Clinical pathological correlations in AKI

Transcription

1 Clinical pathological correlations in AKI Dr. Rajasekara chakravarthi Director - Nephrology Star Kidney Center, Star Hospitals Renown clinical services India

2 Introduction AKI is common entity Community acquired & hospital acquired Is a clinical diagnosis We know what we are treating Outcomes not great AKI to CKD Mechanisms clearly understood

3 Natural history of AKI

4 Spanish registry for glomerulonephritis ( )

5 Analysis of AKI cohort Between 1994 and 2006 Data of native renal biopsies from 112 renal units in Spain AKI was third most common indication for biopsy 16% (2281 biopsies) were diagnosed with AKI Acute tubule-interstitial nephritis was found in 11.3% (second most common) ATN was found in only 5% Clin J Am Soc Nephrol May; 3(3):

6 HISTOPATHOLOGICAL LESION INDICATIONS OF BIOPSY AGE WISE DISTRIBUTION OF LESIONS

7 Pre biopsy clinical suspicion was correct in only 33% of the cases Biopsy enabled a specific diagnosis to be reached in more than 90% of the times

8 CASE SCENARIO 1 A 38 year old female diagnosed to have hypertension one year ago, on dual antihypertensives, recently had fever with burning micturition over a period of two weeks. On evaluation she was found to have Hemoglobin of 13.2 gm/dl Serum albumin of 3.2 gm/dl Serum creatinine of 1.67 mg/dl Proteinuria of 1+ on CUE Bilateral bulky kidneys on ultrasound.

9 Urine culture was positive Provisional diagnosis of acute bilatreral pyelonephritis made She was initially treated with oral antibiotics(cefuroxime) for one week, IV antibiotics for one week (Piperacillin - Tazobactum) and posted for bilateral DJ stenting. However her creatinine worsened and it raised to 7.2 mg/dl in the next 7 days (after stent placement).

10 In view of having rapid decline in renal function, she was initiated on hemodialysis through right IJV HD sheath access. Her autoimmune workup showed negative result for ANA, dsdna, P-ANCA, C-ANCA and she also had normal serum complement levels. After having four hemodialysis sessions she was taken up for renal biopsy. Provisional diagnosis: RPRF

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13 Biopsy showed 12 glomeruli with features suggestive of, glomerulonephritis with 100% crescents, there is tubular injury with interstitial inflammation consistent with tubulointerstitital nephritis. Pt on IV MP, switched to oral steroids Second agent added MMF After two weeks off HD, present s.creatinie 2.7mg%

14 Pt. Mrs. S 59 yrs old lady Presented to ER with breathlessness H/o CLL diagnosed a year ago and treated - Cisplatin/Chlorambucil Had body aches for which she used Piroxicam S. Creat 0.9 mg/dl before this admission

15 Admitted to MICU Hb% 7.2 g/dl TC 5,600 cells S.Creat mg/dl Urine WBC + UO maintained RBC s +

16 Renal biopsy done with Provisional diagnosis - ATN (drug)

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24 CASE SCENARIO 2 A 45 years old male, S/P live related renal transplant recipient on triple immunosupression (DOTx: ) Mother being donor (Haplo match 3/6),with no induction immunosupression except steroids. He presented to OPD clinic for routine post transplant follow up. He was diabetic, hypertensive, suffering from coronary artery disease for which he underwent PTCA + stenting to LCX 6 months prior to the transplantation surgery.

25 On evaluation he was found to have Serum creatinine of 2.05 mg/dl (baseline creatinine 1.1 mg/dl) Bland urinary sediments. He was taken up for graft kidney biopsy to diagnose the cause of acute allograft dysfunction. Provisional diagnosis: Acute allograft nephropathy? Acute rejection?cni toxicity

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29 TUBULAR VACUOLIZATION CHANGES HYPOKALEMIC NEPHROPATHY CNI TOXICITY Coarser and irregular in distribution Isometric, uniform in size Small vacuoles, much smaller than the nucleus.

30 Graft kidney biopsy showed features suggestive of severe acute tubular injury, prominent cytoplasmic vacuolization of tubules with no immune deposits and no C4d stain in the PTC walls and along the GBM. Serum potassium 3.2meq/l Iv correction within a week s. creatinine 1.5 mg%

31 CASE SCENARIO 3 A 60 year old male Dr.RR known diabetic and hypertensive for the last 20 years with normal renal functions (serum creatinine of 1.05 mg/dl and no protein loss in urine), recently had sudden onset of protein loss in urine (as patient noticed increased frothing of urine). He went to local physician for the above complaints, on evaluation he was found to have protein loss of about 12gms/day, serum albumin of 1.2 gm/dl and serum creatinine of 1.7 mg/dl.

32 He was treated with diuretics, fluid restriction and salt restriction. He was also prescribed to take Tab. Ramipril 5mg/day as a part of antiproteinuric medication. However he had rise in serum creatinine and decreased urine output after taking Ramipril and he was found to have serum creatinine of about 7.0 mg/dl. He was then initiated on hemodialysis through right IJV HD sheath access & renal biopsy was done to diagnose the cause of proteinuric kidney disease and rapidly declining renal function.

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35 Renal biopsy showed normal findings on light microscopy and immunofloroscence microscope. No evidence of DN Electron microscopy showed features suggestive of diffuse effacement of foot process of podocytes. Treated as MCD with steroids Off HD Serum creatinine latest 2.2mg%

36 Ms. P child of 14 yrs Admitted with sudden onset of breathlessness at another hospital Shifted to our unit on ventilator, unconscious Anuric S. Creat 9.2 mg/dl on daily dialysis Renal biopsy - provisional diagnosis RPRF

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39 Ms. R 26 yrs Septic shock Anemic In ICU- 3 weeks On daily hemodialysis, ventilator Nephro team requested for biopsy on 5 th day of admission Deferred as platelets count < 1 lakh On Anticoagulants Biopsy after 3 weeks in ICU on ventilator Diagnosed to have Granulomatous Interstitial nephritis

40 Interstitial granulomatous nephritis

41 Obstetric AKI Snake bite induced AKI Pancreatitis - AKI Biopsy must early To prognosticate

42 Patchy Cortical Necrosis

43 Our experience Retrospective analysis of renal biopsy data Total 3293 renal biopsies were analysed The indication of biopsy was AKI in 759 patients out of 3293 biopsies. This cohort of AKI was separated and analysed based on histopathology findings.

44 Results

45 The commonest histopathological lesion was acute interstitial nephritis (AIN) in 28.5% patients (n=216). Proliferative glomerulonephritis (PIGN and DPGN) was found in 17.8% (n=135). Acute tubular necrosis (ATN) was found in 14.1% (n=107) as third most common lesion.

46 Spectrum of Non diabetic renal diseases Among Diabetics Retrospective analysis of biopsies In Diabetics ISN nexus meeting

47 Indications for biopsy in diabetics Short duration (< 5 years) Absence of retinopathy Proteinuria- < 1 gm/day or > 5 gm/day Active urinary sediment Rapidly Pogressive Renal Failure Systemic disease

48 Retrospective analysis of renal biopsy data Total of 1213 biopsies Total DM

49 Total DM 21%

50 Results Total DM NDRD

51 Non diabetic renal disease 60%!

52 Spectrum of non diabetic renal disease Diabetic patients Frequency Percent AIN ATN CGN Cres GN CIN MCD MGN FSGS MPGN IgA N IgM N HTN PIGN Amyloid Cortical necrosis Lupus Transplant kd Normal Total Frequency AIN ATN CGN Cres GN CIN MCD MGN FSGS MPGN IgA N IgM N HTN PIGN Amyloid Cortical necrosis Lupus Transplant kd Normal

53 Summarising results: Total biopsies Diabetics- 254 Non Diabetic Renal Disease AIN 2. CIN 3. IgAN Diabetic Nephropathy- 105

54 AKI DATA FROM NORTH INDIA

55 Five year retrospective analysis of all patients with community acquired AKI From 5499 consecutive patients, 240 patients (2.5%), were diagnosed to have AKI as per specified criteria

56 Biopsy finding of AKI

57 Conclusion AKI- Needs Biopsy early Diagnosis, Treatment, Prognosis AKI leads to CKD ESRD with in weeks Most often we do not know what we are treating Chronic lesions need not be treated with toxic immunosuppressant's Risk of biopsy minimal (specific contraindications)

58 T H A N K Y O U