Chronic Kidney Disease

Mohammad Rudiansyah

Division of Nephrology and Hypertension - Department of Internal Medicine

Medical Faculty of Lambung Mangkurat University – Ulin Hospital
Definition of Chronic Kidney Disease

Criteria
1. Kidney damage for ≥ 3 months, as defined by structural or
functional abnormalities of the kidney, with or without
decreased GFR, manifest by either :

Pathological abnormalities; or

Markers of kidney damage, including
Abnormalities in the composition of the blood or
urine, or abnormalities in imaging tests

2. GFR < 60 mL/min/1.73 m2 for ≥ 3 mounths, with or without

kidney damage
Screening for CKD

Rationale : early detection, early intervention, reduced
associated complications, high prevalence silent kidney
disease

Whom ? Diabetes, hypertension, family of ESRD, family of
nephropathy (DM,HT,glomerulonephritis)

How ?
- standart urine dipstick (spot urine): proteinuria (>=
+1),hematuria, lekosituria
- serum creatinine
- blood pressure
- ultrasound imaging (obstruction,stones,infection,PKD)
- serum electrolytes
- urinary concentration
Clues to the Diagnosis of Chronic Kidney Disease from the Patient’s
History
Clue Potential Diagnosis

Review of System
Symptoms during urination Usually suggest disorders of the urinary tract such as infection, obstruction or stone
Recent infections May suggest post-infection glomerulonephribs or HIV-associated nephropathy
Skin rash of arthritis Suggests autoimmune disease, such systemic lupus arythematosus or cryoglobulinemia
Risk factor for pareneterally May Suggest HIV, Hepatitis B or Hepatitis C infection and associated kidney disease
transmitted disease

Chronic Disease
Heart failure, cirrhosis, or Usually suggest reduced kidney perfusion (*pre-renal factors*)
gastrointestinal fluid losses
Diabetes* As a cause of chronic kidney disease: Diabetic kidney disease usually follows a typical clinical course after
onset, first with microalbuminuria, followed by clinical proteinuria, hypertension and declining GFR.

Hypertension* As a course of chronic kidney disease: Hypertensive nephrosclerosis is usually characterized by severey
elevated blood pressure readings over of long period of time, with associated end-organ damage in
addition to kidney disease. Recent worsening of hypertension, in association with findings of diffuse
atherosclersis, suggests large vesset disease due to atheroscierosis. Recent onset of severe hypertension
in young women suggests large vessel disease due to fibromuscular dysplasia

Past Medical History

Findings from past “routine” May reveal a history of hypertension or proteinuria during childhood, during pregnancy, or on
examinations examinations for school, military service, or insurance

Past urologic evaluations Details may disclose radiologic abnormalities associated with kidney disease

Family History of kidney Diseases

Every generation; equal Suggests an autosomal dominant disease, such as polycystic kidney disease
susceptibility in males and females

Every generation; predominant Suggests a sex-linked recessive disease, such as Alport’s sundrome
male susceptibility

Less frequent than every Suggests an autosomal recessive disease, such as medullary Cystic kidney disease or autosomal
generation recessive polycystic kidney disease

* Extremely commons in elderly patients, and often non-specific

 Interpretation of Proteinuria and Urine Sediment Abnormalities
as Markers of Chronic Kidney Disease

Predominant Urinalysis Abnormality

Granualar Casts

Total Protein to
Cellular Casts
Tubular Cells
RBC Casts*

WBC Casts

Creatiniue
Ratio^
Fat**
WBC
RBC

Associated Kidney Disease

+ + Proliferative glomerulonephritis or hereditary nephritis
+ – + + Hereditary nephritis, or disease of small vessels
(microangiopathy)
+ – – – Cystic kidney disease, kidney neoplasms or urinary tract
lesion other than kidney disease
± – + + 200-1.000 Tubulointerstitial nephritis
mg/g
+ – < 200 Urinary tract lesions other than kidney disease
mg/g
+ + + May be present in all types of kidney disease, but most
abundant in acute tubular necrosis (the most common
kidney disease causing acute kidney failure)
– – + > 1.000 Diabetic kidney disease and non-inflammatory glomerular
mg/g disease
– – – – – – – – 200– Non-inflammatory glomerular disease, non-inflammatory
1.000 tubulointerstitial disease, or disease affecting medium-sized
mg/g arterial)
* Detection of red blood cell casts requires careful preparation and thorough and repeated examination of sediment from freshly obtained urine specimens.
Even under ideal conditions, red blood cell casts may not always be detected patients with proliferative glomerulonephritis.
** Oval fat bodies, fatty casts, free fat
^ Cut-off value are not precise
 Interpretation of Abnormalities on Imaging Studies as Markers of Kidney
Damage

Imaging Modality/Feature Associated Kidney Disease

Ultrasonography
General appearance May show nephrocalcinosis or discrete stone, hydronephrasis, cysts or masses
Increased echogenicity May indicate cystic disease or “medical renal disease”
Small, “hyperechoic” Generally indicate chronic kidney disease
kidney
Large kidney Generally indicate tumors, infiltrating disease or disease causing nephrotic
syndrome.
Size disparities and
Suggest vascular, urologic or tubulointerstial disease due to stones or infection
scarring

May be useful in investigation of venous thrombosis, less so in arterial stenosis

Doppler interrogation
Intravenous pyelography
(IVP) a
Computed tomography (CT) b
Magnetic resonance imaging
(MRI)
Nuclear scans c
May reveal asymmetry of kidney size or function, presence of obstructing stones,
tumors, scars, or dilated colleting ducts medullary sponge kidney.
May show obstruction, tumors (e.g. angiomyolipoma), cysts or ureteral calculi, Helical
CT with contrast may show sites of anatomic renal artery stenosis.
May show mass lesions, renal vein thrombosis, cysts, etc. MR. Angiography using
gadolinium may be useful in patients with decreased kidney function.
May reveal asymmetry of kidney size or function, functional evidence of renal artery
stenosis, acute pyelonephritis, or scars.

a This modality has been largely supplanted be computed tomography, although it remains useful to describe fine detail in the collecting system
b With or without contras
c Captopril renography, mercaptoacetyltriglycine (MAG3), dimereaptrosuccinie acid (DMSA)
 Clinical Presentations of Kidney Disease
GFR (mL/mLn/1.73
Clinical Presentation m2) Proteinuria Urine Sediment Imaging Studies Other Features
Complications due to
Decreased GFR: 15-89 NA NA NA
↓ GFR

< 15 or treated by
Kidney Failure: NA NA NA Uremia
dialysis

Usually >1500 mg/d

Nephritic syndrome
NA or 1000 mg/g RBCs and RBC casts NA Edema, HBP
(“nephritis”) :
creatinine

>3500 mg/d or Fatty casts, oval fat Edema, low serum

Nephrotic syndrome
NA >3000 mg/g bodies, with or without NA albumin, elevated
(“nephrosis”) :
creatinine RBCs and RBC casts serum lipids
fluid and electrolyte
Usually <1500 mg/d
abnormalities,
Tubular syndromes : Usually normal or 1000 mg/d Usually normal Usually normal
inability to
creatinine
concentrate urine
Usually due to
Usually <1500 mg/d
Kidney disease with urinary urinary tract
NA or <1000 mg/g NA Usually normal
tract symptoms : infection, stones or
creatinine
obstruction

RBCs with or without

Asymptomatic urinalysis <3.500 mg/d or <
RBC casts, WBCs with
abnormalities (proteinuria, ≥ 90 3.000 mg/g NA No Symptoms
or without WBC casts,
hematuria, pyuria or others creatinine
tubular cell or casts
Hydronephrosis dilated
calycas, dilated
Asymptomatic radiologic
≥ 90 Usually normal Usually normal collecting ducts (on IVP), No Symptoms
abnormalities
cysts, asymmetry of
kidney size of function
Hypertension due to kidney
NA ± ± ± HBP
disease

Abbreviations and Symbols : RBC, red blood cells; WBC, white blood cells; IVP, intravenous pyelogram; HBP, high blood pressure; NA, not
applicable; ±, may be present or absent
What to do with an abnormality ?
Evaluation and estimating progression
of chronic kidney disease

Determine type of kidney disease

Presence of comorbid conditions

Assessed level of kidney function

The risk for loss of kidney function

Presence of complications

Risk of cardiovascular diseases

Should be referred to nephrologist
Determine type of kidney disease
Disease Major Type (Examples)
Diabetic kidney Type 1 and Type 2 diabetes
disease
Nondiabetic kidney Glomerular disease
disease (autoimmune disease, systemic infections, drugs,
neoplasia)
Vascular disease
(large vessel disease, hypertension,
microangiopathy)
Tubulointerstitial disease
(urinary tract infection, stones, obstruction, drug
toxicity)
Cystic disease
(polycystic kidney disease)
Disease is the Chronic rejection
transplant Drug toxicity (cyclosporine or tacrolimus)
Recurrent disease (glomerular disease)
Transplant glomerulopathy
 Should be referred to nephrologist

When creatinine clearance <30 ml/min/1.73m2

Patients at risk of rapid progression

In whom doubt exists as to their diagnosis and
prognosis

Preparation RRT
 Assesed level of kidney function

Equation
Equation
Author, Year (No of Subjects)
Cockcroft-Gault Equation
Cockcroft 1976 (N = 236) Ccr (ml/min ) =
(140 - Age)x Weight x (0.85 if famele)
72 x Scr

“ Abbreviated” MDRD Study

Equation GFR (ml/min/1.73 m2 ) = 186 x (So)-1.154 x (Age)-0.203
Levey, 1999 (N = 1070 X (0.742 if femele) x (1.210 if African – American)
558 in Validation set)
Schwartz Formula Schwartz
0.55 x Length
1976 (N = 186) Ccr (ml/min) =
S cr
Counahan-Barratt Equation 0.43 x Length
Counahan, 1976 (N = 108) GFR (ml/min/1.73m2 ) =
Scr
 Clinical Situations in Which Clearance Measures May be
Necessary to Estimate GFR
GFR= urine Cr(mg/kg) x urine vol (ml)
plasma Cr (mg/kg)

Extremes of age and body size

Severe mainutrition or obesity
Disease of skeletal muscle
Paraplegia or quadriplegia
Vegetararian diet
Rapidly changing kidney function
Prior to dosing drugs with significant toxicity that are excreted
by the kidneys
Years Until Kidney Failure (GFR < 15 mL/min/1.73 m2)
Based on Level of GFR and Rate of GFR Decline

Rate of GFR Decline (mL/min/1.73 m2 per year)

Level of GFR
(mL/min/1.73 m2)
10 8 6 4 2 1*

90 7.5 9.4 13 19 38 75

80 6.5 8.1 11 16 33 65

70 5.5 6.8 9.2 14 28 55

60 4.5 5.6 7.5 11 23 45

50 3.5 4.4 5.8 8.8 16 35

40 2.5 3.1 4.2 6.3 13 25

30 1.5 1.9 2.5 3.8 7.5 15

20 0.5 0.6 0.8 1.3 2.5 5

•Average age-related GFR decline after age 20-30 year
•MDRD Study: average rate of decline in GFR is 4 ml/min/year. 85% declined,15% stabile or improvement
 The risk for loss of kidney function
Type Definition Examples
Susceptibility Increased susceptibility to Older age, family history
factors kidney damage
Initiation factors Directy initiate kidney damage Diabetes, high blood
pressure, autoimmune
diseases, systemic
infections, urinary tract
infections, urinary stones,
lower urinary tract
obstruction, drug toxicity
Progression Cause worsening kidney Higher lavel of proteinuria,
factors damage and faster decline in higher blood pressure
kidney function after initiation level, poor glycemic
of kidney damage control in diabetes,
smoking
Endstage Increase morbidity and Lower dialysis dase (KW),
factors mortality in kidney failure temporary vascular
access, anemia, low serum
albumin, late referral
Attemps to prevent and correct acute
decline on chronic renal failure

Volume depletion

IV radiographic contrast

Antimicrobial agent (aminoglycoside,amphotericine B)

NSAID (including Cox2)

ACE/ARB

Cyclosporine and tacrolimus

Obstruction of the urinary tract
 Interventions that have been proven to be effective

Diabetic Kidney Non diabetic Kidney disease

Disease Kidney disease In the transplant
Strict giycemic Yes * I:80-120 NA Not tested
control II:100-140
HbA1C(%):<7

ACE – inhibitors or Yes Yes Not tested

angletensin-receptor (greater affect in patients with
blockers proteinuria)
Strict blood pressure Yes Yes Not tested
control < 125/75 mm <130/80 mm Hg
Hg (greater affect in patients with
proteinuria)
<125/75 mm Hg
(greater affect in patients with
proteinuria)

* Prevents or delays the onset of diabetic kidney discase.

 Interventions that have been studied, but the
result of which are inconclusive

Dietary protein restriction (0.6 – 0,8 gr/kgBB/day)

Lipid lowering therapy (LDL<100 mg/dl)

Partial correction anemia

Changes in GFR measured as the plasma
clearance in patients prescribed a
protein-restricted diet or an unrestricted
diet.
16
16
14
14 LPD
LPD
12
12
GFR
GFR 10
10
(%)
(%) 88
66
44

1.0
1.0
0.9
Protein Intake 0.9
Protein Intake
(g/kg/day)
(g/kg/day) 0.8
0.8 LPD
LPD
0.7
0.7
0.6
0.6
00 66 12
12 18
18
Months
Months
(Ihle, 1989)
Low HDL-C and high LDL is an Independent
Predictor of CHD Risk

1
25
45
65
0 85 mg/l
100 mg/l 160 mg/l 220 mg/l

LDL-
LDL-C
Gordon T et al. Am J Med. 1977;62:707
The risk of anemia

Anemia :
- men,post menopause women : < 12 g/dl
- women : < 11 g/dl

Retrospective study (75.000 US HD): HB 9-9.9 g/dl
had mortality hazard ratio 1.33 than 10-10.9 g/dl. (J
Am Soc Nephrol 1999;10;610-619)

2-year longitudinal study 58 058 HD (J Am Soc Nephrol
2006 ;17;1181-1191)
- 12-13 g/dl the best survival
- 11-11.5 g/dl the lowest survival
- > 13.5 risk of myocardial infarct and thrombosis
Kapan dilakukan
hemodialisis ?
 Konsep lama : KK < 5 ml/menit,
Kreatinin >10, BUN > 100

Sudah ditinggalkan, karena :

Sisa ginjal terlampau sedikit

Sudah muncul gejala berat : edema
paru,koma,asidosis dan hiperkalemi, gagal
jantung, hipertensi berat, oliguri,anemia berat

Mortalitas tinggi
 INDIKASI DIALYSIS PADA
CHRONIC KIDNEY DISEASE

Kliren kreatinin <10 ml/menit pada non DM,

atau <15 ml/menit apabila sudah terdapat
uremia

Kliren kreatinin <15 ml/menit apabila
nefropati diabetik

Lebih awal bila didapatkan komplikasi uremia
berat : malnutrisi, atau chronic overload
 PARAMETER KUALITAS
HIDUP PASIEN CKD
KLINIS
LABORATORIUM
1. Berat badan 1. Hb ≥ 11-12 g/dl
kering 2. Albumin ≥ 3 g/dl
tercapai(ultrafil
3. Calsium 8,8 – 11
trasi) mg/dl
2. Status Gizi baik 4. Phospat < 6 mg/dl
5. Ca x P: < 70
3. Tekanan darah
≤130/80 6. Kalium < 5 mEq/L
(ACE/AIIRA) 7. Gula darah terkendali
8. Kadar lemak normal
4. Tak ada gejala
uremia (Kt/V
>1,2)

KU AL IT AS HIDUP BAIK

PANJANG UMUR