Transcript The kidney in systemic disease

The kidney in systemic
disease
Dr Saad Al Shohaib
Associate professor of medicine
and nephrology KAUH
The kidney in systemic
disease
The kidney can be affected in different
diseases including autoimmune diseases
diabetes infections cardiac and liver
diseases
Kidney involvement usually affect
mode of therapy response to therapy
and outcome
Renal function in CHF
CHF is a common disorder and
alteration in renal function affect
mortality and morbidity
Renal impairment make treatment more
difficult since the response to diuretics
is decreased
In CHF there is Na retention in spite of
extra cellular volume expantion
Case presentation
A 55 year old lady known to have CHF and
CRF of unknown etiology . Her serum
creatinine had been maintained in the range
of 350 umol/l .Maintained on diuretics and
enalapril 20 mg /day. Presented to the
emergency room with progressive dyspnea
and orthopnea . On examination she looked
ill dyspnic and orthopnic BP 160/105 JVP
raised and she had basal crackles . CXR
showed pulmonary edema
Case presentation
Lab data Na 133 K 5.3 BUN 26
mmol/l Cr 425umol /l HCO3 18 Hb
11.0
WBC 10 LFT normal ECG no
new changes given 40mg of
frusemide iv with no response this was
repeated an hour later with no response
then nephrology team was contacted
for possible dialysis
Renal function in CHF
There is increase in the nuerohormonal
vasoconstrictors in CHF ( A2 Aldosterone
and vasopressin )
This lead to afferent arteriolar
vasoconstriction Na and K retention and
water retention
There is increase in the hormonal vasodilators
as ANP and renal prostaglandins
The kidney in CHF
The nuerohormonal changes lead to decrease
in renal blood flow and GFR and may give a
picture of pre renal azotaemia or lead to
worsening of a pre existing renal impairment
to the point that dialysis may be required
Dialysis and fluid removal in this situation
may improve cardiac output and induce
diuresis
The kidney in CHF
Prolonged diuretic use can lead to
decrease in ANP and increase in A2 and
norepinephren and therefore diuretic
resistance
In this situation a higher dose is
required particularly if there is renal
impairment
Hyponatremia in CHF
In sever CHF hyponatremia may be seen due
to increased vasopressin
Hyponatremia is an indication of severty of
CHF as well as resistance to diuretics
A very low urine Na is a predictor of
decreased response to diuretics
Patients with hyponatremia are more liable to
get hypo tension in response to ACE
inhibitors or A2 receptors antagonists
CRF and CHF
Renal failure may co exist with CHF and
make management difficult
In this situation a higher dose of loop
diuretics is required
Sever renal failure of may limit the use
of ACE inhibitors particularly in the
presence of hyperkalemia
The kidney is very sensitive to
nephrotoxic in the presence of CHF
drugs particularly NSAID ACE inhibitors
and aminoglycosides
The kidney in liver cirrhosis
There is sever Na retention to the point
that the urine may be Na free
Very low urine Na is a marker of disease
severity
Very low urine Na indicate poor
response to diuretics
The kidney in cirrhosis
There is disturbance in Na handling due
increased Na reabsorption related to excess
aldosterone increased renal sympathetic
activity and alteration in ANP and
prostaglandin
If Na intake continue more than loss there
would be sever Na and water retention
Na restriction is vital in the management of
ascities
Hepatorenal syndrome
Progressive oliguric renal failure either
insidious or rapid
Usually occur in hospitalized patients
May be precipitated by bleeding aggressive
diuresis or abdominal paracentesis
Functional renal failure with very low Na
Should differentiated from ATN and pre renal
states
Treatment of HRS
Search for correctable causes
Na and water restriction
Dialysis is not effective except to
support candidates for transplant
Leveen shunt had been tried in small
studies
Renal involvement in systemic
vasculitis
The kidney is affected by many vacultidies
Giant cell
Takayasu
Polyarteritis nodosa
Kawasaki
Microscopic arteritis
Wegeners
HSP
vasculitis
Giant cell and
takaysu
Medium sized
ployarteritis nodosa
Small vessel
vasculitis as HSP
SLE and wegeners
Rarely cause
significant renal
disease
Main renal artery
and cause ifarction
glomerulonephrits
Small vessel vasculitis
In small vessel vasculitis rapidly progressive
glomerulonephrits leading to ARF that may
require dialysis
Aggressive immunosuppressive therapy using
pulse steroids cyclophosophamide and
possibly plasma pharesis can be useful
particularly if used before creatinine exceed
5 mg /dl
ANCA positive disease respond better to
therapy
SLE
Common disease in Saudi Arabia
Renal involvement is variable from mild a
symptomatic proteinuria and hematuria to
ever renal impairment that may require
dialysis
The clinical picture can change rapidly to a
very aggressive disease
There might be a discrepancy between the
clinical picture and histological findings
Case presentation
21 year old lady known to have SLE and
lupus nephritis for the last 4 years . Biopsy
was done at the time of diagnosis and
showed class IV with active disease but no
chronic changes . At that time her serum
creatinine had been kept within normal limit
as well as her clearance 24 h urine protein
was 4 grams. She was treated with monthly
cyclophosphamide for 6 months then every
3 months for tow years
Case presentation
Her proteinuria improved and serum Cr
was normal for tow years . Follow up
was lost for tow years then she came
back for follow up . She was a
symptomatic but serum Cr was 160
umol/l Cr clearance was 45
mls
/min 24 h urine for protein 3 grams
renal ultrasound was normal
SLE
1. Normal
2. Mesangial
nephropathy
3. Focal proliferative
4. Diffuse proliferative
Steroids
Steroids
cyclophosphamide
SLE
Class IV is treated with monthly
cyclophosphmide for 6 months then every 3
months for two years
Azathioprine is not effective
In resistant nephritis cyclosporine and
cellcept may be usefull
Repeat biopsy may be indicated to assess
further immunosuppressive therapy
Case presentation
A 48 years Egyptian male presented
with mild lower limb edema for the last
tow months. On examination he looked
well B P 160/90and the rest of the
exam was unremarkable except for mild
lower limb edema . Urinalysis showed
protein and red cells but no casts . 24
h urine protein was 4 grams
Case presentation
Seum Cr 85 umol/l Hb 14.2 gm LFT
normal . Serum albumin 32 cholesterol
7 mmol/l ANA negative C3 normal
hep C Ab positive PCR positive
Genotpype 1 cryglobolin negative .
.NKidney biopsy showed membranous
G . N.
Case presentation
He was treated with peg interferon for
six months and proteinuria subsided to
less than one gram
Glomerulonephritis with
hepatitis C and B
Membranous
MPGN
Mesangial proliferative
Nephrotic syndrome
May respond to interferone
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
HSP
Cutaneous vasculitis
Ig A deposits in the skin and kidneys
Transient hematuria and proteinuria
occur in 50% of the cases
Acute proliferative glomerulonephritis
with Ig A deposit may occur but would
rarely require dialysis and this would
indicate aggressive therapy
Rhuematoid arthritis and gout
There is no specific renal lesion in gout
and R A
In R A the renal lesion is usually
secondary to therapy amyloid or
vasculitis
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