This document provides an introduction to renal allograft pathology. It discusses the key topics of harvest injury, rejection including hyperacute, acute T-cell mediated, acute antibody-mediated and chronic rejection. It also covers infections, drug toxicity, and recurrence or new disease that can occur in transplant kidneys. The goal is for students to recognize pathology related to rejection, infections, toxicity and disease processes in renal allografts.
Antibody mediated rejection of solid organ allograftstashagarwal
Objectives:
Introduction of Antibody mediated rejection AMR
Role of C4d in transplant rejection
Donor specific antibodies DSA
Presentation of AMR in kidney, liver, lung and heart.
Plasma cell disorders is a difficult topic where most residents and students confuse with regarding to differentiating between various types of para-proteinemias or plasma cell dyscrasias. This simple presentation will highlight the key points in differentiating, diagnosing these orders. Initial management principles are discussed as well.
Renal Transplantation and Patients managementsachintutor
A kidney transplant is a surgery done to replace a diseased kidney with a healthy kidney from a donor. The kidney may come from a deceased organ donor or from a living donor. Family members or others who are a good match may be able to donate one of their kidneys. This type of transplant is called a living transplant.
Antibody mediated rejection of solid organ allograftstashagarwal
Objectives:
Introduction of Antibody mediated rejection AMR
Role of C4d in transplant rejection
Donor specific antibodies DSA
Presentation of AMR in kidney, liver, lung and heart.
Plasma cell disorders is a difficult topic where most residents and students confuse with regarding to differentiating between various types of para-proteinemias or plasma cell dyscrasias. This simple presentation will highlight the key points in differentiating, diagnosing these orders. Initial management principles are discussed as well.
Renal Transplantation and Patients managementsachintutor
A kidney transplant is a surgery done to replace a diseased kidney with a healthy kidney from a donor. The kidney may come from a deceased organ donor or from a living donor. Family members or others who are a good match may be able to donate one of their kidneys. This type of transplant is called a living transplant.
Basics of kidney_transplant and donor_recepient evaluationJosephN7
This contains basic information on kidney transplant, benefits of transplant , donor_recepient evaluation, immunosuppressive drugs and risk factors
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Pathology of Ectopic pregnancy, spontaneous abortion and gestational trophobl...Sufia Husain
DISORDERS OF PREGNANCY AND PLACENTA.
Pathology of ECTOPIC PREGNANCY, SPONTANEOUS ABORTION AND GESTATIONAL TROPHOBLASTIC DISEASE for medical and health care students
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
1. Introduction to Renal Allograft PathologyAPRIL 2020
REFERENCE: ROBBINS & COTRAN PATHOLOGY AND RUBIN’S PATHOLOGY
SUFIA HUSAIN
ASSOCIATE PROFESSOR
PATHOLOGY DEPARTMENT
COLLEGE OF MEDICINE
KSU, RIYADH
2. Objectives:
• At the end of the lecture the students will be able to:
• Recognize the concept of renal allograft.
• Describe the pathology of rejection and differentiate acute cell-mediated and antibody-mediated rejection.
• Differentiate between acute and chronic rejection.
• Recognize the pathology of the principal infections inherent to renal transplantation.
• Recognize the pathology of acute and chronic drug toxicity.
Key Outlines:
• Acute T-cell mediated rejection.
• Acute antibody-mediated rejection.
• Pathology of chronic rejection.
• Pathology of the principal infections of the renal allograft.
• Pathology of acute and chronic drug toxicity.
3. Lecture outline
Pathology of injury in kidney transplant
• Harvest injury
• Rejection: hyper-acute rejection, acute rejection (T-cell mediated and antibody
mediated) and chronic rejection
• Infections in the renal allograft.
• Drug toxicity, acute and chronic.
• Recurrence of primary disease
• De-novo (new) disease
4. Kidney transplant:
• End-stage renal disease (resulting from any cause) is treated by renal replacement therapy (e.g.
hemofiltration, hemodialysis, peritoneal dialysis) or renal transplant.
• Kidney transplantation is now a routine procedure in most large hospitals in the world.
• The first kidney transplant between humans was conducted in 1933 by a Russian surgeon in Ukraine.
The kidney was implanted in the groin under local anesthesia and the host survived four days.
• The patient who donates the kidney is called as the “donor”.
• The patient who receives the “new” transplant kidney is called as the “recipient”.
• The transplanted (“new”) kidney is called “donor kidney”, “allograft” or “graft”.
• The antigens present in the allograft kidney are called “alloantigens”.
• The antibodies that are against alloantigens (that target the alloantigens) are anti-allograft antibodies
and they are called “alloantibodies”.
5. Kidney transplant
• The donor kidney is placed in the recipients
iliac fossa or groin region. The donor ureter is
inserted into the bladder. The blood vessels
are anastomosed.
• The donor of the kidney can be from a living
or a deceased person.
6. Pathology of injury in kidney transplant
• Harvest injury
• Rejection: hyper-acute rejection, acute rejection (T-cell mediated and
antibody mediated) and chronic rejection
• Infections in the renal allograft.
• Drug toxicity, acute and chronic.
• Recurrence of primary disease
• De-novo (new) disease
8. HARVEST INJURY
• At the time of transplant there can be tubular injury to the transplanted
allograft kidney.
• It is generally due to cold ischemia time or the mode of death of the donor.
• It can lead to non-functioning kidney immediately after transplant (the
patient develops anuria).
• The good thing is that harvest kidney usually recover with appropriate
management.
9. Pathology of injury in kidney transplant
• Harvest injury
• Rejection: hyper-acute rejection, acute rejection (T-cell mediated and
antibody mediated) and chronic rejection
• Infections in the renal allograft.
• Drug toxicity, acute and chronic.
• Recurrence of primary disease
• De-novo (new) disease
11. REJECTION
Rejection is a major complication seen post-transplantation.
Transplant rejection occurs when transplanted tissue is rejected by the recipient's immune system
and the recipient's immune system destroys the transplanted tissue.
There are different types of rejection:
a) Hyper-acute rejection
b) Acute rejection
acute T-cell mediated rejection
and acute antibody-mediated rejection.
c) Chronic rejection
chronic T-cell mediated rejection
and chronic antibody-mediated rejection.
Rejection has been classified by a system called as the Banff Classification
12. a) HYPERACUTE REJECTION
• Rare
• It is rejection of the allograft occurring immediately after
implantation and perfusion of graft.
• Occurs within minutes to hours after transplantation.
Gross
• Cyanosis of graft minutes to hours after perfusion
• Graft becomes swollen, hemorrhagic, and necrotic
Microscopic
• Vasculitis, thrombosis, fibrinoid necrosis of blood vessels
• Thrombi in glomeruli
• Interstitial edema and hemorrhage
• Infarct of the kidney (coagulative necrosis) and loss of graft.
https://tpis.upmc.com/tpis/images/H00021k.jpg
13. b) ACUTE REJECTION
• Acute Rejection is the most common type of rejection in the newly transplanted
kidney patient. It can occur within days or the first few months after surgery.
Sometimes it can occur after years.
• 2 types
• Acute T-cell mediated rejection/ acute cellular rejection.
• Acute antibody-mediated rejection.
14. b) ACUTE REJECTION
Acute T-cell mediated rejection (acute TCMR)
• It is a common form of rejection. It is an acute immune reaction by the recipient against
the antigens present in the allograft (called alloantigens). It is mediated by T cells.
• Classically it develops in the first 3 months after transplantation, but may erupt at any time,
even after many years.
• Clinically there is loss of graft function and it presents as rising creatinine.
• In acute TCMR there is infiltration of allograft by lymphocytes (mainly T-cells) and other
inflammatory cells. The inflammation is primarily in the tubules (tubulitis) and the
interstitium (together called tubulointerstitial inflammation) and may also involve the
arteries called vasculitis/arteritis (+/- fibrinoid necrosis of arteries).
• Acute TCMR responds well to immunosuppressive drug therapy.
15. b) ACUTE REJECTION
Acute T-cell mediated rejection.
MICROSCOPY
1. Tubulointerstitial inflammation with or without arteritis
2. Interstitial edema and sometimes hemorrhage
Note: glomerular usually not involved
https://pathology.uic.edu/assets/1/6/c4d_web.png
Pathology of Renal Transplantation by Javed I. Kazi and Muhammed Mubarak from
Topics in Renal Biopsy and Pathology. April 2012. DOI: 10.5772/39182. Source: InTech
18. A) ACUTE REJECTION
Acute antibody-mediated rejection (acute ABMR)
• Also called as acute humoral rejection.
• It is an acute antibody mediated immune reaction.
• It is mediated by the anti-allograft antibodies (alloantibodies) called donor
specific antibodies (DSA).
• In it the recipient already has preformed (i.e. present before transplantation)
circulating anti-donor specific antibodies (DSA). These antibodies are directed
against the endothelial cells in the allograft kidney they attack the allograft
endothelial cells in the blood vessels (esp. the endothelial cells of the glomeruli
and peritubular capillaries) resulting in rejection.
• The microvasculature of the kidney (i.e. glomeruli and peritubular capillaries) is
the main target.
• Clinically there is loss of graft function presenting as rising creatinine.
19. Acute rejection
Acute antibody-mediated rejection (acute ABMR)
• Microscopy:
Glomerulitis, capillaritis of the peritubular
capillaries (peritubular capillaritis).
Positive C4d immunostain in the peritubular
capillaries.
Acute tubular injury/ necrosis.
Arteritis +/- fibrinoid necrosis.
Acute thrombotic microangiopathy like picture
NOTE: arteritis/ vasculitis can be seen in both acute TCMR
and acute ABMR.
Glomerulitis & peritubular capillaritis
20. c) CHRONIC REJECTION
• Chronic rejection is the type of rejection that happens over an extended period of time and can eventually
lead to loss of the graft.
• Usually occurs after the first year of transplantation.
• Persistent or recurrent episodes of TCMR or ABMR lead to chronic changes in allograft chronic
rejection (chronic TCMR and chronic ABMR) end stage allograft kidney (graft loss).
• Clinically: gradual rise in serum creatinine. Patients presents with chronic graft dysfunction/ chronic renal
failure, proteinuria and hypertension.
• It does not respond to immunosuppressive therapy.
• Additional information Microscopy can show any or all of the following
Tubulitis and tubular atrophy.
Interstitial inflammation and fibrosis.
Arteries show intimal fibrosis with chronic inflammation called chronic transplant arteriopathy.
Glomeruli: global or focal segmental glomerulosclerosis
Chronic ABMR also shows a unique type of glomerular injury called transplant glomerulopathy.
21. Pathology of injury in kidney transplant
• Harvest injury
• Rejection: hyper-acute rejection, acute rejection (T-cell mediated and
antibody mediated) and chronic rejection
• Infections of the renal allograft.
• Drug toxicity, acute and chronic.
• Recurrence of primary disease
• De-novo (new) disease
23. INFECTIONS OF THE RENAL ALLOGRAFT
• The patients who are recipients of allograft kidney are given various immunosuppressive
drugs and are therefore immunosuppressed (immunocompromised). This makes such
patients predisposed to various renal infections like Polyomavirus (SV40 virus),
Adenovirus, Cytomegalovirus and Epstein–Barr virus (EBV).
• They primarily infect the tubules and cause tubulointerstitial inflammation and acute
tubular injury. The infected tubular epithelial cells show viral nuclear changes.
• Theses infections can lead to graft loss.
• Infection with EBV can also lead to post transplant lymphoproliferative disorder (PTLD).
24. Renal tubules showing Polyomavirus infection in
allograft kidney (arrows)
By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=17821564
25. Pathology of injury in kidney transplant
• Harvest injury
• Rejection: hyper-acute rejection, acute rejection (T-cell mediated and
antibody mediated) and chronic rejection
• Infections of the renal allograft.
• Drug toxicity, acute and chronic.
• Recurrence of primary disease
• De-novo (new) disease
27. Drug toxicity
• Calcineurin inhibitors (CNIs) are immunosuppressive drugs given to the recipients in order to
decrease the recipients immune system's response to the transplanted kidney and therefore
help suppress acute rejection.
• Examples of CNI drugs: cyclosporine and tacrolimus
• The problem is that CNIs are also nephrotoxic and can cause acute or chronic damage to the
graft. They can cause acute CNI toxicity and chronic CNI toxicity in the kidney
• Blood tests show:
Rising serum creatinine,
Elevated levels of CNI in blood
29. Pathology of injury in kidney transplant
• Harvest injury
• Rejection: hyper-acute rejection, acute rejection (T-cell mediated and
antibody mediated) and chronic rejection
• Infections of the renal allograft.
• Drug toxicity, acute and chronic.
• Recurrence of primary disease
• De-novo (new) disease
31. RECURRENT & DE-NOVO DISEASE
5) RECURRENCE OF PRIMARY DISEASE
• The primary disease which
lead to end stage kidney
and eventual transplant can
recur as early as 6 months
post-transplant.
6) DE-NOVO (NEW) DISEASE/
GLOMERULONEPHRITIS
• It is the development of
another kidney disease in the
renal allograft, different from
the disease the patient
originally suffered from.
• It is rare.
Occurs within minutes to hours after transplantation in a pre-sensitized host (i.e. a preformed anti-donor antibody is already present in the recipient’s circulation and it is directed against some antigen that is present on the donor kidney). It leads to blood vessel damage, vasculitis, arterial thrombosis, fibrinoid necrosis of the blood vessel, hemorrhage, odema, infarct of the kidney (coagulative necrosis) and loss of graft.
These preformed antibodies that react against donor antigens, develop during a prior exposure of the recipient to donor derived antigens in connection with a blood transfusion, pregnancy or abortion.
HLA and endothelium associated ABO blood group antigens of the donor are the usual target for antibody mediated rejection. Immune reactions mediated by antibodies to the ABO blood group system have now become uncommon and are usually the result of technical errors.
Hyperacute rejection causes immediate and complete failure of the newly transplanted kidney. Prevention for this type of rejection is careful analysis of the match between the donor and the recipient.
Clinically: no urine output.
Grossly: kidney is cyanotic. The capsule bulges out due to marked edema and rupture of the graft may occur. Necrosis.
LM: acute arteritis and arteriolitis with fibrionoid necrosis of the vessels, thrombosis and ischemic/coagulative necrosis of renal parenchyma.
Clinical: rising serum creatinine over a few days, folllowed by signs of renal failure. Fever and graft tenderness +/-.
Gross: variable
LM: T-lymphocytes are the principal agents of acute cellular rejection. They travel to and recognize the allograft. In the allograft (new transplanted kidney) they infiltrate and damage the tubules (called as tubulitis) and the interstitium. The damage can be mild, moderate or severe depending on the extent of tubulitis and T-cell infiltration in the interstitium. This extent has been classified by Banff classification into grade I (A and B), grade II (A and B) and grade III.
Clinical: rising serum creatinine over a few days, folllowed by signs of renal failure. Fever and graft tenderness +/-.
Gross: variable
LM: T-lymphocytes are the principal agents of acute cellular rejection. They travel to and recognize the allograft. In the allograft (new transplanted kidney) they infiltrate and damage the tubules (called as tubulitis) and the interstitium. The damage can be mild, moderate or severe depending on the extent of tubulitis and T-cell infiltration in the interstitium. This extent has been classified by Banff classification into grade I (A and B), grade II (A and B) and grade III.