Dr eslam osama case

1. Dr . Eslam Osama Ibrahim Sabri
Resident doctor of nephrology
NMGH

2. Personal history
22 years old female ptn named khadiga
Ayman Mohamed Ali from El Mahala ,
single , student.
No smoking , no special habit.

3. Past history
.History of CKD for 2 years with
basal creatinine 3.9
.History of HTN for 2 years on
aldomet ,capozide
No history of DM.
No history of IHD.
No previous surgical intervention.

4. In 8/2016 ptn admitted in Tanta University hospital due to
.fits , squint , HTN (200/ 120) not responding to ttt
MRI of brain show CNS vasculitis.
.Fundoscope show optic neuritis and macular edema
Mammography on breast mass show fibroadenoma .
There was no skin lesions .
ANA , ANCA was negative.
C3 , C4 within normal.
Ptn take pulse of steroid and cyclophosphamide .

5. - Doppler on renal arteries show
normal renal arteries with no
stenosis .
- Thyroid profile was normal.
-Catecholamines and Aldosteron
.profile was normal

6. Discharge after one week on follow up and ttt
( Epilat retard , Concor 10 ,.Capozide,
Solupred 20 , Tiratam , Tegretol )
Ptn referred to psychiatric clinic and take
( Haloperidol , Cogintol , Achtenon )

7. Drug history
Solupred 20
Aldomet
Concor 5
Epilat retard
Tegretol 200
Haloperidol
Achtenon
Cogintol
tiratam

8. Family history
No family history of similar
conditions .
.No consangunity

9. complain
Genralized fatigue , nausea , loss of appetite
and hallucinations.

10. Present history
Ptn referred to our department from
Mansoura Emergency Hospital on
24/2 for preparing Ptn for Renal
Biopsy.
Ptn admitted to our department
complaining of fatigue , nausea ,
loss appetite , hallucinations
Ptn was pallor and depressed .

11. GENERAL EXAMINATION
Ptn was fully conscious , alert , oriented ,
cooperative but looks very ill , pallor and
.depressed

12. Vital signs
BP 150/100
HR 80/ min
RR 18/min
Temp 37.6

13. Local examination
Chest : bilateral fine basal crepitations and wheezy chest.
Heart : normal s1 , s2 no murmur or added sounds .
Abdomen : normal contour of abdomen , no scars , no
.pigmentations , lax and soft
LL: bilateral mild pitting edema below knee with intact
.peripheral pulsations
.CNS : normal reflexes , powers and tones

14. Investigations
Blood chemistry and electrolytes
S.creat : 12.7 s.urea : 243
Na : 128 Ca : 4.4 po4 : 10.9 k : 3.8
CBC
TLC : 14.1 HGB : 4 PLT : 215
ABG
PH : 7.37 Pco2 : 20 Hco3 :
11.6

15. -Rt kid : average size , increase in
echogenicity , grade 2 with poor CMD.
-Lt kid : average size , increase in
echogenicity , grade 2 with good CMD.
-Ub : full.
-Bilateral pleural effusion and mild
amount of ff in plevis.

16. Chest x-ray
Mild bilateral
pleural effusion

17. ECHO
.Degenrative HD with MR , TR
Mild pericardial effusion
( anterior 0.5 cm , posterior 0.5
cm , behind RV 1.2 cm , inferior
1.7 cm )

18. Lab sequence before dialysis
28/227/226/225/224/2
87.77.14.54HGB
101010.91215TLC
1413.613.213.212.7S.Creat
247247244245243Urea
136132130128128Na
4.54.54.13.93.8K
7.287.287.37.337.37PH
1111.812.314.715.6HCO3
1820202430Pco2
2.82.82.833.4S.albumin

19. Hospital course
Ptn has been admitted in our department on 24/2 with the
:following ttt
.1- ptn take 3 units of washed RBCS for correction of anemia
.2-solupred 20 /24 H
3- aldomet , concor and epilat for HTN.
4-NaHco3 cap / 8H
h12/5- zantac vial
6- ceftriaxone 1g /24 h
7-nebulizer / 8h

20. 8- we order for the following investigations
(ANA ,ANCA, Anti DS Dna , CRP , C3,C4, Anti
smith ,urine analysis , urine albumin
creatinine ratio,bleeding time, clotting
.time , iron profile , s.albumin )
9- Ptn refuse insertion of catheter and
dialysis for 4 days .
10- Insertion of IJ catheter on 1/3 and ptn
.take 5 sessions of dialysis untill now
11- biopsy has been done on 3/3 and ptn show
haematuria as a common complication of
renal biopsy.

21. 12-Abd pelvic US show collection of blood in UB .
13- Ptn take kapron , dicynone and washing with
500 cm saline / 8h through foley catheter
14- haematuria decreased.
15- diagnosis of biopsy :
Chronic tubulointerstitial nephritis (hypertensive
.nephrosclerosis ) with focal acute tubular injury

23. Lab sequence after dialysis
13/312/311/310/39/3
6.56.87.27.57.5Hgb
6.36.36.18.29.2TLC
5.17.85.37.18.7S.Creat
44546796116Urea
3.54.13.93.63K
7.447.437.447.447.37PH
11.113.720.217.423.2Hco3
3024232619Pco2

24. Hypertensive Nephropathy
-Def : secondary renal disease caused by
poor cotrolled high blood pressure for 5-10
years. Chronic high blood pressure causes
the heart working harder. Overtime, it
damages the blood vessels throughout the
body. Once the kidney blood capillary
vessels are involved, kidney disease
appears.
•

25. -Types : There are 2 types of hypertensive nephropathy
1-benign nephrosclerosis : is most present in people
over 60 years old
2-malignant nephrosclerosis: occurs only in 1 to 5
percent of people with hypertension. in a case of
hypertension with diastolic blood pressure exceeding
130mm Hg. This is present in patients that already
have an existing kidney disease that develop into
malignant hypertension.
Malignant nephrosclerosis has bad prognosis due to rapid
deterioration on kideny that lead to ESRD.

26. THANK
YOU