A 15-year-old male presented with back pain and malaise after taking ibuprofen and naproxen the previous week. His serum creatinine was elevated at 3.6 mg/dL. The most likely urinalysis finding would be bland urine with trace protein, as nonsteroidal anti-inflammatory drugs (NSAIDs) can cause acute kidney injury through mechanisms such as acute tubular necrosis or acute interstitial nephritis, presenting as a non-oliguric elevation in creatinine with a bland or minimally abnormal urinalysis.
Detailed mechanisms of certain antimicrobials that cause renal failure
ANTIMICROBIALS CAUSING RENAL FAILURE
Aminoglycosides
Amphotericin – B
Trimethoprim
B – lactam antibiotics
Fluoroquinolones
Vancomycin
Acyclovir
Tetracycline
Many medicines can cause acute kidney injury (which used to be called acute renal failure), such as:
Antibiotics. These include aminoglycosides, cephalosporins, amphotericin B, bacitracin, and vancomycin.
Antihypertensive: ACE inhibitors, such as lisinopril and ramipril; Angiotensin receptor blockers, such as candesartan and valsartan.
Anticancer drugs (chemotherapy): Examples are cisplatin, carboplatin, and methotrexate.
Dyes (contrast media):These are used in medical imaging tests.
Illegal drugs: Examples are heroin and methamphetamine.
Antiviral drugs: Examples are indinavir and ritonavir, acyclovir
Non-steroidal anti-inflammatory drugs: These include ibuprofen, ketoprofen, and naproxen.
Anti Ulcer medicines: One example is cimetidine.
Drug-induced kidney disease or nephrotoxicity (DIN) is a relatively common complication of several diagnostic and therapeutic agents.
Any drug in the blood will eventually reach the highly vascularized kidneys
It may potentially cause drug induced renal failure
If the drug is primarily cleared by the kidney, the drug will become increasingly concentrated as it moves from the renal artery into the smaller vasculature of the kidney
The drug may be filtered or secreted into the lumen of the renal tubules
The concentrated drug exposes the kidney tissue to far greater drug concentration per surface area
Detailed mechanisms of certain antimicrobials that cause renal failure
ANTIMICROBIALS CAUSING RENAL FAILURE
Aminoglycosides
Amphotericin – B
Trimethoprim
B – lactam antibiotics
Fluoroquinolones
Vancomycin
Acyclovir
Tetracycline
Many medicines can cause acute kidney injury (which used to be called acute renal failure), such as:
Antibiotics. These include aminoglycosides, cephalosporins, amphotericin B, bacitracin, and vancomycin.
Antihypertensive: ACE inhibitors, such as lisinopril and ramipril; Angiotensin receptor blockers, such as candesartan and valsartan.
Anticancer drugs (chemotherapy): Examples are cisplatin, carboplatin, and methotrexate.
Dyes (contrast media):These are used in medical imaging tests.
Illegal drugs: Examples are heroin and methamphetamine.
Antiviral drugs: Examples are indinavir and ritonavir, acyclovir
Non-steroidal anti-inflammatory drugs: These include ibuprofen, ketoprofen, and naproxen.
Anti Ulcer medicines: One example is cimetidine.
Drug-induced kidney disease or nephrotoxicity (DIN) is a relatively common complication of several diagnostic and therapeutic agents.
Any drug in the blood will eventually reach the highly vascularized kidneys
It may potentially cause drug induced renal failure
If the drug is primarily cleared by the kidney, the drug will become increasingly concentrated as it moves from the renal artery into the smaller vasculature of the kidney
The drug may be filtered or secreted into the lumen of the renal tubules
The concentrated drug exposes the kidney tissue to far greater drug concentration per surface area
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Nephrotoxins.pptx
1. S L I D E 0
Nephrotoxins and drug interactions
Ibrahim Sandokji
2. S L I D E 1
15 y/o male presents with back pain and malaise. He took
ibuprofen and naproxen last week. No fever. Normal urine
output. Normal BPs. No edema. Serum creatinine 3.6
mg/dL.
The most likely finding on urinalysis would be:
a) 1+ heme, 1+ LE, >100 WBC/hpf
b) Bland urine with trace protein
c) Dysmorphic RBCs, RBC casts, heavy protein
d) Muddy brown casts, debris
3. S L I D E 2
ABP Content Specifications
• Nephrotoxins and drug interactions:
– Know common nephrotoxins, their mechanisms of
nephrotoxicity, and their clinical manifestations
– Know the natural history of kidney injury caused by
common nephrotoxins
– Recognize drugs that potentiate nephrotoxicity
– Know the management of different types of
nephrotoxicity
• Nephrotoxic Injury Negated by Just-in-time Action (NINJA)
4. S L I D E 3
Kidney Vulnerability
• Final pathways for xenobiotics excretion (particularly, hydrophilic
drugs)
• Proximal tubular cells possess specific secretory pathways -> high
concentrations during transcellular transport -> cytotoxicity
• Large amount of energy consumption. Alterations of blood supply -
> profound cellular damage
• Large amount of oxygen requirement -> high susceptibility to
oxidative stress
• Several medications alter renal hemodynamics -> ischemic damage
• Some drugs are highly concentrated in the tubular lumen and can
crystallize -> obstructive nephropathy
5. S L I D E 4
Natural History of Nephrotoxic-induced AKI
• Usually non-oliguric AKI
• Typically dose-dependent (except AIN which is
idiosyncratic) and more likely to occur with
nephrotoxin combinations
• Urinalysis is often bland
• Might see WBCs & possibly eosinophils in the
urine
• Recovery after removing offending agent(s)
7. S L I D E 6
Acyclovir
• Nephrotoxicity can be seen in 17–35% of children receiving IV
acyclovir. (Rao 2015)
Mechanism of toxicity:
• Rapidly excreted in the urine (both filtered and secreted)
• Crystallization in tubular lumen -> obstructive nephropathy
• Direct tubular toxicity
• Transported by shared organic acid transporters with certain beta-
lactam antibiotics (particularly ceftriaxone) -> increase
nephrotoxicity risk
8. S L I D E 7
Acyclovir
• Prevention of nephrotoxicity:
– Optimize hydration
– Administer over 1–2 hours
– Adjust dose if decreased renal function
– Avoid concurrent nephrotoxic medication exposure
9. S L I D E 8
Amphotericin B
• AKI occurs in 49–65% of adult receiving amphotericin B
Mechanism of toxicity:
• Direct distal tubular toxicity: affect ergosterol in the epithelial cell
membrane -> forms pores in the epithelial cell membrane
• Renal vasoconstriction
• Increased tubular membrane permeability lead to hypokalemia,
hyponatremia, acidosis & hypomagnesemia
• Risk factors:
– Cumulative dose
– Treatment duration
– Dosing schedule
– Dehydration
– Concomitant diuretics or other nephrotoxic drugs
– Impaired glomerular filtration at baseline
10. S L I D E 9
Amphotericin B
• Lipid formulations of amphotericin B (liposomal, lipid complex,
colloidal dispersion):
• A European multicenter prospective open-label study with 134
adults and 204 children with fever and neutropenia compared the
use of liposomal and conventional amphotericin B:
– Similar efficacy, defined as resolution of fever in 3 consecutive days &
recovery of neutrophils
– Nephrotoxicity (doubling of baseline creatinine) occurred in 3% of
liposomal amphotericin, compared to 23% of conventional
amphotericin B group (P<0.01)
– Time to develop nephrotoxicity was longer in liposomal amphotericin
than amphotericin B (P<0.01) and severe hypokalaemia was observed
less frequently in liposomal amphotericin (P<0.01)
Prentice 1997
11. S L I D E 10
Aminoglycosides
Mechanism of toxicity:
• In the kidney, aminoglycosides exclusively accumulate in proximal
tubular cells via endocytic pathways -> transported to the
endosomal compartment -> accumulates in the lysosomes ->
secretory pathway to the Golgi apparatus and ER
• ER stress: disruption of normal protein folding -> accumulation of
misfolded and unfolded proteins induces their aggregation and
subsequent cytotoxicity -> acute tubular necrosis
• Destabilize intracellular membranes -> redistribution of the drug
throughout the cytosol -> acts on the mitochondria -> induce
apoptosis
• In the lysosomes, aminoglycosides bind to phospholipids ->
inhibition of phospholipase activity -> phospholipid accumulation -
> tubular cell death
12. S L I D E 11
Aminoglycosides
• Factors associated with increased risk of nephrotoxicity:
– Drug dosage
– Duration of administration
– Dosing interval
– Preexisting renal disease
– Dehydration
– Hepatic dysfunction
– Sepsis
– Concomitant nephrotoxic and diuretic drugs Patzer (2008)
• Cochrane review of 13 RCT showed:
• Once- and three-times-daily equally effective in CF pulmonary
exacerbations
• The percentage change in creatinine significantly favoured once-
daily treatment in children, MD -8.20 (95% CI -15.32 to -1.08), but
showed no difference in adults, MD 3.25 (95% CI -1.82 to 8.33).
Smyth AR (2010)
13. S L I D E 12
Vancomycin
• Nephrotoxicity occurs in 12–43% of adults treated with
vancomycin. (Rybak 2009)
Mechanism of toxicity:
• Proximal renal tubular cells are the main nephron segment
impaired by vancomycin
• Energy-dependent transport of vancomycin from the blood to the
proximal tubular cells across the basolateral membrane
• Exposure to high doses over long time -> oxidative stress and
mitochondrial damage
14. S L I D E 13
Vancomycin
• Factors associated with increased risk of nephrotoxicity:
– Drug dosage
– Duration of administration
– Preexisting renal disease Patzer (2008)
– Critical illness
– Concomitant nephrotoxic
• A retrospective chart review in NICU
• AKI occurred in 2.7% of patients
(increase in SCr of at least 0.5 mg/L
or an increase of at least 100% from
lowest trough previously available)
Bhargava (2017)
Fit plot between vancomycin trough concentrations and post vancomycin creatinine.
The plot depicts a positive co-relation between the two parameters
15. S L I D E 14
Calcineurin Inhibitor (Cyclosporin A)
• Acute toxicity (reversible):
– Afferent arteriolar vasospasm
– Renal hypoperfusion and decreased GFR
– Reversible with decrease the dose or discontinuation
• Tubular toxic effects:
Renal cell apoptotic mechanisms of CyA-induced
16. S L I D E 15
Calcineurin Inhibitor (Cyclosporin A)
• CNI Nephropathy:
– Proximal tubular injury -> tubular atrophy
– Diffuse interstitial fibrosis or striped interstitial fibrosis
– Arteriopathy: constrictive proliferation with mucoid thickening
and arterial hyalinosis
17. S L I D E 16
CNI Nephropathy
(a) proximal tubular epithelial cell showing the fine isometric vacuoles; (b) typical striped fibrosis pattern (c) an afferent
arteriole showing the characteristic nodular hyaline arteriosclerosis; (d) similar nodule in a non-afferent arteriole
18. S L I D E 17
Calcineurin Inhibitor
• Tacrolimus
– Similar side effect profile
– Less cosmetic effects
• Gingival hyperplasia
• Hirsutism
– Less hyperlipidemia
• In a Prospective study of 41 patients divided
• Hirsutismus and gingival hyperplasia were seen in 10%, and 15% of
CsA group, while it wasn’t observed at all in the Tac group
• No difference in nephrotoxicity or hepatotoxicity
(Ozan 2013)
20. S L I D E 19
NSAIDs
Medical Pharmacology, TMWeb, Tulane University
21. S L I D E 20
NSAIDs
• Case series of 7 children aged 13–17.5 years developed AKI after
treatment with various NSAIDs
– (6/7) used more than one kind of NSAID
– 1 to 4 days between NSAID use and symptoms
– Flank pain (4/7), abdominal pain (3/7), and vomiting (3/7)
– All patients had nonoliguric AKI
– Microscopic hematuria and proteinuria (5/7) patients
– Biopsy done in three patients:
• Mild interstitial inflammation in one patient
• Normal in two patients
– All patients were treated with intravenous fluids
• One patient received corticosteroids
– Renal function was completely normalized in all patients within 7–16
days
Krause 2005
22. S L I D E 21
Acute Interstitial Nephritis
• 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
• UA: WBC casts, hematuria, mild proteinuria, or bland urine
• Non-Oliguria AKI, tubular dysfunction and even Fanconi syndrome
• Treatment:
– Discontinuation of offending agent
– Rarely might need a biopsy if:
• Unclear diagnosis
• When considering steroid therapy
• Or, if started steroids but no response in one week
23. S L I D E 22
Singh AK, Colvin RB. N Engl J Med 2003;349:2055-2063.
Acute Interstitial Nephritis
24. S L I D E 23
White Blood Cell Casts Red Blood Cell Casts
Hyaline Casts Muddy Brown Granular Casts
Waxy Casts
Fatty Casts
25. S L I D E 24
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
26. S L I D E 25
Nephrotoxic Injury Negated by Just-in-time Action (NINJA)
• Automated system using EHR data in patients with 3+ nephrotoxic
medications or 3+ days of IV aminoglycoside exposure
27. S L I D E 26
• 1,749 patients with 2,358 admissions were included. 575 individual
AKI episodes were observed (47% stage 1, 33% stage 2, and 20%
stage 3)
• Nephrotoxic medication exposure rate decreased by 38% (from
11.63 to 7.24 patients/1000 patient days)
Nephrotoxic Injury Negated by Just-in-time Action (NINJA)
28. S L I D E 27
• AKI rates decreased by 64% (from 2.96 to 1.06 patients with
AKI/1000 patient days) during the study period.
Nephrotoxic Injury Negated by Just-in-time Action (NINJA)
29. S L I D E 28
15 y/o male presents with back pain and malaise. He took
ibuprofen and naproxen last week. No fever. Normal urine
output. Normal BPs. No edema. Serum creatinine 3.6
mg/dL.
The most likely finding on urinalysis would be:
a) 1+ heme, 1+ LE, >100 WBC/hpf
b) Bland urine with trace protein
c) Dysmorphic RBCs, RBC casts, heavy protein
d) Muddy brown casts, debris
31. S L I D E 30
References
• Avner, et al. Pediatric Nephrology. 2016
• Bhargava, et al. The association between vancomycin trough concentrations and acute kidney injury in
the neonatal intensive care unit. BMC Pediatr. 2017 Feb 11;17(1):50.
• Ekmekçioğlu, et al. Comparison of tacrolimus with a cyclosporine microemulsion for
immunosuppressive therapy in kidney transplantation. Turkish journal of urology. 2013;39(1):16-21.
• Goldstein SL, Mottes T, Simpson K, Barclay C, Muething S, Haslam DB, Kirkendall ES. A sustained
quality improvement program reduces nephrotoxic medication-associated acute kidney injury. Kidney
Int. 2016 Jul;90(1):212-21
• Krause, et al. Acute renal failure, associated with non-steroidal anti-inflammatory drugs in healthy
children. Pediatr Nephrol. 2005 Sep;20(9):1295-8.
• Patzer L. Nephrotoxicity as a cause of acute kidney injury in children. Pediatr Nephrol.
2008;23(12):2159–73.
• Prentice, et al. A randomized comparison of liposomal versus conventional amphotericin B for the
treatment of pyrexia of unknown origin in neutropenic patients. Br J Haematol. 1997;98: 711–718
• Rao, et al. Intravenous acyclovir and renal dysfunction in children: a matched case control study. J
Pediatr. 2015 Jun;166(6):1462-8.
• Rybak, et al. Therapeutic monitoring of vancomycin in adult patients: a consensus review of the
American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the
Society of Infectious Diseases Pharmacists. Am J Health Syst Pharm. 2009;66(1):82–98.
• Smyth, et al. Once-daily versus multiple-daily dosing with intravenous aminoglycosides for cystic
fibrosis. Cochrane Database Syst Rev. 2014;2.
• Uijtendaal, et al. Once-daily versus multiple-daily gentamicin in infants and children. Ther Drug Monit.
2001;23 (5):506–13.
• Vandecasteele, et al. Recent changes in vancomycin use in renal failure. Kidney Int. 2010;77(9):760–4.