2. Glomerular diseases account for a significant proportion of
acute and chronic kidney disease. There are many causes of
glomerular damage, including immunological injury, inherited
diseases such as ,metabolic diseases), and deposition of abnormal
proteins such as amyloid in the glomeruli. The response of the
glomerulus to injury and hence the predominant clinical features
vary according to the nature of the insult. Most patients with
glomerular disease do not present acutely and are asymptomatic
until abnormalities are detected on routine screening of blood or
urine samples.
3. Diagnosis of glomerular diseases Urine tests The urinalysis
may show red blood cells (which are seen when there is damage or
inflammation in the glomeruli), white blood cells ( indicate
inflammation), or increased protein levels ( indicator of
glomerular damage). Blood tests Blood tests are used to measure the
level of creatinine and blood
4. Nephritic syndrome 1. Haematuria (red or brown urine) Oedema
and generalised fluid retention Hypertension Oliguria Nephrotic
syndrome 1. Overt proteinuria: usually > 3.5 g/24 hrs (urine may
be frothy) 2. Hypoalbuminaemia (< 30 g/L) 3. Oedema and
generalised fluid retention 4. Intravascular volume depletion with
hypotension, or intravascular expansion with hypertension, may
occur
5. Clinical and laboratory features of glomerular injury
Leakage of cells and macromolecules across the glomerular
filtration barrier Proteinuria: characteristic of diseases that
affect the podocyte, scarring and deposition of foreign material
Haematuria: characteristic of inflammatory and destructive
processes Impaired renal function and reduced GFR Hypertension
6. glomerulonephritis describe all types of glomerular disease,
even though some of these (such as minimal change nephropathy) are
not associated with inflammation Glomerulonephritis is generally
classified in terms of the histopathological appearances
7. Minimal change nephropathy may occur at all ages but
accounts for nephrotic syndrome in most children and about one-
quarter of adults. caused by reversible dysfunction of podocytes.
It is postulated that MCD is a disorder of T cells, which release a
cytokine that injures the glomerular epithelial foot processes.
This, in turn, leads to a decreased synthesis of polyanions that
constitute the normal charge barrier to the filtration of
macromolecules, such as albumin. When the polyanions are
8. Focal segmental glomerulosclerosis Primary focal segmental
glomerulosclerosis (FSGS) can occur in all age groups. In some
patients, FSGS can have specific causes, such as HIV infection,
podocyte toxins and massive obesity, but in most cases the
underlying cause is unknown (primary FSGS). Patients with primary
FSGS present with massive proteinuria and idiopathic nephrotic
syndrome. Histological analysis shows
9. Membranous glomerulonephritis
10. Membranous glomerulonephritis, also known as membranous
nephropathy _common cause of nephrotic syndrome in adults. _
antibodies (usually autoantibodies) directed at antigen(s)
expressed on the surface of podocytes. _other causes, such as heavy
metal poisoning, drugs, infections and tumours but most are
idiopathic. Approximately one-third of patients with idiopathic
membranous glomerulonephritis undergo spontaneous remission;
one-third remain in a nephrotic state, and one-third go on to
develop CKD. - _Short-term treatment with high doses of
corticosteroids and cyclophosphamide may improve both the nephrotic
syndrome and the long-term prognosis. _ toxicity of these regimens:
nephrologists reserve such treatment for those with severe
nephrotic syndrome or deteriorating renal function.
11. IgA nephropathy
12. sangial deposition pattern
13. _One of the most common types of glomerulo nephritis and
can present in many ways. _Haematuria is the earliest sign and is
almost universal, and hypertension is also very common.
_Proteinuria can also occur but is usually a later feature. In many
cases, there is slowly progressive loss of renal function leading
to ESRD. _Clinical presentations are protean and vary with age. _A
particular hallmark of IgA nephropathy in young adults is the
occurrence of acute self limiting exacerbations, often with gross
haematuria, in association with minor respiratory
14. HenochSchnlein purpura most commonly occurs in children but
can also be observed in adults. It is characterised by a systemic
vasculitis that often arises in response to an infectious trigger.
characteristic petechial rash typically affecting buttocks and
lower legs, and abdominal pain due to the occurrence of vasculitis
involving the gastrointestinal tract. The presence of
glomerulonephritis is usually indicated by the occurrence of
haematuria.
15. Mesangiocapillary glomerulonephritis "
membranoproliferative " MPGN increase in mesangial cellularity with
thickening of glomerular capillary walls and subendothelial
deposition of immune complexes and/or components of the complement
pathway. The typical presentation is with proteinuria and
haematuria. can be classified into two main subtypes:
16. Post-streptococcal glomerulonephritis case: 12 year old
girl present in distress to the doctor : complaint: rusty color
urine , puffy face on physical exam she had high blood pressure and
a urine test stripe revealed proteinuria. On hearing past history
the physician noted that she had recovered from a strep trhoat
infection following an antibiotic treatment. Blood tests suggested
an autoimmune response damaging the nephrons.
17. _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. _also reduction of GFR,
proteinuria, haematuria and reduced urine volume.
Characteristically, this gives the urine a red or smoky appearance.
As in other causes of post-infectious glomerulonephritis, serum
concentrations of C3 and C4 are typically reduced, reflecting
complement consumption and evidence of streptococcal infection may
be found. _ Renal function begins to improve spontaneously within
1014 days, and management by fluid and sodium restriction with
diuretic and hypotensive agents is usually adequate. Remarkably,
the renal lesion in almost all children and many adults seems to
resolve com-pletely, despite the severity of the glomerular
inflamma-tion and proliferation seen histologically.
18. Rapidly progressive glomerulonephritis Rapidly progressive
glomerulonephritis ( crescentic glomerulonephritis) is
characterised by rapid loss of renal function over days to weeks.
Renal biopsy shows crescentic lesions, often associated with
necrotising lesions within the glomerulus, termed focal segmental
(necrotising) glomerulonephritis. It is typically seen in
Goodpastures disease, where the underlying cause is the
development
19. crescentic glomerulonephritis
20. Inherited glomerular diseases AIports syndrome most
important one affecting adults is Alports syndrome. -Most cases
arise from a mutation or deletion of the COL4A5 ( X-linked
recessive disorder.) -Mutations in COL4A3
21. ACE inhibitors may slow but not prevent loss of kidney
function. Patients with Alports syndrome are good candidates for
RRT, as they are young and usually otherwise healthy. They can
develop an immune response to the normal collagen antigens present
in the GBM of the donor kidney and, in a small minority, anti-GBM
disease develops and destroys the allograft.
22. Thin glomerular basement membrane disease In thin
glomerular basement membrane disease there is glomerular bleeding,
usually only at the microscopic or dipstick level, without
associated hypertension, proteinuria or a reduction in GFR. The
glomeruli appear normal by light microscopy but, on electron
microscopy, the GBM is abnormally thin. The condition may be
familial and some patients are carriers of Alport mutations. This
does not appear to account for all cases, and in many