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.
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 hepatitisadvanced liver cell failure.
A. The renal disease associated with hepatitis c due to advanced liver cell failure:
• Prerenal (Hypovolemia , shock and hepatorenal syndrome )
• ATN ( sepsis or shock)
B. Drugs used for treatment of hepatitis c:
• Interstitial nephritis secondary to Interferon
C. Hepatitis c itself
o Hepatitis c is RNA flavivirus( single strand)
o Has extrahepatic manifestation like arthritis, DM, cryglobulinemia and glomerulonephritis
o Renal diseases associated with hepatitis C
1. The most common types is MPGN with cryoglobulinemia
2. Others are
MPGN without cryoglobulinemia
Membranous nephropathy (MN)
Focal segmental glomerulosclerosis
IgA nephropathy
Fibrillary glomerulopathy
Immunotactoid glomerulopathy
Thrombotic microangiopathy
Amyloid
Vasculitis
Interstitial nephritis secondary to virus
HCV-associated PAN
Infection-related Glomerulonephritis (KDIGO 2021 Guidelines) - Dr. GawadNephroTube - Dr.Gawad
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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 hepatitisadvanced liver cell failure.
A. The renal disease associated with hepatitis c due to advanced liver cell failure:
• Prerenal (Hypovolemia , shock and hepatorenal syndrome )
• ATN ( sepsis or shock)
B. Drugs used for treatment of hepatitis c:
• Interstitial nephritis secondary to Interferon
C. Hepatitis c itself
o Hepatitis c is RNA flavivirus( single strand)
o Has extrahepatic manifestation like arthritis, DM, cryglobulinemia and glomerulonephritis
o Renal diseases associated with hepatitis C
1. The most common types is MPGN with cryoglobulinemia
2. Others are
MPGN without cryoglobulinemia
Membranous nephropathy (MN)
Focal segmental glomerulosclerosis
IgA nephropathy
Fibrillary glomerulopathy
Immunotactoid glomerulopathy
Thrombotic microangiopathy
Amyloid
Vasculitis
Interstitial nephritis secondary to virus
HCV-associated PAN
Infection-related Glomerulonephritis (KDIGO 2021 Guidelines) - Dr. GawadNephroTube - Dr.Gawad
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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.
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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.
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Etiology- genetic mutations, infection, toxin exposure, autoimmunity, atherosclerosis, hypertension, emboli, thrombosis, or diabetes mellitus.
Even after careful study, however, the cause often remains unknown, and the lesion is called idiopathic.
Inflammation of the glomerular capillaries is called glomerulonephritis.
Persistent glomerulonephritis that worsens renal function is always accompanied by interstitial nephritis, renal fibrosis, and tubular atrophy.
Steal syndrome
• Dialysis access–associated hand ischemia, “steal syndrome,” complicates 1%–20% of accesses
• Is stealing سرقة of (arterial) blood which would normally flow to the palmar arch.
• Common in upper arm AVFs (~4%) compared with both AVGs and forearm AVFs (~1%).
• Risk factors
Upper arm access
Peripheral arterial disease
Diabetes
• Patient can complain of:
Hand numbness, pain, or weakness
Cold sensation and pale or cyanosis of the fingers
Diminished or absent pulses
Ulceration or dry gangrene of the finger tips in severe cases infection.
Pt start to wear gloves in fistula hand
• Examination requires comparison with the temperature, pulse, and function of the opposite hand.
• Investigations
Pulse oximetry
Doppler flow
Angiography
• Differential diagnosis
Carpal tunnel syndrome
Peripheral vascular disease
Neuropathy DM or Uremia
Nerve trauma
Ischemic monomelic neuropathy due to the loss of blood supply to nerves.
• Treatment Options (Depending on Severity)
Symptomatic coldness or paresthesia but without sensory or motor loss (e.g., gloves)
Surgical, with preservation of vascular access- in "steal” effect (pain at rest) or the appearance of nonhealing ulcers: banding to reduce flow, distal revascularization–interval ligation (DRIL) procedure
Surgical, with loss of vascular access- in motor loss: ligation
Renal papillary necrosis ( RPN)
• Definition
o Disorder of the kidneys in which all or part of the renal papillae die.
• Causes
Analgesic nephropathy
Diabetic nephropathy
Kidney infection (pyelonephritis)
Sickle cell anemia (common cause of RPN in children)
Urinary tract obstruction
Renal tuberculosis
Renal vein thrombosis
Kidney transplant rejection
• Symptoms
Dysuria, painful urination.
Fever and chills.
Hematuria, macroscopic or microscopic.
Nocturia, frequent urination at night.
Pyuria, unusually high amount of white blood cells in urine.
Severe flank pain on either side of your back.
Urinary tract infections.
• Diagnosis
Urography involves an X-ray, CT scan or MRI of kidneys. (Radiologic findings include an irregular papillary tip; dilated calyceal fornix; extension of contrast material into the parenchyma; and a separated crescent-shaped papilla surrounded by contrast, called the ring sign
Ureteroscopy
Kidney biopsy
Kidney function tests
Urinalysis red blood cells and broken-off pieces of renal papillae
• Complications:
Kidney infection
Kidney stones
Chronic kidney disease (CKD)
Transitional cell cancer of the kidney or ureter.
• Prevention
Controlling diabetes or sickle cell anemia.
Use only the recommended dose of analgesic
• Treatment
There is no specific treatment for renal papillary necrosis.
Treatment depends on the cause.
Cerebral Salt Wasting (CSW)
• Typically associated with subarachnoid hemorrhage,
• The causes may be:
o Impaired sympathetic neural input (SNS normally promotes proximal tubular Na, uric acid, and water reabsorption and renin–aldosterone release),
o Increased brain natriuretic peptide → impairs renal tubular Na reabsorption and inhibits renin release
• Clinical manifestations:
o Volume depletion,
o Orthostatic hypotension
• Laboratory findings:
o Hyponatremia,
o Low serum uric acid,
o high urine osmolality,
o U [Na] > 40 mmol/L,
o low renin and aldosterone levels (similar to those seen with SIADH)
• CSW patients present with volume depletion, in contrast to
SIADH patients who present with euvolemia or mild hypervolemia.
• Treatment of CSW:
o Volume repletion (NS)
(Note: NS may worsen hyponatremia in SIADH but would improve hyponatremia in CSW.
o Consider mineralocorticoids, for example, fludrocortisone 0.2 mg twice daily.
• Common features between SIADH and CSW:
o High ADH and Natriuretic peptide levels.
o High U [Na].
o Low renin and aldosterone levels.
o Low uric acid levels.
o ADH level decreases after volume repletion in CSW but not in SIADH.
Diabetic Ketoacidosis/Hyperosmolar Coma in ESRD
• Clinical Picture of hyperglycemia is modified (due to absence of renal function).
o The absence of polyuria and glycosuria “safety valve” severe hyperglycemia (serum glucose level >1,000 mg/dL)
o Alteration of mental status is unusual (Due to absence of water loss induced by osmotic diuresis).
o Asymptomatic mostly in spite of severe hyperglycemia
o Thirst, weight gain, and may be pulmonary edema or coma
o Severe hyperkalemia in DKA in insulin-dependent dialysis patients.
• Diagnosis in the ESKD patient is based on hyperglycemia, positive serum ketones, metabolic acidemia, and an increased anion gap.
o Which is not easy due to the plasma reaction for ketones may be negative, the anion gap may not be affected and the clinical presentation itself of severe hyperglycemia and ketoacidosis are atypical.
• Management of hyperglycemia with or without ketoacidosis differs from that in patients without renal failure in that administration of large amounts of fluid is unnecessary and generally contraindicated.
o Insulin is the only treatment needed can correct all clinical and laboratory abnormalities of hyperglycemia.
o Can administer a continuous infusion of low-dose regular insulin (starting at 2 units/hr) with close clinical monitoring and measurement of serum glucose and potassium concentrations at 2- to 3-hour intervals.
o Urgent dialysis if pulmonary edema and hyperkalemia.
• IV bicarbonate is not indicated may exacerbate volume overload.
• No phosphate replacement is generally needed.
• Hypophosphatemia is not expected.
• Magnesium deficiency is absent.
Emphysematous pyelonephritis
• Def: Life-threatening necrotizing acute pyelonephritis and/or obstruction, predominantly seen in diabetic patients
• Causes: Mostly gas-forming organisms such as Escherichia coli, Klebsiella pneumonia, Pseudomonas aeruginosa, and Proteus mirabilis
• Symptoms of pyelonephritis and may be a flank mass.
• Urine analysis→ Pyuria and a positive urine culture
• Diagnosis: Gas pockets may be detected on plain abdominal radiograph, ultrasound, or CT.
• CT is the diagnostic modality of choice
• Management: Parenteral broad-spectrum antibiotics and percutaneous catheter drainage with relief of obstruction may be adequate for less severely ill patients, but nephrectomy in severely ill or not responding to other line of medication
• Medical treatment is associated with mortality of 60% to 80%,
Xanthogranulomatous pyelonephritis
• Def: Condition associated with chronic obstruction (e.g., staghorn calculi) and urinary tract infections with resulting destructive granulomatous inflammation
• CT: low-density masses with calcifications mimicking renal malignancy
• Histology: granulomatous inflammation with diffuse cellular infiltrate of lipid-laden foam cells (lipid-laden macrophages)→ replacing normal renal parenchyma
• Clinical manifestations: commonly affect middle-aged women who may present with fevers/chills, chronic flank pain, and, possibly, palpable mass.
• Urine cultures: may reveal gram-negative organisms such as E. coli, Klebsiella, or Proteus and, less commonly, Staphylococcal species.
• Management: organism-specific antibiotics, relief of obstruction, but total or partial nephrectomy as needed
Sickle cell nephropathy (SCN) is presence of sickled erythrocytes in the renal medulla that result in decreased medullary blood flow, ischemia, microinfarcts and papillary necrosis in the kidneys
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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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!
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.
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
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
1. Hepatitis C and renal diseaseHepatitis C and renal disease
Dr. Mohamed AbbassDr. Mohamed Abbass
NephrologistNephrologist
PGDD, CARDIFF, UKPGDD, CARDIFF, UK
2. Hepatitis C virus infection is associated with manyHepatitis C virus infection is associated with many
renal diseases.renal diseases.
Renal disease caused by :Renal disease caused by :
•Virus itself•Virus itself
•Drugs used for treatment of hepatitis c•Drugs used for treatment of hepatitis c
•Associated condition with hepatitis →•Associated condition with hepatitis →
advanced liver cell failure.advanced liver cell failure.
3. 1–The renal disease associated with hepatitis c
due to advanced liver cell failure:
•Prerenal →(Hypovolemia , shock and
hepatorenal syndrome)
•ATN →(sepsis or shock)
2– Drugs used for treatment of hepatitis c:
Interstitial nephritis secondary to interferon
4. 3–Hepatitis c itself:3–Hepatitis c itself:
••Hepatitis c is RNA flavivirus(single strand)Hepatitis c is RNA flavivirus(single strand)
•Has extrahepatic manifestation like arthritis, DM,•Has extrahepatic manifestation like arthritis, DM,
cryglobulinemia and glomerulonephritiscryglobulinemia and glomerulonephritis
5.
6. 11..The most common types isThe most common types is MPGN with cryoglobulinemia
2. Others are:2. Others are:
MPGN without cryoglobulinemiaMPGN without cryoglobulinemia
Membranous nephropathy (MN) Membranous nephropathy (MN)
Focal segmental glomerulosclerosisFocal segmental glomerulosclerosis
IgA nephropathy IgA nephropathy
Fibrillary glomerulopathyFibrillary glomerulopathy
Immunotactoid glomerulopathy Immunotactoid glomerulopathy
Thrombotic microangiopathyThrombotic microangiopathy
Amyloid Amyloid
VasculitisVasculitis
Interstitial nephritis secondary to virus Interstitial nephritis secondary to virus
HCV-associated PANHCV-associated PAN
7.
8. There are many methods of renal diseases in hepatitis c:There are many methods of renal diseases in hepatitis c:
1-1- Formation of immune complexesFormation of immune complexes
2- Formation of mixed cryoglobulinemia2- Formation of mixed cryoglobulinemia
3-3- Direct injury→ HCV has the ability to bind and penetrate theDirect injury→ HCV has the ability to bind and penetrate the
parenchyma cells by the CD 81 and SR-B1 receptors → HCVparenchyma cells by the CD 81 and SR-B1 receptors → HCV
endocytosis!endocytosis!
4- Some time the HCV RNA causes podocytes injury!4- Some time the HCV RNA causes podocytes injury!
5- HCV react with Toll –like receptors (TLR3)→ IL6, IL8!5- HCV react with Toll –like receptors (TLR3)→ IL6, IL8!
6- HCV causes hyperisulinemia and insulin resistance → increases the6- HCV causes hyperisulinemia and insulin resistance → increases the
IGF-1 (insulin like growth factor -1) and TGF-B (transforming growthIGF-1 (insulin like growth factor -1) and TGF-B (transforming growth
factors beta- 1)→ increase the oxidative stressfactors beta- 1)→ increase the oxidative stress!!
9. Mechanism of renal disease in HCV patientsMechanism of renal disease in HCV patients
↓↓
1-Immune
complexes
2-Mixed
cryogulobinemia
3-Direct injury
CD 81
4-Injury to
podocytes
5-Toll –like
receptors
6-Hyper
isulinemia and IR
10. The immune complexes mechanism:The immune complexes mechanism:
The HCV escape from immune system this leading to chronicThe HCV escape from immune system this leading to chronic
viremiaviremia →→immune complex will be formedimmune complex will be formed →→ will deposit inwill deposit in
glomeruliglomeruli→→ attract the platelets, neutrophils, andattract the platelets, neutrophils, and
macrophagesmacrophages →→ complement activation with chemokinecomplement activation with chemokine
generationgeneration
and leukocyte adhesion molecule expressionand leukocyte adhesion molecule expression
11. Capillary wall damage Cytokine and growth factorCapillary wall damage Cytokine and growth factor
Stimulation of mesangial cellsStimulation of mesangial cells
Proteinuria Mesangial cell proliferationProteinuria Mesangial cell proliferation
12. The formation of mixed cryoglobulinemia:The formation of mixed cryoglobulinemia:
The chronic infection of HCV leads to excessive proliferation andThe chronic infection of HCV leads to excessive proliferation and
stimulation of B cells and formation of type II cryoglobulin→ type IIstimulation of B cells and formation of type II cryoglobulin→ type II
mixed cryoglobulinemiamixed cryoglobulinemia
1-1-Deposition of cryoglobulin in the glomerular capillary and mesangiumDeposition of cryoglobulin in the glomerular capillary and mesangium
2-2-Causes vasculitis and fibrinoid necrosisCauses vasculitis and fibrinoid necrosis
3-3-Cryoglobulin can cause nephrotoxicity by attack the cellular fibronectinCryoglobulin can cause nephrotoxicity by attack the cellular fibronectin
in the mesangial matrixin the mesangial matrix
4-4- Cryoglobulins cause vasculitis by deposition in the small-sizedCryoglobulins cause vasculitis by deposition in the small-sized arteriesarteries
→ fix complement →cause local inflammation and injury→ fix complement →cause local inflammation and injury
13. Clinical pictures of renalClinical pictures of renal
diseases due to HCVdiseases due to HCV
14. Patients with chronic hepatitis c may hasPatients with chronic hepatitis c may has
1-Proteinuria1-Proteinuria
2-Hematuria (microscopic)2-Hematuria (microscopic)
3-Deterioration of kidney functions3-Deterioration of kidney functions
4-HTN4-HTN
5-Triad of purpura , asthenia , arthralgia ( GN with cryoglobulinemia)5-Triad of purpura , asthenia , arthralgia ( GN with cryoglobulinemia)
6-The purpura is palpable , which consists of leukocytoclastic vasculitis,6-The purpura is palpable , which consists of leukocytoclastic vasculitis,
this lesions mostly found in the lower limb or can found anywhere, thisthis lesions mostly found in the lower limb or can found anywhere, this
represent small vessel vasculitisrepresent small vessel vasculitis
7-Low serum C4 ,C1q and CH50 but normal C37-Low serum C4 ,C1q and CH50 but normal C3
8-There are different presentation of renal disease according to types of8-There are different presentation of renal disease according to types of
glomerulonephritisglomerulonephritis
16. Laboratory tests +Renal biopsyLaboratory tests +Renal biopsy
1-Anti-HVC antibody and HCV RNA in serum1-Anti-HVC antibody and HCV RNA in serum
2-Elevated serum transaminase in > 70% of patients2-Elevated serum transaminase in > 70% of patients
3-Cryoglobulin can be detected in > 50% of patients3-Cryoglobulin can be detected in > 50% of patients
4-Rheumatoid factors may be +ve4-Rheumatoid factors may be +ve
18. 11--Renal biopsy show changes according to type ofRenal biopsy show changes according to type of
glomerulonephritisglomerulonephritis
2-Membranoproliferative glomerulonephritis type I is2-Membranoproliferative glomerulonephritis type I is
the most commonthe most common
3-Or any other types3-Or any other types
19. The Membranoproliferative glomerulonephritis type IThe Membranoproliferative glomerulonephritis type I
Light microscopy:Light microscopy:
1-Glomerular hypercellularity1-Glomerular hypercellularity
2-Increased matrix and mesangial proliferation2-Increased matrix and mesangial proliferation
3-Splitting of capillary basement membranes (double3-Splitting of capillary basement membranes (double
contouring- tram tracks )contouring- tram tracks )
4-Intracapillary thrombosis due to cryoglobulin deposition4-Intracapillary thrombosis due to cryoglobulin deposition
5-Vasculitis and fibrinoid necrosis5-Vasculitis and fibrinoid necrosis..
21. EM:EM:
1-Large subendothelial deposits (different from1-Large subendothelial deposits (different from
idiopathic MPGN where the subendothelial depositsidiopathic MPGN where the subendothelial deposits
are much smaller)are much smaller)
2-These subendothelial deposits are so large they2-These subendothelial deposits are so large they
may protrude into the capillary lumen, causingmay protrude into the capillary lumen, causing
thrombosisthrombosis..
23. The policy of treatment depend on the renal function
1-In non- nephrotic , normal renal function1-In non- nephrotic , normal renal function →→ interferon alfainterferon alfa
2-In nephrotic syndrome , renal impairment or with cryoglobulinemia →2-In nephrotic syndrome , renal impairment or with cryoglobulinemia →
pegylated interferon alfapegylated interferon alfa (1 ug/kg week )+(1 ug/kg week )+ ribavirinribavirin(15 mg/kg/day) for 12(15 mg/kg/day) for 12
months then short course of low-dose corticosteroidsmonths then short course of low-dose corticosteroids
3-In Rapidly progressive renal failure:3-In Rapidly progressive renal failure: methylprednisolonemethylprednisolone (1 g/ day) for(1 g/ day) for
3 days, followed by3 days, followed by oral prednisoneoral prednisone (60 mg/day) with slow taper over 2-3(60 mg/day) with slow taper over 2-3
monthsmonths
4-4-Plasma exchangePlasma exchange to remove cryoglobulins (3/week for 2 – 3 weeks)to remove cryoglobulins (3/week for 2 – 3 weeks)
24. 5-5-RituximabRituximab to stop further B cell productionto stop further B cell production
(375mg/m 2 weekly for 4 weeks) or in resistance(375mg/m 2 weekly for 4 weeks) or in resistance
casescases
6-6-CyclophosphamideCyclophosphamide for 2 – 4 months ) 1.5 –for 2 – 4 months ) 1.5 –
2.0mg/kg daily orally)2.0mg/kg daily orally)
7-Use7-Use erythropoietinerythropoietin to keep Hb>110 g/L (ribavirinto keep Hb>110 g/L (ribavirin
causes red cell fragility)causes red cell fragility)
8-8-ACE-1/ARBACE-1/ARB to reduce proteinuria ( uPCR<50to reduce proteinuria ( uPCR<50
mg/mmol) also to control blood pressure ( aim <mg/mmol) also to control blood pressure ( aim <
130/80mmHg130/80mmHg