CHRONIC RENAL FAILURE
The Clinical Approach
Dr. Manoj Chaudhary
Consultant Nephrologist
Kidney Hospital, Jalandhar
Why to know about CRF/CKD
• IndiaWorld’s sharpest due to Type II DM,
Hypertension (CAUSE-VASCULAR
DYSFUNCTION)
• Death from communicable disease - 20
million-starting to decline,
• CVS disease to 26 million in 2020,
• DM-150 million in 2000 will to 370 million in
2030 (75% in developing world)
• Estimation of CRF/CKD - 1 lakh/yr
Minority seen by Nephrologists
• CRD - Pathophysiologic process with multiple
etiologies, resulting in inexorable attrition of
nephron number and function frequently leading
to End stage renal disease.
• ESRD - Clinical state or condition that has
irreversible loss of endogenous renal function of
sufficient degree to render the patient
dependent on Dialysis or Transplantation in
order to avoid Uraemia.
• Uraemia - Clinical and laboratory syndrome,
reflecting all organ system dysfunction as result
of untreated or treated Acute or CRF.
STAGES OF CHRONIC RENAL DISEASE
STAGE
GFR,ML/MIN/1.73M2
1
KIDNEY DAMAGE WITH
NORMAL OR INCREASED GFR
90
2
KIDNEY DAMAGE WITH MILDLY 60-89
DECREASED GFR
3
MODERATELY DECREASED GFR
30-59
4
SEVERLY DECREASED GFR
15-29
5
RENAL FAILURE
<15(OR DIALYSIS)
COCKROFT AND GAULT EQUATION
CREATININE.CLEARENCE (ml/min.)
= (140 - AGE) X BODY WT. (kg)
72 X PCr (mg/dl)
Multiply 0.85 for women
CAUSES OF CRF: [SGPGI,PGI,AIIMS]
DIABETIC NEPHROPATHY
34.98%
CGN
CIN
PKD
HYPERTENSIVE NEPHROSCLEROSIS
26.98%
24.69%
3.96%
5.34%
CALCULUS DISEASE
0.92%
REFLUX NEPHROPATHY
0.85%
OBSTRUCTIVE UROPATHY
1.86%
UNSPECIFIED CAUSE
0.51%
DIAGNOSIS OF CRF
• HISTORY
• FACTORS SUGGESTING CHRONICITY
– Duration of symptoms for months.
– Nocturia
– Absence of acute illness in face of high urea and
creatinine.
– Anaemia of chronic disorders
– Bone disease
– Sexual dysfunction
– Nail changes, Pruritis
– Neurological complications
– Small kidneys on renal imaging
•LAB
- Hb, Ca 2+, PO43-, Alk. Phos., HCO3, Alb.,
24hrs. U.protein, Urine R/M, Broad Cast,
PTH levels.
•IMAGING
- USG, MCU (Reflux), Renal Doppler, MRA
•RENAL BIOPSY
- If clear cut Dx not possible in kidney of
Normal size.
SODIUM AND WATER HOMEOSTATIS
• Stable CRD- Increased Total Body Na & H2O
-Not clinical apparent
• Hyponatremia-Restrict water intake
• Wt. gain offset by concomitant loss of lean body
mass
• Expanded ECFV
Restrict salt
Restrict fluid
Loop diuretics + Metalozone (distally acting
diuretics)
• Volume depletion-resuscitated with normal saline.
ANAEMIA
• CLINICAL EFFECTS
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O2 delivery & utilization
CO
Cardiac enlargement
Ventricular hypertrophy
Angina
CHF
Cognition & mental acuity
Altered menstrual cycles
Bleeding diathesis
Impaired host defence against infection
Growth retardation in children
ANAEMIA Contd…..
• Normocytic Normochromic Anaemia
• Reticulocyte count low
• Reduced, Normal or Bone marrow cellularity,
 M:E
• Reduced red cell life span,  Erythropoiesis
IRON STUDIES
• S.Fe, TIBC, S.Ferritin
• If TSAT<20% S.Ferritin<100ng/l give
Fe(50-100mg iv) Thrice weekly x 5weeks
• If still low repeat same course
• Withhold therapy TSAT>50%
S.Ferritin>800mg/ml (>800g/L)
ERYTHROPOIETIN
• Starting dose 50-150 units/kg/wk IV or
S.C (once, twice or thrice/ wk)
• TARGET Hb-11-12gm/dl
• Optimal rate of correction-1-2gm/dl
over 4 wks.
EPO BENEFITS
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Increased Exercise tolerance
Normalization of elevated Cardiac Output
Increased BP in 30% of patients
Decreased Symptom of Angina
Decreased LVH
Decreased Cardiac size on chest X-Ray PA
Improved quality of life
Decreased Uraemic bleeding
Improved platelet function
Enhanced immune function
Decreased Uraemic pruritis
ADVERSE EFFECT OF EPO
• Hypertension
• Seizures/ Encephalopathy
• Clotting of dialysis lines
• Hyperkalemia
• Myalgia/ Influenza like syndrome
DARBOPOIETIN ALPHA
• Analogue of EPO
-Greater biological activity
-Prolonged half life
• Starting dose
-0.45mg/kg iv or s.c. weekly or single dose
0.75mg/kg single iv or s.c. every 2 wks.
• Optimal rate of correction
-Hb by 1-2 gm/dl over 4 wk period
ORAL IRON
• POOR ABSORPTION
• INTOLERANCE
• DIALYSIS  Adequate dialysis.(CAPD
better HD for 3 yrs., then same.)
BLOOD TRANSFUSION
• Suppresses residual EPO production
• Iron overload  deleterious effect on heart,
liver, pancreas
• Infection HepB, HepC, HIV, CMV
• Exposure to wide range of HLA  Cytotoxic Ab
 Risk of +ve crossmatch and Ac. rejection
ANDROGEN THERAPY
• Effective in mild cases only
S/E-Virilization, Muscle & Liver
damage, Cholestasis
BONE DISEASE AND DISORDERS OF
CALCIUM AND PHOSPHATE
METABOLISM
• High turnover bone disease
• Low turnover bone disease
– Osteomalacia
– Adynamic bone disease
• LABS: Ca2+, Phosporous, Alk. Phosphatase, S.PTH
PRACTICAL RECOMMENDATION
• Early CRF  CaCO3 2gms/day
Dietary Phosphate<1000 mg
• Advanced CRF (Cr.Cl-60-40 ml/min)
– Phosphate 800-900 mg/day
Ca supplement
– If S.Calcediol < 20ng/ml
Add the metabolite 2mg/day
- Metabloic acidosis - Ca Co3/ and or bicarbonate
- Avoid citrate - increased absorption of aluminum
• FAR advanced stages
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Daily phosphate - 600-750 mg/day
CaCo3 - 3gm /day
Watch for Metabolic acidosis - NaHCO3
Plasma calcidiol – Add Calcitriol 0.25 pg daily
If hypercalcemia - restrict or half the dose
calcidiol
– hyperphosphatemia
- target PTH around 2-3 times the
upper limit
• Sevalamer
– Non reabsorbable,
– Non calcium containing polymer,
– No Hypercalcemia
• Attenuates calcium deposition in
coronary arteries and aorta.
• Adynamic bone disease
Overzealous suppression of secondary
Hyperparathyroidism (keep PTH<120 pg/ml)
CARDIOVASCULAR ABNORMALITIES
Leading cause of mortality and morbidity
• IHD
Classical risk factors
• Hypervolumia
• Dyslipidemia
• Sympathetic overactivity
• S Hyperhomocysteinemia
• Tt - HMG COA if + Gem fibozil
 Risk of Myositis
CRD RELATED
• Anaemia
• Hyperphosphatemia
• Hyperparathyroidism
• Microinflammation-IL6, CRP
• NO
CHF
• Abnormal cardiac function secondary to IHD or
LVH, Salt and Water retention
• Unique feature - Even in absence of volume
overload there is normal or increased Intracardiac
or PCWP
• Butterfly wing distribution due to increased
permeability of capillary alveolar membrane
leading to low pressure pulmonary edema.
- Treatment by vigorous dialysis
HYPERTENSION
• Most common complication
• Develop early in course associated with
adverse outcome
• LVH & Cardiovascular morbidity
• Anaemia & LVF
If Hypertension absent
Salt wasting renal disease, Medullary cystic
disease, Chronic T1 disease, Volume depletion
or Reduced cardiac index.
Treatment:
• Slow progression of disease
• Prevent complication - CVS disease and stroke
• Target BP – 130/ 80 – 85 (Protenuria < 1gm/
24hrs)
• If protenuria > 1gm/ 24hrs – Target BP 125/ 75
• Volume Control
- Salt restriction
- Diuretics
• Ace inhibitor can be used
• Avoid direct Vasodilators – Minoxidil
Hydralaizne
• If increased Cardiac hypertrophy
- Use only in Refractory hypertension
- Target BP-->130/80-85
(Protenuria<1gm/24hrs)
• If protenuria>1gm/24hrs-Target BP 125/75
• Volume control--> Salt restriction
--> Diuretics
• ACE or ARB ? Or both ?
• Avoid direct vasodilators
– Minoxidil
– Hydralazine
Leads to Cardiac hypertrophy
– Use only in refractory hypertension
NUTRITION
PEM- Common problem
Indian scenario-malnutrition widely prevalent
CAUSES:
• Anorexia
• Altered taste sensation
• Intercurrent stress
• Unpalatable prescribed diets
• Catabolic response to superimposed illness
• Endocrine disorders of uraemia (resistance to
IgF, hyperglucagonemia, hyperparathyroidism)
Energy - 35 k cal/kg/day
On vegetarian diet
-Av. Protein intake 0.64 + 0.15 gms/kg/day
Diabetic pt.- 30-35 kcal/kg of IBW/day,
60% carbohydrates, 30% - fats
15% from mono unsaturated fats.
For MHD- Calories - same
Protein -1.2 gm/kg. (50% HBV)
INDICATIONS OF RENAL REPLACEMENT THERAPY
• Anorexia & nausea
• Fluid & Electrolytes abnormalities that are
refractory to conservative means
– Volume overload refractory to diuretics
– Hyperkalemia unresponsive to protein restricted
– Progressive metabolic acidosis that cannot be
managed by alkali
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Pericarditis
Progressive neuropathy attributable to ureamia
Encephalopathy
Muscle irritability
CLINICAL CLUES INDICATING DEVELOPMENT
OF URAEMIC COMPLICATIONS
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Morning nausea
Vomiting
Intractable pruritis
H/O Hiccuping
Muscle twitching & cramps
Presence of asterixis
Pt’s whose follow up and compliance with
conservative management is difficult- considered
for earlier management
Considerable interindividual variability in severity of
uraemic symptoms and renal function
It is ill advised to assign a certain usual level of
BUN, S.creatinine, GFR to need to start Dialysis
Recent controlled studies failed to show a
survival advantage for early initiation of
RRT prior to onset of clinical indications.
Modality of RRT
• Haemodialysis
• Chronic Ambulatory Peritoneal
Dialysis
• Renal Transplantation
HD- most common modality of ESRD
(USA- 80%)
PD- Younger pt-because of better
manual dexterity and greater
visual acuity
Difficult vascular access
Larger pt-Truncal obesity (>80kg)
suited for HD