The kidney in systemic disease Dr Saad Al Shohaib Associate professor of medicine and nephrology...
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Transcript of The kidney in systemic disease Dr Saad Al Shohaib Associate professor of medicine and nephrology...
The kidney in systemic disease
Dr Saad Al Shohaib Associate professor of medicine and nephrology KAUH
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
The kidney in systemic disease
Renal function in CHF
CHF is a common disorder and alteration in renal function affect mortality and morbidityRenal impairment make treatment more difficult since the response to diuretics is decreasedIn 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 retentionThere 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 resistanceIn 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 requiredSever 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 freeVery 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 prostaglandinIf Na intake continue more than loss there would be sever Na and water retentionNa restriction is vital in the management of ascities
Hepatorenal syndrome
Progressive oliguric renal failure either insidious or rapidUsually occur in hospitalized patientsMay be precipitated by bleeding aggressive diuresis or abdominal paracentesis Functional renal failure with very low NaShould differentiated from ATN and pre renal states
Treatment of HRS
Search for correctable causesNa and water restrictionDialysis is not effective except to support candidates for transplantLeveen shunt had been tried in small studies
Renal involvement in systemic vasculitis
The kidney is affected by many vacultidies Giant cellTakayasu
Polyarteritis nodosaKawasaki
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 diseaseMain renal artery and cause ifarction
glomerulonephrits
Small vessel vasculitis
In small vessel vasculitis rapidly progressive glomerulonephrits leading to ARF that may require dialysisAggressive immunosuppressive therapy using pulse steroids cyclophosophamide and possibly plasma pharesis can be useful particularly if used before creatinine exceed 5 mg /dlANCA positive disease respond better to therapy
SLE
Common disease in Saudi ArabiaRenal 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. Normal2. Mesangial
nephropathy3. 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 yearsAzathioprine is not effectiveIn resistant nephritis cyclosporine and cellcept may be usefullRepeat 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 MPGNMesangial proliferativeNephrotic syndromeMay respond to interferone
Post infectious G N
Immune complex nephritis can follow any bacterial viral fungal or parasitic infections Can follow infected shunts and endocarditsMay complicate deep abscesses Usually present 3 weeks post infection
Post infectious G N
Hematuria edema Oliguria hypertensionFeverUncommonly ARF requiring dialysis
HSP
Cutaneous vasculitisIg A deposits in the skin and kidneysTransient 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 diabeticsLong standing diabetesGenetic predisposition hypertension poor glycemic control are important risk factorsStrongly associated with retinopathy
Diabetic nephropathy stages
1. Increased GFR and hyperfiltration2. Normal GFR and mild mesangial
expansion3. Microalbumiuria 4. Overt proteinuria5. CRF
Diabetic nephropathy diagnosis
Clinical diagnosisLong standing D M particularly in type 1Proteinuria or microalbumiuria RetinopathyInactive urinary sedimentNormal 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 importantStrict glycemic control can reverse glomerular changesBlood pressure control is vital and the ACE inhibitor dose should be titrated to the degree of proteinuria