UNUSUAL CASE OF ARF Dr SAAD AL SHOHAIB KAUH. CASE PRESENTATION 58 Y old Yemeni male Diabetic for 5...
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Transcript of UNUSUAL CASE OF ARF Dr SAAD AL SHOHAIB KAUH. CASE PRESENTATION 58 Y old Yemeni male Diabetic for 5...
UNUSUAL CASE OF ARF
Dr SAAD AL SHOHAIB
KAUH
CASE PRESENTATION
58 Y old Yemeni male Diabetic for 5 years with no obvious
diabetic complications particularly no retinopathy
Admitted with fever and pain in both legs for 4 days
CASE PRESENTATION
He had no other symptoms particularly no dyspnea cough or chest pain
He had no GI symptoms and no urinary symptoms
CASE PRESENTATION
P.M.H Hypertension for 5 years on enalapril 5
mg once daily No history of IHD
Case presentation
Social history
Non smoker married 3 children
Case presentation
On examination He looked well B P 135/80 Temp 38.5 pulse 90/min regular JVP normal chest clear CVS normal Abdomen normal
Case presentation
Cellulitis both legs extending from ankles to both knees
No obvious collection Good peripheral pulses No evidence of peripheral nueropathy
Case presentation
Lab work WBC 17 Mainly nuetrophils Hb 13.1 Na 138 K 4.1 urea 18 mmol/l Cr 212 umol/l Ca 2.1 mmol/l P 1.6mmol/l Urinalysis proteinuria no hemturia no
casts LFT normal
Case presentation
Lab data U/S normal size kidneys C 3 and C4 normal ANA negative Hepatitis screen negative
Course in hospital
Started on ceftrixone and clindamycin with his usual medications
His temprature subsided and cellulitis improved
Course in hospital
His urine output had been maintained within normal range but his renal function got worse and finally his creatinine reached 1100 umol/l and urea 45 mmol/l
K 5.5 but no fluid over load Dialysis was started
Diff diagnosis
Post infectious GN Drug induced Pre existing diabetic nephropathy got
worse with sepsis
Kidney biopsy
Normal glomeruli No interstilal infeltrate
Course in hospital
He was dialysed for 10 days then his renal function stated to improve and creatinine decreased and reached normal value tow weeks after stopping dialysis
At that time he became polyuric for one week
He was sent home in good medical condition
Post infectious G N
Immune complex nephritis can follow any bacterial viral fungal or parasitic infections
Can follow infected shunts and endocardits
May complicate deep abscesses Usually present 3 weeks post infection
Post infectious G N
Hematuria edema Oliguria hypertension Fever Uncommonly ARF requiring dialysis
NSAIDHEMODYNAMICALLY-MEDIATED ACUTE RENAL FAILURE
Although renal prostaglandins are primarily vasodilators, they do not play a major role in the regulation of renal hemodynamics in normal subjects
the release of these hormones (particularly prostacyclin and prostaglandin E2) is increased by underlying glomerular disease, renal insufficiency, hypercalcemia, and the vasoconstrictors angiotensin
NSAIDHEMODYNAMICALLY-MEDIATED ACUTE RENAL FAILURE
Inhibition of prostaglandin synthesis with an NSAID in any of the above settings can lead to reversible renal ischemia, a decline in glomerular hydraulic pressure and ARF
ACUTE INTERSTITIAL NEPHRITIS
Any drug can induce AIN however it is seen more with antibiotics
Affected patients typically present with hematuria, pyuria, white cell casts, proteinuria, and an acute rise in the plasma creatinine concentration.
Fever, rash, eosinophilia, eosinophiluria – can be seen but not always present
. Spontaneous recovery generally occurs within days weeks to a few months after therapy is discontinued
Acute interstitial nephritis
The clinical picture is usually suggestive however the diagnosis is confirmed by renal biopsy
Gallium scan may be helpful High dose steroid is useful to speed up
recovery
ATN
Any pre renal cause can lead to ATN if not corrected on time
The renal medulla is very sensitive to ischemia particularly in old dehydrated diabetic patients or those with CHF or liver cirrhosis
Nephrotoxic drugs would aggravate renal damage
ATN
Mostly seen in the ICU setting It is a clinical diagnosis Biopsy is usually not indcated
ATN
Fluid challenge is an important therapeutic and diagnostic approach
Examination of the urine Na and osmolarity are very important
The condition is potentially reversible but the mortality is still 50% since it happens in very sick patients
Diabetic nephropathy
Diabetes is common in Saudi Arabia This mainly related to genetic factors as
well as the life style 40% of patients with ERSD are diabetics
Dialysis in Saudi Arabia
There are 6700 patients on dialysis in Saudi Arabia
There is 130 haemodialysis centres in Saudi Arabia
The incidence of hepatitis B is 6.7%and 50% for HCV
SCOT data Saudi J kid 2001 12 (3)
Diabetic nephropathy
Common problem 30 - 40% of dialysis patients are diabetics
Long standing diabetes Genetic predisposition hypertension
poor glycemic control are important risk factors
Strongly associated with retinopathy
Diabetic nephropathy stages
1. Increased GFR and hyperfiltration
2. Normal GFR and mild mesangial expansion
3. Microalbumiuria
4. Overt proteinuria
5. CRF
Diabetic nephropathy diagnosis
Clinical diagnosis Long standing D M particularly in type 1 Proteinuria or microalbumiuria Retinopathy Inactive urinary sediment Normal sized kidneys
Diabetic nephropathy
Microalbumiuria is a sign of cariovscular disease and is a very important finding since interference with strict glycemic control and ACE inhibitors is important
Strict glycemic control can reverse glomerular changes
Blood pressure control is vital and the ACE inhibitor dose should be titrated to the degree of proteinuria
The Kidney’s
Type 1
Strict glycaemic control can decrease the nephropathy and progression of rena disese
It has been suggested that 25 to 45 percent of these patients will, during their lifetime, develop clinically evident disease
Type one DM
Strct blood pressure control is very imprtant
Genetic factors play major role in diabetic nephropathy
Most patients have retinopathy Most are asymptomatic
Urinary albumin excretion
Mogensen CE et al. Lancet 1995; 346: 1080–1084
Clinical proteinuria>300 mg/24 hrs (>200 µg/min)
Microalbuminuria30–300 mg/24 hrs (20–200 µg/min)
Normal excretion<30 mg/24 hrs (<20 µg/min)
Microalbuminuria: Prevalence and predictive power in diabetics
Type 1 diabetes• Prevalence: 50%
• Predictive value for the development of nephropathy: 75%
Type 2 diabetes• Prevalence: 25–60% (depending on ethnic
origin)
• Predictive value for the development of nephropathy: 25%
Savage MW et al. Br J Hosp Med 1995; 54: 429–435Viberti GC et al. In: International Textbook of Diabetic Medicine, 1992
Serum creatinine level of 1.4 mg/dl:What is the renal function?
Ser
um
cre
atin
ine
(mg
/dl)
12
10
8
6
4
2
0
Large muscular maleNormal maleSmall female
120 60 30 15
Fraction of normal renal function (%)Sica DA. Unpublished data
100 50 25 0
GFR (ml/min)
ACE inhibitors in hypertension and heart failure
In hypertension, ACE inhibitors Lower blood pressure Reduce the progression of end-organ damage
In heart failure, ACE inhibitors Improve cardiovascular hemodynamics Improve symptomatolgy and exercise capacity Decrease morbidity and mortality
ACE inhibitors and renal impairment: Considerations
Occasional cases of renal
impairment and hyperkalemia
have been reported with ACE
inhibitors
Dose modifications are a consideration
in patients with renal impairment
(except for fosinopril)
ACE inhibitors show
renoprotective effects over and
above blood pressure control
ACE inhibitors
Renoprotection: ACE inhibitors vs. other antihypertensives
Calcium antagonists ACE inhibitors Diuretics and/or -blockers
Urinary protein
Mean systemic
blood pressure
0 –10 –20 –30 –40 –50
Decrease from baseline (%)Böhlen L et al. Am J Hypertens 1994; 7: 84S–92S
ACE inhibitors are renoprotective
Patients with type 2 diabetes Patients with type 1 diabetes Non-diabetic patients with nephropathy Non-diabetic patients with hypertension and
nephropathy Non-diabetic hypertensive patients without
pre-existing nephropathy
ACE inhibitors have demonstrated renoprotective potential in:
ACE inhibition: Renoprotection in type 2 diabetes
Init
ial
valu
e o
f re
cip
roca
l cr
eati
nin
e (%
) 105
100
95
90
85
800 1 2 3 4 5 6
7 Treatment (years)
Ravid M et al. Arch Intern Med 1996; 156: 286–289
ACE inhibitor (years 1–5) and placebo (years 6 and 7)
ACE inhibitor (years 1–7)
Placebo (years 1–5) and ACE inhibitor (years 6 and 7)
Placebo (years 1–7)
ACE inhibition: Renoprotection in type 1 diabetes
PlaceboCaptopril
50
40
30
20
10
0
Die
d o
r n
eed
ed d
ialy
sis
or
tran
spla
nta
tio
n (
%)
0 1 2 3 4Follow-up (years)
Placebo n=202 198 192 186 171 121 100 59 26Captopril n=207 207 204 201 195 140 103 64 37
Lewis EJ et al. N Engl J Med 1993; 329: 1456–1462
p=0.006
ACE inhibitors are renoprotective
Patients with type 2 diabetes Patients with type 1 diabetes Non-diabetic patients with nephropathy Non-diabetic patients with hypertension and
nephropathy Non-diabetic hypertensive patients without
pre-existing nephropathy
ACE inhibitors have demonstrated renoprotective potential in:
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