Minimal change nephropathy and primary focal segmental glomerulosclerosis (FSGS) represent opposite ends of a spectrum of idiopathic nephrotic syndrome. Minimal change disease often responds well to corticosteroids, while FSGS typically shows little response and often progresses to renal failure. Membranous nephropathy is the most common cause of nephrotic syndrome in adults, with one-third of cases remitting spontaneously, one-third remaining nephrotic, and one-third progressing to renal failure. IgA nephropathy is the most common type of glomerulonephritis and can cause hematuria, proteinuria, hypertension, and end-
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
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
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
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
Symptomatic presence of micro-organisms within the urinary tract i.e., kidney, ureters, bladder and urethra.
• Associated with inflammation of urinary tract.
Rapidly progressive glomerulonephritisajith joseph
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function,[4][5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months)[5] with glomerular crescent formation seen in at least 50%[5] or 75%[4] of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure[6] and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents (crescent-shaped scars)
Symptomatic presence of micro-organisms within the urinary tract i.e., kidney, ureters, bladder and urethra.
• Associated with inflammation of urinary tract.
Rapidly progressive glomerulonephritisajith joseph
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function,[4][5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months)[5] with glomerular crescent formation seen in at least 50%[5] or 75%[4] of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure[6] and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents (crescent-shaped scars)
Chest pain and implications for EMS. Review the history, physical and treatment of chest pain. Learn the most important causes of chest pain in the EMS setting and see great EKG examples of MI and the EKG mimics of cardiac ischemia.
Basic EKG and Rhythm Interpretation Symposia - The CRUDEM FoundationThe CRUDEM Foundation
Basic EKG and Rhythm Interpretation Symposia presented in Milot, Haiti at Hôpital Sacré Coeur.
CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
Nephrotic syndrome happens when damage to your kidneys causes these organs to release too much protein into your urine.
Nephrotic syndrome isn’t itself a disease. Diseases that damage blood vessels in your kidneys cause this syndrome.
Nephrotic syndrome is characterized by the following:
A high amount of protein present in the urine (proteinuria)
high cholesterol and triglyceride levels in the blood (hyperlipidemia)
Low levels of a protein called albumin in the blood (hypoalbuminemia)
Swelling (edema), particularly in your ankles and feet, and around your eyes.
This is about glomerulonephritis and all that you need to know. It contains different images illustrating this subject matter, well defined outline, different aspect of glomerulonephritis, which include acute and chronic glomerulonephritis, nephritic and nephrotic syndrome, investigations, how to diagnose glomerulonephritis, treatment and important discussions on Glomerulonephritidis. It is a presentation you need to check out.
Similar to Medicine 5th year, 6th & 7th lectures (Dr. Rasool) (20)
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
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.
- 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
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
2. MINIMAL CHANGE NEPHROPATHY AND PRIMARY
FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)
• Patients with minimal change nephropathy and
a subgroup of patients with FSGS can be seen
as opposite ends of a spectrum of conditions
causing idiopathic nephrotic syndrome .
Minimal change disease occurs at all ages but
accounts for nephrotic syndrome in most
children and about one-quarter of adults.
Proteinuria usually remits on high-dose
corticosteroid therapy (1 mg/kg prednisolone
for 6 weeks), although some patients who
respond incompletely or relapse frequently
need maintenance corticosteroids, cytotoxic
therapy or other agents. Minimal change
disease does not progress to CRF; the main
problems are those of the nephrotic syndrome
and complications of treatment.
3. • FSGS is a histological description with
many causes. The primary FSGS group
that present with idiopathic nephrotic
syndrome and no other cause of renal
disease typically show little response to
corticosteroid treatment and often
progress to renal failure; the disease
frequently recurs after renal
transplantation, and sometimes
proteinuria recurs almost immediately.
However, a proportion of patients with
FSGS do respond to corticosteroids (a
good prognostic sign). As FSGS is a focal
process, abnormal glomeruli may not be
seen on renal biopsy if only a few are
sampled, leading to an initial diagnosis of
minimal change nephropathy.
Juxtamedullary glomeruli are more likely
to be affected in early disease.
4. Cont.
• In other patients with the
histological appearances of FSGS
but lesser proteinuria, focal
scarring reflects healing of previous
focal glomerular injury, such as
haemolytic uraemic syndrome,
cholesterol embolism or vasculitis.
In others, it seems to represent
particular types of nephropathy: for
example, those associated with
heroin misuse, HIV infection and
massive obesity. Associations with
numerous other forms of injury and
renal disorders are reported. There
is no specific treatment for most of
5. MEMBRANOUS NEPHROPATHY
• This is the most common cause of
nephrotic syndrome in adults. A
proportion of cases are associated with
known causes but most are idiopathic.
Of this group, approximately one-third
remit spontaneously, one-third remain in
a nephrotic state, and one-third show
progressive loss of renal function. Short-
term treatment with high doses of
corticosteroids and alkylating agents
(e.g. cyclophosphamide) may improve
both the nephrotic syndrome and the
long-term prognosis. However, because
of the toxicity of these regimens, most
nephrologists reserve such treatment for
those with severe nephrotic syndrome or
deteriorating renal function.
6. IgA NEPHRO AND HENOCH-SCHÖN PURPURA
• IgA nephropathy is the most commonly
recognised type of glomerulonephritis and can
present in many ways . Haematuria is almost
universal, proteinuria usual, and hypertension
very common. There may be severe proteinuria
and nephrotic syndrome, or in some cases
progressive loss of renal function. The disease
is a common cause of ESRF. A particular
hallmark in some individuals is acute
exacerbations, often with gross haematuria, in
association with minor respiratory infections.
This may be so acute as to resemble acute
post-infectious glomerulonephritis, with fluid
retention, hypertension and oliguria with dark
or red urine. Characteristically, the latency
from clinical infection to nephritis is short: a
few days or less. These episodes usually
subside spontaneously
7. IgA/ HSP
• In children, and occasionally in adults, a
systemic vasculitis occurring in response to
similar infections is called Henoch-Schönlein
purpura. A characteristic petechial rash
(cutaneous vasculitis, typically affecting
buttocks and lower legs) and abdominal pain
(gastrointestinal vasculitis) usually dominate the
clinical picture, with mild glomerulonephritis
being indicated by haematuria. When the disease
occurs in older children or adults, the
glomerulonephritis is usually more prominent.
Renal biopsy shows mesangial IgA deposition
and appearances indistinguishable from acute
IgA nephropathy. Occasionally, IgA nephropathy
progresses rapidly and crescent formation may
be seen. The response to immunosuppressive
therapy is usually poor. The management of less
acute disease is largely directed towards the
control of blood pressure in an attempt to
prevent or retard progressive renal disease.
8. GLOMERULONEPHRITIS ASSO WITH
INFECTION
• CAUSES OF GLOMERULONEPHRITIS
ASSOCIATED WITH LOW SERUM
COMPLEMENT
• Post-infection glomerulonephritis
• Subacute bacterial infection-
especially endocarditis
• SLE
• Cryoglobulinaemia
• Mesangiocapillary glomerulonephritis-
usually type II
9. • Bacterial infections, usually subacute (typically
subacute bacterial endocarditis), may cause a
variety of histological patterns of
glomerulonephritis, but usually with plentiful
immunoglobulin deposition and often with
evidence of complement consumption (low
serum C3. In the developed world, hospital-
acquired infections are now a common cause of
these syndromes. World-wide, glomerulonephritis
associated with malaria, hepatitis B, hepatitis C,
schistosomiasis, leishmaniasis and other chronic
infections is very common. The usual histological
patterns are membranous and mesangiocapillary
lesions, although many other types may be seen.
FSGS associated with HIV infection is prevalent
in black races. Proving a causative relationship
between renal disease and infection in individual
cases is extremely difficult. Acute and chronic
infections may also cause interstitial renal
disease .
10. Acute post-infectious glomerulonephritis
• This is most common following infection with certain
strains of streptococcus and therefore is often called post-
streptococcal nephritis, but it can occur following other
infections. It is much more common in children than adults
but is now rare in the developed world. The latency is
usually about 10 days after a throat infection or longer
after skin infection, suggesting an immune mechanism
rather than direct infection. An acute nephritis of varying
severity occurs. Sodium retention, hypertension and
oedema, are particularly pronounced. There is also
reduction of GFR, proteinuria, haematuria and reduced
urine volume. Characteristically, this gives the urine a red
or smoky appearance. There are low serum
concentrations of C3 and C4 and evidence of
streptococcal infection (perform antistrepto-lysin O (ASO)
titre, culture of throat swab, and other swab tests if skin
infection is suspected). Renal function begins to improve
spontaneously within 10-14 days, and management by
fluid and sodium restriction and use of diuretic and
hypotensive agents is usually adequate. Remarkably, the
renal lesion in almost all children and most adults seems
to resolve completely despite the severity of the
glomerular inflammation and proliferation seen
11. RAPIDLY PROGRESSIVE GLOMERULONEPTIS
• This describes an extreme
inflammatory nephritis which causes
rapid loss of renal function over days
to weeks. Renal biopsy shows
crescentic lesions often associated
with necrotising lesions within the
glomerulus (focal segmental
(necrotising) glomerulonephritis). It
is typically seen in Goodpasture's
disease, where there are specific
anti-GBM antibodies, and in small-
vessel vasculitides , but can also be
seen in SLE and occasionally IgA
and other nephropathies
12. INHERITED GLOMERULAR DISEASES
• Alport syndrome
• A number of uncommon diseases may affect the
glomerulus in childhood, but the most important one
affecting adults is Alport's syndrome. Most cases
arise from a mutation or deletion of the COL4A5 gene
on the X chromosome which encodes type IV
collagen, resulting in inheritance as an X-linked
recessive disorder. Mutations in COL4A3 or COL4A4
genes are less common and cause autosomal
recessive disease. The accumulation of abnormal
collagen results in a progressive degeneration of the
GBM. Affected patients progress from haematuria to
ESRF in their late teens or twenties. Female carriers
of COL4A5 mutations usually have haematuria but
rarely develop significant renal disease. Some other
basement membranes containing the same collagen
isoforms are similarly affected, notably in the
cochlea, so that Alport's syndrome is associated with
sensorineural deafness and ocular abnormalities. No
specific treatment has been devised to slow the
progress of this condition, but patients with Alport's
syndrome are good candidates for renal replacement
therapy as they are young and usually otherwise
healthy. Some of these patients develop an immune
response to the normal collagen antigens present in
13. THIN GBM DISEASE
• In 'thin GBM' disease there is glomerular
bleeding, usually only at the microscopic
or stick-test level, without associated
hypertension, proteinuria or reduction of
GFR. The glomeruli appear normal by
light microscopy, but on electron
microscopy the GBM is abnormally thin.
This autosomal dominant condition
accounts for a large proportion of
'benign familial haematuria' and has an
excellent prognosis. Some families may
be carriers of autosomal recessive
Alport's syndrome, but this does not
14. TUBULO-INTERSTITIAL DISEASES
• INTERSTITIAL NEPHRITIS A group of
inflammatory, inherited and other
diseases affect renal tubules and the
surrounding interstitium. The clinical
presentation is often renal failure,
but electrolyte abnormalities are
common, especially hyperkalaemia
and acidosis. Proteinuria (and
albuminuria) is rarely > 1 g/24 hrs but
low molecular weight proteinuria
(e.g. retinol-binding protein, β2-
microglobulin, lysozyme) with
haematuria and pyuria are common.
15. ACUTE INTERSTITIAL
NEPHRITIS (AIN)
• Acute inflammation within the tubulo-
interstitium is most commonly allergic,
particularly to drugs, but other causes
include toxins and a variety of systemic
diseases and infections . Renal biopsies
show intense inflammation, with
polymorphonuclear leucocytes and
lymphocytes surrounding tubules and
blood vessels and invading tubules
(tubulitis), and occasional eosinophils
(especially in drug-induced disease).
16. Cont.
• CAUSES OF ACUTE INTERSTITIAL
NEPHRITIS Allergic
• Penicillins
• NSAIDs
• Allopurinol
• Many other drugs
18. Cont.
• Only a minority (perhaps 30%) of patients
with drug-induced AIN have a generalised
drug hypersensitivity reaction (e.g. fever,
rash, eosinophilia) and dipstick testing of
the urine is usually unimpressive. However,
leucocyturia is common, and eosinophils
are found in the urine in up to 70% of
patients. Deterioration of renal function in
drug-induced AIN may be dramatic and
resemble rapidly progressive
glomerulonephritis. Renal biopsy is usually
required to confirm the diagnosis. The
degree of chronic inflammation in a biopsy
is a useful predictor of the eventual
outcome for renal function. Many patients
are not oliguric despite moderately severe
ARF, and AIN should always be considered
in patients with non-oliguric ARF.
19. Cont.
• Management Some patients with
drug-induced AIN recover
following withdrawal of the drug
alone, but corticosteroids (e.g.
prednisolone 1 mg/kg/day)
accelerate recovery and may
prevent long-term scarring.
Dialysis is sometimes necessary,
but is usually only short-term.
Other specific causes should be
treated where possible
20. CHRONIC INTERSTITIAL NEPHRITIS
• Aetiology Chronic interstitial nephritis (CIN)
is caused by a heterogeneous group of
diseases, summarised in . However, it is
quite common for the condition to be
diagnosed late and for no aetiology to be
apparent. Toxic causes of CIN The
combination of interstitial nephritis and
tumours of the collecting system is seen in
Balkan nephropathy, so called because of
where cases are found, and has been
controversially attributed to ingestion of
fungal toxins, particularly ochratoxin A,
present in food made from stored grain. A
plant toxin, aristolochic acid, has been
blamed for a rapidly progressive syndrome
caused by mistaken identity of ingredients
in herbal preparations
21. Cont/CIN
• CAUSES OF CHRONIC INTERSTITIAL
NEPHRITIS Acute interstitial nephritis
• Any of the causes of AIN if persistent
•
• Glomerulonephritis
• Varying degrees of interstitial inflammation
occur in association with most types of
inflammatory glomerulonephritis
• Immune/inflammatory
• Sarcoidosis
• Sjögren's syndrome
• SLE, primary autoimmune
• Chronic transplant rejection
22. • Toxic
• Mushrooms
• Lead
• Chinese herbs
• Balkan nephropathy
• Drugs
• All drugs causing AIN
• Lithium toxicity
• Analgesic nephropathy
• Ciclosporin, tacrolimus
• Infection
• Consequence of severe pyelonephritis
• Congenital/developmental
• Vesico-ureteric reflux-is associated; causation not clear
• Renal dysplasias-often associated with reflux
• Inherited-now well recognised but mechanisms unclear
• Other-Wilson's disease, medullary sponge kidney, sickle-cell
nephropathy
• Metabolic and systemic diseases
23. Cont.
• Long-term ingestion (years to decades) of
analgesic drugs can cause renal papillary
necrosis and CIN. As the papillae are at the
end of the capillary distribution in the
kidney, they become ischaemic most easily
and may necrose in this condition, in sickle-
cell disease and occasionally in diabetes
and other conditions. Necrosed papillae
may cause ureteric obstruction and renal
colic. Papillary necrosis is difficult to
identify other than on IVU or retrograde
pyelography. In animals, lesions can be
induced with almost any NSAID; however,
there has been a dramatic fall in the
incidence of this disease following
withdrawal of phenacetin from compound
analgesics. If it is diagnosed, cessation of
analgesic intake may arrest progression
24. Cont.
• Clinical and biochemical features Most
patients present in adult life with CRF,
hypertension and small kidneys. CRF is
often moderate (urea < 25 mmol/l or 150
mg/dl) but, because of tubular dysfunction,
electrolyte abnormalities are typically
more severe (e.g. hyperkalaemia,
acidosis). Urinalysis abnormalities are
non-specific. A minority of patients
present with hypotension, polyuria and
features of sodium and water depletion
(e.g. low blood pressure and jugular
venous pressure)-salt-losing nephropathy.
Impairment of urine-concentrating ability
and sodium conservation places patients
with CIN at risk of superimposed ARF with
even moderate salt and water depletion
during an acute illness. Hyperkalaemia
may be disproportionate in CIN or in
diabetic nephropathy because of
25. Glomerulonephritis / Glomerulosclerosis
• Glomerulonephritis - An
inflammatory condition that
affects predominantly the
glomeruli.
• Causes
•IgA nephropathy
• Streptococcus bacteria
•Autoimmune
• Glomerulosclerosis - scarring of
the glomeruli
26. GN/GS
Signs and Symptoms
• Blood or protein in urine
• Frothy urine (signifying protein in
urine)
• Dark or pink-coloured urine
• Leg swelling
• Systemic disease like diabetes or
autoimmune disease will have
systemic manifestations, e.g.
weight loss, arthritis, or skin rash
27. GN/GS
Treatment
Specific
• Suppression of inflammation
may be achieved by certain
medications (eg steroids).
General
• Medications to decrease
excretion of urinary protein
• Control of blood pressure
• Dietary modifications
29. Nephr I / O tic ????
• NephrOtic
(PrOtein)
• 3 Systemic
Diseases
• Diabetes
• SLE
• Amyloidosis
• 1 “membrane”
• Membranous
GN
• 2 others
• Minimal Change
• NephrItic (RBC +/-
casts)
• 3 Autoimmune
• Poststrep GN
(Type III)
• IgA Nephropathy
(Type III)
• Goospasture’s
(Type II)
• 1 “membrane”
• Membranoproliferati
ve
• 2 others
• Crescentic
• Alport’s (collagen IV
30. Hypersensitivity Essentials of GN
• Type I – IgE cross-linking on
presensitizes mast cells
inflammatory mediators released
• Type II – Antibodies directed
against specific “enemies.”
Damage cells via complement
mediated “MAC” Inflammatory
response NOT necessarily present
• Type III – Immune complex
deposits (eg SLE) activates
complement C5a chemotactic to
neutrophils damage
• Type IV – T-cell mediated
33. NephrItic – Autoimmune
• Poststrep GN (#1 acute) – type III
(“small” – subepithelial “humps”) –
follows sore throat or cellulitis
•Peripheral & periorbital edema
(autoimmune)
• IgA – post-infectious – type III
•Mild, self-limiting, assoc w/
Henoch-Sch
• Goodpastures – type II
•Men in mid 20’s
34. NephrItic – Other 3
• Membranoproliferative –
MESANGIAL CELLS proliferate.
Assoc w/ Hep C, SLE, a1-
antitrypsin.
• Crescentic GN – Fibrin deposition
in Bowman’s. Assoc w/ post-strep
& membranous GN.
• Alport’s – Hereditary, type IV
collagen defect, CN VIII defective
36. Linear – Type II
Goodpasture’s
(anti-GBM)
Capillary BM of glomerulus & alveolar walls
37. Granular – Type III
IgA
Nephropathy
(mesangial
deposits)
Post-Strep GN
(Subepithelial)
Membranous GN
(deposits are in
the GBM)
SLE GN
(Subendothelial)
Colon CA (anti-
CEA deposits)