Glomerulonephritis & nephrotic syndrome

1 mil nephrons in each kidney

mesangial cells : connecting tissue
podocytes : epithelial cells that makes up layer of Bowman’s cpsule extend foot
process that cover capillaries

Clinical presentation of renal disease

1. nephrotic syndrome
2. acute nephritic syndrome
3. AKI
4. CKD

Nephrotic syndrome

- collection of sign & symptoms, not a disease

 Proteinuria >3.5g/24 hrs

 Hypoalbuminaemia < 25 g/L
 Generalised oedema
Associated with hyperlipidaemia

Pathophysiology
‘Underfill hypothesis’

Loss of prtein in urine  Low serum albumin levels

Decrease in plasma oncotic P – cause leaking of plasma water into interstitial
space – contraction in plasma volume leads to stimulation of RAAS axis & ADH –
retention of Na & H2O by renal tubules contribute to existence & maintenance of
oedema

‘Overfill hypothesis’
Primary increase in renal Na retention
massive proteinuria leads to tubulointerstital inflammation, release local
vasoconstrictor & inhibition of vasodilation
dimisned response to atrial natriuretic hormone

Hyperlipidaemia

Disordered lipid metabolism.Apolipoprotein-B containing lipoprotein elevated.

Elevated total cholesterol & LDL-cholestrol
Increase synthesis of lipoprotein that accompany increased hepatic albumin
synthesis due to hypoalbuminaemia
Decreased plasma oncotic P cause increased hepatic lipoprotein synthesis
Abnrmalities in regulatory enzymes
Causes of nephrotic syndrome

1) Primary (starting in kidney)

 Primary GN
- minimal change disease
- Focal segmental glomerulosclerosis
- Membranous nephropathy
- membranoproliferative GN

2) Secondary (kidney involvement secondary to systemic disease)

1. Systemic
 DM
 SLE : lupus nephritis
2. Infection
 Hep B, C, HIV
3. Drugs
4. Malignancy
 Myeloma, lymphoma, leukaemia

Clinical Presentation

1. Swelling (symmetrical, generalized)

- facial swelling (periorbital edema)
- abdominal swelling
- scrotal swelling
2. Fluid overload (breathless due to pleural effusion, abdominal swelling)
3. frothy urine

Complications

1. Infection
- Why? Urinary loss of Ig : increased risk of encapsulated organisms eg
Strep pneumonia due to urinary loss of factor B that play role in
opsonization of encapsulated organisms
- Medications used further suppress immune system (CCS, alkylating
agents)
2. eg fever, pontaneous bacterial peritonitis
3. Thrombosis + thromboembolism
- due to urinary loss of anti-thrombin III, protein C, protein S
- increased platelet activation & aggregation
- the more proteinuria, more is risk of thrombosis
eg renal vein thrombosis,
4. AKI
5. CKD
6. protein malnutrition
7. drug therapy complications
8. hyperlipidaemia

Investigations
history : dm, vascular disease, drugs, family hx
examination : BP lying & standing, PR, RR, SaO2, weight

Urinalysis
24 hr urine protein
renal profile
fasting lipids
serum albumin
ultrasound kidneys
CXR

Look for secondary cause : hepatitis Bs Ag, Hep C Ab, HIV Ab

ANA & anti-ds DNA : SLE
FBS
C3, C4 : GN, SLE
Myeloma screening
-
Renal impairment is caused by the accumulation and precipitation of light
chains, which form casts in the distal tubules, resulting in renal obstruction
.
US
- look at kidney size, renal vein trhmbosis

Renal bisopy
- histopathology

diuretics resistance

high Na intake
redued bioavailabily
avoid NSAIDS, COX-2 inhbitors