This document discusses various medication-induced kidney injuries. It covers:
1. Risk factors for drug nephrotoxicity including patient factors like age, sex, CKD/AKI status.
2. Pathophysiology of drug nephrotoxicity including how single drugs can affect different kidney sites and how multiple drugs can affect the same site.
3. Classification of drug-induced kidney injury including prerenal AKI, acute tubular necrosis, acute/chronic interstitial nephritis, glomerular disease, and obstructive nephropathy.
4. Specific nephrotoxic drugs that can cause the different types of injury through various mechanisms are discussed along with
DILI is possible consequence of ingestion of OTC drugs like PCM.
so it require careful clinical knowledge before taking drugs without doctors prescriptions...
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
DILI is possible consequence of ingestion of OTC drugs like PCM.
so it require careful clinical knowledge before taking drugs without doctors prescriptions...
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
hepatorenal syndrome is a one of the complication of cirrhosis of liver. It causes hepatic decompensation of liver. It has high risk of mortality. HRS has two types and type 1 usually present as a acute kidney injury. so, at first HRS should exclude from AKI. HRS type 2 present as a refractory ascites. As this has worst prognosis, only valuable management is liver transplantation.
hepatorenal syndrome is a one of the complication of cirrhosis of liver. It causes hepatic decompensation of liver. It has high risk of mortality. HRS has two types and type 1 usually present as a acute kidney injury. so, at first HRS should exclude from AKI. HRS type 2 present as a refractory ascites. As this has worst prognosis, only valuable management is liver transplantation.
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
In this presentation i have tried to thoroughly discuss about the concept of Drug induced kidney disease or injury, the mechanism behind it, its classification and how to access it.
The kidney maintains the vital functions of clearing excess body fluid and removing metabolic and exogenous toxins from the blood
The kidney is particularly vulnerable to drugs and other agents that cause renal damage
The heart pumps approximately 25% of cardiac output into the kidneys
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
Drug-induced kidney disease or nephrotoxicity (DIN) is a relatively common complication of several diagnostic and therapeutic agents.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- 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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
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!
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
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.
Follow us on: Pinterest
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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
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
3. Introduction
Medications are a common cause of kidney injury .
The medication history is an absolutely fundamental component of renal
medicine.
Consideration should be given when any drug prescribed for patient with
renal insufficiency .
4. Risk factors for drug nephrotoxicity
The innate kidney
toxicity of the offending
agent.
Drug factorsKidney factors Patient factors
Old age
Female sex
CKD
AKI
High renal blood flow,
which approximates 25% of
cardiac output, exposes the
kidney to significant drug
conc
Insoluble drug and/or
metabolite with
intratubular crystal
Precipitation
Combination between
nephrotoxic drugs
Volume depletion:
Vomiting, diarrhea, poor
fluid intake, fever,
diuretic use, or effective
volume depletion (CHF,
liver disease with ascites)
Immune response genes
increasing allergic drug
response
Biotransformation of drugs
to nephrotoxic metabolites
and reactive oxygen species
(aminoglycoside –platinum )
Extensive tubular cell
uptake of potential
nephrotoxic drugs via
transport systems
5. Pathophysiology of drug-induced nephropathy
Multiple drugs can affect the same site, e.g. acute tubular necrosis, can be
caused by aminoglycosides and amphotercin B
dyes and many other drugsA single drug can affect different sites in the kidney, e.g. NSAIDs can cause
interstitial nephritis ,glomeruloral disease and prerenal azotemia
6. Classification of drug induced kidney
Injury
Therapeutic agents associated with kidney injury can be classified based
on the category of the agent or the clinical kidney syndrome .
2-Acute
3-Acute
1-Prerenal/
functional
2-Acute
tubular
necrosis
(ATN )
3-Acute
interstitial
nephritis
(AIN )
5-
Glomerular
Disease
6-
Obstructive
nephropathy
4-Chronic
interstitial
nephritis
7. 1- Drug induce Functional
(Hemodynamically mediated) AK I
Caused by a decrease in intraglomerular pressure through the
vasoconstriction of afferent arterioles or the vasodilation of efferent
arterioles
NSAIDsNSAIDs
Cyclosporin
Tacrolimus
ACEI
ARB
8. 1-Functional (Hemodynamically mediated) AK I
NSAID Calcineurin inhibitor
Cyclosporin
Tacrolimus
ACE I /ARB
Mechanism VC (afferent
arteriole)
VC (afferent
arteriole)
VD of the efferent arteriole
presentation Increase, SCr
Can occur within
days of starting
therapy
Increase, SCr
Can occur within
days of starting
therapy
S.Cr increases within 3-5
days up to 30%
therapy therapy
Prevention Paracetamol Monitor serum
cyclosporine and
tacrolimus
concentrations
-Initiate low dose+ gradual
titration
-Monitor SCr
-Avoid use of concomitant
NSAIDs.
10. 2-Drugs induce acute tubular necrosis
Aminoglycosides Cisplatin & carboplatin Amphotercin
Gradual rise in SCr
concentrations after 6–10
days of therapy
-Electrolyte wasting
SCr peaks 10–12 days
after therapy starts
-Electrolyte wasting
-scr increase after
administration of 2-
3 gm
-Electrolyte wasting
-Avoid use in high-risk Use smallest dose possible Intravenous
Presentation
afferentafferent
arteriolar vc ,
causing
a hemodynamic
reduction in the
GFR.
-Avoid use in high-risk
patients.
-Maintain adequate
hydration.
-Use extended-interval
(once-daily)
Use smallest dose possible
and decrease frequency of
administration
-Aggressive intravenous
hydration: 1–4 L within
24 hours of high-dose
cisplatin or carboplatin
Intravenous
hydration:Nacl
0.9%
At least 1 L/day
before each dose
prevention
11. 3-Tubulointerstitial disease
Involves the renal tubules and the surrounding interstitium
1-Acute (allergic)
-Allergic hypersensitivity reaction that affects the
interstitium of the kidney
-Classic” presentation of skin rash, arthralgia,
and eosinophilia is more commonly occurs in association
with certain drugs, such as penicillin derivatives,
2-Chronic
(Irreversible )
-Shows interstitial
fibrosis
with certain drugs, such as penicillin derivatives,
compared with NSAIDs
No clinical symptoms or signs are sensitive
or specific enough to establish a definitive diagnosis.
-The GFR typically falls 7 to10 days after starting the
medication.
-Drugs such as the NSAIDs and proton pump inhibitors
(PPIs) may not develop AIN for many weeks or months
after initial exposure
-Slow decline in
kidney function
-No systemic
Symptoms
14. Lithium
Lithium
Chronic tubulointerstitial nephritis
Most commonly encountered after >= 10 years of therapy
Risk factor Long duration of use
Elevated serum concentrations
Repeated episodes of AKI from lithium toxicity.
presentation (a) Often asymptomatic, with slow progression over years
(b) May be recognized by slow increases in blood pressure (BP) or
BUN and SCr
Prevention Maintaining the lowest serum lithium concentrations possible,
avoiding dehydration, and monitoring kidney function closely
15. 5-Glomerular disease
Proteinuria is the hallmark of glomerular disease and may occur with or
without a decrease in GFR.
NSAIDs Minimal change ( most common ) -membranouse
nephropathy is a relatively rare complication
Lithium Minimmal change -focal segmental glomerulosclerosisLithium Minimmal change -focal segmental glomerulosclerosis
Interferon (α, β, γ) A variety of glomerular lesions, including minimal
change disease and focal segmental glomerulosclerosis
16. 6-Postrenal
(obstructive nephropathy )
Renal tubular obstruction Extrarenal urinary tract obstruction
Tissue degradation
product
Drugs precipitation
Uric acid Sulfonamides
Results from obstruction of the flow of urine after glomerular filtration
BPH can
worsened by
anticholinergic
Bladder outlet or
ureteral
obstructionUric acid
intratubular
precipitation after
tumor lysis after
chemotherapy
Sulfonamides
Methotrexate
Acyclovir
Ascorbic acid
Myoglobin
intratublar
precipitatons after
drugs induce
rhabdomyolysis
(Statin-fibrate)
Needle like crystals
observed in
leukocytes found on
urinalysis can
prompt diagnosis
anticholinergic obstruction
from fibrosis
after
cyclophosphamide
for hemorrhagic
cystitis
--------------------- Prevention
Hydration and
concomitant
Mesna
administration
17. Pseudo-nephrotoxicity
Drugs that inhibit the
tubular secretion of Cr
Trimethoprim, cimetidine
Drugs that increase BUN Corticosteroids, tetracycline
Drugs that interfere with SCr
assay
Cefoxitin and other cephalosporins
20. Sodium phosphate preparations
Agent Use Adverse events Comment
Sodium
phosphate
preparations
as purgatives
for bowel
cleansing before
diagnostic
colonoscopy.
-AKI
-Hypocalcemia and
hyperphosphatemia
Occur with excessive
dosing or use in
patients with underlying
kidney disease.
oral sodium
phosphate-based
products should not be
used in patients with
underlying
kidney disease, volume
depletion, or
electrolyte
abnormalitiesabnormalities
Recently, the
possibility of CKD
developing in patients
receiving phosphate-
containing enemas was
raised. Clinicians
should remain vigilant
for this possibility.
21. Case 2
.
Iv acyclovir 10 mg/kg /dose q 8hr
Duration 14- 21 day
30 -year-old man with CNS infection (encaphlitis)
75 kg
Normal kidney function
No hepatic impairment
Duration 14- 21 day
Do you need any precautions during
administration ?
22. Case 2 cont.,
.
For iv infusion
Avoid rapid IV infusion
Infuse over 1 hr to avoid renal damage
Maintain adequate hydration of the patient
Crystal nephropathy
Typically develops within 24 to 48 hours of acyclovir administration,
with an incidence of 12% to 48% when acyclovir is administered as a
rapid IV bolus .
23. Case 3
.
Regarding vancomycin adverse effects, which one of the following choices
is CORRECT?
A. Acute kidney injury (AKI)
B. Ototoxicity in combination with aminoglycosides
C. Red man syndrome
D. Thrombocytopenia
E. All of the above
24. Case 4
.
-Both triamterene and amiloride are potassium sparing
diuretics, but triamterene is more likely to cause what
problem not seen with amiloride?
1. Increased calcium nephrolithiasis
2. Increased uric acid nephrolithiasis
3. Less diuresis compared to Amiloride3. Less diuresis compared to Amiloride
4. Metabolite caused nephrolithiasis
25. Case 5
Which one of the following drugs is associated with stone
formation?
A. Vitamin C
B. Acyclovir
C. Indinavir
D. All of the above
26. Case 6
72-year-old man with bipolar disorder and hypertension is treated
with lithium (Li). His physician added enalapril 10 mg/day for
improvement of his hypertension and possible congestive heart
failure.
Two months later, he was confused and admitted to the hospital withTwo months later, he was confused and admitted to the hospital with
LI toxicity.
27. Case 6 cont.,
Which one of the following choices explains his Li toxicity?
A. Combination of Li and an angiotensin converting enzyme-inhibitor (ACE-
I) enhances Li toxicity
B. No relationship exists between Li and ACE-Is
C. Combination of an ACE-I and Li enhances estimated glomerular filtration
rate (eGFR)
D. Combination of an ACE-I and Li has no effect on eGFRD. Combination of an ACE-I and Li has no effect on eGFR
E. None of the above
28. Case 7
.
A 26-year-old woman with sickle cell disease with serum creatinine of 1.4
mg/dL (eGFR <30 mL/dL) is admitted for seizure disorder.
She is on meperidine 50 mg BID for pain by his primary care physician. Her
pain was controlled for many weeks. She does not want to change her
medication.
What is the cause of seizure ?
29. Case 8
.
60 year old male admitted to nephrology department
begun on ciprofloxacin for UTI, patient on theophylline for
asthma .
Patient developed confusion , seizure after 3 days of admission .
What is the cause of seizure ?
30. Quinolone antibiotic may decrease the metabolism of
theophylline
Theophylline / Quinolone may augment the seizure producing
potential of each individual agent
Case 8 cont.,
An empiric reduction in the dosage of theophylline ( 25 – 50 % )
Consider using another antibiotic ( other than ciprofloxacin)
32. Case 9
56 year old female CKD – Spontaneous bacterial peritonitis
weight 60 kg - height 160 cm- sCr 2mg/dl
(ceftrixone- cefotaxime)
..
Ceftrixone not avialable in the pharmacy ?
33. Case 9 cont.,
Renal impairment may necessitate a dose reduction, an extension in
the dosing interval, or a combination of both.
Such alterations will depend on the degree of renal dysfunction (or form of
renal replacement therapy).
35. Case 10
.
Oseltamiver dose as a treatment for influenza in different
modalities of dialysis
IHD CAPD
30 mg Immediately and then 30 mg 30 mg immediately as a single dose30 mg Immediately and then 30 mg
after every HD session for 5 days
( Assume 3 hemodialysis sessions in
the 5-days period )
30 mg immediately as a single dose
(Single dose provide a 5days
duration)
36. Case 11
.
Do you need special precautions for this patient ?
60 year old female on regular hemodialysis has catheter realted
blood stream infection(CRBSI ) on tineam (imipenem /
cilastatin ) 500 mg q 12 hr (based on blood culture )
Do you need special precautions for this patient ?
37. Case 11 cont.,
.
Dosing changes in patients with HD may be necessary because of
Drug dosing in hemodialysis
Dosing changes in patients with HD may be necessary because of
-Accumulation caused by kidney failure
-or because the procedure may remove the drug from the circulation
38. Case 12
.
Which is not effectively removed by hemodialysis?
1. Amphetamines
2. Phenobarbital
3. Digoxin
4. Chlorpropamide
39. Case 13
.
Which one of the following drugs does NOT need supplementation
following hemodialysis (HD)?
A. Vancomycin
B. Gentamicin
C. Piperacillin/tazobactam
D. Meropenam
E. PhenytoinE. Phenytoin
40. Case 14
.
55 year old male on Peritoneal dialysis ( PD) admitted to
nephrology
department with Peritonitis
His current medications
Ciprofloxacin Iv
Vancomycin Iv
Calcium carbonate
Ciprofloxacin 250 mg oral q 12hr
Vancomycin Iv
Calcium carbonate
????????
Calcium carbonate
Calcium carbonate
41. Interaction
oral calcium
Salts
ScurlfateSevelemer
Ciprofloxacin should be separated by 2 hr to prevent chelation interactionCiprofloxacin should be separated by 2 hr to prevent chelation interaction
reducing ciprofloxacin absorption .
(Administer ciprofloxacin 1st )
Oral zinic Milk
Oral
magnesium
and alumnium
antacid
42. Case 15
.
35 year old female admitted to nephrology department
Current medication sheet
Azathiopurine
Prednisone ( oral )
Allopurinol
Calcium carbonate
Comment on current medications
Calcium carbonate
43. Case 15 cont.,
.
Azathiopurine
Allopurinol may
increase serum
conc of active
Reduce dose of
azathiopurine to
1/3
To ¼ the usual
dose
Allopurinol
conc of active
metabolite (s) Monitor
Systemic toxicity
(heamatologic
toxicity
, nasuea and
vomiting )
45. Case 16
.
35 year old female , renal transplant , HCV admitted to nephrology department
seek advice due to increase in the serum level of tacrolimus
Current medication sheet
-Tacrolimus
-Myfortic
-Prednisone
Patient has start qureveo for hcv
The nephrologist ask for tacrolimus level
46. Case 16 cont.,
.
Tacrolimus
Ombitasvir
Paritaprevier
Avoid combination
May increase serum conc
of tacrolimus
Management
-When combination
the typical
tacrolimus dose
required to
maintain
therapeutic
ConcParitaprevier
Ritonavir
of tacrolimus Conc
was 0.5 mg
q 7 days