Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, and edema. It results from increased permeability of the glomerular basement membrane. Nephritic syndrome involves inflammation of the glomeruli that causes hematuria, hypertension, and sometimes reduced kidney function. While nephrotic syndrome presents with proteinuria and edema, nephritic syndrome presents with hematuria and red blood cell casts with proteinuria generally less than 3g per day. Both require diagnostic tests including urine analysis, blood work, and often renal biopsy for diagnosis and management.

1. Nephrotic And Nephrotic
Syndrome

3. NEPHROTIC NEPHRITIC
• Loss of foot processes  Proliferative changes and
inflammation of the glomeruli
Bottom line- “increased permeability of the glomeruli”
Pathophysiology

4. What is Nephrotic syndrome
 Increased permeability of the glomerulus leading to loss of proteins into the
tubules

5. How many pathological types causes
nephrotic syndrome?

7. Proteinuria
(>3.5g/24/hr in adults
or 40mg/m2 /hr in
children)
Hypoalbuminemia
<2.5gm/dl
Hyperlipidemia
Edema Nephrotic
Syndrome

8. PRESENTATION
 New-onset oedema
Initially periorbital or peripheral
Later genitals, ascites, anasarca
 Frothy urine
 Generalised symptoms –
lethargy, fatigue, reduced
appetite

10. Further Possible Presentations
 Oedema
 BP normal/raised
 Leukonychia
 Breathlessness:
Pleural effusion, fluid overload,
AKI
 DVT/PE/MI
 Eruptive xanthomata/
xanthalosmata

11. Differential Diagnosis for Oedema
 Congestive Cardiac Failure
Raised JVP, pulmonary oedema, mild proteinuria
 Liver disease
Hypoalbuminaemia, ascites/oedema

12.  Most children (90%) with nephrotic syndrome have a form of
the idiopathic nephrotic syndrome.

13. Investigations
 Urine dipstick for protein
 Urine microscopy
 Bloods – the usual ones, plus renal screen
Immunoglobulins, electrophoresis (myeloma
screen), complement (C3, C4) autoantibodies (ANA,
ANCA, anti-dsDNA, anti-GBM)
 Renal ultrasound
 Renal biopsy (all adults)
Children generally trial of steroids first

14. Investigations:-
1-Urine analysis:-
 Proteinuria : 3-4 + SELECTIVE.
 Urine collection for protein
>40mg/m2/hr for children
 volume: oliguria (during stage of edema formation)
 Microscopically:-
microscopic hematuria 20%, large number of hyaline cast

15. Investigations:-
2-Blood:
 Serum protein: decrease >5.5gm/dL , Albumin levels are low
(＜2.5gm/dL).
 Serum cholesterol and triglycerides:
Cholesterol ＞5.7mmol/L (220mg/dl).
 ESR↑＞100mm/hr during activity phase
3.Serum complement: Vary with clinical type.
4.Renal function

16. Management
 Conservative
Monitor U&E, BP, fluid balance, weight
Salt and fluid restriction
Treat underlying cause

17. Management
 General (non-specific )
 *Corticosteroid therapy

18. General therapy:-
 Hospitalization:- for initial work-up and evaluation of
treatment.
 Activity: usually no restriction , except
massive edema,heavy hypertension and infection.
 Diet
Hypertension and edema: Low salt diet (<2gNa/ day) only
during period of edema or salt-free diet.
Severe edema: Restricting fluid intake
 Avoiding infection: very important.
 Diuresis: Hydrochlorothiazide (HCT) ：2mg/kg.d
Antisterone ： 2～4mg/kg.d
Dextran ： 10～15ml/kg , after 30～60m,
followed by Furosemide (Lasix) at 2mg/kg .

19. Induction use of albumin:-
Albumin + Lasix (20 % salt poor)
 1-Severe edema
 2-Ascites
 3-Pleural effusion
 4-Genital edema
 5-Low serum albumin

20. Corticosteroid—prednisone therapy:-
 Prednisone tablets at a dose of 60 mg/m2/day
(maximum daily dose, 80 mg divided into 2-3 doses) for
at least 4 consecutive weeks.
 After complete absence of proteinuria, prednisone dose
should be tapered to 40 mg/m2/day given every other
day as a single morning dose.
 The alternate-day dose is then slowly tapered and
discontinued over the next 2-3 mo.

21. Treatment of relapse in NS:
 Many children with nephrotic syndrome will
experience at least 1 relapse (3-4+proteinuria plus
edema).
 daily divided-dose prednisone at the doses noted earlier
(where he has the relapse) until the child enters
remission (urine trace or negative for protein for 3
consecutive days).
 The pred-nisone dose is then changed to alternate-day
dosing and tapered over 1-2 mo.

22. According to response to prednisone
therapy:
 *Remission: no edema, urine is protein free for 5 consecutive
days.
 * Relapse: edema, or first morning urine sample contains > 2 +
protein for 7 consecutive days.
 *Frequent relapsing: > 2 relapses within 6 months (> 4/year).
 *Steroid resistant: failure to achieve remission with
prednisolone given daily for 28 days.

23. Side Effects With Long Term Use of
Steroids “Steroid toxicity
 hyperglycemia
 myopathy
 peptic ulcer
 poor healing of wound.
 Hirsutism
 Thromboembolism
-Stunted growth
Cataracts
- Pseudotumor cerebri
-Psycosis
-Osteoporosis
- Cushingoid features
-Adrenal gland suppression

24. Alternative agent:-
 When can be used:
 Steroid-dependent patients, frequent relapsers, and steroid-
resistant patients.
 Cyclophosphamide Pulse steroids
 Cyclosporin A
 Tacrolimus
 Microphenolate

25. Complications
Thromboembolism
Hyperlipidaemia
Increased
Susceptibility to
infection

26. What is nephritic syndrome?
 Refers to a specific set of renal diseases in which an
immunologic mechanism triggers inflammation
and proliferation of glomerular tissue that result in
damage to the basement membrane, mesangium or
capillary endothelium
It is a syndrome associated with severe glomerular
injury, but does not denote a specific etiologic form of
glomerulonephritis

28. Pathophysiology
 Thin glomerular basement membrane with pores that allow protein and blood
into the tubule.

30. Hematuria
Red cell casts
Hypertension
Proteinuria
<3gm/day
Oliguria
Nephritic
Syndrome

31. Signs and Symptoms
 Haematuria (E.g. cola coloured)
 Proteinuria
 Hypertension
 Oliguria
 Flank pain
 General systemic symptoms
 Post-infectious = 2-3 weeks
after strep-throat/URTI

32. Investigations
 Urine dipstick and send sample to lab
 Bloods – the usual plus renal screen
Immunoglobulins, electrophoresis, complement (C3,
C4) autoantibodies (ANA, ANCA, anti-dsDNA, anti-
GBM); blood culture; ASOT (anti-streptolysin O titre)
 Renal ultrasound
 Renal biopsy
 Urine microscopy – red cell casts

33. Investigations
 U&E – ?Elevated urea ± creatinine
 Urinalysis – haematuria, Red cell casts present, 24
hour collection helpful
 ASOT (increased in 60-80%), anti-DNAse b
 ESR ?CRP
 Cultures (throat, blood, urine)Complement
(Decreased C3, normal C4

34. Management
 Correct electrolyte abnormalities if present
 Post Streptococcal – penicillin therapy
 Admission if oliguria and renal failure
 Fluid restriction with significant oedema

35. Management
 Conservative
o Monitor U&E, BP, fluid balance, weight
o Salt and fluid restriction
o Treat underlying cause
 Medical
o Diuretics
o Treat hypertension
Corticosteroids/immunosuppression
o Dialysis
 Surgical
o Renal transplant

36. NEPHROTIC NEPHRITIC
 Negligible RBC’s /
WBC’s
 Absence of cellular
casts
 Free lipid droplets
 Lipid laden
macrophages
 RBC’s abundant
 RBC casts
 Lipid elements usually
absent
URINANALYSIS

37. Summary
 Nephrotic syndrome = MASSIVE proteinuria
 Nephritic syndrome = haematuria/red cell casts
 May be a mixed presentation
 New oedema? Dipstick that urine!
 Haematuria? Exclude malignancy!

42.  THE END….
THANK YOU….