1. Red Red Wine That’s not normal

2. A 12-year-old boy is brought in by his mother, who says that he reluctantly admitted this morning that he had had red urine several times since the previous day. She says he had a sore throat about two weeks ago, which lasted for a couple of days, but she didn’t think anything of it as “it has been going around.” She says however, that he has not really “picked up” since then, and has seemed tired. She adds that he seems a bit “puffy” around the eyes since getting up this morning. You examine the child, and find him to be afebrile, and in no obvious distress. His blood pressure however is 145/95. Your clinical diagnosis is that he has acute glomerulonephritis.

3. Q1. What type of glomerulonephritis is most likely, given the scenario?

4. Acute Poststreptococcal Glomerulonephritis (aka Acute Proliferative Glomerulonephritis/ Postinfectious Glomerulonephritis) NEPHRITIC glomerulopathy caused by IgG/C3 immune complex/ M-protein (capsule part) cross-reaction when it deposits inside the glomerulus, under the epithelium (But not inside the GBM), normally after b-haemolytic group A streptococcal infection (can be other causative infections and SLE too). Neutrophil and monocyte, and endothelial and mesangial cell proliferation inside the glomerulus leads to nephritic syndrome of HTN, and haematuria.

5. Q2. What specific test would help you to confirm this?

6. Elevated antistreptolysin O titres (ASO) is just an Ig against streptolysin (responsible for all the haemolysis going on), an enzyme produced by group A streptococci (also can look at hypocomplementemia, DNase, hyaluronidase). This is the main Ig that cross-react with autoantigens. ASO peaks in 3 to 5 weeks correlating to onset of nephritic syndrome.

7. Q3. What would you expect to find in his urine (other than blood)?

8. Blood is expected to be found in his urine, with RBC casts because cellular proliferation damages capillary walls, leaking RBC’s everywhere. These become trapped inside the tubules and pushed into mould of the lumen – then pressure behind it releases them into the collecting duct and out into the urine.

9. Q4. What is the most common outcome of this form of glomerulonephritis?

10. In children: >95% of cases have complete recovery, 1% go on to have Rapidly Progressive GN and about 2% go on to have chronic GN.

11. Q5. What finding in the urine would indicate a poorer prognosis?

12. Persistent heavy proteinuria

13. Q6. Briefly describe the pathophysiologic process which is happening in his kidneys.

14. Group A streptococci produce antigenic proteins (e.g. M protein, NSAP and NAPlr)  These proteins have a predilection for sites within the glomerulus  once bound to these sites they cause local tissue destruction and activate complement  Neutrophil and monocyte proliferation within glomerulus  followed by endothelial and mesangial cell proliferation  expanding cell mass leads to collapse and damage to capillary walls  leading to reduced glomerular perfusion (HTN) and RBC leaking into bowman’s capsule