acute glomerulonephritis

Question 1

Nephritic Syndrome

Answer 1

Hematuria ( RBC cast)
High Blood pressure
Azotemia ( high Cr and BUN ) and oliguria (renal impairment)
Edema (real overload , loss of GFR)

Question 2

most common cause of gross hematuria in children

Answer 2

PSGN used to be the most common cause of gross hematuria in children; now IgA nephropathy is most common ..because of aggressive ttt of tonsillitis

Question 3

ETIOLOGY of PSGN

Answer 3

follows infection of the throat or skin with certain “nephritogenic” strains of group A beta-hemolytic streptococci.
Pharynigitis mostly in winter and skin infection in summer
throat (serotype 12).
skin (serotype 49) infections.

Question 4

PATHOLOGY of PSGN ang microscope

Answer 4

Crescents and interstitial inflammation may be seen in severe cases..
Immunofluorescence : deposits of immunoglobulin and complement on the glomerular basement membranes (GBMs) and in the mesangium.
On electron microscopy, electron-dense deposits, or “humps,” are observed on the epithelial side of the GBM

Question 5

PATHOGENESIS.of PSGN

Answer 5

The precise mechanisms by which nephritogenic streptococci induce the disease remain to be determined.
A depression in the serum complement (C3) and deposition of Ig strongly suggest that poststreptococcal glomerulonephritis is mediated by immune complexes.

Question 6

CLINICAL MANIFESTATIONS of PSGN

Answer 6

most common in children 5-15 yr
rare before the age of 3 yr.

an acute nephritic syndrome 1-2 wk after an URTI or 3-4 wk after skin streptococcal infection.

Renal involvement may vary from asymptomatic microscopic hematuria with normal renal function to full nephritic presentation or rarely progress to acute renal failure requiring dialysis. (very rare)
Nonspecific symptoms such as malaise, lethargy, abdominal or flank pain, and fever are common
Encephalopathy / heart failure if malignant HTN develop. (not common)
The edema is a result of salt and water retention due to decreased GFR(real)
Nephrotic syndrome may also occur .. 10-20%
The acute phase generally resolves within 2 months after onset, (if more than 2 m then you have to take biopsy)
Urinary abnormalities may persist for 1 yr.(microscopic hematuria)

Question 7

DIAGNOSIS of psgn

Answer 7

Urinalysis
demonstrates red blood cells (RBCs), with RBC casts
Proteinuria. (no proteinurea if present it might be not infectoius – rare

                     Cultures  Throat swab  

CBC  (no thrombocytopenia and no anemia)
ASO titer – high 
Anti DNAase B level 
The serum C3 level is usually reduced
With normal C4! Or maybe low 
Example of nephritic syndrome with low complement :
 Post.inf\ lupus\memb.prolifrative
Staph (shunt nephritis )  , infective endocarditis and  cryoglobulinemia
Confirmation of the diagnosisBlood tests

Question 8

Renal biopsy indication in psgn

Answer 8

renal biopsy is not indicated in a classical PSGN presentation
It is important if SLE nephritis or MPGN is suspected
Acute Renal Failure
Nephrotic syndrome
the absence of evidence for streptococcal infection
the absence of hypocomplementemia, or
persistent low C3 and C4 for more than 3 mo after onset …..( SLE) ??
Or if they not low at presentation

Question 9

COMPLICATIONS of psgn

Answer 9

are those of acute renal failure and include 
volume overload,
 heart failure, 
hypertension,
 hyperkalemia, 
hyperphosphatemia,
 hypocalcemia, 
acidosis, 
Seizures (maybe related to hypeertension or to uremia0,
 and uremia

Question 10

TREATMENT of psgn

Answer 10

no specific therapy for acute poststreptococcal glomerulonephritis.
the management is that of acute renal failure .
Although a 10-day course of systemic antibiotic therapy, generally with penicillin, is recommended to limit the spread of the nephritogenic organisms, no evidence shows that antibiotic therapy affects the natural history of glomerulonephritis.
Supportive therapy for HTN, electrolyte disturbances
medications (diuretics, Ca Channel Blockers and angiotensin-converting enzyme inhibitors)

Question 11

PROGNOSIS psgn

Answer 11

Excellent outcome with Complete recovery occuring in more than 95% .
0-5 % mortality was reported in some studies in the acute stage due to acute renal or cardiac failure and hypertension.
They end with dialysis or chronic proteinuria or chronic hypertension
Recurrences are extremely rare
Urinary abnormalities may pertsist for one year
C3 level is back to normal by 2-3 months .

Question 12

PREVENTION psgn

Answer 12

Early systemic antibiotic therapy of streptococcal throat and skin infections does not eliminate the risk of glomerulonephritis.
Family members of patients with acute glomerulonephritis should be cultured for group A beta-hemolytic streptococci and treated if culture positive.

Question 13

IgA Nephropathy presentation

Answer 13

Most commonly present with recurrent gross hematuria following  URTI ( 1-2 days post infection)
Other modes of presentations:
    -Asymptomatic microscopic hematuria
    -Proteinuria
    -Nephrotic syndrome 
    -Acute Nephritis 
    -Mixed Nephritic/Nephrotic

Question 14

Diagnosis IgA Nephropathy

Answer 14

Definite diagnosis is renal Biopsy
Increase serum IgA in < 20% of patients
Normal serum C3 and C4
Renal Biopsy:
LM: focal segmental mesangial proliferation
EM and IF : deposition of IgA and sometimes lesser amount IgG, IgM and C3.

Not complement mediator

Question 15

Prognosis iga

poor prognosis

Answer 15

Prognosis :
30 %  of patients will progress to ESRD 
The recurrence of hematuria and the persistent microscopic hematuria does not correlate with the prognosis
Poor prognosis: 
   - Hypertension
    -Heavy proteinuria > 1g/L
    -Diffuse GN with Crescents on Biopsy

Question 16

Treatment iga

Answer 16

Fish oil
Steroids : Prednisone & pulse Methyl Prednisone (RF|Nephrotic range proeinurea)
So when to give steroid ?
Heavy proteinuria , high createnine , nephrotic
ACE inhibitors and ARBs for hypertension and control of proteinuria Drug of choice for IgA
Tonsillectomy..