Acute Post-Streptococcal Glomerulonephritis Clinical Case Study

These flashcards cover the clinical presentation, diagnosis, pathophysiology (including renal anatomy and filtration mechanisms), and treatment of Acute Post-Streptococcal Glomerulonephritis based on Case 4.

What were the chief complaints and primary history of the 9-year-old boy in Case 4?

• scanty urine (oliguria) and edema

• history of coffee-colored urine for 2 days

• diagnosed with streptococcal pharyngitis 2 weeks prior.

What were the patient's vital signs and physical findings regarding blood pressure and chest sounds?

BP was $220/130\text{ mm Hg}$ and chest auscultation revealed coarse breath sounds.

What white blood cell (WBC) count and differential were recorded for the patient?

The WBC count was $23,500/\text{µl}$ with 77\text{%} neutrophils (neu.) and 12\text{%} lymphocytes (lym.).

How did the patient's Anti-streptolysin-O titer (ASO) compare to the normal range?

The patient's ASO was $295\text{ IU/ml}$, which is significantly higher than the normal range of $0\text{-}166\text{ IU/ml}$.

What are the clinical indications of a higher-than-normal plasma level of Lactate Dehydrogenase (LDH)?

It may indicate tissue damage such as heart attack, stroke, or damage to the liver, kidneys, or muscles.

How is the Erythrocyte Sedimentation Rate (ESR) used as a measure of inflammation?

It is a non-specific measure where inflammatory proteins cause RBCs to stick together into rouleaux, making them settle faster in a Westergren tube.

What is the primary site of synthesis for C-Reactive Protein (CRP) and what is its role in the immune response?

CRP is synthesized by the liver; it binds to damaged cells or bacteria to activate the complement system, increasing antibody functions and phagocytosis.

Which specific organism is the common cause of Acute Post-Streptococcal Glomerulonephritis (PSGN)?

Group A beta hemolytic streptococci.

Why is the renal perfusion rate maintained at a high level (approximately 22\text{%} of cardiac output)?

High renal blood flow is required to maintain a high Glomerular Filtration Rate (GFR), which is necessary for the kidneys to work properly.

Trace the vascular pathway in the kidney from the renal artery to the peritubular capillaries.

Renal artery $\rightarrow$ interlobar artery $\rightarrow$ arcuate a. $\rightarrow$ interlobular a. $\rightarrow$ afferent arteriole $\rightarrow$ glomerulus $\rightarrow$ efferent arteriole $\rightarrow$ peritubular capillary.

What is the typical Net Filtration Pressure in the glomerulus?

$$+10\text{ mm Hg}$$

What value of Glomerular Filtration Rate (GFR) typically indicates lower kidney function?

$$< 90\text{ ml/min}$$

List the three layers of the glomerular filtration barrier.

1. Fenestrated glomerular capillary endothelium, 2. Glomerular basement membrane (basal lamina), and 3. Podocytes (visceral epithelial cells).

What substance provides the negative charge to the glomerular basement membrane?

Heparan sulfate.

What are the four basic nephron processes regarding the handling of substances?

Glomerular filtration, tubular reabsorption, tubular secretion, and tubular synthesis (e.g., $NH_3$).

What is the molecular size cutoff for substances to pass through the glomerular barriers?

Substances with a diameter smaller than $8\text{ nm}$ can pass through.

How do glomerular mesangial cells influence the Glomerular Filtration Rate (GFR)?

They contain myofilaments that can contract to decrease glomerular surface area or relax to increase it.

Explain the pathogenesis of hypocomplementemia in PSGN.

Deposition of IgG/anti-IgG immune complexes in the glomeruli activates the classical complement pathway, exhausting plasma complements like C3 and CH50.

What does the CH50 test (Total Hemolytic Complement) measure specifically?

The ability of serum to lyse antibody-sensitized sheep RBCs via the classical complement pathway.

Why does oliguria occur in patients with PSGN?

Infiltration of inflammatory cells and proliferation of mesangial and endothelial cells compress the glomerular capillaries, reducing surface area and GFR.

Where does almost all protein reabsorption occur in the nephron, and how are the proteins processed?

In the proximal tubules (PT) via endocytosis; proteins are degraded in lysosomes into amino acids.

Explain the mechanism of edema in PSGN based on fluid movement forces.

Proteinuria leads to hypoalbuminemia, which decreases plasma colloid osmotic pressure ($\rho_p$), leading to fluid accumulation in the interstitial space.

What are the diagnostic components of Nephrotic Syndrome?

Proteinuria ($> 3.5\text{ g/day}$), hypoalbuminemia, edema, hyperlipidemia, and hypercoagulability.

Why do patients with nephrosis have an increased risk of bacterial infections?

Due to the urinary loss of IgG and complement factors, as well as the loss of zinc, transferrin, and cytokines which are needed for immune cell function.

What dietary and pharmacological treatments are standard for PSGN?

Dietary: low salt, high-quality protein, and limited water. Pharmacological: Antibiotics for infection, ACE inhibitors or calcium channel blockers for hypertension, and diuretics.