1. Acute Nephritic Syndrome
Dr.Gudigunti Gopi
Dept of Nephrology,
Rustaq Hospital.

2. 1) Overview
2) Synonymous Conditions
3) Etiology of Ac Nephritic Synd
4) APSGN/APIGN
5) Ac Nephritic Synd Clinical Presentation
6) Workup
7) Management.

3. ● Acute Nephritic Synd comprises a specific set of renal diseases in
which an immunologic mechanism triggers inflammation and
proliferation of glomerular tissue that can result in damage to the
basement membrane, mesangium, or capillary endothelium.
● Bright initially described acute glomerulonephritis (GN) in 1927. Acute
poststreptococcal glomerulonephritis (APSGN) is the archetype of
acute nephritic Synd. Acute nephritic syndrome is the most serious
and potentially devastating form of the various renal syndromes.
Over view

4. RPGN
● Rapidly progressive GN (RPGN) describes the clinical situation in which
glomerular injury is so acute and severe that renal function deteriorates
during days or weeks
● The histologic counterpart of RPGN is crescentic GN. The proliferative
cellular response seen outside the glomerular tuft but within Bowman's space
is known as a crescent because of its shape on histologic cross section
● Unfortunately, not all patients with a nephritic urine sediment and acute
kidney injury (AKI) will fit this syndrome. For example, AKI may also occur in
milder forms of glomerular disease if it is complicated by accelerated
hypertension, renal vein thrombosis, or acute tubular necrosis. This
emphasizes the need to obtain histologic confirmation of the clinical
diagnosis.

6. Aetiology of Ac Nephritic Synd

7. APSGN/APIGN
Etiology
● The offending organisms are virtually always
group A streptococci ( GAS ).
● Acute poststreptococcal glomerulonephritis
(APSGN) follows pyodermatitis with streptococci
M types 47, 49, 55, 2, 60
● Acute poststreptococcal glomerulonephritis
(APSGN) throat infection with streptococci M
types 1, 2, 4, 3, 25, 49, and 12.

8. APSGN/APIGN
● Occurs 10-14 days after URTI
● NOT SYNPHARYNGITIC
● CAN OCCUR IN EPIDEMICS
● Epidemic poststreptococcal glomerulonephritis occurs
mainly in developing countries in areas such as Africa,
the West Indies, and the Middle East.
● Incidence is declining in the West due to better
antibiotics/hygeine- similar to Ac Rh Heart Disease
● M : F 2:1

9. Ac Nephritic Syndrome
Clinical Presentation
● History
A history suggestive of preceding streptococcal infection may include a
preceding infective episode such as pharyngitis, tonsillitis, or pyoderma.
This is the sine qua non for the diagnosis of APSGN.
In general, the latent period is 1-2 weeks after a throat infection and 3-6
weeks after a skin infection.
The onset of signs and symptoms at the same time as pharyngitis (also
called synpharyngitic nephritis) is more likely to be immunoglobulin A
(IgA) nephropathy rather than APSGN.

10. Ac Nephritic Syndrome
Clinical Presentation
Classic Triad
Haematuria
Edema
Hypertension
40 % Classical – 95%
have atleast 2 of these
Hematuria
This is present universally.
In 30% of cases, gross hematuria is present.
Edema
Edema is present in 80-90% of cases, and it is the presenting complaint in
60% of cases.
Reduced blood flow to the glomerulus that manifests as low fractional
excretion of sodium and concentrated urine. This salt and water retention
leads to edema.

11. Ac Nephritic Syndrome
Clinical Presentation
Hypertension
Hypertension occurs in 60-80% of cases and is more common among elderly individuals.
In 50% of cases, the hypertension can be severe; however, more often it is transient, with
normalization of blood pressure upon restoration of the glomerular filtration rate, loss of
edema, and normalization of plasma volume.
If hypertension persists, it is more indicative of the progression to a more chronic stage or
that the disease is not poststreptococcal glomerulonephritis.
Hypertension is thought to be the result of excessive salt and water retention.
Hypertensive encephalopathy occurs in no more than 5-10% of patients. Usually, clinical
improvement occurs without any neurological sequelae.
Oliguria
This is present in 10-50% of cases, and, in 15%, urine output is less than 200 mL.
Oliguria is indicative of the severe crescentic form of the disease.
It is often transient, with diuresis occurring within 1-2 weeks.

12. Acute Nephritic Syndrome

13. D/D
● Membranoproliferative glomerulonephritis (MPGN) — The
presentation of MPGN may be indistinguishable initially from PSGN. It
typically presents with hematuria, hypertension, proteinuria, and
hypocomplementemia following an upper respiratory infection.
However, patients with MPGN continue to have persistent nephritis
and hypocomplementemia beyond four to six weeks and possibly a
further elevation in serum creatinine. In contrast, patients with PSGN
typically have resolution of their disease and a return of normal C3
and CH50 levels
● IgA nephropathy — Patients with IgA nephropathy often present
after an upper respiratory infection, similar to the presentation of
patients with PSGN. Potential distinguishing features from PSGN
include a shorter time between the antecedent illness and hematuria
is (less than 5 versus more than 10 days in PSGN) and a history of
prior episodes of gross hematuria since recurrence is rare in PSGN
● Lupus nephritis and Henoch-Schönlein purpura (IgA vasculitis)
nephritis share similar features to PSGN. However, extrarenal
manifestations of the underlying systemic diseases and laboratory
testing should differentiate them from PSGN..

14. Ac Nephritic Syndrome
Work Up
● RFT'S :-
This reflects the decrease in the glomerular filtration rate that
occurs in the acute phase.
The elevations are usually transient. Most common in
APSGN.
Prolonged Elevation S/O other causes.
Patients who have the crescentic form of
glomerulonephritis( RPGN) have rapid deterioration and,
often, incomplete recovery of renal function

15. Ac Nephritic Syndrome
Work Up
Urinalysis
Results are always abnormal.
Hematuria and proteinuria are present in all cases.
Urine sediment has red blood cells, red blood cell casts, white blood cells, granular casts,
and, rarely, white blood cell casts.
Dysmorphic red blood cells indicative of glomerular hematuria can usually be detected by
performing phase-contrast microscopy.
Red blood cell casts are best detected in first, early-morning urine specimens examined by
the physician immediately after the patient voids.
Hematuria usually resolves within 3-6 months but may persist as long as 18 months.
Microscopic hematuria may be present in patients in whom the disease has otherwise
clinically resolved.
Proteinuria may be mild or so severe that it causes nephrotic syndrome.
Approximately 5-10% of patients with APSGN have nephrotic-range proteinuria.
Proteinuria usually disappears in 6 months. A mild increase in urinary protein excretion is
present in 15% at 3 years and 2% at 10 years.
Patients with nephrotic-range proteinuria in the acute phase or persistent heavy proteinuria
have a worse prognosis. This is often associated with an evolution to a garlandlike pattern
of immune deposits as the disease progresses.

16. Phase contrast micrograph
showing dysmorphic red cells
in urine sediment
Scanning electron micrograph
showing dysmorphic red cells
in urine sediment
Photomicrograph of
urine sediment with a
red cell cast

17. Evidence of preceding streptococcal infection
Antibody titers to extracellular products of streptococci are positive in more than
95% of patients with pharyngitis and 80% of patients with skin infections.
The antistreptolysin (ASO), antinicotinamide adenine dinucleotidase (anti-NAD),
antihyaluronidase (AHase), and anti–DNAse B are commonly positive after
pharyngitis, and anti–DNAse B and AHase titers are more often positive
following skin infections.
ASO titers are frequently used to document streptococcal infection, but a more
sensitive test is the streptozyme test, which tests antibodies to ASO, anti–
DNAse B, AHase, and anti-NAD.
Studies suggest that the relatively unavailable antizymogen titer test is superior
to both anti–DNAse B and ASO titers.
In general, the antibody titers are elevated at 1 week, peak at 1 month, and fall
toward preinfection levels after several months.
Ac Nephritic Syndrome
Work Up

18. Understanding Serology In Ac
Nephritis

19. Ac Nephritic Syndrome
Work Up
UltraSound
Renal ultrasound images usually reveal normal-sized
kidneys bilaterally.
Nephromegaly/ Echogenic Kidneys rarely seen and is S/O
Ac Inflamation
Renal Biopsy
APSGN is often a clinical diagnosis and requires the detection of glomerulonephritis and
evidence of preceding streptococcal infection.
Atypical features in the early phase that suggest the need for renal biopsy include the
following:
✔ Absence of the latent period between streptococcal infection and acute
glomerulonephritis
✔ Anuria
✔ Rapidly deteriorating renal function
✔ Normal serum complement levels
✔ No rise in antistreptococcal antibodies
✔ Extrarenal manifestations of systemic disease-- S/O LUPUS NEPHRITIS
✔ No improvement or continued decrease in the glomerular filtration rate at 2 weeks
✔ Persistence of hypertension beyond 2 weeks

20. APSGN- LM STUDY

21. APSGN- EM
Humps

23. Necrosis

24. Cellular Crescent Glomerulus

25. Ac Nephritic Synd
Rx
Symptomatic therapy is recommended for patients with Ac Nephritic Synd, and it
should be based on the clinical severity of the illness. The major goal is to
control edema and blood pressure.
During the acute phase of the disease, restrict salt and water.
If significant edema or hypertension develops, administer diuretics.
Loop diuretics increase urinary output and consequently improve cardiovascular
congestion and hypertension.
For hypertension not controlled by diuretics, usually calcium channel blockers or
angiotensin-converting enzyme inhibitors are useful. For malignant hypertension,
intravenous nitroprusside or other parenteral agents are used.
Indications for dialysis include life-threatening hyperkalemia and clinical manifestations
of uremia.
Restricting physical activity is appropriate in the first few days of the illness but is
unnecessary once the patient feels well.
Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated.