HCT not

desiring transf.

1. Softwa.

sourc

2. Infections3. Mechanical

4. Obesity

HDReadily Not affordable 1. Easy

2. Time constr.

3.

1. Hypotensn.

2. Reactions

3. Inf transm.

4. Blood loss

TX Readily Not affordable 1. Best QOL2. Cheap ultim.

3. Best profile

1. Planning

2. Organ Sourc

3. Infrastruc.

4. Donor Probl

Reference

s

Akinsola et al,

2000

Arije et al, 1992&95,

Bamgboye 2002,

Arogundade et al,

2005

Arije et al,

1992&95,

Arogundade et

al, 2004 & 2005

Arije et al,

1992&95,

Arogundade et

al, 2004 & 2005


41/52

Fig 1: COMPARING HRQOL IN THE PATIENT'S GROUPS

0

5

10

15

20

25

30

Livingre

lated

Rec

ipien

ts(Group

II)

Emo

tiona

lly

relatedRec

ipien

ts

(Gro

up

III)

Main

tenance

haem

odialys

is

Pa

tient

s(Group

I)

Patients Groups

Num

bero

fPa

tien

ts

Karnofsky Score =90 Karnofsky Score = 80 Karnofsky score = 70 Karnofsky score = 50

Fi 2 C l ti b t Q lit f Lif


42/52

Fig 2: Correlation between Quality of Life

Scores and Age in all studied subjects

(r=-0.363, P


43/52


Scores and Serum Creatinine in all subjects

(r=-0.502, P


44/52


Scores and Haemoglobin (g/dL) in all subject

(r=0.705, P


45/52


46/52

Preventive Nephrology

Primary Prevention Aims at preventing kidney disease from occurring at all

Calls for knowledge of risk factors that predispose to renal disease

risk factors that initiate renal damage.

modification, removal, or avoidance of factors. development of a positive health seeking attitude and

behaviour

Secondary Prevention Aims at identifying factors that aid or hasten progression

of kidney disease and/or accelerate loss of kidney

function, and preventing or removing such factors. Whilea few of these factors are not modifiable, majority of themcould be modified, controlled or completely avoided.

Tertiary Prevention

Ri k F /M k f i CKD


47/52

CKDHypertension

Proteinuria

Lipids

Smoking

alcohol

Weight

Risk Factors/Markers for progressive CKD

Cal-phos

Anaemia

Nutrition

Gender

Race

Ageing

Card.VD

CKDDM

Infectns

Non ModifiableModifiable


48/52

Hypertension


49/52

Tertiary Prevention

Hypertension


50/52

Tertiary Prevention Contd

Control of HT

Use of EPO & Parenteral Iron

Use of Vit D analogues

Use of Phosphate sequestering agents

Control of hyperlipidaemia

Control of Infections Control of Heart Failure


51/52

When do we refer to Nephrologists

CKD 4 & 5

Resistant HT

Persistent proteinuria / haematuria

Difficulty achieving Bld sugar control

Established CKD

Uraemia

Heart failure

Anaemia


52/52

Documents

Predisposing Conditions, Management and Prevention of Chronic Kidney Disease..ppt