This document presents a case study of a 50-year-old male patient with chronic kidney disease due to diabetic nephropathy. The patient has a 15-year history of type 2 diabetes and non-proliferative diabetic retinopathy. Diagnostic tests show elevated blood sugar, creatinine, and signs of kidney damage. The patient is assessed as having progressed chronic kidney disease due to diabetic nephropathy. His treatment plan includes insulin, medications to protect the kidneys and manage symptoms, and lifestyle changes to control his diabetes and slow disease progression.

1. CASE PRESENTATION ON CHRONIC KIDNEY
DISEASE WITH DIABETIC NEPHROPATHY
Presented By
Percy Arpitha.B
Pharm-D IIIYr
12Y01T0019
1

2. DEMOGRAPHIC DATA
NAME: xxx
AGE: 50 yrs
GENDER: male
I.P. NO: 8998/14
D.O.A: 8-1-14
D.O.D: Not Known
WARD: Delux Ward
CONSULTANT: Dr. V. Venkata Ranga Reddy
REFERRED TO : Dr. Nemali Ravi Kumar Reddy
Dr. Venkata Pakkir Reddy
2

3. SUBJECTIVE
3

4. CHIEF COMPLAINTS
C/O loss of appetite( anorexia) since
a month
C/O Generalized weakness &
fatigue
HISTORY OF PRESENT ILLNESS
H/O fever (night time) since 15
days
4

5. PAST MEDICAL HISTORY:
 Type II diabetes mellitus(DM) since
15 yrs and not on regular medication
 NPDR(Non Proliferative Diabetic
Retinopathy)
PAST MEDICATION HISTORY: not known
PAST SURGICAL HISTORY: Nil
5

6. PERSONAL HISTORY AND HABITS:
Chronic smoker and alcoholic since
20yrs
FAMILY HISTORY:
Father suffered with DM &
HTN
6

7. OBJECTIVE
7

8. GENERAL EXAMINATION
PHYSICALEXAMINATION
Date 8-1-15 9-1-15 10-1-15
Temp N N N
B.P in mm of
Hg
120/80 140/90 110/70
P.R 92/min 86/min 86/min
R.R 24/min 22/min 24/min
SYSTEMEXAMINATION
Cvs: s1,s2 +
Rs: ↓↓ breath sounds (dull note)
8

9. DIAGNOSTIC INVESTIGATIONS
COMPLETE BLOOD PICTURE
TEST TEST VALUE NORMAL VALUE
Hb 10 g/dl 13-17g/dl
RBC 3.79 million/cumm 4.5-5.5million/cumm
TLC(WBC) 15600 cells/cumm 4000-
11000cells/cumm
Differential Leukocyte
Count
Neutrophils 89 % 40-80%
Lymphocytes 08 % 20-40%
Eosinophils 01 % 0-6%
Monocytes 02 % 2-10%
ESR 38 mm/hr 0-20mm/hr
9

10. TEST TEST VALUE NORMAL VALUE
TOTAL BILIRUBIN 0.7 mg/dl 0.0-1.0mg/dl
DIRECT BILIRUBIN 0.2 mg/dl 0.0-0.25mg/dl
INDIRECT BILIRUBIN O.5 mg/dl 0.3-1.0 mg/dl
SGPT 55 IU/L 0-45 IU/L
SGOT 23 IU/L 0-40 IU/L
ALKALINE
PHOSPHATASE
222 IU/L 30-170 IU/L
TOTAL PROTEIN 7.8 g/dl 6-8g/dl
ALBUMIN 3.0 g/dl 3.5-5.5g/dl
GLOBULIN 4.8 g/dl 2.3-3.6g/dl
LIVER FUNCTION TESTS
10

11. TEST 8-1-15 9-1-15 10-1-15 NORMAL
VALUE
FASTING 240 mg/dl 210 mg/dl 60-110mg/dl
RANDOM 255 mg/dl 315 mg/dl 80-150mg/dl
BLOOD SUGAR TEST
RENAL FUNCTION TESTS
TEST 8-1-15 9-1-15 Normal value
BUN 67 mg/dl 10-50mg/dl
Creatinine 1.8 mg/dl 1.9 mg/dl 0.6-1.6mg/dl
11

12. URINE ANALYSIS
Color : Light yellow
Reaction : Acidic
Albumin : Traces
Sugar : ++(two plus)
Deposit cells : 4-5 pus cells/HPF
3-4 epithelial cells/HPF
Casts : Nil
Crystals : Nil
Ketone : -ve
RBC : -ve
12

13. ELECTROLYTES
TEST 9-1-15 Normal value
Sodium 139 135-145 mEq/l
Chloride 105 98-105 mEq/l
Potassium 5.2 3.5-5.5 mEq/l
Calcium 9.0 9-11 mg/dl
13

14. X-ray Chest PA View
Impression : normal
CPB Peripheral Smear
WBC : Neutrophillic leucocytosis
RBC : Normocytic hypochromic with mild anisocytosis
PLATELETS : Mild thrombocytosis
Impression: normocytic normochromic anemia with neutrophillic
leucocytosis
14

15. ASSESMENT
15

16. Based On Subjective And Objective Evidence The Patient Is A
Known Case Of Diabetes Mellitus And Newly Diagnosed To Have
Progressed Chronic Kidney Disease Due To Diabetic Nephropathy
16

17. PLANNING
17

18. S.N
O BRANDNAME GENERICNAME DOSE ROA FREQUEN
CY
DATE
BEGIN
DATEEND
1 Inj. Rabeloc RABEPRAZOLE 20mg IV OD 8-1-15 NotKnown
2 Inj. Humanmixtard INSULIN(Shortacting+ longacting) 24 U S/C BD 9-1-15 NotKnown
3 Tab.Renosave N-Acetylcysteine-150mg+Taurine-500mg 1 tab Oral OD 8-1-15 NotKnown
5 Tab.Supradyn MULTI VITAMIN& MULTI MINERAL
SUPPLEMENT
1 tab Oral OD 9-1-15 NotKnown
6 Syp.Aristozyme PEPSIN-10mg/5ml+ FUNGAL
DIASTASE-50mg
5ml Oral TID 8-1-15 NotKnown
7 Inj.Emeset ONDENSETRON 2mg/2m
l
IV BD 10-1-15 NotKnown
18

19. DISEASE DISCUSSION
DIABETIC NEPHROPATHY
 Microvascular complication
 Progressive kidney disease
 Angiopathy of capillaries
19

20. EPIDEMIOLOGY
Over 40% of new cases of end-stage renal disease (ESRD) are attributed
to diabetes.
In 2001, 41,312 people with diabetes began treatment for end-stage renal
disease.
In 2001, it cost $22.8 billion in public and private funds to treat patients
with kidney failure.
Minorities experience higher than average rates of nephropathy and
kidney disease
20

21. PATHOPHYSIOLOGY
Three major histologic changes occur in the glomeruli of persons with diabetic
nephropathy.
1. Mesangial cell expansion directly induced by hyperglycemia
2. Thickening of the glomerular basement membrane
3. Glomerular sclerosis is caused by intraglomerular hypertension
21

22. Uncontrolled diabetes leading to persistent Hyperglycemia induces ,
 Endothelial NO uncoupling
 Activation of Pkc
 Formation of advanced glycation end products
 Activation of polyol pathway
22

23. 23

24. 24

25. 25

26. 26

27. 27

28. GLOMERULOSCLEROSIS
-Hardening of glomerulus due to scarring
-Disturbs filtering process
-2 types
• Focal segmental
• Nodular (significant in diabetes)
-Nodules of pink hyaline material formed in glomerular capillary
loops
28

29. CLINICAL PRESENTATION
You may not experience any symptoms until your kidney
disease progresses to ESRD. Symptoms of ESRD may include:
 Microalbuminuria
-First laboratory finding of DN
-Moderate increase in level of urine albumin
-Occurs when kidney leaks small amount of albumin into
urine
 Anorexia
 Nausea and vomiting
 General ill feeling
 Fatigue
 Headache
 Itchy and dry skin
 Swelling of arms and legs 29

30. Chronic Kidney Disease (CKD)
Or
Chronic Renal Failure(CRF)
DEFINITION
Chronic kidney disease (CKD), also known as chronic renal disease, is a
progressive loss in renal function over a period of time. The three most common
causes of CKD are,
-Diabetes mellitus
-Hypertension and
-Glomerulonephritis.
 Together, these cause about 75% of all adult cases.
30

31. 31
PATHOPHYSIOLOGY
Involves 2 broad sets of mechanisms
 Initiating mechanisms specific to underlying etiology
 Progressive mechanisms, involving hyperfiltration and
hypertrophy of viable nephrons

32. 32

33. 33
Endocrine-metabolic disturbances
2ᵒ hyperparathyroidism
Vitamin-D deficient osteomalacia
Hypertriglyceridemia
CVS and Pulmonary disturbances
HTN
CHF
Pericarditis
Pulmonary edema
Accelerated atherosclerosis
Hematological & Immuological
disturbances
Anemia
Lymphocytopenia
Platelet disorders
Fluid & electrolyte disturbances
Hyponatremia
Hyperkalemia
Hypophosphatemia
Dermatological disturbances
Pallor
Pruritus
GIT disturbances
Anorexia
Nausea &vomiting
Peritonitis
Ulceration
Neuromuscular disturbances
Fatigue
Sleep disorders
Seizures
Coma
CLINICAL
PRESENTATION

34. 34

35. 35
COMPLICATIONS
 Cardiovascular complications
-Hypertension
-Coronary artery disease
-Heart failure
-Pericarditis
 Disorders of mineral metabolism
 Hematological complications
-Anemia
-Coagulopathy
 Hyperkalemia
 Acid-base disorders
 Neurologic complications
 Endocrine disorders

36. 36

37. 37
Complications Related To Case
Uremic pericarditis
o Results frominflammationof visceral & parietal membranes of the pericardialsac.
o There is a correlation b/wdegree of azotemia(BUNis usually>60)althoughpathogenesis
is poorlyunderstood
Emphysematous pyelonephritis(EPN)
o Severe infection of renal parenchymathat causes gas accumulation in the tissues.
o However UTI’sare common in persons withdiabetes, but not all of these infections lead
to EPN
o Factors predisposing to EPN
-Uncontrolled diabetes
-High levels of glycated Hb
-Impaired host immune mechanism

38. 38
Typical presenting features of EPN include thefollowing:
• Fever (79%)
• Abdominal or flankpain(71%)
• Nausea and vomiting (17%)
• Dyspnea (13%)
• Acute renal impairment (35%)
• Alteredsensorium(19%)
• Shock(29%
Laboratory findings include the following:
• Leukocytosis with a left shift
• Pyuria

39. 39
TREATMENT
SLOWING PROGRESSION
 Treatment of underlying cause
 Glycemic targets need to be relaxed
 Blood pressure control is vital. Agents that block RAAS are imp in
proteinuric disease
 Oral alkali therapy in slowing CKD progression if acidemia is
present
 Modify Loading And Maintenance Doses Of Drugs That Are
Excreted Through Renal Route.

40. 40
NON PHARMACOLOGICAL
Dietary management
 Protein restriction : Decrease protein intake to 0.6-0.8g/kg/day in
patients with GFR <30ml/min
 Phosphate restriction : Food like cola beverages,nuts,beans,meat
should be limited.To reduce soft tissue calcification (avoid milk, egg)
 Salt & water restriction : Moderate sodium restriction to control BP
and edema
 Potassium restriction : If CKD is moderate to severe (avoid food like
banana,citrus,coconut water, papaya etc.)

41. 41
o Smoking and alcohol cessation
o Diet and weight management
o Regular exercise
PHARMACOLOGICAL
o Target BP in both diabetic and non-diabetic patients is <140/90 mm of Hg
and in patients with urine albumin excretion >/=30mg/24hrs,target BP is
consistently <130/80mm of Hg
 Tab.Furosemide 40-160mg/day or
 Tab.Amlodipine 5-20mg/day or
 Tab.Atnelol 50-100mg/day (contraindicated if concomitant
cardiomyopathy with failure.
o In both diabetic and non diabetics with albuminuria >300mg/24hrs –
ACE inhibitor/ARB with or without a diuretic is preferred.

42. 42
Treatment Of ESRD
When GFR declines to 5-10ml/min with or without uremic
symptoms
Renal Replacement Therapy
• Hemodialysis
• Peritoneal dialysis
• Kidney transplantation
Pancreatic Transplantation
can produce insulin independence which slow or reverse microvascular
disease
Medical Management

43. 43
Treatment Of Pericarditis
• Uremic pericarditis is an absolute indication for initiation of dialysis.
• Heparin-free dialysate should be used.
Treatment Of Anemia
• Look for common aggravating causes of anemia eg: GI blood loss, iron
deficiency and chronic infections & treat accordingly.
• Iron supplementation to ensure adequate response to EPO
• Inj.EPO s/c 80-120units/k/week(divided into 2-3 times a week)
• The target Hb should be 10-12g/dl

44. 44
Monitoring And Interventions
 Treatment with metformin should be withdrawn
when creatinine is ↑ than 1.7mg/dl.This increases
lactic acidosis
 Long acting sulphonyl urea's are replaced by short
acting which are metabolised rather than excreted
 Monitor dosing of renally eliminated drugs
 Drug toxicity may develop as renal clearence
worsens;in particular ,since insulin is renally cleared
,hypoglycemia may develop& can be life theatening in
patients with diabetes

45. 45
 In DN for reducing arterial HTN
- In type I DM - ACE inhibitors provide
greater benefit
-In type II DM – ARB’s shows same effect
• But these cause hyperkalemia and renal artery
stenosis sometimes hence Non dihydropyridine
ca+2 antagonists (diltiazem, verapamil)are
suitable alternatives.

46. 46
Reference
1.Aminoff.M.J,Andreadis.L.B,Barbour.D.M,Baron.R.B,Barrows.K,B
ashore.T.M,et.al.53rded.Current Medical diagnosis and
Treatment.2014
2.Fauci.S.A,Kasper.D.L,Longo.D.L,Braunwald.E,Hauser.S.L,Jameso
n.J.L et.al.17th ed.USA:Mc Graw Hill companies;2008.
3.Colledge.N.R,Walker.B.R,Raltson.S.H.Davidsons principles and
practice of medicine.21st ed.US:elsevier;2010.

47. THANK YOU
47