Patients with HIV are at risk for both acute kidney injury and chronic kidney disease due to various factors like medication toxicity, HIV-associated nephropathy, and immune complex kidney diseases. The risk factors for acute kidney injury in HIV patients are similar to the general population but also include factors specific to HIV like low CD4 count and co-infection with hepatitis C virus. Timely screening for chronic kidney disease is important in HIV patients to monitor for decline in kidney function and proteinuria, in order to guide management and reduce risk of end-stage renal disease.
Theodoros Katsivas, MD (UC San Diego Owen Clinic), Shira Abeles, MD (UC San Diego Owen Clinic) and Robyn Cunard, MD (UC San Diego) present "Renal Disease in HIV/AIDS"
Theodoros Katsivas, MD (UC San Diego Owen Clinic), Shira Abeles, MD (UC San Diego Owen Clinic) and Robyn Cunard, MD (UC San Diego) present "Renal Disease in HIV/AIDS"
Infectious diseases are the second most common cause of death in end-stage renal disease (ESRD) patients. Patients with ESRD are at high risk for several infections, due to exposure to blood products and frequent dialysis. The increased susceptibility to infections among these patients is indicative of a complex and varied state of immunodeficiency manifested by abnormal phagocytosis, T and B lymphocytes abnormalities and impaired response to T cell dependent pathogens such as hepatitis B and influenza viruses. These immunologic abnormalities are complicated by the use of immunosuppressive drugs used to treat and control underlying disease and exacerbated by nutritional deficiency and the dialysis procedure. Though many of these infections can be prevented by appropriate vaccination, the usual schedules of vaccination may be less effective.
The aim of this paper is to review the studies on the use of vaccines in ESRD patients
and summarize the vaccines required in this population.
Hepatitis C virus infection is associated with many renal diseases. Renal disease caused by :•Virus itself •Drugs used for treatment of hepatitis c •Associated condition with hepatitis → advanced liver cell failure.
Renal Replacement Therapy: modes and evidenceMohd Saif Khan
Renal replacement therapy is a supportive care often required in critically ill patients who develop acute renal failure and its complications. Complexity arises when such patients become hemodynamically unstable and pose special challenge to critical care clinicians in ICU to carefully choose dialytic modality to tackle volume and solute overload. This presentation is about short description of modalities of RRT and current evidence regarding initiation, dose and type of modality.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
Infectious diseases are the second most common cause of death in end-stage renal disease (ESRD) patients. Patients with ESRD are at high risk for several infections, due to exposure to blood products and frequent dialysis. The increased susceptibility to infections among these patients is indicative of a complex and varied state of immunodeficiency manifested by abnormal phagocytosis, T and B lymphocytes abnormalities and impaired response to T cell dependent pathogens such as hepatitis B and influenza viruses. These immunologic abnormalities are complicated by the use of immunosuppressive drugs used to treat and control underlying disease and exacerbated by nutritional deficiency and the dialysis procedure. Though many of these infections can be prevented by appropriate vaccination, the usual schedules of vaccination may be less effective.
The aim of this paper is to review the studies on the use of vaccines in ESRD patients
and summarize the vaccines required in this population.
Hepatitis C virus infection is associated with many renal diseases. Renal disease caused by :•Virus itself •Drugs used for treatment of hepatitis c •Associated condition with hepatitis → advanced liver cell failure.
Renal Replacement Therapy: modes and evidenceMohd Saif Khan
Renal replacement therapy is a supportive care often required in critically ill patients who develop acute renal failure and its complications. Complexity arises when such patients become hemodynamically unstable and pose special challenge to critical care clinicians in ICU to carefully choose dialytic modality to tackle volume and solute overload. This presentation is about short description of modalities of RRT and current evidence regarding initiation, dose and type of modality.
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
Liver diseases are very common in HIV infected patients. This presentation summarized common conditions related to HIV, Hepatitis virus coinfections, hepatotoxicities and other related causes.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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.
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.
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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 ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
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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
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.
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2. Patients with HIV are at risk for both acute kidney injury (AKI)
and chronic kidney disease (CKD), secondary to:
Medication nephrotoxicity.
HIV-associated nephropathy (HIVAN).
Immune complex kidney diseases.
Thrombotic Microangiopathy (less commonly).
3.
4. Prior to the introduction of combination antiretroviral therapy
(ART), acute kidney injury (AKI) was commonly attributed to
septicemia, or volume depletion.
5. The incidence of AKI in HIV-positive patients is higher than it is in
patients without HIV.
The incidence of AKI in patients with HIV has also increased over
time.
Acute renal failure in hospitalized patients with HIV: risk factors and impact on in-hospital mortality, Wyatt CM, Arons RR, 2006;20(4):561
6. The risk factors for AKI among HIV-positive patients are similar to
risk factors for AKI in the general population:
Older age.
Diabetes mellitus.
Chronic kidney disease (CKD).
Acute or chronic liver disease.
7. Risk factors are specific to HIV:
Receiving ART.
AIDS-defining illness.
Co-infection with hepatitis C virus (HCV).
Low CD4 count.
High viral load.
Incidence and etiology of acute renal failure among ambulatory HIV-infected patients, Franceschini N, Napravnik S, Kidney Int. 2005;67(4):1526.
8. As in the general population, the development of AKI increases
the risk of morbidity and mortality in HIV-positive patients
(Inpatient mortality and Long-term mortality).
Acute renal failure in hospitalized patients with HIV: risk factors and impact on in-hospital mortality, Wyatt CM, Arons RR, 2006;20(4):561
9. The most common types of AKI in patients with HIV infection,
similar to patients without HIV, are prerenal states and acute
tubular necrosis.
10. 1. Prerenal states:
2. Acute tubular necrosis:
3. Crystalluria with obstruction:
4. Interstitial nephritis:
Incidence and etiology of acute renal failure among ambulatory HIV-infected patients, Franceschini N, Kidney Int. 2005;67(4):1526.
11. Patients with HIV infection are at risk for nephrotoxicity from ART,
as well as from medications used to treat opportunistic infections
or hepatitis virus co-infection.
Medication nephrotoxicity may present with acute or chronic
kidney injury or with acid-base and electrolyte disturbances.
12. Some of the more commonly agents include the following:
Protease inhibitors :
Indinavir and atazanavir are protease inhibitors that can cause
crystalluria and AKI.
13. Tenofovir disoproxil fumarate (TDF) –
Tenofovir is a nucleoside reverse transcriptase inhibitor, can
cause AKI, proximal tubular dysfunction, or both in combination.
According to expert guidelines, TDF should be avoided in patients
with an (eGFR) less than 60 mL/min/1.73 m2, and should be
discontinued in patients who experience a 25 percent or greater
decline to an eGFR less than 60 mL/min/1.73 m2.
The risk of kidney toxicity with TDF has varied across different
studies, with estimates ranging from 2-10 %.
The significance of antiretroviral-associated acute kidney injury in a cohort of ambulatory human immunodeficiency virus-infected patients, Wikman P, Nephrol Dial
Transplant. 2013;28(8):2073.
14. Other antiviral agents – Acyclovir, foscarnet, and cidofovir are
drugs used to treat herpes simplex virus or cytomegalovirus
infection. Each of these agents can be associated with the
development of AKI.
Anti-Pneumocystis drugs – Trimethoprim-sulfamethoxazole and,
less commonly, pentamidine are agents used to treat
Pneumocystis infection. Trimethoprim-sulfamethoxazole can
produce interstitial nephritis, while approximately 25 percent of
patients treated with pentamidine develop reversible AKI that is
likely due to nephrotoxic acute tubular necrosis.
15. In addition, several antiretroviral agents can interfere with the
tubular secretion of creatinine, producing an increase in serum
creatinine (and decline in estimated glomerular filtration rate
[eGFR]) without a true decline in kidney function.
These include the boosting agent, cobicistat, and the integrase
inhibitor, dolutegravir; the increase in serum creatinine with these
drugs occurs early and is typically in the range of 0.05 to 0.2
mg/dL.
16. HIV-associated thrombotic microangiopathy can present with
significant AKI.
Results of a large observational cohort study suggest that
systemic thrombotic microangiopathy is a rare complication of
HIV infection in the ART era.
HIV-associated thrombotic microangiopathy in the era of highly active antiretroviral therapy: an observational study, Becker S, Clin Infect Dis. 2004;39 Suppl 5:S267.
17.
18. The prevalence and incidence of HIV-related end-stage renal
disease (ESRD) are projected to increase as the prevalence of
HIV infection continues to rise.
Highly active antiretroviral therapy and the epidemic of HIV+ end-stage renal disease, Schwartz EJ, J Am Soc Nephrol. 2005;16(8):2412.
19. Risk factors for incident or progressive CKD in HIV-positive
adults include hepatitis C virus (HCV) co-infection, low CD4 T cell
count, high HIV viral load, and traditional CKD risk factors such
as diabetes and hypertension.
Treatment with tenofovir disoproxil fumarate (TDF) and boosted
protease inhibitors has also been associated with GFR decline or
decreased GFR in several studies, while ART in general appears
to slow the rate of renal function decline.
20. The etiology of CKD in patients with HIV:
HIV-independent disorders (such as hypertension, diabetes).
Incomplete recovery from an episode of acute kidney injury.
HIV-related disorders, including HIVAN.
HIV immune complex kidney disease (HIVICK).
In addition, many HIV-positive adults are also at risk for
glomerulonephritis secondary to HCV co-infection.
21. The classic kidney disease of HIV infection, HIV-associated
nephropathy (HIVAN), was first described in 1984 in patients with
advanced HIV infection.
HIVAN is a collapsing form of focal segmental glomerulosclerosis
(FSGS) with associated tubular microcysts and interstitial
inflammation.
22. HIVAN classically presents with significant proteinuria and rapidly
progressive kidney disease in the setting of normal blood
pressure and normal to enlarged kidneys, although the
presentation may be less dramatic in the ART era.
HIVAN is usually not seen in patients on ART who have a normal
CD4 T cell count and an undetectable HIV viral load.
23. Nearly 40% of HIV-positive patients with proteinuric kidney disease
and suspected HIVAN will have an alternative diagnosis on biopsy.
Renal pathology of human immunodeficiency virus infection, D'Agati V, Appel GB, Semin Nephrol. 1998;18(4):406.
24. A number of immune complex kidney diseases have been
reported in patients with HIV infection, including:
Membranous nephropathy.
Membranoproliferative.
Mesangial proliferative glomerulonephritis.
"lupus-like" proliferative glomerulonephritis.
Though rare, IgA nephropathy has also been reported in the
setting of HIV infection.
25. HCV co-infection has been associated with the development of
acute and chronic kidney disease.
The classic clinical findings of cryoglobulinemia and
hypocomplementemia may be less common in co-infected
patients.
26.
27. Expert guidelines that recommend screening and early
identification of CKD in patients with HIV.
HIV-positive individuals should have their GFR estimated at least
twice yearly and should have either a urinalysis or quantitative
assessment of urine protein excretion at least once yearly in order
to monitor for the development of kidney disease.
Such patients whose eGFR has declined by 25 percent or more
to a level below 60 mL/min/1.73 m2, or who have protein
excretion greater than 300 mg/day, should be referred for
nephrology evaluation.
28. Identification of CKD in a patient with HIV should prompt initiation
of ART (if not already started) and tight control of comorbid
diabetes and hypertension (if present).
Medication doses should be adjusted for the calculated creatinine
clearance, with particular attention to nucleoside and nucleotide
reverse transcriptase inhibitors.
29. Analyses of data from the US Renal Data System (USRDS) have
demonstrated similar outcomes in HIV-positive ESRD patients
treated with hemodialysis or peritoneal dialysis, as well as
significant improvements in survival in the ART era.
Editor's Notes
This was documented in a study of hospitalized adults in New York state which compared administrative data from 1995 (before the introduction of ART) to data from 2003 (after the introduction of ART) [17]. Compared with HIV-negative hospitalized patients, AKI was documented in a significantly greater proportion of HIV-positive hospitalized patients, both in 1995 (2.9 versus 1 percent) and 2003 (6 versus 2.7 percent). Among HIV-positive patients, the proportion with documented AKI was two-fold higher in 2003, although in-hospital mortality was lower.
In the study of 754 HIV-positive patients : receiving ART (12 versus 4 percent) and those with an AIDS-defining illness (30 versus 7 percent).
BACKGROUND: Acute renal failure (ARF) is a cause of renal dysfunction in human immunodeficiency virus (HIV)-infected patients. Its incidence and causes have not been studied since the introduction of highly active antiretroviral therapy (HAART) in HIV ambulatory patients.
METHODS: This is a prospective cohort study of 754 HIV patients, 18 years or older, seen at a university-based infectious disease clinic between 2000 and 2002. ARF was identified using proportional increases in serum creatinine from baseline and by chart review. Clinical conditions were assessed at the time of the ARF event. ARF incidence rates (IR) were calculated by dividing the number of events by person time at risk. To compare patients with and without ARF, t test or chi-square test were used.
RESULTS: Patient's mean age was 40 years; 68% were male and 61% were black. One hundred-eleven ARF events occurred in 71 subjects (IR 5.9 per 100 person-years; 95% CI 4.9, 7.1). ARF was more common in men, in those with CD4 cell count<200 cells/mm(3), and HIV RNA levels>10,000 copies/mL. These patients more often had acquired immunodeficiency syndrome (AIDS), hepatitis C infection (HCV), and have received HAART. ARF was mainly community-acquired, due to prerenal causes or acute tubular necrosis, and associated with opportunistic infections and drugs. Liver disease was a cause of ARF in HCV-infected patients.
CONCLUSION: ARF is common in ambulatory HIV patients. Immunosuppression, infection, and HCV are important conditions associated with ARF in the post-HAART era
Inpatient mortality was significantly more frequent among HIV-positive patients who had AKI than among HIV-positive patients without AKI in a 2003 sample of hospitalized patients in New York state (27 versus 4 percent).
The best data come from a prospective study of 754 HIV-positive patients followed at a single center; 111 episodes of AKI developed in 71 patients during a two-year period. The major types of AKI in this population included:
In the study of 754 HIV-positive patients : receiving ART (12 versus 4 percent) and those with an AIDS-defining illness (30 versus 7 percent).
BACKGROUND: Acute renal failure (ARF) is a cause of renal dysfunction in human immunodeficiency virus (HIV)-infected patients. Its incidence and causes have not been studied since the introduction of highly active antiretroviral therapy (HAART) in HIV ambulatory patients.
METHODS: This is a prospective cohort study of 754 HIV patients, 18 years or older, seen at a university-based infectious disease clinic between 2000 and 2002. ARF was identified using proportional increases in serum creatinine from baseline and by chart review. Clinical conditions were assessed at the time of the ARF event. ARF incidence rates (IR) were calculated by dividing the number of events by person time at risk. To compare patients with and without ARF, t test or chi-square test were used.
RESULTS: Patient's mean age was 40 years; 68% were male and 61% were black. One hundred-eleven ARF events occurred in 71 subjects (IR 5.9 per 100 person-years; 95% CI 4.9, 7.1). ARF was more common in men, in those with CD4 cell count<200 cells/mm(3), and HIV RNA levels>10,000 copies/mL. These patients more often had acquired immunodeficiency syndrome (AIDS), hepatitis C infection (HCV), and have received HAART. ARF was mainly community-acquired, due to prerenal causes or acute tubular necrosis, and associated with opportunistic infections and drugs. Liver disease was a cause of ARF in HCV-infected patients.
CONCLUSION: ARF is common in ambulatory HIV patients. Immunosuppression, infection, and HCV are important conditions associated with ARF in the post-HAART era
BACKGROUND: To determine the incidence and significance of acute kidney injury (AKI) after initiating highly active antiretroviral therapy (HAART).
METHODS: A prospective cohort study of 271 consecutively treated HIV-infected patients, initiating first (75) or sequential HAART (196) from January 2008 to June 2011. AKI was diagnosed according to the Risk, Injury, Failure, Loss of kidney function, End-stage renal disease (RIFLE)/Acute Kidney Injury Network (AKIN) criteria, and the risk of progression to chronic kidney disease (CKD) was evaluated.
RESULTS: A greater estimated glomerular filtration rate (eGFR) decrease after 1 year was observed for patients initiating a tenofovir disoproxil fumarate (TDF)-based regimen (-6.45 versus +0.98 mL/min/1.73 m(2) when compared with patients without TDF; P<0.01), both in the case of the first (-8.5 versus -2.27; P = 0.04) or successive regimens (-5.3 versus + 1.18 mL/min/1.73 m(2); P<0.01). AKI, as defined, was observed in 10% (28 cases, 6.98 episodes/100 patients-year), mostly stage I (27 cases), in a median time of 6 (3-16.5) months. Four cases (14%), having a worse baseline renal function progressed to CKD, whereas four recovered completely. In the multivariate analysis, AKI was associated with the concomitant use of cotrimoxazole prophylaxis and to low CD4+ count. CKD was diagnosed in 2% (six cases) of patients. Therefore, the overall rate of HAART-associated renal disorders was 11% (30 cases, 7.46 episodes/100 patients-year (95% confidence interval, 6.09-8.83).
CONCLUSIONS: The initiation of a tenofovir-based regimen is followed by a significant decline in eGFR, although it could be misinterpreted by the concomitant use of cotrimoxazole. A substantial proportion of patients develop AKI, but only a minority progress to CKD. Patients initiating HAART and developing AKI should be carefully monitored for progression of renal disease.
Other antiviral agents – Acyclovir, foscarnet, and cidofovir are drugs used to treat herpes simplex virus or cytomegalovirus infection. Each of these agents can be associated with the development of AKI. (See "Crystal-induced acute kidney injury (acute renal failure)", section on 'Acyclovir' and "Foscarnet: An overview", section on 'Renal insufficiency' and "Cidofovir: An overview", section on 'Toxicity'.)
HIV-associated thrombotic microangiopathy in the era of highly active antiretroviral therapy: an observational study.
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Becker S, Fusco G, Fusco J, Balu R, Gangjee S, Brennan C, Feinberg J, Collaborations in HIV Outcomes Research/US Cohort
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Clin Infect Dis. 2004;39 Suppl 5:S267.
The prevalence and predisposing factors of thrombotic microangiopathy (TMA) in the era of highly active antiretroviral therapy (HAART) were evaluated among patients in the Collaborations in Human Immunodeficiency Virus (HIV) Outcomes Research/US cohort. Of 6022 patients, 17 (0.3%) had TMA, with unadjusted incidences per 100 person-years of 0.079 for TMA, 0.009 for thrombotic thrombocytopenic purpura, and 0.069 for hemolytic-uremic syndrome. Compared with patients without TMA, patients with TMA had lower mean CD4(+) cell counts (197 vs. 439 cells/mm(3); P=.0009) and higher mean log(10) HIV-1 RNA levels (4.6 vs. 3.3 copies/mL; P=.0001) at last follow-up and a significantly greater incidence of acquired immune deficiency syndrome (82.4% vs. 55.3%; P=.025), Mycobacterium avium complex infection (17.6% vs. 3.3%; P=.018), hepatitis C (29.4% vs. 11.3%; P=.001), and death (41.2% vs. 7.4%; P<.0001). The prevalence of herpes and use of antiherpetics were slightly higher for patients with TMA, but unadjusted distributions were not statistically significant. TMA in a cohort surveyed after the introduction of HAART was rare and was associated with advanced HIV disease.
Highly active antiretroviral therapy and the epidemic of HIV+ end-stage renal disease.
Schwartz EJ, Szczech LA, Ross MJ, Klotman ME, Winston JA, Klotman PE
J Am Soc Nephrol. 2005;16(8):2412.
The rise in the number of patients with HIV-associated nephropathy and HIV-infection with end-stage renal disease (HIV+ ESRD) continues to be a substantial concern for the ESRD program. In order to assess the impact of highly active antiretroviral therapy (HAART) on the progression of patients with AIDS to the development of ESRD and to project the prevalence of HIV+ ESRD through 2020, a mathematical model of the dynamics of HIV+ infection in the ESRD population was developed. Epidemiologic data on AIDS and HIV+ ESRD among black individuals in the United States were obtained since 1991 from the Centers for Disease Control and Prevention and US Renal Data System, respectively. The model was constructed to predict the prevalence of HIV+ ESRD incorporating the current rate of growth in AIDS prevalence. Two possible trends were considered: linear AIDS growth and exponential AIDS growth. The likely effectiveness of HAART in slowing progression to HIV+ ESRD was estimated from the best fit of the model to the data after 1995, when HAART was introduced. The model was then used to evaluate recent data and to project the prevalence of HIV+ ESRD through 2020. The model suggested that HAART has reduced the rate of progression from AIDS to HIV+ ESRD by 38%. The model projected an increase in HIV+ ESRD prevalence in the future as a result of the increase in the AIDS population among black individuals. This increasewas predicted even assuming a 95% reduction in the progression from AIDS to HIV+ ESRD. Despite the potential benefit of HAART, the prevalence of HIV+ ESRD in the United States is expected to rise in the future as a result of the expansion of the AIDS population among black individuals. It is concluded that prevention of progression to ESRD should focus on early antiretroviral treatment of HIV-infected patients who have evidence of HIV-associated nephropathy.