Primer: histopathology of calcineurin-inhibitor toxicity in renal allografts
|
|
- Felicity Pearson
- 5 years ago
- Views:
Transcription
1 Primer: histopathology of calcineurin-inhibitor toxicity in renal allografts Peter Liptak and Bela Ivanyi* SUMMARY Calcineurin inhibitors (ciclosporin and tacrolimus) can cause acute and chronic nephrotoxicity. The serum levels of these drugs do not correlate well with the extent of renal damage caused, and the clinical manifestation is nonspecific. Renal biopsy is a reliable tool with which to diagnose calcineurin-inhibitor-induced nephrotoxicity. Ciclosporin and tacrolimus produce identical lesions, which are focal in nature and can be overlooked, necessitating the evaluation of serial tissue sections. Acute toxicity is characterized histologically by necrosis and early hyalinosis of individual smooth muscle cells in the afferent arterioles, and/or isometric vacuolation of the proximal straight tubules; thrombotic microangiopathy is a rare manifestation. In chronic toxicity, the damaged media smooth muscle cells in afferent arterioles are replaced by beaded medial hyaline deposits that bulge into the adventitia; the interstitium displays striped fibrosis and tubular atrophy. As maintenance doses of calcineurin inhibitors in renal transplant recipients have been lowered during the past decade, the incidence of acute toxicity has decreased markedly. Chronic toxicity, however, is still prevalent, and causes chronic allograft damage. KEYWORDS arteriolopathy, calcineurin inhibitor, ciclosporin, nephrotoxicity, tacrolimus REVIEW CRITERIA Terms used for Pubmed searches were as follows: arteriolopathy, arteriolar hyalinosis, calcineurin inhibitor nephrotoxicity, ciclosporin, haemolytic uraemic syndrome, histology, morphology, renal allograft, tacrolimus, thrombotic microangiopathy, tubulopathy. CME P Liptak is currently a trainee at the Glasgow School of Pathology, Glasgow, UK, and B Ivanyi is Professor of Pathology in the Department of Pathology at the University of Szeged, Szeged, Hungary. Correspondence *Department of Pathology, University of Szeged, Allomás utca 2, Szeged H-6720, Hungary ivanyi@patho.szote.u-szeged.hu Received 5 September 2005 Accepted 8 May doi: /ncpneph0225 This article offers the opportunity to earn one Category 1 credit toward the AMA Physician s Recognition Award. INTRODUCTION The introduction in 1983 of a new class of immuno suppressive agents, the calcineurin inhibitors (CNIs), has dramatically improved renal allograft survival rates. The two agents in this class, ciclosporin and tacrolimus, prevent T-cell activation by inhibiting calcineurin. Calcineurin is a cytoplasmic phosphatase required for the transcription of interleukin-2 and other cytokines that are upregulated when antigen is presented to T cells. Unfortunately, the CNIs also have adverse effects, including nephro toxicity, hypertension, hyperlipidemia, glucose intolerance, hirsutism and gum hypertrophy. Combination therapy has been used to achieve adequate immunosuppression and to lower the risk of drug-related toxicity. The most frequently administered regimens include a corticosteroid plus either ciclosporin or tacrolimus plus a lymphocyte-proliferation inhibitor (e.g. mycophenolate mofetil). As CNI nephrotoxicity can occur even when the serum concentration of the drug is within the therapeutic range, toxicity-induced renal impairment can be diagnosed only if a renal biopsy is performed. During standard evalua tion (of two tissue cores whenever possible) special light microscopic staining of serial sections and immunostaining for complement (C)4d are used. To extract optimum interpretative power from histological changes, comparison with a time-zero biopsy is strongly advised. 1 3 Some pathologists also perform elastin staining with the full immuno fluorescence panel (IgG, IgA, IgM, C3, C1q, and fibrinogen), and investigate upregula tion of tubular human leukocyte antigen (HLA)-DR. 4 5 These additional stains sometimes provide extra diagnostic information. Sampling of tissue for electron microscopy is recommended if there is a clini cal suspicion of de novo or recurrent glomerular 398 NATURE CLINICAL PRACTICE NEPHROLOGY JULY 2006 VOL 2 NO 7
2 disease. Ultrastructural examination of glomerular and peritubular capillaries facilitates more definitive identification of lesions of chronic rejection, 6 but it is not routinely performed because of cost benefit concerns. This introductory survey will discuss the histopathology, clinicopathological aspects and differential diagnostics of CNI nephrotoxicity. Ciclosporin and tacrolimus nephrotoxicity occur in acute and chronic forms that can affect arterioles, glomeruli, tubules and interstitium. These drugs apparently produce identical lesions. 7 The pathogenetic pathways underlying CNI nephrotoxicity are complex, and beyond the scope of this paper. ACUTE CNI-INDUCED NEPHROTOXICITY Acute CNI-related nephrotoxicity can take the form of functional toxicity, delayed recovery from post-transplantation acute tubular necrosis (ATN), toxic tubulopathy or vascular toxicity. 4,8,9 Functional toxicity CNIs administered at pharmacological doses can cause vasoconstriction, a drop in glomerular filtration rate and elevation of serum creatinine level, in the absence of structural abnormalities in the biopsy specimen. This condition is most common in the early post-transplantation period. Clinical correlation: functional toxicity is reversible in response to a lowering of the dose of the drug. Delayed recovery from post-transplantation ATN Prolonged warm or cold ischemia causes ATN in renal allografts, and manifests as oligoanuria in the immediate postoperative period. This condition is a common complication of cadaveric renal transplantation. Morphological features include dilation and flattening of tubular profiles, loss of brush borders, necrosis of individual tubular epithelial cells, cytoplasmic basophilia and enlarged regenerative nuclei. Desquamation of tubular epithelial cells into the tubular lumen might be observed. Tubular changes are accompanied by interstitial edema and sparse lymphocytic infiltrates. 4 Allografts with any degree of ATN are markedly sensitive to CNIs, which can prolong recovery from the ATN. Biopsy findings of CNI-induced nephrotoxicity are the same as those of post-transplantation ATN (above). Clinical correlation: patients are maintained on dialysis until urine output has been restored and renal function recovered. Because of the potential for CNIs to exaggerate ischemic tubular damage, a drug of this class is introduced only when allograft function has been established. Toxic tubulopathy Patients with CNI-induced toxic tubulopathy present with acute allograft dysfunction, usually associated with an elevated serum drug level. As a consequence of the lowering of maintenance CNI doses over the past decade, the incidence of tubulo pathy has fallen markedly. Morphologically, isometric tubular vacuolation is observed focally, predominantly affecting the proximal straight tubules (Figure 1). The vacuoles are small, clear and evenly distributed throughout the cytoplasm. Ultrastructurally, the vacuoles correspond to dilations of the endoplasmic reticulum. 10 Focal tubular calcification might also be present. The features of this type of tubulopathy are indistinguishable from those of radiocontrast nephrotoxicity and osmotic nephrosis, conditions to be considered when making the diagnosis. Clinical correlation: toxic tubulopathy can be reversed by lowering the CNI dose. Vascular toxicity CNIs can have a direct toxic effect on endothelial cells, with or without the involvement of platelet aggregation. Two types of vascular toxicity have been identified, acute arteriolopathy and thrombotic microangiopathy. Acute arteriolopathy Patients present with acute allograft dysfunction. The serum level of CNI is usually elevated. On biopsy, lesions are confined to afferent arteriolar profiles. There is swelling and vacuolation of endothelial cells, vacuolation, necrosis and/or apoptosis and sometimes dropout of individual myocytes, and early replacement of damaged myocytes with rounded plasma protein insudates (hyalinization). Immunohistochemically, the insudates are positive for IgM and C3. Acute arteriolo pathy and toxic tubulopathy can co-exist. Clinical correlation: the clinical outcome of CNI-induced acute arteriolopathy varies. Some patients recover renal function after the dose of CNI has been reduced, while in others renal damage is irreversible. In clinical practice, the diagnosis of arteriolopathy frequently leads to cessation of CNI administration. JULY 2006 VOL 2 NO 7 LIPTAK AND IVANYI NATURE CLINICAL PRACTICE NEPHROLOGY 399
3 Box 1 Summary of lesions of acute calcineurininhibitor-induced nephrotoxicity, acute rejection and post-transplantation acute tubular necrosis. Acute calcineurin-inhibitor-induced nephrotoxicity Acute afferent arteriolopathy: endothelial swelling/vacuolation; necrosis and early-stage hyaline replacement of individual myocytes Tubulopathy: small, evenly distributed vacuoles mainly in the proximal straight tubules Thrombotic microangiopathy (rare) Acute cellular rejection Interstitial infiltrates of activated lymphocytes Lymphocytic tubulitis; HLA-DR expression in tubules Figure 1 Acute calcineurin-inhibitor-induced nephrotoxicity. Isometric vacuolation of proximal straight tubular profiles (arrows). Trichrome; 200. Lymphocytic intimal arteritis Acute humoral rejection Fibrinoid necrosis of small arteries and/or afferent arterioles Glomerular microthrombi Neutrophils in peritubular capillaries Ischemic tubular damage Complement 4d localized along peritubular capillaries Acute tubular necrosis Dilation and flattening of tubules Loss of brush border Necrosis and desquamation of individual tubular epithelial cells Figure 2 Ciclosporin-induced thrombotic microangiopathy. Hyaline thrombi in the lumen of glomerular capillary loops (arrows). Hematoxylin eosin; 400. Enlarged regenerative nuclei Interstitial edema Thrombotic microangiopathy A rare manifestion of CNI-related vascular nephrotoxicity is a clinical picture resembling the hemolytic uremic syndrome. Biopsy reveals thrombotic microangiopathy (TMA), characterized by thrombi in the lumina of arterioles and glomerular capillaries (Figure 2). Pronounced arterial intimal changes are not typical of CNIinduced TMA. It is important to bear in mind, however, that CNI-induced TMA cannot be differentiated from other forms of TMA on the basis of morphology alone. The following possibilities should therefore be considered: acute humoral rejection (C4d positivity), bacterial or viral infection, recurrent hemolytic uremic syndrome, and anticardiolipin antibody-induced TMA. Clinical correlation: diagnosis of CNI-induced TMA should prompt withdrawal of the drug because, if lesions are widespread and associated with extensive arterial mural necrosis and luminal thrombosis, graft loss develops. Differential diagnosis The main clinical conditions to be differ entiated from acute CNI-induced nephrotoxicity are acute rejection, post-transplantation ATN (Box 1) 400 NATURE CLINICAL PRACTICE NEPHROLOGY LIPTAK AND IVANYI JULY 2006 VOL 2 NO 7
4 Figure 5 Interstitial fibrosis and tubular atrophy in a band-like pattern indicative of chronic calcineurin-inhibitor-induced nephrotoxicity (area between the arrows). Hematoxylin eosin; 100. Figure 3 Chronic calcineurin-inhibitor-induced nephrotoxicity. Beaded medial hyalinosis in afferent arteriolar profiles (arrow). Periodic acid- Schiff; 400. H E and, on occasion, acute pyelonephritis. Carefully derived clinical pathological correlations are required to ensure correct diagnosis. Acute rejection Acute rejection of a grafted kidney can be cellular and/or humoral. Cellular rejection is characterized by the presence of interstitial infiltrates predominantly composed of activated lymphocytes, tubulitis (lymphocytes infiltrate the tubular wall) and upregulation of HLA-DR by tubular epithelial cells. Lymphocytic intimal arteritis, also termed endothelialitis, might be A H A 5μm Figure 4 Hyaline arteriolopathy on electron microscopy. Endothelial cells are swollen. Hyaline material is present subendothelially and at sites where media smooth muscle cells have dropped out previously. Hyaline material bulges into the adventitia (asterisk). 2,500. Abbreviations: A, apoptotic myocytes; E, endothelial cells; H, hyaline material. E * evident. Diagnosis of humoral rejection is based on histological features (ATN-type tubular damage, neutrophilic peritubular capillaritis or fibrinoid necrosis of the arteries) and bright, linear C4d-positivity along the peritubular capillaries. 1 4 Post-transplantation ATN See section above. Acute pyelonephritis This condition is characterized by an interstitial infiltrate of neutrophils and monocytes macrophages, and is associated with neutrophilic tubulitis and neutrophilic casts. CHRONIC CNI-INDUCED NEPHROTOXICITY This form of CNI-related toxicity occurs several months after renal transplantation. Characterized by a slow, insidious increase in the serum creatinine level, patients usually have hypertension and sometimes moderate to nephrotic-range proteinuria. Some patients have an elevated serum level of ciclosporin or tacrolimus. The incidence of chronic CNIinduced nephrotoxicity increases with time since transplantation. 11 The histological indicators of chronic CNI-induced nephro toxicity are hyaline arteriolopathy, striped interstitial fibrosis and tubular atrophy. 4,9,12 Hyaline arteriolopathy This lesion is the marker of chronic CNIinduced nephrotoxicity. It affects the afferent arterioles and distal portions of small interlobular arteries. Damaged smooth muscle cells are replaced by beaded hyaline deposits on the outer aspect of the media that bulge into the adventitia (Figures 3 and 4). Beaded JULY 2006 VOL 2 NO 7 LIPTAK AND IVANYI NATURE CLINICAL PRACTICE NEPHROLOGY 401
5 medial hyalinosis is focal and can be overlooked as a result. Evaluation of two cores of kidney tissue and serial sections overcomes the problem of sampling error. In advanced cases, the entire wall is replaced by the hyaline material and the lumen is severely narrowed. Immunohistochemistry detects IgM and C3 at the sites of insudation. Staining is in a pearl necklace pattern. Hyaline arteriolopathy must be differentiated from the arteriolar hyalinosis that is a feature of aging, hypertension and diabetes. In these three conditions, hyalinosis is primarily subendothelial and rarely extends into the adventitia, and necrosis of myocytes is not observed. Interstitial fibrosis and tubular atrophy In chronic CNI-induced nephrotoxicity, the interstitium shows prominent patchy fibrosis and corresponding tubular atrophy, with preferential and early involvement of the medullary rays. This results in a band-like pattern (Figure 5). This striped pattern is characteristic of, but not specific to, chronic CNI-induced nephro toxicity; hyper tensive kidney disease can produce a similar lesion. Glomerular changes The effects of chronic CNI-induced toxicity on glomeruli tend to be nonspecific. Compensatory glomerular hypertrophy, mesangial matrix expansion, capillary collapse, and focal segmental and/or focal global sclerosis can be observed. Focal segmental glomerulo sclerosis seems to result from hyperfiltration in response to loss of functioning nephrons, rather than being a direct effect of toxicity to podocytes and/or endo thelial cells. Focal segmental glomerulosclerosis related to CNI use should be distinguished from recurrent or de novo idiopathic focal sclerosis. The presence of hyaline arteriolopathy, striped fibrosis and tubular atrophy with or without isometric vacuolation of proximal straight tubules, and absence of fullblown nephrotic syndrome are evidence against idiopathic focal sclerosis. Clinical correlation: chronic CNI-induced kidney damage is irreversible. Appropriate management is dose reduction or discontinuation of ciclosporin or tacrolimus, and administration of alternative immunosuppressive agents. Differential diagnosis The main clinical conditions to be differentiated from chronic CNI-induced nephrotoxicity are chronic rejection/chronic allograft nephro pathy (CAN), de novo or recurrent glomerulo nephritis, and polyomavirus nephropathy. The symptoms of chronic CNI-induced nephrotoxicity are similar to those of chronic rejection/can. Chronic rejection involves ongoing, smoldering damage to the allograft, mediated by cellular and/or humoral alloimmune mecha nisms. In addition to chronic allo immune damage to renal parenchyma, a variety of non-immunological factors (e.g. advanced donor age, ischemic injury to the graft during implanta tion, hypertension, chronic CNI-induced nephro toxicity, infection, increased ureteral pressure, hyperfiltrating glomeruli) deplete nephrons. Alloimmune and non-immunological mechanisms act in parallel. Ultimately, these processes cause sclerosing changes in arteries and glomeruli, interstitial fibrosis and tubular atrophy. As chronic rejection, chronic CNI-induced nephrotoxicity, hypertensive vascular disease and chronic infection and/or reflux cannot always be distinguished in the biopsy specimen, the panel that compiled the Banff classification of kidney transplant pathology 1 coined the term CAN to emphasize the multi factorial nature of transplantation-related chronic renal injury. Presently, there is no therapeutic consequence by which chronic rejection can be distinguished from CAN. The usual diagnostic label is either chronic rejection/can or CAN with or without features of chronic rejection. 3,4 Some pathologists believe that use of the term CAN as a histological descriptor should be restricted as much as possible because it generates uncertainty rather than precision. Box 2 summarizes the main features of chronic CNI-induced nephro toxicity, chronic rejection and CAN. Chronic rejection A diagnosis of chronic allograft rejection is made 4,6 if there are light microscopic and/or ultrastructural and/or immunohistochemical signs of chronic alloimmune injury; that is, transplant arteriopathy (new-onset intimal fibrosis with or without foam cells and/or mononuclear cells in the intima), transplant glomerulopathy (thickening and double contours of the glomerular basement membrane), transplant capillaropathy (peritubular capillary profiles with five or more circumferential basement 402 NATURE CLINICAL PRACTICE NEPHROLOGY LIPTAK AND IVANYI JULY 2006 VOL 2 NO 7
6 Box 2 Summary of lesions of chronic calcineurin-inhibitor-induced nephrotoxicity, chronic rejection and chronic allograft nephropathy. Chronic calcineurin-inhibitor-induced nephrotoxicity Hyaline arteriolopathy: myocytes are replaced by beaded hyaline deposits that bulge into the adventitia Nonspecific segmental or global glomerular sclerosis Striped interstitial fibrosis and tubular atrophy Chronic rejection Transplant arteriopathy: new-onset intimal fibrosis; foam cells and/or mononuclear cells in the intima Transplant glomerulopathy: double-contoured glomerular capillaries Transplant capillaropathy: peritubular capillaries with five or more circumferential basement membrane layers on electron microscopy; complement 4d positivity Interstitial fibrosis and tubular atrophy Chronic allograft nephropathy Intimal fibroelastosis in arteries No change, or subendothelial hyalinosis, in arterioles Nonspecific segmental or global glomerular sclerosis Interstitial fibrosis and tubular atrophy membrane layers detected by electron microscopy), and C4d-positivity along the thickened walls of peritubular capillaries. The interstitium is fibrotic and tubules are atrophic. Chronic rejection is frequently accompanied by active cellular and/or humoral rejection. Chronic CNI-induced nephrotoxicity and rejection can co-exist. Verification of marker lesions facilitates correct reporting of coincidental conditions. CAN CAN is diagnosed 6 if there is intimal fibroelastosis in arteries, arterioles exhibit no or eccentric subendothelial hyalinosis, glomeruli are sclerosed in a nonspecific segmental or global pattern, the interstitium is fibrotic, and tubules in the fibrotic areas are atrophic. Recurrent or de novo glomerulonephritis These forms of glomerulonephritis can be readily detected if a full immunohistochemical panel is applied and electron microscopy performed. Polyomavirus nephropathy This form of renal damage is characterized by viral cytopathic effects in tubules (inclusion bodies and tubular epithelial injury), a varying degree of interstitial inflammation, interstitial fibrosis and tubular atrophy. 4 CONCLUSIONS CNI-induced nephrotoxicity is a clinicopathological entity. The histological features indicative of acute toxicity are necrosis and dropout of individual myocytes, onset of replacement of these myocytes with hyaline insudates in afferent arterioles, and isometric vacuolation, predominantly in the straight proxi mal tubules. A TMA-like presentation is rare. In chronic toxicity, beaded medial hyalinization of afferent arterioles, striped interstitial fibrosis and tubular atrophy are observed. Careful analysis of the morphology of arteriolar lesions is necessary, and comparison with time-zero biopsies is advised. KEY POINTS Immunosuppressants of the calcineurin inhibitor (CNI) class (tacrolimus and ciclosporin) can have acute and chronic deleterious effects on transplanted kidneys Renal biopsy and microscopy of serial tissue sections provide information that is essential to diagnosis of CNI-induced nephrotoxicity Histological features of acute CNI-induced nephrotoxicity include early-stage hyalinization and dropout of individual myocytes in afferent arterioles, and isometric vacuolation of proximal straight tubules Histological features of chronic CNI-induced nephrotoxicity include replacement of myocytes in afferent arterioles with beads of hyaline that bulge into the adventitia, striped interstitial fibrosis and tubular atrophy References 1 Solez K et al. (1993) International standardization of criteria for the histologic diagnosis of renal allograft rejection: the Banff working classification of kidney transplant pathology. Kidney Int 44: Racusen LC et al. (1999) The Banff 97 working classification of renal allograft pathology. Kidney Int 55: JULY 2006 VOL 2 NO 7 LIPTAK AND IVANYI NATURE CLINICAL PRACTICE NEPHROLOGY 403
7 Acknowledgments The nephropathological activities of B Ivanyi are supported by the Hungarian Scientific Research Fund (OTKA) via grant T Competing interests The authors declared they have no competing interests. 3 Racusen LC et al. (2003) Antibody-mediated rejection criteria an addition to the Banff 97 classification of renal allograft rejection. Am J Transplant 3: D Agati VD et al. (Eds; 2005) Pathology of renal transplantation. In AFIP Atlas of Non Tumor Pathology: Non-Neoplastic Kidney Diseases, Silver Spring: ARP Press 5 Nickeleit V et al. (1998) Histological characteristics of interstitial renal allograft rejection. Kidney Blood Press Res 21: Ivanyi B (2003) Transplant capillaropathy and transplant glomerulopathy: ultrastructural markers of chronic renal allograft rejection. Nephrol Dial Transplant 18: Solez K et al. (1998) Histopathologic findings from 2-year protocol biopsies from a US multicenter kidney transplant trial comparing tacrolimus versus cyclosporine: a report of the FK506 Kidney Study Group. Transplantation 66: Mihatsch MJ et al. (1994) Cyclosporine nephropathy. In Renal Pathology With Clinical and Functional Correlations, edn 2, (Eds Tisher CC and Brenner BM) Philadelphia: JB Lippincott 9 Colvin RB (1998) Renal transplant pathology. In Heptinstall s Pathology of the Kidney, edn 5, (Eds Jennette JC et al.) Philadelphia: Lippincott-Raven 10 Mihatsch M et al. (1988) Cyclosporine nephrotoxicity. Adv Nephrol Necker Hosp 17: Nankivell BJ et al. (2004) Calcineurin inhibitor nephrotoxicity: longitudinal assessment by protocol histology. Transplantation 78: Mihatsch MJ et al. (1994) Cyclosporin A nephropathy: standardization of the evaluation of kidney biopsies. Clin Nephrol 41: NATURE CLINICAL PRACTICE NEPHROLOGY LIPTAK AND IVANYI JULY 2006 VOL 2 NO 7
Pathology of Kidney Allograft Dysfunction. B. Ivanyi, MD Department of Pathology, University of Szeged, Szeged, Hungary
Pathology of Kidney Allograft Dysfunction B. Ivanyi, MD Department of Pathology, University of Szeged, Szeged, Hungary The renal biopsy is a powerful tool in the diagnostic evaluation of allograft dysfunction
More informationPathology of Kidney Allograft Dysfunction. B. Ivanyi, MD Department of Pathology, University of Szeged, Szeged, Hungary
Pathology of Kidney Allograft Dysfunction B. Ivanyi, MD Department of Pathology, University of Szeged, Szeged, Hungary The gold standard for exploration of the cause of an allograft dysfunction is to perform
More informationInterpretation of Renal Transplant Biopsy. Arthur H. Cohen Wake Forest University School of Medicine Winston-Salem, North Carolina USA
Interpretation of Renal Transplant Biopsy Arthur H. Cohen Wake Forest University School of Medicine Winston-Salem, North Carolina USA Renal Transplant Biopsies Tissue Processing Ideal world process as
More informationBiopsy Features of Kidney Allograft Rejection Banff B. Ivanyi, MD Department of Pathology, University of Szeged, Szeged, Hungary
Biopsy Features of Kidney Allograft Rejection Banff 2017 B. Ivanyi, MD Department of Pathology, University of Szeged, Szeged, Hungary Treatment of allograft dysfunction should rely on the biopsy findings
More informationDr Ian Roberts Oxford. Oxford Pathology Course 2010 for FRCPath Illustration-Cellular Pathology. Oxford Radcliffe NHS Trust
Dr Ian Roberts Oxford Oxford Pathology Course 2010 for FRCPath Plan of attack: Diagnostic approach to the renal biopsy Differential diagnosis of the clinical syndromes of renal disease Microscopy Step
More informationEvolution of the approaches toward grading and classifying chronic changes in the renal allograft: Banff classification updates III
EDITORIAL Advance Access publication 24 February 2014 Evolution of the approaches toward grading and classifying chronic changes in the renal allograft: Banff classification updates III Histopathology
More informationOrdering Physician. Collected REVISED REPORT. Performed. IgG IF, Renal MCR. Lambda IF, Renal MCR. C1q IF, Renal. MCR Albumin IF, Renal MCR
RenalPath Level IV Wet Ts IgA I Renal IgM I Renal Kappa I Renal Renal Bx Electron Microscopy IgG I Renal Lambda I Renal C1q I Renal C3 I Renal Albumin I Renal ibrinogen I Renal Mayo Clinic Dept. of Lab
More informationAcute renal failure (ARF) in the transplanted kidney represents a
Acute Renal Failure in the Transplanted Kidney Kim Solez Lorraine C. Racusen Acute renal failure (ARF) in the transplanted kidney represents a high-stakes area of nephrology and of transplantation practice.
More informationManagement of Rejection
Management of Rejection I have no disclosures Disclosures (relevant or otherwise) Deborah B Adey, MD Professor of Medicine University of California, San Francisco Kidney and Pancreas Transplant Center
More informationHistopathology: Glomerulonephritis and other renal pathology
Histopathology: Glomerulonephritis and other renal pathology These presentations are to help you identify basic histopathological features. They do not contain the additional factual information that you
More informationSurgical Pathology Report
Louisiana State University Health Sciences Center Department of Pathology Shreveport, Louisiana Accession #: Collected: Received: Reported: 6/1/2012 09:18 6/2/2012 09:02 6/2/2012 Patient Name: Med. Rec.
More informationKidneytransplant pathologyrelatedto immunosuppressiveagents
Kidneytransplant pathologyrelatedto immunosuppressiveagents Helmut Hopfer Pathologie Women, 53 years old. 16 months after kidney transplantation for diabetic nephropathy. Metabolicsyndromeandcoronaryheartdisease.
More informationIndex. electron microscopy, 81 immunofluorescence microscopy, 80 light microscopy, 80 Amyloidosis clinical setting, 185 etiology/pathogenesis,
A Acute antibody-mediated rejection (Acute AMR) clinical features, 203 clinicopathologic correlations, 206 pathogenesis, 205 206 204 205 light microscopy, 203 204 Acute cellular rejection (ACR) clinical
More informationRENAL HISTOPATHOLOGY
RENAL HISTOPATHOLOGY Peter McCue, M.D. Department of Pathology, Anatomy & Cell Biology Sidney Kimmel Medical College There are no conflicts of interest. 1 Goals and Objectives! Goals Provide introduction
More informationCase Presentation Turki Al-Hussain, MD
Case Presentation Turki Al-Hussain, MD Director, Renal Pathology Chapter Saudi Society of Nephrology & Transplantation Consultant Nephropathologist & Urological Pathologist Department of Pathology & Laboratory
More informationRENAL EVENING SPECIALTY CONFERENCE
RENAL EVENING SPECIALTY CONFERENCE Harsharan K. Singh, MD The University of North Carolina at Chapel Hill Disclosure of Relevant Financial Relationships No conflicts of interest to disclose. CLINICAL HISTORY
More informationA clinical syndrome, composed mainly of:
Nephritic syndrome We will discuss: 1)Nephritic syndrome: -Acute postinfectious (poststreptococcal) GN -IgA nephropathy -Hereditary nephritis 2)Rapidly progressive GN (RPGN) A clinical syndrome, composed
More informationYear 2004 Paper one: Questions supplied by Megan
QUESTION 53 Endothelial cell pathology on renal biopsy is most characteristic of which one of the following diagnoses? A. Pre-eclampsia B. Haemolytic uraemic syndrome C. Lupus nephritis D. Immunoglobulin
More informationHistopathology: Hypertension and diabetes in the kidney These presentations are to help you identify basic histopathological features.
Histopathology: Hypertension and diabetes in the kidney These presentations are to help you identify basic histopathological features. They do not contain the additional factual information that you need
More informationReview of Rituximab and renal transplantation. Dr.E Nemati. Professor of Nephrology
Review of Rituximab and renal transplantation Dr.E Nemati Professor of Nephrology Introductio n Rituximab is a chimeric anti-cd20 monoclonal antibody. The CD20 antigen is a transmembrane nonglycosylated
More informationInteresting case seminar: Native kidneys Case Report:
Interesting case seminar: Native kidneys Case Report: Proximal tubulopathy and light chain deposition disease presented as severe pulmonary hypertension with right-sided cardiac dysfunction and nephrotic
More informationSome renal vascular disorders
Some renal vascular disorders Introduction Nearly all diseases of the kidney involve the renal blood vessels secondarily We will discuss: -Hypertension (arterionephrosclerosis in benign HTN & hyperplastic
More informationHistopathological evaluation of renal allograft biopsies in Nepal: interpretation and significance
Nepal Medical Association Building Exhibition Road, Kathmandu Journal of Pathology of Nepal (2012) Vol. 2, 172-179 Association of Clinical Pathologist of Nepal-2010 Journal of PATHOLOGY of Nepal www.acpnepal.com
More informationRenal Pathology- Transplantation. Eva Honsova Institute for Clinical and Experimental Medicine Prague, Czech Republic
Renal Pathology- Transplantation Eva Honsova Institute for Clinical and Experimental Medicine Prague, Czech Republic eva.honsova@ikem.cz Kidney has a limited number of tissue reactions by which the kidney
More informationHistopathology: Vascular pathology
Histopathology: Vascular pathology These presentations are to help you identify basic histopathological features. They do not contain the additional factual information that you need to learn about these
More informationGlomerular pathology in systemic disease
Glomerular pathology in systemic disease Lecture outline Lupus nephritis Diabetic nephropathy Glomerulonephritis Associated with Bacterial Endocarditis and Other Systemic Infections Henoch-Schonlein Purpura
More informationStatement of Disclosure
Statement of Disclosure Mark Haas serves as a paid consultant on pathology adjudication committees for two industry-sponsored clinical trials: Shire ViroPharma Treatment of Acute ABMR AstraZeneca Treatment
More informationMonoclonal Gammopathies and the Kidney. Tibor Nádasdy, MD The Ohio State University, Columbus, OH
Monoclonal Gammopathies and the Kidney Tibor Nádasdy, MD The Ohio State University, Columbus, OH Monoclonal gammopathy of renal significance (MGRS) Biopsies at OSU (n=475) between 2007 and 2016 AL or AH
More informationDr Ian Roberts Oxford
Dr Ian Roberts Oxford Oxford Pathology Course 2010 for FRCPath Present the basic diagnostic features of the commonest conditions causing renal failure Highlight diagnostic pitfalls. Crescentic GN: renal
More informationThe Banff Classification for Diagnosis of Renal Allograft Rejection: Updates from the 2017 Banff Conference
The Banff Classification for Diagnosis of Renal Allograft Rejection: Updates from the 2017 Banff Conference Mark Haas Cedars-Sinai Medical Center Los Angeles, California, USA Statement of Disclosure Mark
More informationDr Ian Roberts Oxford. Oxford Pathology Course 2010 for FRCPath Illustration-Cellular Pathology. Oxford Radcliffe NHS Trust
Dr Ian Roberts Oxford Oxford Pathology Course 2010 for FRCPath Present the basic diagnostic features of the commonest conditions causing proteinuria & haematuria Highlight diagnostic pitfalls Nephrotic
More informationRecognition and Treatment of Chronic Allograft Dysfunction
Recognition and Treatment of Chronic Allograft Dysfunction Alexander Wiseman, M.D. Associate Professor, Division of Renal Diseases and Hypertension Medical Director, Kidney and Pancreas Transplant Programs
More informationRenal Pathology 1: Glomerulus. With many thanks to Elizabeth Angus PhD for EM photographs
Renal Pathology 1: Glomerulus With many thanks to Elizabeth Angus PhD for EM photographs Anatomy of the Kidney http://www.yalemedicalgroup.org/stw/page.asp?pageid=stw028980 The Nephron http://www.beltina.org/health-dictionary/nephron-function-kidney-definition.html
More informationGlomerular diseases mostly presenting with Nephritic syndrome
Glomerular diseases mostly presenting with Nephritic syndrome 1 The Nephritic Syndrome Pathogenesis: proliferation of the cells in glomeruli & leukocytic infiltrate Injured capillary walls escape of RBCs
More informationKidney Summary. Mark Haas Cedars-Sinai Medical Center Los Angeles, California, USA
Kidney Summary Mark Haas Cedars-Sinai Medical Center Los Angeles, California, USA Key Issues to Address re: the Classification 1. Incorporation of i-ifta + tubulitis into the TCMR classification - Defining
More informationImmunopathology of T cell mediated rejection
Immunopathology of T cell mediated rejection Ibrahim Batal MD Columbia University College of Physicians & Surgeons New York, NY, USA Overview Pathophysiology and grading of TCMR TCMR is still a significant
More informationThe Value of Electron Microscopy in the Diagnosis of Chronic Renal Allograft Rejection
The Value of Electron Microscopy in the Diagnosis of Chronic Renal Allograft Rejection B. Ivanyi, M.D., E. Kemeny, M.D., E. Szederkenyi, M.D., F. Marofka, M.D., P. Szenohradszky, M.D. Departments of Pathology
More informationCase Report A Clinical and Pathological Variant of Acute Transplant Glomerulopathy
Case Report A Clinical and Pathological Variant of Acute Transplant Glomerulopathy Miklos Z. Molnar, 1 G. V. Ramesh Prasad, 2 Darren A. Yuen, 2,3 Serge Jothy, 4 and Jeffrey S. Zaltzman 2,5 1 Division of
More informationHistopathological findings in transplanted kidneys
Katsuma et al. Renal Replacement Therapy (2017) 3:6 DOI 10.1186/s41100-016-0089-0 REVIEW Histopathological findings in transplanted kidneys Ai Katsuma, Takafumi Yamakawa, Yasuyuki Nakada, Izumi Yamamoto
More informationHLA and Non-HLA Antibodies in Transplantation and their Management
HLA and Non-HLA Antibodies in Transplantation and their Management Luca Dello Strologo October 29 th, 2016 Hystory I 1960 donor specific antibodies (DSA): first suggestion for a possible role in deteriorating
More informationRecurrent Idiopathic Membranous Glomerulonephritis After Kidney Transplantation and Successful Treatment With Rituximab
TRANSPLANTATION Recurrent Idiopathic Membranous Glomerulonephritis After Kidney Transplantation and Successful Treatment With Rituximab Khadijeh Makhdoomi, 1,2 Saeed Abkhiz, 1,2 Farahnaz Noroozinia, 1,3
More informationThe Natural History of Chronic Allograft Nephropathy
The new england journal of medicine original article The Natural History of Chronic Allograft Nephropathy Brian J. Nankivell, M.D., Ph.D., Richard J. Borrows, M.B., B.Chir., Caroline L.-S. Fung, M.B.,
More informationClassification of Glomerular Diseases and Defining Individual Glomerular Lesions: Developing International Consensus
Classification of Glomerular Diseases and Defining Individual Glomerular Lesions: Developing International Consensus Mark Haas MD, PhD Department of Pathology & Laboratory Medicine Cedars-Sinai Medical
More informationGlomerular pathology-2 Nephritic syndrome. Dr. Nisreen Abu Shahin
Glomerular pathology-2 Nephritic syndrome Dr. Nisreen Abu Shahin 1 The Nephritic Syndrome Pathogenesis: inflammation proliferation of the cells in glomeruli & leukocytic infiltrate Injured capillary walls
More informationRECURRENT AND DE NOVO RENAL DISEASES IN THE ALLOGRAFT. J. H. Helderman,MD,FACP,FAST
RECURRENT AND DE NOVO RENAL DISEASES IN THE ALLOGRAFT J. H. Helderman,MD,FACP,FAST Vanderbilt University Medical Center Professor of Medicine, Pathology and Immunology Medical Director, Vanderbilt Transplant
More informationPathological back-ground of renal transplant pathology and important mile-stones of the Banff classification
Banff 1 Banff Pathological back-ground of renal transplant pathology and important mile-stones of the Banff classification Department of Nephrology, Japanese Red Cross Nagoya Daini Hospital Morozumi Kunio,
More informationRECURRENT AND DE NOVO RENAL DISEASES IN THE ALLOGRAFT
RECURRENT AND DE NOVO RENAL DISEASES IN THE ALLOGRAFT HISTOPATHOLOGIC DISORDERS AFFECTING THE ALLOGRAFT OTHER THAN REJECTION RECURRENT DISEASE DE NOVO DISEASE TRANSPLANT GLOMERULOPATHY Glomerular Non-glomerular
More informationChronic Active Thrombotic Microangiopathy in Native and Transplanted Kidneys
Available online at www.annclinlabsci.org Annals of Clinical & Laboratory Science, vol. 36, no.3, 2006 319 Case Reports: Chronic Active Thrombotic Microangiopathy in Native and Transplanted Kidneys Ping
More informationLight-Chain Mediated Acute Tubular Interstitial Nephritis. A Poorly Recognized Pattern of Renal Disease in Patients With Plasma Cell Dyscrasia
Light-Chain Mediated Acute Tubular Interstitial Nephritis A Poorly Recognized Pattern of Renal Disease in Patients With Plasma Cell Dyscrasia Xin Gu, MD; Guillermo A. Herrera, MD Context. Acute renal failure
More informationLight and electron microscopical studies of focal glomerular sclerosis
J. clin. Path., 1971, 24, 846-850 Light and electron microscopical studies of focal glomerular sclerosis A. H. NAGI, F. ALEXANDER, AND R. LANNIGAN From the Department of Pathology, Queen's University of
More informationOverview of glomerular diseases
Overview of glomerular diseases *Endothelial cells are fenestrated each fenestra: 70-100nm in diameter Contractile, capable of proliferation, makes ECM & releases mediators *Glomerular basement membrane
More informationCase # 2 3/27/2017. Disclosure of Relevant Financial Relationships. Clinical history. Clinical history. Laboratory findings
Case # 2 Christopher Larsen, MD Arkana Laboratories Disclosure of Relevant Financial Relationships USCAP requires that all planners (Education Committee) in a position to influence or control the content
More informationCrescentic Glomerulonephritis (RPGN)
Crescentic Glomerulonephritis (RPGN) Background Rapidly progressive glomerulonephritis (RPGN) is defined as any glomerular disease characterized by extensive crescents (usually >50%) as the principal histologic
More informationGlomerular Pathology- 1 Nephrotic Syndrome. Dr. Nisreen Abu Shahin
Glomerular Pathology- 1 Nephrotic Syndrome Dr. Nisreen Abu Shahin The Nephrotic Syndrome a clinical complex resulting from glomerular disease & includes the following: (1) massive proteinuria (3.5 gm /day
More informationFußzeile (Titel der Präsentation) 1. Thrombotic Microangiopathy: The German Experience 4. Conflictof interest: none
Thrombotic Microangiopathy: The German Experience 3 Nephropathology Section, Institute of Pathology, Hamburg, Germany Agenda 1. Difficulties in the diagnosis TMA 2. Previous efforts to reach consensus
More informationProgressive histological damage in renal allografts is associated with expression of innate and adaptive immunity genes
http://www.kidney-international.org & 2011 International Society of Nephrology see commentary on page 1254 Progressive histological damage in renal allografts is associated with expression of innate and
More informationImpact of Subclinical Rejection on Transplantation
Trends in Transplantation 2007;1:56-60 Impact of Subclinical Rejection on Transplantation David N. Rush for the Winnipeg Transplant Group Transplant Manitoba Adult Kidney Program, University of Manitoba,
More informationTHE URINARY SYSTEM. The cases we will cover are:
THE URINARY SYSTEM The focus of this week s lab will be pathology of the urinary system. Diseases of the kidney can be broken down into diseases that affect the glomeruli, tubules, interstitium, and blood
More informationrenoprotection therapy goals 208, 209
Subject Index Aldosterone, plasminogen activator inhibitor-1 induction 163, 164, 168 Aminopeptidases angiotensin II processing 64 66, 214 diabetic expression 214, 215 Angiotensin I intrarenal compartmentalization
More informationInterstitial Inflammation
Interstitial Inflammation Currently considered to be T cell-mediated process Plasma cell rich acute rejection often associated with AMR Preliminary data suggests that interstitial follicular helper T cells
More informationTHE URINARY SYSTEM. The cases we will cover are:
THE URINARY SYSTEM The focus of this week s lab will be pathology of the urinary system. Diseases of the kidney can be broken down into diseases that affect the glomeruli, tubules, interstitium, and blood
More informationEndothelitis in cardiac allograft biopsy specimens: Possible relationship to antibody-mediated rejection
http://www.jhltonline.org ORIGINAL CLINICAL SCIENCE Endothelitis in cardiac allograft biopsy specimens: Possible relationship to antibody-mediated rejection Fabio Tavora, MD, a Raghava Munivenkatappa,
More informationPost-Transplant Monitoring for the Development of Anti-Donor HLA Antibodies
Post-Transplant Monitoring for the Development of Anti-Donor HLA Antibodies Lorita M Rebellato, Ph.D., D (ABHI) Associate Professor Department of Pathology The Brody School of Medicine at ECU Scientific
More informationDeján Dobi, MD. PhD Thesis
Clinicopathologic Relevance of Vascular Changes Associated with Transplant Glomerulopathy Secondary to Chronic Antibody-mediated Rejection in the Renal Allograft Deján Dobi, MD PhD Thesis Szeged, 2018
More informationThe Banff Conferences on renal allograft pathology the latest 2013 report
615245PSH0010.1177/2010105815615245Proceedings of Singapore HealthcareLoh research-article2015 Review Article PROCEEDINGS OF SINGAPORE HEALTHCARE The Banff Conferences on renal allograft pathology the
More informationAs outlined under External contributions (see appendix 7.1), the group of Prof. Gröne at the
3 RESULTS As outlined under External contributions (see appendix 7.1), the group of Prof. Gröne at the DKFZ in Heidelberg (Dept. of Cellular and Molecular pathology) contributed to this work by performing
More informationSupplementary appendix
Supplementary appendix This appendix formed part of the original submission and has been peer reviewed. We post it as supplied by the authors. Supplement to: Lefaucheur C, Loupy A, Vernerey D, et al. Antibody-mediated
More informationMembranoproliferative Glomerulonephritis
Membranoproliferative Glomerulonephritis MPGN is characterizedby alterations in the GBM and mesangium and by proliferation of glomerular cells. 5% to 10% of cases of 1ry nephrotic syndrome in children
More informationNephritic vs. Nephrotic Syndrome
Page 1 of 18 Nephritic vs. Nephrotic Syndrome Terminology: Glomerulus: A network of blood capillaries contained within the cuplike end (Bowman s capsule) of a nephron. Glomerular filtration rate: The rate
More informationMayo Clinic/ RPS Consensus Report on Classification, Diagnosis, and Reporting of Glomerulonephritis
Mayo Clinic/ RPS Consensus Report on Classification, Diagnosis, and Reporting of Glomerulonephritis Sanjeev Sethi, MD, PhD Department of Laboratory Medicine and Pathology Disclosure Relevant Financial
More informationRENAL HISTOPATHOLOGY FOLLOWING RUSSELL'S VIPER (VIPERA RUSSELLI) BITE
RENAL HISTOPATHOLOGY FOLLOWING RUSSELL'S VIPER (VIPERA RUSSELLI) BITE Soe ~oe', May Mya win2, Than Than Htwe', Myint win', Swe Swe ~het* and Wynn Wynn Kyawl 'Department of Medical Research No. 5. Ziwaka
More informationElevated Serum Creatinine, a simplified approach
Elevated Serum Creatinine, a simplified approach Primary Care Update Creighton University School of Medicine. April 27 th, 2018 Disclosure Slide I have no disclosures and have no conflicts with this presentation.
More informationCKD in Other Organ Transplants
CKD in Other Organ Transplants Alexander Wiseman, M.D. Associate Professor, Division of Renal Diseases and Hypertension Medical Director, Kidney and Pancreas Transplant Programs University of Colorado
More informationQUANTITATIVE HISTOCHEMISTRY OF THE NEPHRON. V.
QUANTITATIVE HISTOCHEMISTRY OF THE NEPHRON. V. ALKALINE PHOSPHATASE AND LACTIC DEHYDROGENASE ACTIVITIES IN LUPUS NEPHRITIS * By VICTOR E. POLLAK,t SJOERD L. BONTING, ROBERT C. MUEHRCKE AND ROBERT M. KARK
More informationClinical and pathologic characteristics of focal segmental glomerulosclerosis pathologic variants
original article http://www.kidney-international.org & 2006 International Society of Nephrology Clinical and pathologic characteristics of focal segmental glomerulosclerosis pathologic variants DB Thomas
More informationII.Tubulointerstitial diseases
II.Tubulointerstitial diseases two major groups of processes (1) ischemic or toxic tubular injury, leading to acute kidney injury (AKI) and acute renal failure, and (2) inflammatory reactions of the tubules
More informationChapter 6: Idiopathic focal segmental glomerulosclerosis in adults Kidney International Supplements (2012) 2, ; doi: /kisup.2012.
http://www.kidney-international.org chapter 6 & 2012 KDIGO Chapter 6: Idiopathic focal segmental glomerulosclerosis in adults Kidney International Supplements (2012) 2, 181 185; doi:10.1038/kisup.2012.19
More informationINTRODUCTION TO GLOMERULAR DISEASES
INTRODUCTION TO GLOMERULAR DISEASES Goal: to explain the general mechanisms leading to glomerular diseases and to analyze what is known about their relationship to morphologic and clinical manifestations
More informationFocal peritubular capillary C4d deposition in acute rejection
Nephrol Dial Transplant (2006) 21: 1382 1388 doi:10.1093/ndt/gfk028 Advance Access publication 5 January 2006 Original Article Focal peritubular capillary C4d deposition in acute rejection Alexander B.
More informationDiabetic Nephropathy. Introduction/Clinical Setting. Pathologic Findings Light Microscopy. J. Charles Jennette
12 Diabetic Nephropathy J. Charles Jennette Introduction/Clinical Setting Diabetic nephropathy is a clinical syndrome in a patient with diabetes mellitus that is characterized by persistent albuminuria,
More informationFundamentals of Renal Pathology
Fundamentals of Renal Pathology Fundamentals of Renal Pathology Agnes B. Fogo, Arthur H. Cohen, J. Charles Jennette, Jan A. Bruijn, Robert B. Colvin Agnes B. Fogo, M.D. Vanderbilt University Medical Center
More informationHistological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load
American Journal of Transplantation 2004; 4: 2082 2092 Blackwell Munksgaard Copyright C Blackwell Munksgaard 2004 doi: 10.1111/j.1600-6143.2004.00603.x Histological Patterns of Polyomavirus Nephropathy:
More informationThe topic of normal vascular and glomerular anatomy is introduced
Normal Vascular and Glomerular Anatomy Arthur H. Cohen Richard J. Glassock The topic of normal vascular and glomerular anatomy is introduced here to serve as a reference point for later illustrations of
More informationSection Title. Subject Index
Section Title Subject Index Acute kidney injury definitions 287 289 hypoxia 287, 290 overview 286, 287 sublethal tubular injury adaptive responses 292, 293 combination of sublethal injuries 291, 292 detection
More informationDisorders of the kidney. Urine analysis. Nephrotic and nephritic syndrome.
Disorders of the kidney. Urine analysis. Nephrotic and nephritic syndrome. Azotemia and Urinary Abnormalities Disturbances in urine volume oliguria, anuria, polyuria Abnormalities of urine sediment red
More informationC1q nephropathy the Diverse Disease
C1q nephropathy the Diverse Disease Danica Galešić Ljubanović School of Medicine, University of Zagreb Dubrava University Hospital Zagreb, Croatia Definition Dominant or codominant ( 2+), mesangial staining
More informationThe Histology of Kidney Transplant Failure: A Long-Term Follow-Up Study
CLINICAL AND TRANSLATIONAL RESEARCH The Histology of Kidney Transplant Failure: A Long-Term Follow-Up Study Maarten Naesens, 1,2,6 Dirk R.J. Kuypers, 1,2 Katrien De Vusser, 1,2 Pieter Evenepoel, 1,2 Kathleen
More informationUrinary System Laboratory
Urinary System Laboratory 1 Adrenal gland Organs of The Urinary System Renal artery and vein Kidney Ureter Urinary bladder Figure 26.1 2 Urethra Functions of the urinary system organs: Urethra expels urine
More informationJames E. Cooper, M.D. Assistant Professor, University of Colorado at Denver Division of Renal Disease and Hypertension, Kidney and PancreasTransplant
James E. Cooper, M.D. Assistant Professor, University of Colorado at Denver Division of Renal Disease and Hypertension, Kidney and PancreasTransplant Program Has no real or apparent conflicts of interest
More informationChronic renal allograft rejection: Pathophysiologic considerations
Kidney International, Vol. 68 (2005), pp. 1 13 PERSPECTIVES IN RENAL MEDICINE Chronic renal allograft rejection: Pathophysiologic considerations SIMONE A. JOOSTEN,YVO W.J. SIJPKENS,CEES VAN KOOTEN, and
More informationC3 GLOMERULOPATHIES. Budapest Nephrology School Zoltan Laszik
C3 GLOMERULOPATHIES Budapest Nephrology School 8.30.2018. Zoltan Laszik 1 Learning Objectives Familiarize with the pathogenetic mechanisms of glomerular diseases Learn the pathologic landscape and clinical
More information2017 CST-Astellas Canadian Transplant Fellows Symposium. Management of Renal Dysfunction in Extra Renal Transplants
2017 CST-Astellas Canadian Transplant Fellows Symposium Management of Renal Dysfunction in Extra Renal Transplants Jeffrey Schiff, MD Dr. Jeffrey Schiff is an Assistant Professor of Medicine at the University
More informationSegmental glomerulonephritis
M. S. DUNNILL AND P. R. MILLARD From the Gibson Laboratories, Radcliffe Infirmary, Oxford J. clin. Path., 1975, 28, 167-175 SYNOPSIS The renal biopsy findings in 40 patients with segmental glomerulonephritis
More informationClinical and pathological characteristics of patients with glomerular diseases at a university teaching hospital: 5-year prospective review
Clinical and pathological characteristics of patients with glomerular diseases at a university teaching hospital: 5-year prospective review KW Chan, TM Chan, IKP Cheng Objective. To examine the prevalence
More informationPathology of Complement Mediated Renal Disease
Pathology of Complement Mediated Renal Disease Mariam Priya Alexander, MD Associate Professor of Pathology GN Symposium Hong Kong Society of Nephrology July 8 th, 2017 2017 MFMER slide-1 The complement
More informationVASCULITIS. Case Presentation. Case Presentation
VASCULITIS Case Presentation The patient is a 24 year old woman who presented to the emergency room with left-sided weakness. She was confused and complained of a severe headache. She was noted to have
More informationCASE OF THE WEEK 1
www.nephro-pathology.com CASE OF THE WEEK 1 Clinical Presentation: A 17 year old Indian boy presented with anasarca, decreased urine output and episodes of nausea and vomiting over the last three weeks.
More informationJournal of Nephropathology
www.nephropathol.com DOI: 10.15171/jnp.2018.24 J Nephropathol. 2018;7(3):101-105 Journal of Nephropathology Relationship of CD147 kidney expression with various pathologic lesions, biochemical and demographic
More informationAlterations of Renal and Urinary Tract Function
Alterations of Renal and Urinary Tract Function Chapter 29 Urinary Tract Obstruction Urinary tract obstruction is an interference with the flow of urine at any site along the urinary tract The obstruction
More informationThe Banff 2015 Kidney Meeting Report: Current Challenges in Rejection Classification and Prospects for Adopting Molecular Pathology
The Banff 2015 Kidney Meeting Report: Current Challenges in Rejection Classification and Prospects for Adopting Molecular Pathology The Harvard community has made this article openly available. Please
More information