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Unusual cause of Renal failure

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  • 1. Physicians Meet – M2 Case Presentation Prof. Dr. S. Sundar’s Unit Presented by Dr. Deepu Sebin
  • 2.  Ponnammal , 55 yr old female  House wife  First admitted with complaints of  Abdominal distention – 1 month  Swelling of legs – 1 month
  • 3.  Gradually progressing abdominal distention over one month.  Breathlessness with moderate exertion.  No orthopnea / PND.  Sweling of both legs for 1 month  Swelling of legs mainly in the evenings.  No history of nausea or vomiting.  No history of malena/hematemesis.  No history of decreased urine output.  No history arthralgia/ oral ulcers
  • 4.  Past History  No history DM/SHT/PTB/ Jaundice/ CAD/ Surgeries/Drug Intake  No history of blood transfusions  Personal History  Post Menopausal status  Mixed Diet  Family History  Nil Specific
  • 5.  General Examination  PR – 80/min  BP - 110/70 mmHg  JVP – elevated  No pallor/cyaosis/clubbing/lymphadenopathy  BPPE +  No Signs of liver cell failure
  • 6.  Systems  P/A  Distented  Free Fluid +  No organomegaly  BS +  Chest  Clear  AEBE  CVS  S1 S2 normal  CNS  NFND  PEARL
  • 7. Investigations  Hb - 10 mg/dl  TC – 5600  DC – P60 L30  ESR – 10mm/hr  Platelet Count – 1.4 lakh  RBS – 128 mg/dl  Blood Urea – 42 mg/dl  S. Creatine – 1.2 mg/dl  Na+ - 139  K+ - 3.7
  • 8.  Urine Rountine  Albumin - +  Sugar – Nil  Depostis – 1 -4 pus cells
  • 9.  Bilirubin – 1.0 mg/d  SGOT- 83u/l  SGPT – 49u/l  ALP – 146u/l  Total Protein – 6.1 g.dl  Albumin – 4.0 g/dl  Globulin – 1.8 g/dl  INR 1.2
  • 10.  USG Abdomen :  Liver 10.1 cm shrunken, coarse echo texture, surface nodular.  GB wall thickened  Spleen 13 cm enlarged, no focal lesions  Kidneys  Rt 8.8 x 4.3  Lt 8.4 x 4.0 Normal echotexture, CMD maintained  Bladder normal  Impression : Cirrhosis with Portal Hypertension
  • 11.  HbSAg – positive  Anti HCV – negative  HIV – negative  OGDscopy – Grade 2 fundal varices
  • 12.  Impression : DCLD with Portal Hypertension HBV Related
  • 13. 2nd admission  Patient got readmitted with increasing abdominal distention and breathlessness of 1 wk duration.  Vitals Stable  General Examination – Facial puffiness  BPPE +  Systems  P/A  Distended  Free fluid  No organomegaly
  • 14.  Hb- 11mg/dl  TC – 6400  DC – P60 L30  ESR – 10mm/hr  Platelet Count – 1.1lakh  RBS – 111 mg/dl  Blood Urea – 67 mg/dl  S. Creatine – 1.8 mg/dl  Na+ - 136  K+ - 3.7
  • 15.  Bilirubin – 1.0 mg/d  SGOT- 90 u/l  SGPT – 53 u/l  ALP – 145 u/l  Total Protein – 5.9g.dl  Albumin –2.9 g/dl  Globulin – 1.8 g/dl  INR 1.2
  • 16.  Urine Rountine  Albumin - +  Sugar – Nil  Depostis –1-3 pus cells  10-12 RBCs
  • 17.  DCLD – Portal Hypertension , HBV related  AKI - ? Cause to r/o HRS  Non oliguric
  • 18.  Urine Sodium – 22meq  (<20 pre renal & >40 ATN)  UNa x PCr  FENa, percent = — — — — — —x 100 —  PNa x UCr  FeNa – 0.8  (<1 prerenal , > 2 ATN )
  • 19.  Plasma Urea / Creatine Ratio – 37.2  (>30 prerenal)  Urine to plasma creatine ratio - 24  (<20 ATN , >40 pre renal )  Urine Creatininre – 43mg/dl
  • 20.  Diuretics including Spironolactone stopped  Syrup Laculose temporarly withdrawn  Antibiotics ( Cefotaxime, Metrogyl ) initiated  Maintained adequate fluid intake orally  Hypovolemia ruled out  No hematemesis or malena  No loose stools
  • 21. 1st adm Day 14 Day15 Day 18 Day 20 Day 22 Day 28 Day 29 Blood Urea 42 67 56 60 49 56 63 59 S.Creati nine 1.2 1.8 1.7 1.6 1.4 1.8 1.7 1.8 Urine Albumin + Nil ++ ++ +++ +++ ++ +++ 24 hour urine protein – 2gm Volume 1500 ml
  • 22.  In view of the  Elevated renal parameters  Which is static  Not resolving with conservative management  Proteinuria  Proceeded with Renal Biopsy after Nephrology Review
  • 23.  Sections show renal tissue with eight glomeruli per sections. These are enlarged and hypercellular with endothelial and mesangial proliferation with infiltration by few neutrophils. Focal splitting of capillary wall noted. No capillary wall thickening is seen. There is no tubular atropy. Blood vessels appear unremarkable  Immunofluorescence stains show peripheral granular deposits in IgM, IgG, IgA, C3c, and C1q  Impression : Renal Biopsy showing Diffuse Proliferative Glomerulonephritis and mild exudation and no significant tubuointerstitial changes.
  • 24.  Full House pattern  IgM, IgG, IgA, C3c, and C1q  Possibility of Lupus Nephritis, vasculitis and other connective tissue disorders with DPGN – full house pattern.
  • 25.  ANA – negative (Repeated)  ds DNA – negative  ASO titer - < 100  p-ANCA and c- ANCA – Negative  C3 – 53.04 (90 – 180mg/dl)  C4 – 13. 78 (10- 40 mg/dl)
  • 26.  HBsAg – Postive  HBeAg – Positive  HBV DNA levels – > 20,000 IU/mL
  • 27.  In Hepatits B virus related Glomerular pathology we expect  membranous glomerulonephritis, or membranoproliferative glomerulonephritis  Here we have Active Hepatitis  HbeAg postivity  High Viral Load  Absence of other infection, Connetive tissue disorders clinically and radiologicaly.  This is a case of HBV related DPGN
  • 28.  Final Diagnosis  HBV infection related Diffuse Proliferative Glomerulonepheritis  HBV related DCLD and PHT Am J Gastroenterol. 1995 Jun;63(6):476-80. Hepatitis-B-antigenemia with panarteritis, diffuse proliferative glomerulitis and malig Razzak IA, Bauer W, Itzel W. Full-house nephropathy in a patient with negative serology for lupus Esra Baskin, Pınar Isik Agras, Nurcan Menekşe, Handan Ozdemir and Nurcan Cengiz
  • 29. Treated with  T. Lasix 40mg BD  T. Lamividine 100mg OD  T. Propranalol 20 BD  T. Rantac 50mg BD  Syp. Lactulose 15ml TID  Pulse Methylprednisolone therapy reserved if patient develops worsening of her renal failure.
  • 30. Simplified Appraoch to Glomerular Disease  Glomerular Disease a diagnosis before biopsy  — Although there are many causes of glomerular disease, the patient's age and the characteristics of the urine sediment usually allow the differential diagnosis to be narrowed prior to renal biopsy
  • 31. Focal Nephritic Diffuse Nephritic Nephrotic
  • 32. Focal nephritic  Focal nephritic —  Focal glomerulonephritis is associated with inflammatory lesions in less than one-half of glomeruli on light microscopy.  The urinalysis reveals  red cells (which often have a dysmorphic appearance)  red cell casts, and  mild proteinuria (usually less than 1.5 g/day).  The findings of more severe disease are usually absent, including nephrotic range proteinuria, edema, hypertension, and renal insufficiency. These patients often present with asymptomatic hematuria and proteinuria discovered on routine examination.
  • 33. Focal Nephritic - DDs  Active urine sediment without renal insufficiency or nephrotic syndrome  Less than 15 years - Mild postinfectious glomerulonephritis, IgA nephropathy, thin basement membrane disease, hereditary nephritis, Henoch- Schönlein purpura, mesangial proliferative glomerulonephritis  15 to 40 years - IgA nephropathy, thin basement membrane disease, lupus, hereditary nephritis, mesangial proliferative glomerulonephritis  Greater than 40 years - IgA nephropathy
  • 34. Diffuse Nephritic  Diffuse nephritic —  Diffuse glomerulonephritis, in comparison, affects most or all of the glomeruli.  Thus, the urinalysis is similar to focal disease, but heavy proteinuria (which may be in the nephrotic range), edema, hypertension, and/or renal insufficiency may be seen.
  • 35. Diffuse Nephritic - DDs  Active urine sediment with renal insufficiency and variable proteinuria, which can include nephrotic syndrome  Less than 15 years - Postinfectious glomerulonephritis, membranoproliferative glomerulonephritis  15 to 40 years - Postinfectious glomerulonephritis, lupus, rapidly progressive glomerulonephritis, fibrillary glomerulonephritis, membranoproliferative glomerulonephritis  Greater than 40 years - Rapidly progressive glomerulonephritis, vasculitis (including mixed cryoglobulinemia), fibrillary glomerulonephritis, diffuse proliferaive nephritis, postinfectious glomerulonephritis
  • 36.  Nephrotic —  Heavy proteinuria and lipiduria,  But few cells or casts  Bland proteinuria  Patients who also have edema and hyperlipidemia (the full-blown nephrotic syndrome) tend to have a more marked glomerular leak than those with heavy proteinuria alone.  Differntial Diagnosis – all the range of nephrotic disorders  Patients with Nephrotic proteinuria but no hypoalbuminemia or edema – Suspect some form of secondary focal glomerulosclerosis (as with reflux nephropathy)
  • 37.  The relatively bland sediment in the nephrotic disorders results from the  lack of inflammatory cell infiltration in the glomeruli  absence of immune complex deposition in most of these disorders  The lack of inflammation also results in the plasma creatinine concentration being normal or only slightly elevated at presentation in the nephrotic disorders !
  • 38. Renal Failure + Nephrotic Syndrome  Concurrent acute tubular necrosis, esp in MCD  Tubular injury in collapsing focal glomerulosclerosis, either idiopathic or associated with HIV infection. (Collapsing FSG)  Minimal change disease with acute interstitial nephritis due to NSAIDs  Crescentic glomerulonephritis superimposed upon membranous nephropathy.  Nephrotic syndrome secondary to monoclonal immunoglobulin deposition disease may also develop myeloma cast nephropathy and acute renal failure.
  • 39. Nephrotic - DDs  Heavy proteinuria, bland sediment although some hematuria allowed .  Less than 15 years - Minimal change disease, focal glomerulosclerosis, mesangial proliferative glomerulonephritis  15 to 40 years - Focal glomerulosclerosis, minimal change disease, membranous nephropathy (including lupus), diabetic nephropathy, preeclampsia, postinfectious glomerulonephritis (later stage)  Greater than 40 years - Focal glomerulosclerosis, membranous nephropathy, diabetic nephropathy, minimal change disease, IgA nephropathy, primary amyloidosis or the related disorder light chain deposition, benign nephrosclerosis, postinfectious glomerulonephritis (later
  • 40. References  Comprehensive Clinical Nephrology 3rd edition  Rose, BD. Pathophysiology of Renal Disease, 2d ed, McGraw- Hill, New York, 1987, p. 16  Rose, BD. Clinical characteristics of glomerular disease. In: Scientific American Medicine, Rubinstein, E, Federman DD (Eds), Scientific American, New York, 1989, section X (IV):1. Praga, M, Borstein, B, Andres, A, et al. Nephrotic proteinuria without hypoalbuminemia:  Clinical characteristics and response to angiotensin-converting enzyme inhibition. Am J Kidney Dis 1991; 17:330.  Rivera, F, Lopez-Gomez, JM, Perez-Garcia, R, et al. Clinicopathologic correlations of renal pathology in Spain. Kidney Int 2004; 66:898. Iseki, K, Miyasato, F, Urhara, H, et al.  Outcome study of renal biopsy patients in Okinawa, Japan. Kidney Int 2004; 66:914
  • 41. Renal Failure in Cirrhosis  Hepatorenal Syndrome  Psuedohepaorenal Syndrome
  • 42.  HRS – DIAGNOSIS  Major Criteria — :  Chronic or acute hepatic disease with advanced hepatic failure and portal hypertension  A plasma creatinine concentration above 1.5 mg/dL that progresses over days to weeks.  The absence of any other apparent cause for the renal disease, including shock, ongoing bacterial infection, current or recent treatment with nephrotoxic drugs,  The absence of ultrasonographic evidence of obstruction or parenchymal renal disease.  Urine red cell excretion of less than 50 cells per high power field (when no urinary catheter is in place)  Protein excretion less than 500 mg/day.  Lack of improvement in renal function after volume expansion with intravenous albumin (1 g/kg of body weight per day up to 100 g/day) for at least two days and withdrawal of diuretics.  Minor Criteria  Urine Volume < 500mg/dl  Urine Sodium < 10 mmol/l  Urine RBC < 50/hpf  Serum Sodium concentration < 130 mmol/l
  • 43.  Type I hepatorenal syndrome is the more serious type; it is defined as at least a 50 percent lowering of the creatinine clearance to a value below 20 mL/min in less than a two week period or at least a twofold increase in serum creatinine to a level greater than 2.5 mg/dL  Type II hepatorenal syndrome is defined as less severe renal insufficiency than that observed with type I disease; it is principally characterized by ascites that is resistant to diuretics.
  • 44. Liver and Kidney Potential Causes Tubular Involvement Glomerular involvement Infections Sepsis, Leptospirosis, Brucellosis, B, EBV, Hepatitis B Hepatitis B and C Shistosoma Mansoni, HIV Drugs and Toxins Nephrotoxic Drugs Systemic Diseases Sarcoidosis, Sjogren Syndrome SLE, vasculitis, cryoglobulinemian, Amyloidosis Circulaory Failure Hypovolemia / shock Congenital and Genetic PCKD, Nephrolithiasis, Congenital hepatic fibrosis Malignancy Lukemia Lymphoma Misc Fatty liver of pregnancy, Reyes Syndrome Eclampsia, HELLP
  • 45. References  Comprehensive Clinical Nephrology , 3rd edition- Feehaly  Brenner and Recotor – The Kindey  Gines, P, Schrier, RW. Renal failure in cirrhosis. N Engl J Med 2009; 361:1279. Gines, P, Guevara, M, Arroyo, V, Rodes, J  Hepatorenal syndrome. Lancet 2003; 362:1819.
  • 46. Hepatits B virus and Kidney  Infection with hepatitis B virus (HBV) may be directly associated with a variety of renal diseases, including polyarteritis nodosa, membranous glomerulonephritis, and membranoproliferative glomerulonephritis
  • 47. Treatement  Antiviral therapy targeted against HBV.  Steroids and Immunosuppressants and/or Plasma exchange in cases with RPGN features or vasculitis.  Conservative management in rest.
  • 48.  Mukhtyar C, Guillevin L, Cid, MC, et al. EULAR recommendations for the management of primary small and medium vessel vasculitis. Annals of Rheumatic Diseases April 2008.  Guillevin, L, Mahr, A, Cohen, P, et al. Short-term corticosteroids then lamivudine and plasma exchanges to treat hepatitis B virus-related polyarteritis nodosa. Arthritis Rheum 2004; 51:482.  Wen, YK, Chen, ML. Remission of hepatitis B virus- associated membranoproliferative glomerulonephritis in a cirrhotic patient after lamivudine therapy. Clin Nephrol 2006; 65:211.
  • 49. Thank you
  • 50. Membranous nephropathy  HBV can induce the nephrotic syndrome due to membranous nephropathy. It has been proposed, although not proven,  deposition of HBeAg and anti-HBe is responsible for the formation of pathogenic subepithelial immune deposits  Membranous nephropathy is most common in children and resolves spontaneously in many cases,  However, resolution is relatively uncommon in adults, most of whom appear to have progressive disease over time
  • 51. Membranoproliferative glomerulonephritis  The deposition of circulating antigen-antibody complexes in the mesangium and subendothelial space characterizes the membranoproliferative glomerulonephritis associated with HBV. Both  HBsAg and HBeAg deposition have been implicated in this  Some patients may have a membranoproliferative pattern due to mixed cryoglobulinemia; concurrent infection with hepatitis C to be ruled out.
  • 52.  Polyarteritis nodosa — A large vessel vasculitis can be induced by HBV, in which circulating antigen- antibody complexes may be deposited in the vessels.  The vasculitis, which is called secondary PAN and has the same clinical features as idiopathic PAN that is not associated with HBV, typically occurs within four months after the onset of HBV infection
  • 53. Diffuse Proliferative Glomerulonephritis  A distinct form of glomerulonephritis common to  Autoimmune Disorder (eg SLE)  Vasulitis Syndrome ( eg Wegeners Granulomatosis)  Infectious Process  More than 50 % of glomeruli shows an increase in mesangial, epithelial and enothelial proliferaive and inflammatory cells  If less than 50% focal proliferative
  • 54. When to suspect DPGN  Suspect DPGN in patients with SLE, infectious disease processes, a recent streptococcal throat infection, or in patients with sinopulmonary disease who have recent onset of the following:  Hypertension  Microscopic or gross hematuria  Nonnephrotic or nephrotic range proteinuria or an increase in proteinuria from baseline  Serum creatinine of more than 0.4 mg/dL from the reference range or the baseline  Oligoanuria and symptoms of uremia in severe cases of RPGN with crescent formation
  • 55.  A history of rash; photosensitivity; oral ulcers; arthralgias; arthritis; serositis; or a renal, neurologic, hematologic, or immunologic disorder suggests SLE as the primary disease.  A history of cough, dyspnea, hemoptysis, and renal disease suggests Goodpasture syndrome, but other pulmonary-renal syndromes must be ruled out, including SLE pneumonitis, Wegener granulomatosis, cryoglobulinemia, renal vein thrombosis with pulmonary embolism, legionella infection, and congestive heart failure.  Patients with Wegener granulomatosis present with sinopulmonary  Atypical Presentations of Ig A Nephropathy