This document summarizes tubulointerstitial nephritis (TIN). It begins with questions about drug-induced acute TIN (ATIN). It then describes a case of suspected amoxicillin-induced ATIN in a 5-year old girl. The next question concerns management and follow-up of a boy with nonoliguric AKI and biopsy-proven severe interstitial inflammation treated with corticosteroids. The document goes on to define TIN and classify it as primary or secondary, acute or chronic. It discusses etiologies, pathophysiology, clinical features, investigations, treatment including corticosteroids, and prognosis of ATIN and chronic TIN. Specific conditions
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
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Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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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.
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
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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.
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
TIN.pptx
1. S L I D E 0
Tubulo-interstitial Nephritis
Ibrahim Sandokji
2. S L I D E 1
Questions
Which of the following is true regarding drug-induced ATIN?
a. ATIN secondary to NSAIDs can present as nephrotic syndrome.
b. The triad of fever, rash, and arthralgia is present in the majority
of patients with drug-induced ATIN.
c. Eosinophiluria is pathognomonic for ATIN.
d. Renal injury always develops soon after starting the offending
drug.
e. Drug-induced ATIN is dose-dependent.
3. S L I D E 2
Questions
A 5-year-old girl presents with fever, fatigue, and abdominal pain
and is admitted to the hospital because of AKI with a creatinine
value of 1.3. According to history obtained, she had been taking
amoxicillin for 4 days for strep throat. Her physical examination is
normal; her urinalysis reveals a specific gravity of 1.009, negative
findings for blood and protein, 10 to 20 white blood cells, and no
casts. You suspect ATIN secondary to amoxicillin. Which of the
following is the next best step in her management?
a. Schedule her for a renal biopsy.
b. Discontinue amoxicillin and follow creatinine trend.
c. Administer pulse corticosteroids followed by oral prednisone.
d. Check eosinophils in the urine, if negative, continue workup
looking for other causes of AKI.
e. Change amoxicillin to a cephalosporin.
4. S L I D E 3
Questions
A 10-year-old boy presents with nonoliguric AKI. He has a renal
biopsy performed that shows severe interstitial inflammation with
predominant mononuclear cell infiltrate and no granulomas;
immunofluorescence is negative. There is no history of medication
use or evidence of any viral or bacterial infection. The patient
receives corticosteroids and his renal function returns to normal.
Regarding further evaluation and follow-up, which of the following
is the most accurate statement?
a. He will need follow-up with a nephrologist for at least 1 year.
b. He can follow up with his primary care physician for yearly
checkups only and does not need specialty care.
c. He needs an ophthalmology evaluation now, in addition to
follow-up with a nephrologist.
d. He needs follow-up with a rheumatologist because of the
possibility of underlying autoimmune disease.
6. S L I D E 5
Definition and Classifications
• TIN is characterized by inflammatory infiltrate, edema, and fibrosis
affecting renal tubules and the interstitium.
Classification
Primary TIN
Inflammation starts in tubules & interstitium
Secondary TIN
Inflammation starts in glomeruli & vessels
The clinical spectrum of tubulointerstitial nephritis. Rastegar (1998) Kidney International
7. S L I D E 6
Classification
Clinicopathologically
Acute TIN
Acute inflammatory cell-
mediated
Rapid decline in renal
function
Chronic TIN
Protracted onset
Slow decline in renal
function
8. S L I D E 7
ATIN
• Epidemiology
– It accounts for 8% to 27% of the reported cases of acute kidney injury
(AKI) in adults and up to 7% in children
• Etiology
Singh AK, Colvin RB. N Engl J Med 2003;349:2055-2063.
9. S L I D E 8
Etiologic Classification of ATIN
Kher et al (2016). Clinical Pediatric Nephrology, 3rd Edition
10. S L I D E 9
Kher et al (2016). Clinical Pediatric Nephrology, 3rd Edition
Drugs-induced ATIN
• Most commonly
– Penicillins
– NSAIDs
– Rifampin
– Sulfonamide
11. S L I D E 10
Pathophysiology
Kher et al (2016). Clinical Pediatric Nephrology, 3rd Edition
12. S L I D E 11
Kher et al (2016). Clinical Pediatric Nephrology, 3rd Edition
13. S L I D E 12
Low power view of severe acute interstitial nephritis
showing diffuse interstitial inflammatory infiltrate
Inflammatory process predominantly in the interstitium.
Insert shows a higher magnification, with arrows
pointing to eosinophils in the interstitium
Pathology
14. S L I D E 13
Pathology
Light microscopy showing acute interstitial
inflammatory infiltrate consisting of mononuclear
cells in a patient with acute interstitial nephritis.
The patient presented with acute kidney injury
and proteinuria.
Inflammatory cell infiltration into +the tubules
resulting in tubulitis
Kher et al (2016). Clinical Pediatric Nephrology, 3rd Edition
16. S L I D E 15
Pathology
Granuloma in the renal interstitium in a patient
with sarcoidosis
Kher et al (2016). Clinical Pediatric
Nephrology
17. S L I D E 16
Pathology
Immunofluorescence
Classification
Pauciimmune
No antibodies or
immune deposits
Immune complex
deposits
Granular deposits
along the basement
membrane
Anti–TBM disease
Linear
immunofluorescence
staining for IgG and
complement along the
TBM
18. S L I D E 17
Pathology
• Immune complex deposits present along the basement membrane
Immunofluorescence microscopy showing intense staining of the
tubular basement membranes (TBMs) and Bowman capsule with
IgG in a finely granular pattern. The glomerular tufts (G) are
negative for immunofluorescence staining. Inset shows the TBMs
with finely granular staining pattern at 400x magnification.
19. S L I D E 18
Pathology
• Anti–tubular basement membrane disease
– Linear immunofluorescence staining for IgG and complement along the TBM
Immunofluorescence microscopy showing linear immunoglobulin
G deposits in a patient with acute interstitial nephritis
20. S L I D E 19
Clinical Features of ATIN
• Usually present with rise in sCr and non-specific symptoms
• Nausea, vomiting, malaise, back/flank pain, or asymptomatic
• Allergic-type symptoms like fevers, rash, peripheral eosinophilia
• 30% to 40% of patients with ATIN have nonoliguric AKI
• Classic triad of fever, arthralgia, and rash occurs only in <10%
• Tubular dysfunction and even Fanconi syndrome
• In drug-induced ATIN, renal manifestations develop on average 10
days after starting the medication; however, they can occur as early
as one day and as late as months after the inciting medication is
started
21. S L I D E 20
Laboratory Findings in ATIN
• Urinalysis
– Hematuria (micro/macro)
– Proteinuria (UPC usually <1)
– Sterile pyuria
– White blood cell casts
– Eosinophiluria
– Or bland urine
• Blood tests
– Increased creatinine
– Tubular defects
• Proximal: proximal RTA, Fanconi syndrome
• Distal: hyperkalemia, Na wasting, distal RTA
• Medullary: concentration defect
– Eosinophilia
– Increased ESR
22. S L I D E 21
• Urinary biomarkers:
– Monocyte chemotactic pep-tide-1 (MCP-1) might correlate with
interstitial edema and inflammatory infiltration
– N-acetyl-β-D-glucosaminidase (NAG) might correlate with more rapid
progression of renal dysfunction in patients with CTIN
– Ongoing studies for novel biomarkers
23. S L I D E 22
White Blood Cell Casts Red Blood Cell Casts
Hyaline Casts Muddy Brown Granular Casts
Waxy Casts
Fatty Casts
24. S L I D E 23
Eosinophiluria
• It is neither sensitive nor specific
• Seen only in ~20-60% of patients
• Present in UTIs, ATN and RPGN
Unstained urine sediment showing
leukocyturia (▴) with cellular casts (↑)
Hansel's stain of urine sediment showing both
free eosinophils (▴) and eosinophils in casts (↑)
25. S L I D E 24
Renal US in ATIN
Diffusely enlarged, echogenic kidney in a patient with acute interstitial nephritis. However, the appearances are
nonspecific and are similar to those seen in several other acute disorders of the renal parenchyma
26. S L I D E 25
Treatment
• Discontinuation of offending agent
• Supportive therapy
• Rarely might need a biopsy if:
– Unclear diagnosis
– When considering steroid therapy
– Or, if started steroids but no response in one week
27. S L I D E 26
Corticosteroids Therapy
• Corticosteroids are the mainstay of treatment
• Although
– No randomized, controlled, prospective studies
– Conflicting studies, some revealed no benefit with corticosteroids and
others showed improvement of serum creatinine and decreased need
for dialysis
• A retrospective study of 60 adults with ATIN with a variety of underlying
etiologies showed no difference in outcome when comparing treatment
with corticosteroids to supportive care alone when assessing serum
creatinine at 1, 6, and 12 months follow-up or dialysis independence
Clarkson et al, Nephrol Dial Transplant (2004)
28. S L I D E 27
Corticosteroids Therapy
– A prospective pediatric study showed that corticosteroids sped up
recovery of TIN (especially in patients with severe nephritis). But the
renal function did not differ significantly at 6-month follow-up.
– They suggested that because TIN may be self-limited, treatment may
be delayed by two weeks in uncomplicated cases
(a) Plasma creatinine (PCr) concentration and (b) urine low molecular weight (LMW) protein/creatinine
ratio at baseline and during follow-up visits in the non-treatment group (circles), in the low creatinine
group (squares), and in the high creatinine group (diamonds).
Jahnukainen et al, Pediatr Nephrol (2013)
29. S L I D E 28
Corticosteroids Therapy
• Corticosteroids use is primarily guided by underlying
pathophysiology and severity of kidney damage
– Drug-induced TIN with mild AKI may recover spontaneously, so a trial
of drug cessation can be done first
– Severe AKI or systemic rheumatologic and inflammatory conditions
associated with TIN are usually treated with corticosteroids
30. S L I D E 29
Mycophenolate mofetil (MMF)
• Mycophenolate mofetil (MMF) has been used in few case reports
and small studies when corticosteroids alone were not effective
– A retrospective study of eight adults with steroid-resistant, biopsy-
proven AIN, treated with MMF
– Mean decline in serum creatinine from 2.3 to 1.6 mg/dl over a mean of
24.3 mo of treatment.
Preddie et al. Clin J Am Soc Nephrol (2006)
31. S L I D E 30
Chronic TIN
• Slowly progressive
• Renal tubular atrophy and
interstitial fibrosis
• Thickened and wrinkled TBM
• Glomeruli often show ischemic
changes with shrinking of the
glomerular tuft and wrinkling of
the Bowman capsule
• Eventually, leading to small and
shrunken kidneys with prominent
parenchymal scarring and
pelvicalyceal dilatation.
Glomerulus in a patient with chronic tubulointerstitial
nephritis showing periglomerular fibrosis and ischemic
glomeruli with collapsed capillary lumens.
Kher et al (2016). Clinical Pediatric Nephrology, 3rd Edition
33. S L I D E 32
Clinical Features
• Asymptomatic proteinuria, or first presentation of CKD
• Nonspecific symptoms:
– Weight loss, growth failure, fatigue, anorexia, vomiting, and
polyuria/polydipsia
• Laboratory evaluation:
– Elevated serum creatinine
– Signs of tubular dysfunction
• Renal ultrasound
– Small, hyperechogenic kidneys
• A kidney biopsy is often needed to confirm the diagnosis
34. S L I D E 33
Treatment
• Discontinuation of offending agent
• Supportive therapy
• No evidence of corticosteroids or immunosuppressive therpaies
35. S L I D E 34
Tubulointerstitial Nephritis & Uveitis (TINU) syndrome
• The pathogenesis is unknown, but evidence suggests
– Autoantigen to modified C-reactive protein (mCRP)
– Delayed-type hypersensitivity
• Presentation
– Bilateral anterior uveitis (ocular pain, redness, photophobia, itching,
and visual impairment)
– Present before, simultaneous with, or up to several months after renal
disease
– Asymptomatic in ~50% of patients
• Laboratory findings
– Markedly elevated ESR +/- autoantibodies (ANA, RF & c-ANCA)
• Treatment
– Early referral to an ophthalmologist
– Uveitis requires topical or systemic corticosteroids
– Recurrences and relapses of uveitis are common
36. S L I D E 35
Questions
Which of the following is true regarding drug-induced ATIN?
a. ATIN secondary to NSAIDs can present as nephrotic syndrome.
b. The triad of fever, rash, and arthralgia is present in the majority
of patients with drug-induced ATIN.
c. Eosinophiluria is pathognomonic for ATIN.
d. Renal injury always develops soon after starting the offending
drug.
e. Drug-induced ATIN is dose-dependent.
37. S L I D E 36
Questions
A 5-year-old girl presents with fever, fatigue, and abdominal pain
and is admitted to the hospital because of AKI with a creatinine
value of 1.3. According to history obtained, she had been taking
amoxicillin for 4 days for strep throat. Her physical examination is
normal; her urinalysis reveals a specific gravity of 1.009, negative
findings for blood and protein, 10 to 20 white blood cells, and no
casts. You suspect ATIN secondary to amoxicillin. Which of the
following is the next best step in her management?
a. Schedule her for a renal biopsy.
b. Discontinue amoxicillin and follow creatinine trend.
c. Administer pulse corticosteroids followed by oral prednisone.
d. Check eosinophils in the urine, if negative, continue workup
looking for other causes of AKI.
e. Change amoxicillin to a cephalosporin.
38. S L I D E 37
Questions
A 10-year-old boy presents with nonoliguric AKI. He has a renal
biopsy performed that shows severe interstitial inflammation with
predominant mononuclear cell infiltrate and no granulomas;
immunofluorescence is negative. There is no history of medication
use or evidence of any viral or bacterial infection. The patient
receives corticosteroids and his renal function returns to normal.
Regarding further evaluation and follow-up, which of the following
is the most accurate statement?
a. He will need follow-up with a nephrologist for at least 1 year.
b. He can follow up with his primary care physician for yearly
checkups only and does not need specialty care.
c. He needs an ophthalmology evaluation now, in addition to
follow-up with a nephrologist.
d. He needs follow-up with a rheumatologist because of the
possibility of underlying autoimmune disease.
Mechanisms whereby a drug (or one of its metabolites) can induce acute interstitial nephritis. (a) The drug can bind to a normal component of the tubular basement membrane (TBM) and act as a hapten. (b) The drug can mimic an antigen normally present within the TBM or the interstitium and induce an immune response that will also be directed against this antigen. (c) The drug can bind to the TBM or deposit within the interstitium and act as a planted (“trapped”) antigen. (d) The drug can elicit the production of antibodies and become deposited in the interstitium as circulating immune complexes.
Hapten is a small molecule that, when combined with a larger carrier such as a protein, can elicit the production of antibodies that bind specifically to it (in the free or combined state)
3M-1 (TIN antigen) is the antigen of anti-TBM disease and has been characterized and mapped to chromosome 6 in humans. TIN antigen is defective in kidney tissues of patients with juvenile nephronophthisis. Genetic deletion of the TIN antigen gene has been identified to cause TIN resulting in CKD.
Tamm-Horsfall protein (uromodulin) may be an inciting antigen, especially following lower tract obstruction.
Tamm-Horsfall protein (Uromodulin) is a tubular glycoprotein normally secreted by the thick ascending limb of loop of Henle and forms the matrix of the urinary casts