CKD

1. 1
History Taking
Particulars of the patients
 Daw Khin Ohn, 61 years old,
 Burmese, Buddhist, who is a dependent
 From Yay Oo township
 was admitted to medical unit (1) of MGH, on 29th
November, 2019
Chief complaints
 Worsening of generalized edema x 1 month
 Breathlessness x 20 days
History of present illness
 Previously she was suffering from generalized edema off and on x 1 year
 Edema worsens in 1 month, with insidious onset
 Starts from the dorsum up to the knee
 More prominent in left leg
 Concomitant abdominal distension and slight puffiness of face
 Which are worsened in the mornings
At that time, she also suffered from
 Shortness of breath

2. 2
 Dyspnoea on exertion (NYHA grading 5)
 Orthopnoea (+)
 PND (+)
 Dyspnoea is precipitated by increased fluid intake, increased salt intake
 It is relieved by diuretics.
Associated symptoms
 Cough x 30 days
 Moderate sputum production
 White to rusty colour
 On the morning we took history taking, the sputum is blood streak sputum
At Yay Oo hospital (12.11.2019 to 27.12.2019),
 Oliguria (+), with 2-3 drops
 Dysuria (+),
 With normal coloured urine
System review
On Cardiovascular System,
 Chest pain (-)
 Breathlessness (+)
 Palpitation (+)
 Oedema (+)
 Dizziness (+)

3. 3
On Respiratory System,
 Shortness of breath (+)
 Cough (+)
 Sputum production (+)
 Wheeze (-)
On Gastrointestinal System,
 Dysphagia (+)
 Nausea, Vomiting (-)
 Vomiting of blood (-)
On Genitourinary System,
 Dysuria (+)
 Polyuria (+) x 15 times per day
 Oliguria (+) while at Yay Oo hospital
On Nervous System,
 Dizziness (+)
 Headache (-)
 Fits (-)
 Numbness (-)
On Musculoskeletal System,
 Joint pain (-)

4. 4
 Muscle stiffness (-)
 Swelling (-)
On Endocrine System,
 Heat or cold intolerance (-)
 Changes in sweating (-)
 Excessive thirst (-)
 No bleeding manifestation
 No skin rash
Past medical history
Diabetes mellitus x 13 years
 Diagnosed by routine medical checkup
 Regular blood glucose level measurement at home
 Maximal RBS level – about 280 mg/dL
Hypertension x 13 years
 Diagnosed by routine medical checkup
 No regular blood pressure measurement
 Maximal blood pressure – she could not remember
 Cold extremities (-)

5. 5
 Claudication (-)
 Previous vascular bypass surgery (-)
 Stroke (-)
 Transient ischaemic attack (-)
 Blurred vision (-)
 Renal disease (+)
 Foot ulcers (+) on both legs
 Numbness of fingers and toes (+) x 10 years
History of hospitalization
 8 times of hospitalization
 The last one – hospitalization at Yay Oo hospital x 15 days
 with chief complaint of shortness of breath x 1 month
Past surgical history
 6 times of surgical operation
 4 times for diabetic foot ulcer
 2 times for sebaceous cyst in the nect
No history of blood transfusion

6. 6
Personal and Social history
 Educated up to primary school level
 She is a dependent.
 Alcohol drinking (-)
 Betel chewing (-)
 Cigarette smoking (-)
 Habit of doing regular physical exercise (-)
 She has habits of having fatty meal and sweet diet.
Drug history
 Regular taking drugs for diabetes mellitus – gliclazide, now stopped by physician
 For hypertension – amlodipine, 5 mg x O.D
 History of taking Sin-Thone-Kaung indigenous drug for DM
 No known drug allergy
ICE
 Idea – She has an idea that she is suffering from renal disease.
 Concern – for financial burden on the family
 Expectation – she expects to relieve the symptoms as fast as possible and believes
that doctors in MGH will treat her well.

7. 7
Physical examination
General examination
 A 61 years old woman with average weight and height is lying on her bed.
 She is well-conscious and well-coperative.
 She seems dyspnoeic.
 She is afebrile.
 No pallor, no jaundice
 No subconjunctival haemorrhage
 No xanthelasma
 No artheroma
 Face – no rash
 Alar nasi are working.
 Mouth – no cyanosis, no dry mouth
 Tongue – no central cyanosis
 No tonsillar enlargement
 Cervical lymph node enlargement of right side of the neck.
Upper extremities
 No features if infective endocarditis such as splincter haemorrhage,
Osler node, Janesway lesions, clubbing
 No palmar erythema
 No skin turgor

8. 8
 No photosensitive rash
 No tendon xanthoma
Lower extremities
 Ankle edema (+) on both legs
 No clubbing
 No cyanosis
 No xanthoma
Systemic Examination
CVS examination
Pulse
 Rate – 90/min
 Rhythm – irregularly irregular
 Volume – low
 No special character
 Vessel walls are not thickening
 Equal on both sides.
Blood pressure – 140/90 mmHg
JVP is not raised.
On inspection, palpation and auscultation of the precordium, no abnormalities are found.
No signs of CHF except pitting edema.

9. 9
Respiratory system examination
On inspection,
 Shape of the chest – pectus carinatum
 Respiratory rate – 20/min
 Chest wall movement is reduced on left side.
On palpation,
 Trachea is deviated to the right side.
 Chest wall movement is reduced on the left side.
 Vocal fremitus is reduced on the left side.
On percussion,
 Dullness is present in left anterior 4th
, 5th
, 6th
ICS and the rest are normal
resonance.
On auscultation,
 Normal vesicular breath sounds are heard but reduced in left lower zone.
 No other added sounds.
Examination of abdomen
On inspection,
 Abdomen is uniformly distended.
 Move with respiration

10. 10
 Umbilicus – flat
 Flanks are full.
 No scars, dilated veins, tapping marks, visible peristalsis
On palpation,
 Light palpation – no tenderness, guarding, rigidity
 Deep palpation – liver and spleen are not palpable.
- kidneys are not ballotable.
On percussion,
 No shifting dullness and fluid thrill
On auscultation,
 Bowel sounds are present and normal.
 No liver bruit
Motor system examination
 Muscle tone is normal.
 Muscle power is normal.
 Reflexes are present and normal.
 Normal coordination is present.

11. 11
Investigations
Haemogram
 WBC 15.9 ↑
 Hb 9.9 ↓
 Platelet 153
 CRP 78.7 ↑
 Urea 33.8 mmol/L ↑
 Creatinine 540 µmol/L ↑
 Electrolytes
Na 138 mmol/L
K 3.31 mmol/L ↓
Cl 97.3 mmol/L
HCO3 26 mmol/L ↑
Phosphate 2.3 mmol/L ↑
UREME
 Leucocytes (-)
 Nitrate (-)
 Urobilinogen (-)
 Protein (++)
 pH 6
 Blood (+)
 Specific gravity 1.012
 Ketone (-)
 Bilirubin (-)

12. 12
 Glucose (-)
 Ascorbic acid (+)
Macroscopic examination
 Colour yellow
 Transparency clear
Microscopic examination
 Epithelial cells 2-4
 Pus cells 1-2
 RBCs 2-4
 Casts Nil
 Crystals Nil
USG (abdomen)
 Fatty liver
 GB sludges
Chest X-ray
 Left pleural effusion
Total & Differential Protein
 Total protein 62
 Albumin 33 ↓
 Globulin 29
 OSPT 14.8 sec (control 12.3 sec)
 INR 1.37
 HBs Ag negative

13. 13
 Anti HCV negative
 HIV Ab non-reactive
Provisional Diagnosis
Chronic kidney disease with fluid overload and chest infection with underlying
type-2 DM and hypertension.
Points for Diagnosis
From history taking,
 Generalized edema with puffiness of face which is worsened in the mornings
 Breathlessness
 Cough with sputum production
 Dysuria
 History of DM and hypertension x 13 years
From examination,
 Dyspnoeic
 Alar nasi are working
 Ankle edema (+) on both legs
Respiratory system,
 Inspection - Chest wall movement is reduced on left side.
 Palpation – Chest wall movement and vocal fremitus are reduced on left side.
 Percussion – Dullness (+) in left anterior ICS.

14. 14
 Auscultation - Normal vesicular breath sounds are heard but reduced in left lower
zone.
From investigation,
 Raised blood urea and creatinine level
 Increased bicarbonate and phosphate level
 Proteinuria ++
 Haematuria
Treatment
 IV Lasix 80 mg IV x 8 Hourly
 IV Co-amoxiclav 600 mg x OD
 Atorvastatin 10 mg x Hs
 Cinoglip x OD
 Solmux x TDS
 Linagliptin x TDS

15. 15
Literature Review
Chronic kidney disease (CKD)
Definition
Chronic kidney disease (CKD) refers to an irreversible deterioration in renal
function that usually develops over a period of years.
Initially, it manifests only as a biochemical abnormality but, eventually, loss of
the excretory, metabolic and endocrine functions of the kidney leads to the clinical
symptoms and signs of renal failure, collectively referred to as uraemia.
Causes of CKD
1. Diabetes: Type II >> Type I
2. Glomerulonephritis: commonly IgA nephropathy, also rarer disorders, eg;
mesangiocapillary GN, systemic disorders, eg SLE, vasculitis
3. Unknown: up to 20% in the UK have no obvious cause of CKD, many of these
present late with small, shrunken kidneys where a biopsy would be uninformative
4. Hypertension or renovascular disease
5. Pyelonephritis and reflux nephropathy
Classification of CKD by GFR (ml/min/1.73 m2
)
Category GFR Notes
G 1
G 2
G 3a
G 3b
G 4
G 5
>90
60-89
45-59
30-44
15-29
<15
Only CKD if proteinuria/haematuria (+)
Pathology on biopsy/imaging
Mild-moderate ↓GFR
Moderate-severe ↓GFR
Severe ↓GFR
Renal failure

16. 16
Clinical features of CKD
Typical presentation Raised urea and creatinine
Most patients Asymptomatic until GFR falls below 30 mL/min/1.73
m2
Early symptom Nocturia due to the loss of renal concentrating ability
GFR < 15–20 mL/min Tiredness or breathlessness, due to renal anaemia or
fluid overload
Worse in renal function Pruritus, anorexia, weight loss, nausea, vomiting and
hiccups
Advanced renal failure Kussmaul breathing due to profound metabolic
acidosis, muscular twitching, fits, drowsiness and coma
Management of CKD
Mild-moderate CKD is usually managed in general practice or physicians.
Refer early to a nephrologist if the patient meets any of the following criteria:
 Stage 4 and 5 CKD
 Moderate proteinuria (ACR >70mg/mmol) unless due to DM and already
appropriately treated
 Proteinuria with haematuria
 Rapidly falling eGFR (>5mL/min in 1yr, or >10mL/min within 5yrs)
 BP poorly controlled despite ≥4 antihypertensive drugs at therapeutic doses
 Known or suspected rare or genetic causes of CKD
 Suspected renal artery stenosis
Management of CKD patients can be split into four main approaches:
1. Investigations
2. Limiting progression/ complications
3. Symptomatic control
4. Renal replacement therapy (RRT)

17. 17
1. Investigation
Identifying and treating reversible causes: relieve obstruction, stop nephrotoxic drugs,
deal with high Ca2+ and cardiovascular risk (stop smoking, achieve a healthy weight),
tight glucose control in DM.
2. Limiting progression/complications
• BP: Even a small BP drop may save significant renal function. Target BP is <130/80.
• Renal bone disease (risk of osteodystrophy or adynamic bone disease): Check PTH and
treat if raised.
• Cardiovascular modification: In CKD stages 1 and 2, risk from cardiovascular death is
higher than the risk of reaching ESRF. Give statins to CKD patients with raised lipids for
any patient. Give aspirin also (CKD is not a contraindication to the use of low-dose
aspirin).
• Diet: Advice on a healthy, moderate protein diet, K+ restriction
if hyperkalaemic, and avoidance of high phosphate foods (eg: milk, cheese,eggs).
3. Symptom control
• Anaemia: Check haematinics and replace iron/B12/folate if necessary. If still anaemic
consider recombinant human erythropoietin.
• Acidosis: Consider sodium bicarbonate supplements for patients with low serum
bicarbonate; this not only improves symptoms but may slow progression of CKD.
Caution in patients with hypertension, as sodium load can raise BP.
• Oedema: High doses of loop diuretics may be needed
(eg: furosemide 250mg–2g/24 hr, metolazone 5–10mg/24h PO each morning), and
restriction on fluid and sodium intake.
• Restless legs/cramps: Check ferritin (low levels worsen symptoms), clonazepam (0.5–
2mg daily) or gabapentin may help.
4. Preparation for renal replacement therapy (RRP)

18. 18
Monitoring renal function in CKD
GFR and albuminuria should be monitored at least annually, according to risk. If
high risk, monitor every 6 months. If very high risk, monitor every 3-4 months.
REFERENCES
• Davidson’s Principles and Practices of Medicine (23rd edition)
• Oxford Handbook of Clinical Medicine (10th edition)
• USMLE Step-2 CK Lecture Notes 2019 Internal Medicine (2018)