APPROACH TO A

PATIENT WITH
Glomerulonephritis
DR. MD. ASIQUR RAHMAN
MBBS(DMC),FCPS(Medicine)
MD (Nephrology)
Definition

Disorder of glomerulus involving both

kidney which is inflammatory or
non inflammatory, usually
immunologically mediated
characterized by haematuria,
proteinuria,hypertension,decrease
renal function.
Terminology

• Focal or diffuse? - Focal lesions affect some

(50%) glomeruli, if not all.
• Segmental or global? - Segmental lesions
affect part of an affected glomerulus.
Global lesions involve most of the glomerular
tuft.
• Proliferative or not? -Proliferative lesions
describe an increase in local cell number;
for instance, an increase in mesangial cells (
‘ mesangial proliferative ’ ) is a feature of
IgA nephropathy.
Presentation

➢ Asymptomatic proteinuria
➢ Asymptomatic haematuria
➢ Nephrotic syndrome
➢ Nephritic syndrome
➢ AKI
➢ CKD
➢ HTN
Classification

Proliferative:
➢ IgA nephropathy
➢ Membranoproliferative GN ( MPGN)
➢ PIGN ( post infectious GN)
➢ RPGN
Non-proliferative:
➢ Minimal change disesase (MCD)
➢ Focal segmental glomerulosclerosis ( FSGS)
➢ Membranous nephropathy
Primary:
➢ IgA nephropathy
➢ Membranoproliferative GN ( MPGN)
➢ Minimal change disesase (MCD)
➢ Focal segmental glomerulosclerosis (
FSGS)
➢ Membranous nephropathy
Secondary:
➢ Infection: Post-streptococcal,Hepatitis B and
C, HIV ,Endocarditis, leprosy,
meningococcal meningitis Malaria,
schistosomiasis, mycoplasma, leishmaniasis.
➢ Systemic disease: DM, SLE, RA, Sjogren ,
MCTD, Vasculitis .
➢ Malignancy:Solid
tumors,leukemia,lymphoma,Myeloma
➢ Drugs: NSAID, penicillamin, heroin, lithium
etc.
Nephritic syndrome

The clinical syndrome associated

with underlying glomerulonephritis ,
presents as:
• Haematuria and proteinuria.
• Impaired renal function.
• Oliguria with signs of salt and water
retention.
Causes:
• IgA nephropathy and Henoch –
Schönlein purpura.
• Lupus nephritis.
• Post-infectious GN.
• Anti-GBM disease.
• ANCA-associated vasculitis.
• Mesangiocapillary GN (MCGN)
Nephrotic syndrome

clinical syndrome defined as proteinuria >3.5g/1.73m2/day that is

associated with hypoalbuminaemia, oedema, hyperlipidaemia,
lipiduria (and thrombotic tendency).
Causes:
 Membranous nephropathy.
• Minimal change nephropathy.
• Focal and segmental glomerulosclerosis.
• SLE
• Mesangiocapillary (or membranoproliferative) glomerulonephritis
(MCGN)
• Renal amyloidosis.
• IgAN.
• Light chain deposition disease.
Approach to suspected GN

History:
▪ Age of onset
▪ Rapidity of onset
▪ Macroscopic haematuria?
▪ Urine output
▪ Fever,sore throat,infected scabies
▪ Joint pain, rash, arthitis
▪ Palpable purpura
▪ Haemoptysis
Physical examination:
▪ Blood pressure
▪ Edema
▪ Anaemia
▪ Rash
▪ Leukonychia
▪ Temperature
▪ JVP
Investigations

➢ Dipstick urine for haematuria, proteinuria.

➢ Urine microscopy for red morphology &
casts
➢ Phase contrast microscopy for dysmorphic
RBC
➢ Quantification of protein – 24 hrs UTP/ uPCR
➢ Serum Albumin
➢ Serum creatinine, S. Electrolytes, Blood urea
➢ CBC
➢ Fasting lipid profile
To exclude secondary cause:
➢ ANA
➢ ANCA
➢ C3,C4
➢ HBsAg
➢ Anti HCV
➢ Anti HIV
➢ ASO titre
Fitness for biopsy:
➢ PT,APTT
➢ USG of KUB to see kidney size,CMD
Confirmation of disease:
Renal biopsy
General Management
(Dietary)
General
management(Edema)
 Management of
hypertension and proteinuria
➢ ACEI or ARB is the first line drug.
➢ Do not stop drug until >30% rises of S. Creatinine
or K+ occurs
➢ Target systolic B.P is < 120 mm Hg
➢ Uptitrate to maximally tolerated dose.
➢ Monitor lab variables regularly.
➢ Lifestyle modifications
➢ Use potassium wasting diuretics or K+ binders if
needed
➢ Non dihydropyridine CCB also reduce
proteinuria independent of B.P.
Management of
hyperlipidemia
➢ Important in patients with CV risk factors
such as DM,HTN.
➢ Lifestyle modifications
➢ Consider statin as first line therapy in patients
with persistent hyperlipidemia
➢ Calculate ASCVD risk using calculator.
➢ Reduced eGFR< 60ml/min/1.73m2 and
albuminuria>30mg/g is independent risk
factor
➢ Non statin therapy if patient is intolerant to
statin or fail to achieve goal with statin
Management of
hypercoagubility
➢ Full warfarin anticoagulation for
thromboembolic events:
- Intravenous heparin followed by warfarin
- Target INR 2-3
➢ Prophylactic anticoagulation during
transient high risk events
- Unfractionated heparin 5000u S/C twice
daily
- LMWH 1mg/kg 12 hourly ( dose
reduction if eGFR< 30)
Infection

• Low IgG levels predispose to infection.

• Treat infections promptly, with appropriate
cover for polysaccharide encapsulated
organisms.
▪ Parenteral antibiotics should be started
once cultures are taken.
▪ If repeated infections occur, serum
immunoglobulins should be measured.
Infection risk is reduced by monthly
administration of intravenous
immunoglobulin 400 mg/kg to keep serum
IgG >600 mg/dl (>6 g/l).
Vaccination

 Use pneumococcal vaccine in patients with

glomerular disease and nephrotic syndrome, as
well as patients with chronic kidney disease
(CKD). Patients and household contacts should
receive the influenza vaccine.
 Screen for tuberculosis (TB), hepatitis B virus
(HBV), hepatitis C virus (HCV), human
immunodeficiency virus (HIV), and syphilis in
clinically appropriate patients
 Prophylactic trimethoprim– sulfamethoxazole
(TMP-SMX) should be considered in patients
receiving high-dose prednisone or other
immunosuppressive agents (rituximab,
cyclophosphamide).
 RPGN
Refers to clinical syndrome characterized by
progressive rise of S. creatinine over days to
weeks with presence of active sediment in
urine microscopy.
Types:
Type 1: Anti GBM disease
Type 2: Immune complex
- IgA nephropathy
- PIGN
- Lupus nephritis
 Type 3: ANCA associated vasculitis
 Tye 4: Double antibody disease
 Type 5: Idiopathic
Management:
1. Glucocorticoid: first line treatment
- Methylprednisolone 1g over 20 minutes for three
days followed by Prednisolone 1-2 mg/kg/day for 2-4
weeks
2. Cyclophosphamide:
IV pulse 0.5-1 g or oral cyclophospamide 1-2 mg/kg/day
3. Plasma exchange
- Pulmonary haemorrage
- S. creatinine rapidly rising
- Anti GBM disease
 Minimal Change
Disease(MCD)
MCD is the cause of nephrotic syndrome in
approximately
➢ 90% of children younger than age 6
➢ 65% of older children
➢ 20-30% of adolescents
➢ 10-25% of adult
C/F:
Edema
HNT (only in 5-7%)
Haematuria is rare
Nephrotic range proteinuria present
MCD terminology
Management in adult
MCD in Children

 We recommend that oral glucocorticoids be given for 8

weeks (4 weeks of daily glucocorticoids followed by 4
weeks of alternate-day glucocorticoids) or 12 weeks (6
weeks of daily glucocorticoids followed by 6 weeks of
alternate-day glucocorticoids) (1B).
 The standard dosing regimen for the initial treatment of
nephrotic syndrome is daily oral prednisone/prednisolone
60 mg/m2 /d or 2 mg/kg/d (maximum 60 mg/d) for 4
weeks followed by alternate day prednisone/
prednisolone, 40 mg/m2 , or 1.5 mg/kg (maximum of 50
mg) for other 4 weeks, or prednisone/prednisolone 60
mg/m2 /d (maximum 60 mg/d) for 6 weeks followed by
alternate day prednisone/prednisolone, 40 mg/m2 , or 1.5
mg/kg (maximum of 50 mg), for other 6 weeks
FSGS

Presentation:
Peak age: Adolescent
Nephrotic range proteinuria: 70-90%
HTN: 30-65%
Haematuria: 30-75%
Reduced GFR: 20-50%
Management
Membranous Nephropathy

Presentation:
➢ Peak age of onset: 4th & 5Th decade
➢ Nephrotic syndrome 70-80%
➢ Subnephrotic asymptomatic
proteinuria: 20-30%
➢ HTN: 10-20%
➢ Haematuria: 30-40%
➢ Renal impairment: <10%
Management
IgA Nephropathy

 Presentation:
Age: 2nd & 3rd decade
Macroscopic haematuria: 40-50%
Asymptomatic haematuria & proteinuria: 30-40%
Nephrotic syndrome: <5%
AKI: < 5%
CKD: 15-40%
Management
MPGN

 Age: 3rd & 4th decade

 Microhaematuria and non nephrotic proteinuria – 35%
 Nephrotic syndrome & mildly reduced GFR – 35%
 HTN 50-80%
Management

➢ For patients with idiopathic ICGN and proteinuria<

3.5g/day the absence of the nephrotic syndrome,
and a normal eGFR, we suggest supportive therapy
with RAS inhibition alone.
➢ : For patients with idiopathic ICGN, a nephrotic
syndrome, and normal or near-normal SCr, try a limited
treatment course of glucocorticoids. Prednisone (or its
equivalent) can be initiated at 1 mg/kg/ d (maximum
dose of 60–80 mg/d) for 12–16 weeks.
 For patients with idiopathic ICGN, abnormal kidney
function (but without crescentic involvements), active
urine sediment, with or without nephrotic-range
proteinuria, add glucocorticoids and
immunosuppressive therapy to supportive care.
 For patients presenting with a rapidly progressive
crescentic idiopathic ICGN, treat with high-dose
glucocorticoids and cyclophosphamide.
Lupus Nephritis

When to suspect:
 known SLE patient who develop an
active urinary sediment with
persistent hematuria (five or more
RBCs, most of which are dysmorphic,
per HPF)
 and/or cellular casts, proteinuria,
 and/or an elevated serum creatinine
(or decrease in estimated glomerular
filtration rate [eGFR])
Thank You