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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