Definition

  • What is AGN?
  • What is cast?
  • Which glomerulopathies present as nephritic syndrome?

Epidemiology

  • How many adults with glomerulonephritis have hypertension?

Etiology and Pathophysiology

  • What are the causes of AGN?
  • What are the mechanisms of nephritic syndrome?
  • In AGN, is streptococcus directly infecting the kidney?
  • Which type of disease is this? (Immune-mediated.)
  • Why there is hypertension in AGN?
  • What is the mechanism of edema formation in AGN?
  • What are the causes of rapidly progressive (crescentic) glomerulonephritis?
  • What are the causes of glomerulonephritis with low serum complement?
  • What is the latency between infection and nephritis?
  • If latency is 3 days, what would you think?  (IgA nephropathy.)

Clinical manifestations

  • What are the clinical features of AGN?
  • What are the common features of AGN in adults?
  • What are the features of nephritic syndrome?

Examinations

  • Q

Investigations

  • What investigations do you suggest in AGN?
  • What are the findings in routine examination of urine in AGN?
  • What is the hallmark of glomerulonephritis?
  • What are the different urinary casts present in different diseases?

Diagnosis

  • What is your differential diagnosis?
  • A 5-year-old boy presented with puffiness of face with scanty micturition for last 3 days. What is your diagnosis?
    • What is the probable cause?
    • What history would you take to detect underlying cause?
    • What history will you take in case of AGN following scabies?
  • Why not nephrotic syndrome?
  • Why this is not IgA nephropaty?
  • Why this is not angioneurotic edema?
  • Why not acute renal failure?
  • How can you differentiate AGN from nephrotic syndrome?

Treatment

  • How to treat?
  • Which antihypertensives are preferred?
  • How can you follow up this patient?
  • What is the prognosis of acute nephritic syndrome?

Complications

  • What are the complications of AGN?
  • Suppose this patient develops severe breathlessness, what is your thinking?
  • Suppose this patient becomes unconscious, what is your thinking?

Topics in relation to AGN a

  • Causes of puffy face
  • Characteristics of edema in different disease
  • Causes of red urine
  • Causes of black urine
  • Causes of painless hematuria
  • Cause of painful hematuria
  • Few common definitions
    • Anuria
    • Oliguria
    • Nocturia
    • Polyuria
    • Frequency of micturition

Rimikri

SOLVES


Definition

What is AGN?

AGN is the inflammation in kidney characterized by hematuria, hypertension, edema (periorbital, leg or sacral) and oliguria. Urine shows proteinuria and red cell cast.

*Long Cases in Clinical Medicine, ABM Abdullah
Which glomerulopathies present as nephritic syndrome?

Glomerulopathies present as nephritic syndrome are:
– Poststreptococcal glomerulonephritis
– Goodpasture’s disease (anti-GBM disease)
– IgA nephropathy
– Henoch-Schönlein purpura.

*Pre-exam preparation for medicine, HN Sarker

Epidemiology

How many adults with glomerulonephritis have hypertension

About 50%.

Etiology and Pathophysiology

What are the causes of AGN?

Causes are:

  1. Infection—post-streptococcal commonest. Other infections include infective endocarditis, infectious mononucleosis, HBV, HCV, etc.
  2. Non-infectious—SLE, Henoch-Schönlein purpura, cryoglobulinemia, etc.
  3. Primary glomerular disease—diffuse proliferative GN, IgA nephropathy, membranous GN, focal segmental GN.
  4. Shunt nephritis.
*Long Cases in Clinical Medicine, ABM Abdullah
What are the mechanisms of nephritic syndrome?

Mechanisms of nephritic syndrome are:
– Inflammation
– Reactive cell proliferation
– Breaks in GBM
– Crescent formation.

*Pre-exam preparation for medicine, HN Sarker
In AGN, is streptococcus directly infecting the kidney?

No, antibody formed against streptococcal antigen cross react with glomerular protein due to molecular mimicry.

Which type of disease is this?

Immune-mediated.

What are the causes of rapidly progressive (crescentic) glomerulonephritis?

Causes are:
– Focal segmental (necrotizing) glomerulonephritis
– SLE
– Goodpasture’s (anti-GBM ) disease
– IgA nephropathy.

*Pre-exam preparation for medicine, HN Sarker
What are the causes of glomerulonephritis with low serum complement?

As follows:

  • Post-streptococcal glomerulonephritis (PSGN)
  • Subacute bacterial infection: Especially infective endocarditis
  • Mesangiocapillary glomerulonephritis, usually type II (90% in type II and 70% in type I)
  • Cryoglobulinemia
  • Lupus nephritis
*Long Cases in Clinical Medicine, ABM Abdul; Pre-exam preparation for medicine, HN Sarker
What is the latency between infection and nephritis?

The latency is usually about 10 days after a throat infection or longer (2–3 weeks) after skin infection.

*Pre-exam preparation for medicine, HN Sarker
If latency is 3 days, what would you think?

IgA nephropathy.

*Pre-exam preparation for medicine, HN Sarker

Clinical manifestations

What are the features of nephritic syndrome?

Features of nephritic syndrome are:
– Hematuria (red or brown urine)
– Edema and generalized fluid retention
– Hypertension
– Oliguria.

*Pre-exam preparation for medicine, HN Sarker
What are the clinical features of AGN?

Symptoms
– Swelling of the face followed by generalized swelling
– Scanty high colored urine (smoky)
– Sometimes history of sore throat/skin infections 2–3 weeks back.
Signs
– Puffy face
– Pitting edema
– Hypertension
– Evidence of skin infection
– Signs of complications.

*Pre-exam preparation for medicine, HN Sarker
Why there is hypertension in AGN?

The mechanisms of hypertension in AGN are:

  • Hypervolemia due to salt and water retention secondary to oliguria.
  • Secondary hyperaldosteronism due to stimulation of renin angiotensin aldosterone axis.
*Long Cases in Clinical Medicine, ABM Abdullah;  Short and Long Cases in Clinical Medicine, HN Sarker
What is the mechanism of edema formation in AGN?

The mechanisms of edema formation in AGN are due to:

  • Retension of salt and water
  • Hypoproteinemia
*Short and Long Cases in Clinical Medicine, HN Sarker
What are the common features of AGN in adults?
  • Presence of oligouria, hematuria and proteinuria (as in child)
  • Edema is not marked.
  • Hypertension may or may not be present
  • There is no history of preceding infection
*Short and Long Cases in Clinical Medicine, HN Sarker

Examinations

Investigations

What investigations do you suggest in AGN?

As follows:

  1. Urine R/M/E:
    • Urine looks smoky.
    • It shows mild to moderate proteinuria, RBC, RBC cast and granular cast (RBC cast is suggestive of AGN)
  2. 24 hours urinary total protein (increases, but less than 3 g/L) and volume is less
  3. Renal function test
    • Blood urea, serum creatinine – may be raised
    • serum electrolytes – Kmay be raised
  4. CBC (leukocytosis may be present)
  5. Serum C3 and C4 level: Decreased
  6. ASO titer (may be high in post-streptococcal glomerulonephritis)
  7. Bacteriological
    • Throat swab for C/S to find streptococcal infection
    • Pus from skin lesion for C/S
  8. USG of the whole abdomen (to look for renal pathology)
  9. CXR (cardiomegaly or pulmonary edema if LVF)
  10. Other investigation according to suspicion of causes:
    • ANA, Anti-dsDNA, C3, C4 (if the history is suggestive of SLE)
    • P-ANCA, c-ANCA (if the history is suggestive of vasculitis)
    • HbsAg, Anti-HCV
    • Renal biopsy may be done in some cases
*Long Cases in Clinical Medicine, ABM Abdullah;  Short and Long Cases in Clinical Medicine, HN Sarker
What are the findings in routine examination of urine in AGN?

Urine— R/M/E

  • RBC ++
  • Cast— RBC and granular cast
  • Albumin +/++
  • Dysmorphic RBC in phase contrast microscopy.
*Pre-exam preparation for medicine, HN Sarker
What is the hallmark of glomerulonephritis?

Presence of dysmorphic RBC under phase contrast microscopy and/or RBC cast in urine.

What is cast?

Casts are cylindrical structures (shape of renal tubule) composed mainly of mucoprotein (the Tamm-Horsefall mucoprotein) which is secreted by epithelial cells lining the loops of Henle, the distal tubules and the collecting ducts.
Common casts include—
Hyaline cast—Nephrotic syndrome
Granular cast—Urinary tract infection
RBC cast—Glomerulonephritis.

*Pre-exam preparation for medicine, HN Sarker
What are the different urinary casts present in different diseases?

As follows:

  • RBC cast—AGN
  • WBC cast—Pyelonephritis
  • Granular cast—GN
  • Hyaline cast—Normal finding.
*Long Cases in Clinical Medicine, ABM Abdullah

Diagnosis

A 5-year-old boy presented with puffiness of face with scanty micturition for last 3 days. What is your diagnosis?

Diagnosis is acute glomerulonephritis.

What is the probable cause?

Poststreptococcal glomerulonephritis is the probable cause.

What history would you take to detect underlying cause?

History of:
– Skin infection (infected scabies)
– Sore throat

What is your differential diagnosis?
  • Nephrotic syndrome
  • Angioneurotic edema
Why not nephrotic syndrome?

Because in nephrotic syndrome, there will be generalized edema, massive proteinuria which are absent in this case. (Serum protein will show hypoalbuminemia).

In this case, there is history of infected scabies, acute onset of facial puffiness followed by scanty smoky urine (oligouria and hematuria), absence of generalized edema, presence of hypertension. These are against NS.

*Long Cases in Clinical Medicine, ABM Abdullah;  Short and Long Cases in Clinical Medicine, HN Sarker
Why this is not IgA nephropaty?

IgA nephropaty usually follows respiratory tract infection and latent period is about 3 days.

Why this is not angioneurotic edema?

Presence of hypertension, oligouria and hematuria, and absence of itchy swelling of eyelids, lips and tongue; no history of atopy – all these exclude angioneurotic edema.

*Short and Long Cases in Clinical Medicine, HN Sarker
Why not acute renal failure?

Because there is no anorexia, nausea or vomiting. Also, previous history of sore throat followed by scanty micturition is in favor of AGN.

*Long Cases in Clinical Medicine, ABM Abdullah
How can you differentiate AGN from nephrotic syndrome?
Traits AGN Nephrotic syndrome
Age 5-15 years usually*

5-12 years**

2-6 years usually*

2-8 years**

History: Pharyngitis or skin infection Present Absent
Clinical features:

Hematuria

Oligouria

Scratch mark

Hypertension

 

Present

Present

May be present

Present

 

Absent

Absent

Absent

May be present

Urine examination

Color

Protein

RBC and RBC cast

Granular cast

 

High color

Mild to moderate

Present

Absent

 

Normal

Massive

Absent

Present

Serum

Albumin

Cholesterol

C3 level

 

Normal

Normal

Low

 

Decreased

Increased

Normal

Relapse Uncommon Common
Treatment Mainly supportive Specific by Prednisolone
*Short and Long Cases in Clinical Medicine, HN Sarker; **Step on to Paediatrics, Md Abid Hossain Mollah

Treatment

How to treat?
  1. General measures
    1. Bed rest—Increases GFR, so helps in reducing hypertension
    2. Diet
      • Salt restricted diet. No added salt in the diet.
      • Protein restricted diet (0.5 gm/kg/day**)
      • Fluid (previous day urine output + 300 mL) / (400 mL/m2 + previous day’s output **)
      • K+ containing food and fruits restriction.
  2. Supportive measures
    1. Edema—Diuretic, e.g. frusemide (1-2 mg/kg/day **) (If renal function impairment, dose of diuretics is single and high. but if renal function is normal, then divided and low dose. ***)
    2. Antihypertensive drug—Calcium channel blocker, ACE inhibitor
      • For rapid reduction of BP: Nifedipine (0.3–0.5 mg/kg) sublingual **
      • For maintenance:
        • Captopril (0.25–6 mg/kg/day) in 2–4 doses **
        • Nifedipine (0.25–0.5 mg/kg/day) in 2–4 doses **
    3. Antibiotic—Phenoxymethylpenicillin/erythromycin for 10 days.
      • Oral Phenoxymethylpenicillin (50 mg/kg/day) in 4 divided doses for 10 days. Penicillin does not alter the course of the disease but prevents spreading of remaining nephritogenic strain of streptococcus to the contacts.**
  3. Treatment of complications if any.
  4. Follow up: Daily to assess the clinical response and to search for any complications.
    1. Pulse
    2. BP
    3. Edema
    4. Weight
    5. Maintain fluid intake output chart
    6. Albumin chart.
* Short and Long Cases in Clinical Medicine, HN Sarker; ** Step on to Paediatrics, Md Abid Hossain Mollah; ***Long Cases in Clinical Medicine, ABM Abdullah.
Which antihypertensives are preferred?

Preferred antihypertensives are:
– Calcium channel blocker, e.g. amlodipine
– ACE inhibitor if S.creatinine is less than 5 mg.

*Short and Long Cases in Clinical Medicine, HN Sarker
How can you follow up this patient?

Follow up: Daily to assess the clinical response and to search for any complications.

  1. Pulse
  2. BP
  3. Edema
  4. Weight
  5. Maintain fluid intake output chart
  6. Albumin chart.
*Short and Long Cases in Clinical Medicine, HN Sarker
What is the prognosis of acute nephritic syndrome?
  1. Complete recovery – 80% of childern and 50% of adults (usually within 2 weeks)
  2. Apparent recovery – 10-15% cases live with persistent proteinuria and hematuria for long periods.
  3. Complications – 5% cases develop complications e.g. Rapidly Progressive Glomerulonephritis (RPGN)

Recurrence are extremely rare.

*Short and Long Cases in Clinical Medicine, HN Sarker.

Complications

What are the complications of AGN?

As follows:

  • Acute renal failure
  • Hypertension and its complications, such as
    • acute left ventricular failure,
    • hypertensive encephalopathy
  • Fluid and electrolyte imbalance (↑K+, ↓Na)
  • Nephrotic syndrome**
  • May lead to chronic glomerulonephritis.**
*Short and Long Cases in Clinical Medicine, HN Sarker; Step on to Paediatrics, Md Abid Hossain Mollah; **Long Cases in Clinical Medicine, ABM Abdullah
Suppose this patient develops severe breathlessness, what is your thinking?

Acute pulmonary edema due to hypertensive LVF.

Suppose this patient becomes unconscious, what is your thinking?

Hypertensive encephalopathy.

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