The kidney in systemic disease

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The kidney in systemic disease

• Dr Saad Al Shohaib
• Associate professor of medicine
• and nephrology KAUH

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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

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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

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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
  

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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

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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

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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

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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

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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

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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

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• The kidney is very sensitive to nephrotoxic in
  the presence of CHF drugs particularly NSAID ACE
  inhibitors and aminoglycosides

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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

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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

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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

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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

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Renal involvement in systemic vasculitis

• The kidney is affected by many vacultidies
• Giant cell
• Takayasu
• Polyarteritis nodosa
• Kawasaki
• Microscopic arteritis
• Wegeners
• HSP

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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

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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

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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

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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

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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

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SLE

1. Normal
2. Mesangial nephropathy
3. Focal proliferative
4. Diffuse proliferative

• Steroids
• Steroids
• cyclophosphamide

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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

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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

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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.

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Case presentation

• He was treated with peg interferon for six
  months and proteinuria subsided to less than one
  gram

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Glomerulonephritis with hepatitis C and B

• Membranous
• MPGN
• Mesangial proliferative
• Nephrotic syndrome
• May respond to interferone

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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

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Post infectious G N

• Hematuria edema
• Oliguria hypertension
• Fever
• Uncommonly ARF requiring dialysis

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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

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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

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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

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Diabetic nephropathy stages

1. Increased GFR and hyperfiltration
2. Normal GFR and mild mesangial expansion
3. Microalbumiuria
4. Overt proteinuria
5. CRF

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Diabetic nephropathy diagnosis

• Clinical diagnosis
• Long standing D M particularly in type 1
• Proteinuria or microalbumiuria
• Retinopathy
• Inactive urinary sediment
• Normal sized kidneys

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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

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thank you