Download to read offline
More Related Content
Similar to Nephro pathological correlation
![De novo microangiopathy after kidney transpanation[3023]](https://cdn.slidesharecdn.com/ss_thumbnails/denovomicroangiopathyafterkidneytranspanation3023-191204163852-thumbnail.jpg?width=640&height=640&fit=bounds)
Nephro pathological correlation
- 1. NEPHRO-PATHOLOGICAL CORRELATION PART 1 (GENERALNEPHROLOGY ) DR SCIENTHIA SANJEEVANI 15/11/19
- 2. APPROACH TO KIDNEYDISEASE REASON FOR PATIENT PRESENTATIONS/REFERRAL TO NEPHROLOGIST To explain abnormalities attributable to kidney disease that have been found in asymptomatic individuals including those at risk of familial conditions. Symptomatic renal disease: renal failure, either acute or chronic; abnormalities of urination including poly- and oliguria, visible haematuria; unexplained loin pain; the classic renal syndromes (nephritic and nephrotic). Renal consequences of systemic conditions: metabolic, inflammatory, infectious; drugs, malignancy, pregnancy, organ failure (especially cardiac and hepatic).
- 3. MAJOR SYNDROMES INNEPHROLOGY
- 4. POSSIBLE INDICATIONS FORRENAL BIOPSY.
- 5. RENAL PATHOLOGISTS RIGHTLYEXPECT NEPHROLOGISTS TO DESCRIBE THE PROBLEM AND HOW THE FINDINGS WILL ALTER MANAGEMENT.
- 6. Examples of treatmentdecisions that may be prompted by renal biopsy results in acute renal failure and nephrotic syndrome
- 7.
- 8. Urinary Leukocytes (Pyuria): An increase in urinary leukocyte count (>20,000 leukocytes/Ml or >5 leukocytes per high-power field) may be due infection other conditions such as acute or chronic interstitial nephritis, renal papillary necrosis and analgesic nephropathy, nephrolithiasis, glomerulonephritis, and polycystic kidney disease.
- 9. Renal Tubular Cells Large numbers of renal tubular cells in the urine can be found in acute tubular necrosis and acute interstitial nephritis
- 10. Urinary Casts Redcell casts most commonly seen in patients with glomerulonephritis may also occur with acute interstitial nephritis. White cell casts pyelonephritis Noninfectious interstitial nephritis proliferative glomerulonephritis. Renal tubular epithelial cell casts acute tubular necrosis or acute interstitial nephritis. Fatty casts nephrotic syndrome Broad casts advanced chronic kidney disease
- 11. HEMATURIA three ormore RBCs per high-power field. can be GLOMERULAR or NON GLOMERULAR Glomerular hematuria is likely if hematuria is accompanied by significant proteinuria red cells have a dysmorphic appearance (i.e., red cells with blebs, budding, vesicle-shaped protrusions, and marked variability in shape and size red cell casts Nonglomerular bleeding red to pink urine microscopically by red cells that are round and uniform in size and shape there may be some “ghost cells,” that is, cells that are losing their hemoglobin
- 12. FAMILY HISTORY of renaldysfunction or renal stones TRAVEL HISTORY -to areas where Schistosoma haematobium infection or tuberculosis
- 14. PROTEINURIA Overflow Proteinuriadue to the filtration of an abnormally large amount of small molecular weight proteins that exceed the capacity of the tubules for reabsorption. Causes intravascular hemolysis (hemoglobinuria) Rhabdomyolysis (myoglobinuria) multiple myeloma (light chains) Tubular Proteinuria damage to the renal tubulointerstitium leading to a failure to reabsorb normally filtered small molecular weight proteins, mostly beta-2 microglobulin, light chains, retinol- binding protein, and breakdown products of albumin less than 1 to 2 g/day, predominance of small molecular weight proteins.
- 15. Glomerular proteinuria–injury to the glomerular filtration barrier more than 3 g/day, primarily albumin Tubular and glomerular proteinuria are not mutually exclusive can be mild, with albumin excretion rates of 30 to 300 mg/day, moderate, in the range of 1 to 3 g/day, or heavy(nephrotic), more than 3 g/day and up to over 20 g/day “Postrenal” Proteinuria occurs with inflammation in the urinary tract, that is, with infection, nephrolithiasis, gross hematuria, and tumors. amounts are small to moderate.
- 19. uACR and uPCR uACRhas been considered superior at low protein concentrations (where there is less noise from physiological urinary proteins), uPCR has been shown to perform well also at levels equivalent to >0.5 g/day as a predictor of outcomes.
- 20. Tubular proteinuriahas also been defined as nonalbumin proteinuria, calculated as the difference between uPCR and Uacr Isolated nonalbumin proteinuria was defined as uPCR ≥17 mg/mmol in the absence of albuminuria (uACR >3 mg/ mmol). Bence Jones proteinuria – should be measured, and look for any identified protein band characterized using electrophoresis with immunofixation
- 21. URINE DIPSTICK Negative: <15mg/dL Trace: 15-30 mg/dL 1+: 30-100 mg/dL 2+: 100-300 mg/dL 3+: 300-1000 mg/dL 4+: >1000 mg/dL
- 22. Causes of SecondaryProteinuria (Due to a Systemic Disorder or Medication)
- 23. Causes of Nephritic(Glomerular) Proteinuria and Hematuria
- 24.
- 25. NEPHRITIC SYNDROME Classic nephriticsyndrome is characterized by glomerular hematuria and an active urine sediment, manifested by dysmorphic RBCs (especially acanthocytes) and RBC casts and often white blood cells (WBCs) and WBC casts glomerular filtration rate (GFR) is reduced variable degrees of hypertension, oliguria, and edema occur. Proteinuria is common but often of relatively low magnitude Hematuria work up already explained
- 26. HISTORY TAKING CLINICAL PRESENTATIONETIOLOGY Overtly red color urologic pathology postpharyngitic hematuria PSGN recent episode of staphylococcal infection particularly in older diabetic patients raises IgA-dominant postinfectious glomerulonephritis synpharyngitic hematuria IgA nephropathy Hearing loss and visual symptoms related to lens abnormalities ALPORTS Hemoptysis vasculitis or anti–glomerular basement membrane (anti-GBM) disease
- 27. PHYSICAL EXAMINATION High-frequency sensorineuralhearing loss Alport’s disease Typical skin findings. SLE, vasculitis, Fabry’s disease, and Henoch-Schönlein purpura Joint findings rheumatologic-collagen vascular disease or vasculitis
- 28.
- 30. OTHER SEROLOGICAL TESTSDEPENDING ON CLINICAL ASSESSMENT Antinuclear antibody (ANA) and anti-DNA, anti-Smith, and anti-Rho antibodies SLE The perinuclear antineutrophil cytoplasmic antibody (P-ANCA) and cytoplasmic antineutrophil cytoplasmic antibody (C-ANCA) -vasculitis. Anti-GBM antibodies -Goodpasture’s syndrome.
- 31. Systemic Diseases withNephritic Clinical Presentation
- 32. CAUSE DIAGNOTIC CLUES GLOMERULONEPHRITISdysmorphic RBCs and/or red cell casts Isolated dysmorphic hematuria without proteinuria Alport syndrome, thin basement membrane nephropathy, or mild IgA nephropathy Alport syndrome, ADPKD Sickle cell disease microscopic or macroscopic hematuria, with positive family history Specific findings-High-frequency sensorineural hearing loss,visual symptoms related to lens abnormalities (ALPORTS) Immunoglobulin A (IgA) nephropathy In children, Alport syndrome /sickle cell disease/sickle cell trait Onset of gross hematuria 2 to 3 days after recent upper respiratory or gastrointestinal infection along with proteinuria, particularly In young adults. Acute poststreptococcal glomerulonephritis If the hematuria appears 2 to 3 weeks after a pharyngitis (or impetigo in children) Henoch–Schönlein purpura Younger subjects with a purpuric rash, arthralgias, and gross or microscopic hematuria IgA-dominant postinfectious glomerulonephritis recent episode of staphylococcal infection particularly in older diabetic patients Vasculitis such as granulomatosis with polyangiitis or microscopic polyangiitis Older patients with hematuria, proteinuria, profound constitutional symptoms, arthralgias, or respiratory symptoms Hemoptysis – anti GBM, GPA
- 33. RENAL LIMITED GLOMERULONEPHRITIS most common form of primary glomerular disease in the world slowly progressive renal disease Hematuria and subnephrotic proteinuria, which is often an incidental finding on urinalysis. Some patients develop gross hematuria, which classically develops in the setting of an upper respiratory tract infection (“synpharyngitic”) Treatment. ACE inhibitors, patients with proteinuria greater than 1 g/day may benefit from treatment with a 6-month course of prednisone (0.5 mg/kg on alternate days) IgA NEPHROPATHY
- 34. Membranoproliferative GN canbe idiopathic or secondary to systemic diseases as in autoimmune diseases ( like lupus nephritis), in infection-associated glomerular disease (e.g., with hepatitis C), and in patients with thrombotic microangiopathy Can present with mild nephritic findings, a rapid decline in renal function, or with the nephrotic syndrome
- 36. RARE CAUSES NHL,RCC, melanoma snake venom splenorenal shunt surgery for portal hypertension alpha 1 antitrypsin deficiency cryoglobulinemic GN idiopathic-diagnosis of exclusion
- 37. TREATMENT Underlyingcauses such as chronic bacterial infection, hepatitis C infection, and cryoglobulinemia, as well as leukemias and lymphomas, all have therapies that may lead to remission of the renal disease. Blood pressure should be controlled in all patients, and treatment should include an ACE inhibitor immunosuppressive drugs
- 38. Nephritic Syndrome withSystemic Manifestations nephritic pattern of injury, and the loss of renal function can be rapid. present with a pulmonary-renal syndrome-can have pulmonary hemorrhage at the time of presentation TREATMENT-high-dose steroids, cyclophosphamide, and plasmapheresis to remove the anti-GBM antibody. Patients who present with oliguria have a poor renal prognosis, but occasionally may avoid chronic dialysis with aggressive and early therapy. ANTI-GBM DISEASE
- 39. Pauci-immune Renal Vasculitis. Granulomatosis with polyangiitis (GPA; formerly called Wegener’s granulomatosis), Churg–Strauss syndrome, and microscopic polyangiitis. All forms of pauci-immune small vessel vasculitis can affect multiple organ systems, including the skin, lungs, and gastrointestinal system. Churg–Strauss syndrome is associated with asthma and eosinophilia. The clinical presentation of small vessel pauci-immune vasculitis is variable, but patients generally present with a nephritic pattern of renal disease. The renal disease can progress rapidly, making it very important to diagnose the disease promptly. Because the lungs are frequently involved in all forms of ANCA-associated vasculitis, patients can present with alveolar capillaritis and pulmonary hemorrhage (“pulmonary-renal syndrome”). GPA is most commonly associated with c-ANCA (anti-PR-3). Churg–Strauss syndrome and microscopic polyangiitis are more commonly associated with p-ANCA (anti- MPO).
- 40. Cryoglobulinemia (MPGN and/orCryoglobulinemia) Cryoglobulins form immune complexes that precipitate in small vessels, causing vasculitis. Most frequently associated with hepatitis C infection palpable purpura, arthralgias, and generalized weakness. Causes immune complex GN. proteinuria, hematuria, and slowly progressive disease, may have nephrotic range proteinuria, and rapid loss of renal function. Cryoglobulinemic GN should be suspected in any patient with known hepatitis C infection who develops renal disease. Labs that support the diagnosis of cryoglobulinemia include a low C4 level and the cryoglobulins often have rheumatoid factor activity. TREATMENT- patients with hepatitis C and symptomatic cryoglobulinemia, antiviral therapy with peginterferon alpha and ribavirin B-cell–depleting therapies, such as rituximab, in patients with an underlying B-cell lymphoproliferative disease and in those with rapidly progressive or resistant disease. Plasmapheresis in patients with rapidly progressive disease
- 41. Infection-Related GN poststreptococcalGN- most common Chronic hepatitis B is associated with MN, nephrotic syndrome HIV infection is associated with FSGS Bacterial endocarditis and infected atrioventricular shunts- immune complex GN Staphylococcus aureus– related GN
- 42. NEPHROTIC SYNDROME High-grade,albumin-dominant proteinuria (generally >3000 mg/day or spot urine protein/creatinine ratio of >3000 mg of protein/gm of creatinine) Hypoalbuminemia Edema Hyperlipidemia Lipiduria
- 43. Causes of SecondaryNephrotic Syndrome
- 44. HISTORY AND REVIEWOF SYSTEMS Clinical clues DIFFERENTIAL DIAGNOSIS malar facial rash, scarring alopecia, mat telangiectasia, nail bed telangiectasia nail fold capillary loops and vascular infarcts, and erythema nodosum. Rheumatological causes erythema nodosum and skin papules. Sarcoidosis (occasionally cause) Scleritis, skin manifestations, including leukocytoclastic rashes and skin infarctions. vasculitides dystrophic nails, hypoplastic patellae, iliac horns Nail-patella syndrome
- 45. LABORATORY INVESTIGATION Additionaltesting directed by the patient’s clinical presentation and findings and the suspicions of the physician. Testing for syphilis, HIV infection, and viral hepatitis (hepatitis B and C) Testing for ANA, anti–double-stranded DNA antibody, and complement levels is indicated, if collagen vascular disease is suspected. Serum immunoelectrophoresis or immunofixation study, if a paraproteinemia disorder (including primary amyloidosis) is suspected
- 46. IMAGING finding ofa single kidney, asymmetric kidney size, or bilaterally small kidneys will direct the subsequent evaluation. Large kidneys are suggestive of diabetes mellitus, amyloidosis, HIV, or renal vein thrombosis. Patients should have routine age-indicated screening studies for malignancy, such as mammography and colonoscopy.
- 47. RENAL BIOPSY Inyoung children with a classic clinical and biochemical presentation, the diagnosis of minimal change disease can usually be assumed and therapy initiated without histologic confirmation.
- 48. RENAL BIOPSY INDIABETIC PATIENTS WITH NEPHROTIC SYNDROME ● Sudden onset of low egfr or rapidly decreasing egfr ● Abrupt increase in albuminuria ● Refractory hypertension ● Signs or symptoms of another systemic disease ● 30% egfr decline within 2–3 months of initiation of a renin-angiotensin system inhibitor ● Very active urine sediment with RBC casts, ● Very short time course (diabetic nephrotic syndrome usually evolves over 15 to 20 years), ● Paraproteinemia or paraproteinuria, ● Hypocomplementemia, ● Absence of retinopathy
- 49. Renal Limited nephroticsyndromes 4th or 5th decade with a 2:1 male predominance. MN is often slowly progressive; however, some patients have spontaneous remission of disease M-type phospholipase A2 receptor (PLA2R) is the target antigen in 70% to 80% of cases of primary MN TREATMENT-ACE inhibitor or ARB therapy/ immunosuppressive agents is indicated for those patients at high risk for progressive loss of renal function PRIMARY MEMBRANOUS NEPHROPATHY
- 50. Primary FSGS Approximately20% of cases of idiopathic nephrotic syndrome in adults are due to FSGS. features of the nephrotic syndrome and often have hypertension. The natural history of primary FSGS is variable, but spontaneous remission in primary FSGS associated with nephrotic syndrome is low (<10%). The strongest predictor of progression to ESRD is resistance to corticosteroids. TREATMENT- steroids
- 51. Nephrotic Syndrome Dueto Systemic Illness Approximately 20% of MN Malignancy (colon, lung, or prostate cancer), autoimmune disease (systemic lupus erythematosus), infectious disease (hepatitis B virus, hepatitis C virus), drugs [nonsteroidal anti-inflammatory drugs (NSAIDs), gold, penicillamine SECONDARY MN
- 52. Secondary MCD. Systemicconditions associated with secondary MCD include Hodgkin’s disease and medications, such as lithium and NSAIDs. PRIMARY AMYLOIDOSIS associated with B-cell lymphoproliferative disorders (as seen in multiple myeloma). Less commonly secondary amyloidosis can be secondary to a chronic inflammatory state, such as rheumatoid arthritis or chronic infections
- 53. SECONDARY FSGS Geneticmutations in key podocyte structural proteins, viral nephropathies (HIV-associated nephropathy and parvovirus B19) drug-induced nephropathy (pamidronate, interferon alpha, heroin) adaptive hemodynamic changes (unilateral renal agenesis, reflux nephropathy, obesity).
- 54. THROMBOTIC MICROANGIOPATHIES. Can presentwith hematuria, hypertension, and proteinuria (although usually less than 1 to 1.5 g/day) Systemic diseases such as Thrombotic thrombocytopenic purpura (TTP) Hemolytic uremic syndrome (HUS), scleroderma, malignant hypertension antiphospholipid antibody syndrome (APS)
- 55. Hemolytic Uremic Syndrome acute renal failure, thrombocytopenia, and hemolysis Result from verotoxin (from Escherichia coli 0157:H7 gastrointestinal infection). Therapy primarily supportive and 90% of cases of diarrhea associated HUS will completely recover, although 5% die within the acute phase and 5% may have persistent renal and extrarenal complications. Patients who develop HUS in the absence of a verotoxin-producing infection are regarded as having atypical HUS, a disease that is usually caused by dysregulated activation of the alternative pathway of complement---- have a worse prognosis than those with diarrhea-associated HUS. Plasma exchange is beneficial in some patients with atypical HUS, eculizumab (a therapeutic complement inhibitor) has been approved for treatment of this disease.
- 56. Thrombotic Thrombocytopenic Purpura The “classic pentad” of signs of TTP includes thrombocytopenia, hemolytic anemia, neurologic abnormalities, fever, and renal failure. Primary TTP is believed to be triggered by endothelial injury in patients who have abnormally large von Willebrand factor (vWF) multimers Secondary forms of TTP exist, and include pregnancy-, malignancy-, and HIVassociated causes. A very low ADAMTS13 level supports the diagnosis of TTP, but it may take several days to get these results and the decision to treat TTP is usually made on clinical grounds. Plasma exchange or infusion is the most effective therapeutic intervention for TTP.
- 57. ACUTE KIDNEY INJURY kidney biopsy can be useful when vasculitis, glomerulonephritis, or allergic interstitial nephritis is considered a possible cause of the AKI.
- 58.
- 59. Ganesh K, NairR R, Seethalekshmy N V, Kurian G, Mathew A, Sreedharan S, Paul Z. A study of clinical presentation and correlative histopathological patterns in renal parenchymal disease. Indian J Nephrol 2018;28:28-3
- 60.
- 61. Nephrotic proteinuria +microhematuria + renal failure
- 62. Subnephrotic proteinuria +microhematuria
- 63. Subnephrotic proteinuria +microhematuria + renal failure
- 64.
- 65. Renal failure +proteinuria
- 68.